Angina pectoris. Clinical pattern. Diagnostics. ECG and ultrasound diagnostics. Treatment. Prophylaxis. Emergency care. Complications.
Myocardial infarction. Definition. Clinical pattern. Diagnostics. Emergency care. Complications of myocardial infarction: cardiogenic shock, acute left ventricular failure. Diagnostics. Emergency care in ambulatory terms. Treatment. Role of a doctor-dentist in primary prophylaxis.
Ischaemic or ischemic heart disease (IHD), or myocardial ischaemia, is a disease characterized by ischaemia (reduced blood supply) of the heart muscle, usually due to coronary artery disease (atherosclerosis of the coronary arteries). Its risk increases with age, smoking, hypercholesterolaemia (high cholesterol levels), diabetes, and hypertension (high blood pressure), and is more common in men and those who have close relatives with ischaemic heart disease.
The blood vessels are narrowed or blocked due to the deposition of cholesterol plaques on their walls. This reduces the supply of oxygen and nutrients to the heart musculature, which is essential for proper functioning of the heart.
This may eventually result in a portion of the heart being suddenly deprived of its blood supply leading to the death of that area of heart tissue, resulting in a heart attack. As the heart is the pump that supplies oxygenated blood to the various vital organs, any defect in the heart immediately affects the supply of oxygen to the vital organs like the brain, kidneys etc.
A multitude of factors are responsible for the development of IHD. The major risk factors are smoking, diabetes mellitusand cholesterol levels.
Those with Hypercholesterolaemia (elevated blood levels of cholesterol) have a much higher tendency to develop the disease. There is also the theory that Hypertension is a risk factor in the development of IHD, Genetic and hereditary factors may also be responsible for the disease. Males are more prone to IHD. However, in post-menopausal women, the risk is almost similar to that of men. Stress is also thought to be a risk factor, though there has been a great deal of debate on this factor of late.
The disease process occurs when an atheromatous plaque forms in the coronary vessels, leading to narrowing of the vessel walls and obstructing blood flow to the musculature of the heart. Complete blockage results in deficient oxygenation and nutrient supply to the heart tissues, leading to damage, death and necrosis of the tissue, which is known as Myocardial Infarction (heart attack).
Symptoms of stable ischaemic heart disease include angina (characteristic chest pain on exertion) and decreased exercise tolerance. Unstable IHD presents itself as chest pain or other symptoms at rest, or rapidly worsening angina. Diagnosis of IHD is with an electrocardiogram, blood tests (cardiac markers), cardiac stress testing or a coronary angiogram. Depending on the symptoms and risk, treatment may be with medication, percutaneous coronary intervention (angioplasty) or coronary artery bypass surgery (CABG).
It is the most common cause of death in most Western countries, and a major cause of hospital admissions. There is limited evidence for population screening, but prevention (with a healthy diet and sometimes medication for diabetes, cholesterol and high blood pressure) is used both to prevent IHD and to decrease the risk of complications.
Signs and symptoms
Ischaemic heart disease may be present with any of the following problems:
Angina pectoris (chest pain on exertion, in cold weather or emotional situations)
Acute chest pain: acute coronary syndrome, unstable angina or myocardial infarction (“heart attack”, severe chest pain unrelieved by rest associated with evidence of acute heart damage)
Heart failure (difficulty in breathing or swelling of the extremities due to weakness of the heart muscle)
Heartburn
Stable Angina Pectoris
The diagnosis of chronic stable angina pectoris includes predictable and reproducible left anterior chest discomfort after physical activity, emotional stress, or both; symptoms are typically worse in cold weather or after meals and are relieved by rest or sublingual nitroglycerin. The presence of one or more obstructions in major coronary arteries is likely; the severity of stenosis is usually greater than 70 percent.
Pathophysiology Angina occurs when there is regional myocardial ischemia caused by inadequate coronary perfusion and is usually but not always induced by increases in myocardial oxygen requirements. Cardinal features of chronic stable angina include complete reversibility of the symptoms and repetitiveness of the anginal attacks over time, typically months to years. New, prolonged, or recent-onset symptoms are characteristic of unstable angina. Coexisting conditions, such as poorly controlled hypertension, anemia, or thyrotoxicosis, can precipitate or accentuate angina.
As coronary atherosclerosis progresses, there is deposition of plaque external to the lumen of the artery; the plaque may extend eccentrically and outward without compromising the lumen. Thus, stress testing or angiography may not suggest coronary disease, even in the presence of significant atherosclerosis. As atherosclerosis worsens, encroachment of the plaque mass into the lumen can result in hemodynamic obstruction and angina. Disordered endothelial vasomotor function of the coronary arteries is common in patients with angina and results in diminished vasodilatation or even vasoconstriction in response to various stimuli, including exercise Occasionally, patients with severe aortic-valve disease or hypertrophic cardiomyopathy have angina-like chest pain in the absence of overt coronary disease.
As the plaque burden increases, the atherosclerotic mass tends to stay external to the lumen, which allows the diameter of the lumen to be maintained; this is known as the Glagov effect, or positive remodeling. As plaque encroaches into the lumen, the coronary artery diameter decreases. Myocardial ischemia results from a discordant ratio of coronary blood supply to myocardial oxygen consumption. Luminal narrowing of more than 65 to 75 percent may result in transient ischemia and angina. In acute coronary syndromes, vulnerable plaque is a more important factor than is the degree of stenosis; acute coronary events result from ulceration or erosion of the fibrous cap, with subsequent intraluminal thrombosis. Vulnerable plaque within the vessel wall may not be obstructive and thus may remain clinically silent until it causes rupture and associated consequences.
Classification of Angina Pectoris
Chest pain is characterized as classic, or typical, angina; as atypical angina, which includes symptoms that have some but not all the features of angina; and as nonanginal chest pain, which has none of the features of angina. Chest pain that occurs during rest or at night8 is well described in persons with chronic stable angina, particularly women.
Atypical presentations of angina are more common in women than in men. Women with ischemia are more likely than men to report variable pain thresholds, inflammatory pain, palpitations, or sharp, stabbing pain. Overall, chest pain in women is quite common and usually is not due to coronary artery disease. Data from the Women’s Ischemia Syndrome Evaluation initiative of the National Heart, Lung, and Blood Institute indicate that many women with anginal symptoms have inducible ischemia and a reduced coronary flow reserve yet no significant obstruction on coronary angiography. Atypical presentations of angina are also more frequent in older patients (who often have exertional dyspnea, weakness, or sweating) than in younger patients and in patients with diabetes (who often have atypical or even silent ischemic episodes) than in those without diabetes; a high level of suspicion for coronary disease is needed in these groups. The severity of angina should be assessed to aid in management decisions. However, there is no direct correlation between the class of angina and the severity of coronary artery disease as determined on angiography.
Diagnostic Strategies
Stress Testing
Various diagnostic tests are available for the evaluation of suspected coronary disease. Summarizes common stress-testing methods. Adults with typical or atypical features of chest pain, especially those with major risk factors for coronary artery disease, should undergo stress testing. False positive and false negative exercise tests occur in up to 20 to 30 percent of persons (more commonly in women); coronary angiography is ofteecessary to resolve equivocal test results. Noninvasive testing may provide useful additional prognostic information, such as total exercise time, the inducibility of left ventricular dysfunction, blood-pressure and heart-rate responses, and, most important, the degree of myocardial ischemia. In general, poor aerobic performance and disordered heart-rate or blood-pressure responses increase the likelihood of subsequent clinical events.
Coronary Angiography
Coronary angiography remains the diagnostic gold standard for obstructive coronary artery disease, but it may miss extraluminal plaque related to coronary remodeling. Indications for angiography include poorly controlled symptoms; abnormal results on stress testing, particularly with a substantial burden of ischemia (e.g.,
Invasive coronary angiography
Conventional invasive coronary angiographic image compared
Atypical chest pain or inconclusive or discordant test results occasionally warrant the use of angiography. Intermediate-grade coronary obstructions (e.g., 50 to 70 percent stenosis) may require additional evaluation, such as assessment of coronary flow reserve. Suspected vasospastic or microvascular angina requires additional specialized testing.
Cardiac Biomarkers
Elevated levels of high-sensitivity C-reactive protein and other markers, including brain natriuretic peptide, have prognostic value with respect to cardiovascular events in patients with stable angina or asymptomatic coronary artery disease. However, the clinical utility of such testing remains uncertain.
Treatment
Lifestyle Modifications
Although obesity and sedentary lifestyles are not listed as CAD risk factors, their presence will increase the likelihood of other risk factors (e.g., diabetes, elevated LDL, low HDL, hypertension). In order to reduce the risk of CAD, interventions aimed at increasing exercise and weight reduction in obese patients should be employed. Even modest weight reduction will improve a patient’s lipid profile and reduce the risk of hypertension, dyslipidemia and diabetes. Exercise also has been shown to have a positive effect on lipid profile by increasing HDL. Smokers with dyslipidemia should be counseled on the added risk of cigarette smoking and referred to a smoking cessation program.
The NCEP guidelines include specific recommendations for diet therapy to reduce intake of saturated fats and cholesterol. Diet therapy has been shown to lower total serum cholesterol between 5% and 10%.NCEP diet therapy is broken down into Step I and Step II diets. Step II diet has a lower saturated fat allowance (7% of total calories vs. 10% in Step I). Increased saturated fat intake has a more adverse effect on lipid profile than do monounsaturated and polyunsaturated fats. TABLE 5 lists common sources of these fats. lists some simple recommendations for decreasing fat intake. In order, to ensure successful implementation of these diets, it is imperative that patients be referred to a dietitian.
Determining the optimal diet in patients with dyslipidaemia is challenging. The ideal goal is to improve the metabolic profile in anyone with a dyslipidaemia and induce weight loss in those who are overweight. Traditional standards of BMI may not be as helpful in guiding appropriate weight loss, and waist circumference may be a better standard. The metabolic syndrome includes abdominal obesity and two of the following abnormalities: high triglycerides (150 mg/dl (1.69 mmol/l) or on triglyceride treatment), low HDL (40 mg/dl (1.02 mmol/l) for men and 50 mg/dl (1.28 mmol/l) for women or on HDL treatment), elevated blood pressure (130/85 mm Hg or on antihypertensive treatment), and elevated fasting blood glucose 100 mg/dl (5.5 mmol/l) (includes diabetes). The metabolic syndrome definition of abdominal obesity is traditionally 40 inches (
Regular exercise reduces the frequency of anginal symptoms, increases functional capacity, and improves endothelial function. Patients with chronic stable angina who are receiving medical therapy should exercise regularly, beginning at low levels for 20 to 30 minutes and increasing as symptoms allow. A recent randomized trial that compared the effects of daily exercise with those of angioplasty and stenting among patients with chronic stable angina and single-vessel coronary artery disease demonstrated better outcomes (in terms of major adverse events and improved exercise capacity) at one year in the exercise group than in the revascularization group.
Although dietary modification has not been studied specifically in patients with chronic stable angina, in a trial involving patients with a history of myocardial infarction who had been randomly assigned to follow either a Mediterranean diet or a prudent Western diet, the rate of cardiovascular events was 47 percent lower in the Mediterranean-diet group than in the Western-diet group, and this difference persisted for four years. Trials involving multifactorial risk modification, including exercise, a low-fat diet, and smoking cessation, have demonstrated improvements in the progression of angina and coronary disease.
Vigorous efforts at smoking cessation and weight control are mandatory in patients with chronic stable angina. For patients with diabetes, a multifactorial approach that includes lifestyle changes and medications for glycemic control and coronary risk factors substantially reduces the risk of cardiovascular events.
Chemotherapy
It is useful to classify therapeutic drugs into two categories: antianginal (anti-ischemic) agents and vasculoprotective agents. Although medications for angina are widely used, therapy to slow the progression of coronary artery disease, to induce the stabilization of plaque, or to do both is a newer concept, and these forms of treatment are underprescribed.
Antianginal Agents
All antianginal drugs — nitrates, beta-adrenergic blockers, and calcium-channel blockers — have been shown to prolong the duration of exercise before the onset of angina and ST-segment depression as well as to decrease the frequency of angina.
– Beta-blockers work primarily by decreasing myocardial oxygen consumption through reductions in heart rate, blood pressure, and myocardial contractility.
– Calcium antagonists dilate coronary and systemic arteries, increase coronary blood flow, and decrease myocardial oxygen consumption.
– Nitrates dilate systemic and coronary arteries, including some coronary stenoses, and particularly the systemic veins; venous pooling of blood decreases cardiac work and chamber size. Sublingual or oral spray nitroglycerin relieves acute episodes of angina within 5 to 10 minutes; prophylactic use before activity can be helpful in persons with frequent angina. Prevention of tolerance requires an intermittent dosing strategy, with a nitrate-free interval of 12 to 14 hours. Phosphodiesterase type 5 inhibitors (e.g., sildenafil, vardenafil, and tadalafil) and nitrates should not be used within 24 hours of one another because of the potential for serious hypotension.
– The use of aspirin at a dose of 81 to 150 mg per day reduces cardiovascular morbidity and mortality by 20 to 25 percent among patients with coronary artery disease.
Inotropic agents (Dopamine, Dobutamine) are indicated in the presence of peripheral hypoperfusion (hypotension, decreased renal function) with or without congestion or pulmonary oedema refractory to diuretics and vasodilators at optimal doses
Revascularization
Revacularization includes either percutaneous coronary intervention (i.e., balloon angioplasty and stenting) or coronary-artery bypass surgery. More than 1 million percutaneous coronary interventions were performed in the United States in 2003, far surpassing the number of surgical revascularizations. More than 80 percent of percutaneous interventions in the United States in 2004 were performed with the use of drug-eluting stents coated with sirolimus or paclitaxel.
Revascularization (performed by any technique) has not been shown to decrease the risk of myocardial infarction or death from coronary artery disease in patients with chronic stable angina and preserved left ventricular function. However, revascularization should be considered for persons with lifestyle-limiting angina who have a good medical regimen or for those with high-risk factors, such as symptomatic multivessel disease, proximal left anterior descending or left main artery disease, left ventricular systolic dysfunction, diabetes, a large ischemic burden ouclear or echocardiographic stress testing, early onset of ischemia on stress testing, or ST-segment depression of
Balloon Angioplasty
Cardioprotective Therapy versus Percutaneous Intervention
Marked regional variability in the use of revascularization procedures suggests excessive use in some geographic areas. Several trials have indicated that treatment with a combination of vasculoprotective agents, along with lifestyle changes — with the option to proceed to percutaneous revascularization if symptoms worsen — results in rates of myocardial infarction and death that are not significantly different from those associated with revascularization in patients with class I or II stable angina whose disease involves one or two vessels.
MYOCARDIAL INFARCTION
Acute coronary syndromes (ACS) include “a broad spectrum of clinical presentations, spanning ST-segment-elevation myocardial infarction, through to an accelerated pattern of angina without evidence of myonecrosis”.
Myocardial infarction, commonly known as a heart attack, is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.
The terminology used to describe ACS continues to evolve, with the emergence of the term “non-ST-segment-elevation acute coronary syndrome” (NSTEACS). This reflects a shift away from establishing a definitive diagnosis at presentation, and towards a more clinically appropriate strategy of forming a rapid working diagnosis with its implications for initial clinical decision making.
At presentation, the initial diagnostic nomenclature focuses on risk stratification to direct treatment strategies. Establishing a definitive diagnosis often requires time, particularly for evidence of myocardial necrosis to emerge, and has important implications pertaining to prognosis, diagnostic coding, and social issues such as insurance and licensure. See for a representation of diagnosis over time, from presentation to final diagnosis.
Patients with typical myocardial Infarction may have prodromal symptoms of fatigue, chest discomfort, or malaise in the days preceding the event; alternatively, typical STEMI may occur suddenly, without warning. Myocardial infarction occurs most often in the early morning hours, perhaps partly because of the increase in catecholamine-induced platelet aggregation and increased serum concentrations of plasminogen activator inhibitor-1 (PAI-1) that occur after awakening. In general, the onset is not directly associated with severe exertion. Instead, it is concomitant with exertion. The immediate risk of myocardial infarction increases 6-fold on average and by as much as 30-fold in sedentary people. A high index of suspicion should be maintained for myocardial infarction especially when evaluating women, patients with diabetes, older patients, patients with dementia, patients with a history of heart failure, cocaine users, patients with hypercholesterolemia, and patients with a positive family history for early coronary disease. A positive family history includes any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who experienced a myocardial infarction.
The patient may recall only an episode of indigestion as an indication of myocardial infarction. In some cases, patients do not recognize chest pain, possibly because they have a stoic outlook, have an unusually high pain threshold, have a disorder that impairs function of the nervous system and that results in a defective anginal warning system (eg, diabetes mellitus), or have obtundation caused by medication or impaired cerebral perfusion. Elderly patients with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.
Physical Examination. For many patients, the first manifestation of coronary artery disease is sudden death likely from malignant ventricular dysrhythmia.
Physical examination findings for myocardial infarction can vary; one patient may be comfortable in bed, with normal examination results, while another may be in severe pain, with significant respiratory distress and a need for ventilatory support.
Patients with ongoing symptoms usually lie quietly in bed and appear pale and diaphoretic. Hypertension may precipitate myocardial infarction, or it may reflect elevated catecholamine levels due to anxiety, pain, or exogenous sympathomimetics. Hypotension may indicate ventricular dysfunction due to ischemia. Hypotension in the setting of myocardial infarction usually indicates a large infarct secondary to either decreased global cardiac contractility or a right ventricular infarct. Acute valvular dysfunction may be present. Valvular dysfunction usually results from infarction that involves the papillary muscle. Mitral regurgitation due to papillary muscle ischemia or necrosis may be present.
The typical chest pain of acute myocardial infarction is intense and unremitting for 30-60 minutes. It is retrosternal and often radiates up to the neck, shoulder, and jaw and down to the ulnar aspect of the left arm. Chest pain is usually described as a substernal pressure sensation that also may be described as squeezing, aching, burning, or even sharp. In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas.
Atypical presentations are common and frequently lead to misdiagnoses. Moreover, any patient may present with atypical symptoms, which are considered the anginal equivalent for that patient. A patient, for example, may present with abdominal discomfort or jaw pain as his or her anginal equivalent. An elderly patient may present with altered mental status. Atypical chest pain is common, especially in elderly patients and patients with diabetes. A low threshold should be maintained when evaluating high- and moderate-risk patients, as their anginal equivalents may mimic other presentations. Women tend to present more commonly with atypical symptoms such as sharp pain, fatigue, weakness, and other nonspecific complaints.
Diaphoresis, weakness, a sense of impending doom, profound restlessness, confusion, presyncope, hiccupping (which presumably reflects irritation of the phrenic nerve or diaphragm), nausea and vomiting, and palpitations may be present. (Nausea and/or abdominal pain often are present in infarcts involving the inferior or posterior wall.)
Decreased systolic ventricular performance may lead to impaired perfusion of vital organs and reflex-mediated compensatory responses, such as restlessness, impaired mentation, pallor, peripheral vasoconstriction and sweating, tachycardia, and prerenal failure.
By contrast, impaired left ventricular diastolic function leads to pulmonary vascular congestion with shortness of breath and tachypnea and, eventually, pulmonary edema with orthopnea. Shortness of breath may be the patient’s anginal equivalent or a symptom of heart failure. In an elderly person or a patient with diabetes, shortness of breath may be the only complaint.
In patients with acute inferior-wall myocardial infarction with right ventricular involvement, distention of neck veins is commonly described as a sign of failure of the RV. (Central venous pressure is most properly estimated independently of venous distension on the basis of the height of the meniscus of venous pulsation above the mid atrium.) Impaired right ventricular diastolic function also leads to systemic venous hypertension, edema, and hepatomegaly with abdominojugular reflux, which may result in saline-response underfilling of the LV and a concomitant reduction in cardiac output.
Elderly patients and those with diabetes may have particularly subtle presentations and may complain of fatigue, syncope, or weakness. The elderly may also present with only altered mental status.
As many as half of myocardial infarctions are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. Myocardial infarction is clinically silent in as many as 25% of elderly patients, a population in whom 50% of myocardial infarctions occur; in such patients, the diagnosis is often established only retrospectively, by applying electrocardiographic criteria or by scanning the patients using 2-dimensional (2D) echocardiography or magnetic resonance imaging (MRI).
On clinical evaluation, ventricular aneurysms may be recognized late, with symptoms and signs of heart failure, recurrent ventricular arrhythmia, or recurrent embolization.
Vital signs
The patient’s heart rate is often increased secondary to sympathoadrenal discharge. The pulse may be irregular because of ventricular ectopy, an accelerated idioventricular rhythm (demonstrated below), ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular arrhythmias. Bradyarrhythmias may be present; bradyarrhythmias may be attributable to impaired function of the sinus node. An AV nodal block or infranodal block may be evident.
In general , the patient’s blood pressure is initially elevated because of peripheral arterial vasoconstriction resulting from an adrenergic response to pain and ventricular dysfunction. However, with right ventricular myocardial infarction or severe left ventricular dysfunction, hypotension is seen.
The respiratory rate may be increased in response to pulmonary congestion or anxiety.
Coughing, wheezing, and the production of frothy sputum may occur.
Fever is usually present within 24-48 hours, with the temperature curve generally parallel to the time course of elevations of creatine kinase (CK) levels in the blood. Body temperature may occasionally exceed
Funduscopic examination
Manifestations of atherosclerotic vascular disease include copper wiring, or narrowing, of arterioles. Hypertension may manifest with arteriovenous nicking, which is a pinching of the veins by small arteries where they cross. Extreme hypertension may cause cupping or loss of the margins of the optical disk. Antecedent long-standing hypertension may be reflected by arterial narrowing and hemorrhages.
Arterial pulsations
Arterial pulsations may exhibit pulsus alternans, which reflects impaired left ventricular function and is characterized by strong and weak alternating pulse waves (the variation in systolic pressure is >
Pulsus bisferiens consists of 2 systolic peaks; it may be palpated in association with hypertrophic obstructive cardiomyopathy (HOCM) or mixed aortic stenosis and regurgitation. A dicrotic pulse is encountered in cases involving hypovolemic shock, severe heart failure, or cardiac tamponade. It manifests as a double pulse, produced by a combination of the systolic wave followed by an exaggerated dicrotic (diastolic) wave.
A bigeminal pulse is observed in the presence of ectopic beats or Wenckebach heart block; it is characterized by regular coupling of 2 beats with the interval between a pair of beats greater than that between the coupled beats themselves.
Pulsus paradoxus is defined as a decline in systolic blood pressure of
In patients with associated aortic regurgitation, a pulse with sharp descent, or a water-hammer pulse, may be observed.
Venous pulsations
Jugular venous distention may accompany right ventricular myocardial infarction or right ventricular failure secondary to profound left ventricular dysfunction and pulmonary hypertension. It may also be elevated as a result of an increase in right atrial pressure in patients with heart failure, decreased right ventricular compliance, pericardial disease, fluid overload, or tricuspid or superior vena cava obstruction. The Kussmaul sign, characterized by a paradoxical increase in jugular venous pressure during inspiration, may occur in patients with constrictive pericarditis, congestive HF (CHF), or tricuspid stenosis.
Chest
Rales or wheezes may be auscultated; these occur secondary to pulmonary venous hypertension, which is associated with extensive acute left ventricular myocardial infarction. Unilateral or bilateral pleural effusions may produce egophony at the lung bases. On chest radiographs, they are evidenced by blunted costophrenic angles; on MRI, they are evidenced by dependent fluid signal intensity; on echocardiography, they are evidenced by echolucent zones adjacent to the heart.
Heart
On palpation, lateral displacement of the apical impulse, dyskinesis (seen in the image below), a palpable S4 gallop, and a soft S1 sound may be found. These indicate diminished contractility of the compromised LV.
Paradoxical splitting of S2 may reflect the presence of left bundle-branch block or prolongation of the preejection period with delayed closure of the aortic valve, despite decreased stroke volume.
Increased S4 and S3 gallops may suggest increased LV stiffness; they represent the rapid filling phase (S3) or atrial contraction (S4).
A mitral regurgitation murmur (typically holosystolic near the apex) indicates papillary muscle dysfunction or rupture or mitral annular dilatation; it may be audible even when cardiac output is substantially decreased.
A holosystolic systolic murmur that radiates to the midsternal border and not to the back, possibly with a palpable thrill, suggests a ventricular septal rupture; such a rupture may occur as a complication in some patients with full-thickness (or Q-wave) myocardial infarctions. With resistive flow and an enlarged pressure difference, the ventricular septal defect murmur becomes harsher, louder, and higher in pitch than before.
A pericardial friction rub may be audible as a to-and-fro rasping sound with 1-3 components; it is produced through sliding contact of inflammation-roughened surfaces.
Neck vein and pulse patterns, splitting of S2, or ECG findings may suggest premature ventricular beats, brief runs of ventricular tachycardia, accelerated idioventricular rhythm, atrial flutter or atrial fibrillation, or conduction delays.
Abdomen
Patients frequently develop tricuspid incompetence; hepatojugular reflux may be elicited even when hepatomegaly is not marked.
Extremities
Peripheral cyanosis, edema, pallor, diminished pulse volume, delayed rise, and delayed capillary refill may indicate vasoconstriction, diminished cardiac output, and right ventricular dysfunction or failure. Pulse and neck-vein patterns may reveal other associated abnormalities, as previously discussed. Dependent edema may be graded 0-4 by assessing the depth of persistent pitting after thumb pressure is applied to the patient’s inner shin for more than 10 seconds or by evaluating the lower back if the patient has had his or her legs elevated.
Rough diagram of pain zones in myocardial infarction; dark red: most typical area, light red: other possible areas; view of the chest
Back view
The diagnosis is based on the clinical presentation and the electrocardiogram (ECG) findings and, in particular, the presence or absence of ST-segment elevation. As the vast majority of patients who present with initial ST-segment elevation develop biochemical evidence of myonecrosis, the term “ST-segment-elevation myocardial infarction” (STEMI) is often used from the outset in these patients.
Electrocardiography
The ECG is the most important tool in the initial evaluation and triage of patients in whom an ACS is suspected. It is confirmatory of the diagnosis in approximately 80% of cases.
Acute anterior myocardial infarction.
Acute inferior myocardial infarction
Posterolateral myocardial infarction
Electrocardiography is necessary to detect ischaemic changes or arrhythmias. It should be noted that the initial ECG has a low sensitivity for ACS, and a normal ECG does not rule out ACS. However, the ECG is the sole test required to select patients for emergency reperfusion (fibrinolytic therapy or direct PCI). Patients with STEMI who present within 12 hours of the onset of ischaemic symptoms should have a reperfusion strategy implemented promptly (grade A recommendation).
Many people who have had a prior MI will have an ECG that appears normal. There may however be typical features of previous MI, and the most conspicuous of these is Q waves. A simplistic explanation of these prominent Q waves is that an appropriately placed lead “sees through” the dead tissue, and visualises the normal depolarisation of the viable myocardial wall directly opposite the infarcted area. Because, in the normal myocardium, depolarisation moves from the chamber outwards, this normal depolarisation is seen as a Q wave
Another feature of previous MI is loss of R wave amplitude. It’s easy to imagine that if muscle is lost, amplitude must be diminished. (Having a pre-infarction ECG for comparison is invaluable).
One can get some idea of the site of infarction from the lead in which abnormalities are seen – inferior, lateral, or anterior.
Ischaemic heart disease – ST changes
One should always remember that more than a quarter of people presenting with an acute myocardial infarction will have no ECG evidence of ischaemia or infarction! The ECG on its own is a blunt-edged tool in the detection of coronary artery disease. Exercise testing to elicit ischaemia is also not very sensitive in detecting this common disease.
Acute myocardial infarction — the `hyperacute phase’
There are four main features of early myocardial infarction (as per Schamroth):
1. increased VAT
2. increased R wave amplitude (!)
3. ST elevation which is sloped upwards!
4. Tall, widened T waves (The ST segment often merges with these)
We now lay great emphasis on ST segment elevation in diagnosing acute MI (In the past, Q waves were remarked on, but as noted above, these are often absent, early on). The features of `full blown‘ MI may be:
1. prominent Q waves;
2. elevated ST segments;
3. Inverted `arrowhead‘ T waves.
Remember our previous warning, that a significant proportion of people having an acute MI will have a normal ECG, so do not rely on any of these features to Posterior MI
The trick in diagnosing this is to realise that posterior wall changes will be mirrored in the leads opposite to the lesion — V1 and V2. S we’ll see a tall R (corresponding to a Q), ST depression, and upright arrowhead T waves:
Right ventricular infarction
This occurs in about 1/3 of patients with inferior MI, but is often missed. It would be distinctly unusual in the absence of inferior MI. Sensitivity can be improved by looking at V4R — V4, but put the lead on the right side of the chest! Look for ST elevation which is higher than that in V1 — V3. Another suggestive feature is lack of ST depression in V1 with evidence of MI in the inferior leads (look for ST depression in V2 under 50% of the ST elevation in AVF).
Non-ST elevation MI
There are no reliable correlates of “subendocardial” or non-ST elevation MI, and the diagnosis is based on the combination of clinical and laboratory criteria (troponin elevation being important). There may be no ECG changes, or even ST segment depression and/or T wave abnormalities.
Angina and stress testing
The most important component of an effort ECG that indicates the presence of coronary artery disease is where exercise reproduces the patient’s chest discomfort or pain. Other findings may be:
ST segment depression (It is customary to apply the Sheffield criteria, that is, 1mm (0.1mV) ST depression 0.08s after the J point;
failure of suppression of ventricular ectopy, or (especially) development of ectopy in the recovery period;
Failure of the blood pressure to rise with exercise (an ominous finding);
ST segment elevation
T-wave changes (which may be rather nonspecific)
Development of inverted U waves, which, although subtle, is said to be specific for the presence of ischaemia
Shows the normal QRS complex in a lead.
Within hours of the clinical onset of an MI, there is ST segment elevation. At this stage no QRS or T wave changes have occurred. This indicates myocardial damage only, not definitive evidence of infarction.
Within days, the R wave voltage falls and abnormal Q waves appear. This is sufficient evidence of an infarction. In addition, T wave inversion will also have appeared but the ST segment elevation may be less obvious than before.
Within one or more weeks, the ST segment changes revert completely to normal. The R wave voltage remains low and the abnormal Q waves persist. Deep, symmetrical T wave inversion may develop at this stage.
Months after the MI, the T waves may gradually return to normal. The abnormal Q waves and reduced R wave voltage persist.
Occasionally, all evidence of infarction may be lost with the passing of time; this is due to shrinkage of scar tissue.
Because primary ECG changes occur in leads overlying the infarct, the location of an infarct can be derived by looking at the primary changes occurring in such leads. This is depicted in the following table:
|
Location of infarction |
Leads showing primary changes |
|
|
Typical changes |
|
Anterior infarction |
|
|
Antero-septal |
V1, V2, V3 |
|
Anterior |
Some of V1-V3 plus some of V4-V6 |
|
Anterior extensive |
V1, V2, V3, V4, V5, V6,I, aVL |
|
Antero-lateral |
V4, V5, V6, I, aVL, possibly II |
|
High lateral |
aVL and/or I |
|
Inferior infarction |
|
|
Inferior |
II, III, aVF |
|
Infero-lateral (= apical) |
II, III, aVF, V5, V6 & sometimes also I, aVL |
|
Infero-septal |
II, III, aVF, V1, V2, V3 |
|
|
Other changes |
|
Posterior infarction |
V1, V2 (inverse of usual changes elsewhere) |
|
Subendocardial infarction |
Any lead (usually multiple leads) |
|
|
|
|
|
|
Diagnostic criteria for MI
A definitive diagnosis of MI from the ECG can only be made on the basis of abnormalities in the QRS complex. The following changes are seen:
q waves which are either 0.04 s or longer in duration (excluding aVR and lead III) or have a depth which is more than 25% of the height of the following R wave (excluding aVR and lead III).
qs or QS complexes (excluding aVR and lead III).
Local area of inappropriately low R wave voltage.
Additional changes frequently associated with MI are:
ST segment elevation (convex upwards) in leads facing the infarcted zone.
ST segment depression occurs as a reciprocal change in leads mutually opposite to the primary leads showing evidence of infarction.
Horizontal ST segment depression may occur as a primary change in subendocardial infarction.
Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA), right coronary artery = RCA
Did you notice the ST segment depression in our section on voltage and timing, above? Prinzmetal’s angina
The simple (and possibly even correct) explanation of why you see ST segment elevation with this variant form of angina is that the predominant area of ischaemia is epicardial. This disorder is thought to be related to vascular spasm, and angiography shows coronaries without a significant burden of atheroma. Many other morphological abnormalities have been described with this disorder.
T waves
T wave abnormalities are common and often rather nonspecific. T-wave changes that suggest ischaemia are a very sudden junction between the ST segment and the T wave, and very symmetrical T waves. A variety of changes may be seen with cardiomyopathies, intracranial haemorrhage and so on. Symmetrical deep T-wave changes most prominent in V3 and V4 suggest ischaemia in the territory of the left anterior descending artery (LAD T0-waves). We should all know the features of hypo- and hyper-kalaemia.
Introduction to ECG Recognition of Myocardial Infarction
When myocardial blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur beginning with subendocardial or transmural ischemia, followed by necrosis, and eventual fibrosis (scarring) if the blood supply isn’t restored in an appropriate period of time. Rupture of an atherosclerotic plaque followed by acute coronary thrombosis is the usual mechanism of acute MI. The ECG changes reflecting this sequence usually follow a well-known pattern depending on the location and size of the MI. MI’s resulting from total coronary occlusion result in more homogeneous tissue damage and are usually reflected by a Q-wave MI pattern on the ECG. MI’s resulting from subtotal occlusion result in more heterogeneous damage, which may be evidenced by a non Q-wave MI pattern on the ECG. Two-thirds of MI’s presenting to emergency rooms evolve to non-Q wave MI’s, most having ST segment depression or T wave inversion.
Most MI’s are located in the left ventricle. In the setting of a proximal right coronary artery occlusion, however, up to 50% may also have a component of right ventricular infarction as well. Right-sided chest leads are necessary to recognize RV MI.
In general, the more leads of the 12-lead ECG with MI changes (Q waves and ST elevation), the larger the infarct size and the worse the prognosis. Additional leads on the back, V7-9 (horizontal to V6), may be used to improve the recognition of true posterior MI.
The left anterior descending coronary artery (LAD) and it’s branches usually supply the anterior and anterolateral walls of the left ventricle and the anterior two-thirds of the septum. The left circumflex coronary artery (LCX) and its branches usually supply the posterolateral wall of the left ventricle. The right coronary artery (RCA) supplies the right ventricle, the inferior
Basically, there can be three types of problems – ischemia is a relative lack of blood supply (not yet an infarct), injury is acute damage occurring right now, and finally, infarct is an area of dead myocardium. It is important to realize that certain leads represent certain areas of the left ventricle; by noting which leads are involved, you can localize the process. The prognosis often varies depending on which area of the left ventricle is involved (i.e. anterior wall myocardial infarct generally has a worse prognosis than an inferior wall infarct)(diaphragmatic) and true posterior walls of the left ventricle, and the posterior third of the septum. The RCA also gives off the AV nodal coronary artery in 85-90% of individuals; in the remaining 10-15%, this artery is a branch of the LCX.
Usual ECG evolution of a Q-wave MI; not all of the following patterns may be seen; the time from onset of MI to the final pattern is quite variable and related to the size of MI, the rapidity of reperfusion (if any), and the location of the MI.
A. Normal ECG prior to MI
B. Hyperacute T wave changes – increased T wave amplitude and width; may also see ST elevation
C. Marked ST elevation with hyperacute T wave changes (transmural injury) D. Pathologic Q waves, less ST elevation, terminal T wave inversion (necrosis)
(Pathologic Q waves are usually defined as duration >0.04 s or >25% of R-wave amplitude)
E. Pathologic Q waves, T wave inversion (necrosis and fibrosis)
F. Pathologic Q waves, upright T waves (fibrosis)
MI Family of Q-wave MI’s
Inferior STEMI with sinus node dysfunction (either sinus arrest or extreme sinus bradycardia) and a slow junctional escape rhythm.
(includes inferior, true posterior, and right ventricular MI’s)
Right Ventricular Infarction
Clinical Significance
Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon.
Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents.
Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.
The ECG changes of RV infarction are subtle and easily missed!
How to spot right ventricular infarction
The first step to spotting RV infarction is to suspect it in all patients with inferior STEMI!
In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of:
ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle.
ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.
Other useful tips for spotting right ventricular MI (as described by Amal Mattu and William Brady in ECGs for the Emergency Physician):
If the magnitude of ST elevation in V1 exceeds the magnitude of ST elevation in V2.
If the ST segment in V1 is isoelectric and the ST segment in V2 is markedly depressed.
NB. The combination of ST elevation in V1 and ST depression in V2 is highly specific for right ventricular MI.
Right ventricular infarction is confirmed by the presence of ST elevation in the right-sided leads (V3R-V6R).
Right-sided leads
There are several different approaches to recording a right-sided ECG:
A complete set of right-sided leads is obtained by placing leads V1-
It may be simpler to leave V1 and V2 in their usual positions and just transfer leads V3-6 to the right side of the chest (i.e. V3R to V6R).
The most useful lead is V4R, which is obtained by placing the V4 electrode in the 5th right intercostal space in the midclavicular line. ST elevation in V4R has a sensitivity of 88%, specificity of 78% and diagnostic accuracy of 83% in the diagnosis of RV MI.
Inferior STEMI. Right ventricular infarction is suggested by:
ST elevation in V1
ST elevation in lead III > lead II
Repeat ECG of the same patient with V4R electrode position:
There is ST elevation in V4R consistent with RV infarction
This ECG shows a full set of right-sided leads (V3R-V6R), with V1 and V2 in their original positions. RV infarction is diagnosed based on the following findings:
There is an inferior STEMI with ST elevation in lead III > lead II.
V1 is isoelectric while V2 is significantly depressed.
There is ST elevation throughout the right-sided leads V3R-V6R.
Posterior Myocardial Infarction
Clinical Significance
Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction.
Isolated posterior MI is less common (3-11% of infarcts).
Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death.
Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed.
Be vigilant for evidence of posterior MI in any patient with an inferior or lateral STEMI.
How to spot posterior infarction
As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3:
Posterior MI is suggested by the following changes in V1-3:
Horizontal ST depression
Tall, broad R waves (>30ms)
Upright T waves
Dominant R wave (R/S ratio > 1) in V2
In patients presenting with ischaemic symptoms, horizontal ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI.
Typical appearance of posterior infarction in V2
Posterior infarction is confirmed by the presence of ST elevation and Q waves in the posterior leads (V7-9).
Explanation of the ECG changes in V1-3
The anteroseptal leads are directed from the anterior precordium towards the internal surface of the posterior myocardium. Because posterior electrical activity is recorded from the anterior side of the heart, the typical injury pattern of ST elevation and Q waves becomes inverted:
ST elevation becomes ST depression
Q waves become R waves
Terminal T-wave inversion becomes an upright T wave
The progressive development of pathological R waves in posterior infarction (the “Q wave equivalent”) mirrors the development of Q waves in anteroseptal STEMI.
This picture illustrates the reciprocal relationship between the ECG changes seen in STEMI and those seen with posterior infarction. The previous image (depicting posterior infarction in V2) has been inverted. See how the ECG now resembles a typical STEMI!
Posterior leads
Leads V7-9 are placed on the posterior chest wall in the following positions (see diagram below):
V7 – Left posterior axillary line, in the same horizontal plane as V6.
V8 – Tip of the left scapula, in the same horizontal plane as V6.
V9 – Left paraspinal region, in the same horizontal plane as V6.
The degree of ST elevation seen in V7-9 is typically modest – note that only
Inferolateral STEMI. Posterior extension is suggested by:
Horizontal ST depression in V1-3
Tall, broad R waves (> 30ms) in V2-3
Dominant R wave (R/S ratio > 1) in V2
Upright T waves in V2-3
The same patient, with posterior leads recorded:
Marked ST elevation in V7-9 with Q-wave formation confirms involvement of the posterior wall, making this an inferior-lateral-posterior STEMI (= big territory infarct!).
In this ECG, posterior MI is suggested by the presence of:
ST depression in V2-3
Tall, broad R waves (> 30ms) in V2-3
Dominant R wave (R/S ratio > 1) in V2
Upright terminal portions of the T waves in V2-3
Inferior MI
Pathologic Q waves and evolving ST-T changes in leads II, III, aVF
Q waves usually largest in lead III, next largest in lead aVF, and smallest in lead II
Example #1: frontal plane leads with fully evolved inferior MI (note Q-waves, residual ST elevation, and T inversion in II, III, aVF)
True posterior MI
ECG changes are seen in anterior precordial leads V1-3, but are the mirror image of an anteroseptal MI:
Increased R wave amplitude and duration (i.e., a “pathologic R wave” is a mirror image of a pathologic Q)
R/S ratio in V1 or V2 >1 (i.e., prominent anterior forces)
Hyperacute ST-T wave changes: i.e., ST depression and large, inverted T waves in V1-3
Late normalization of ST-T with symmetrical upright T waves in V1-3
Often seen with inferior MI (i.e., “inferoposterior MI”)
Right Ventricular MI (only seen with proximal right coronary occlusion; i.e., with inferior family MI’s)
ECG findings usually require additional leads on right chest (V1R to V6R, analogous to the left chest leads)
ST elevation, >1mm, in right chest leads, especially V4R (see below)
Anterior Family of Q-wave MI’s
Anterior Myocardial Infarction
Clinical Relevance
Anterior STEMI results from occlusion of the left anterior descending artery (LAD).
Anterior myocardial infarction carries the worst prognosis of all infarct locations, mostly due to larger infarct size.
A study comparing outcomes from anterior and inferior infarctions (STEMI + NSTEMI) found that on average, patients with anterior MI had higher incidences of in-hospital mortality (11.9 vs 2.8%), total mortality (27 vs 11%), heart failure (41 vs 15%) and significant ventricular ectopic activity (70 vs 59%) and a lower ejection fraction on admission (38 vs 55%) compared to patients with inferior MI.
In addition to anterior STEMI, other high-risk presentations of anterior ischaemia include left main coronary artery (LMCA) occlusion and Wellens’ syndrome.
How to recognise anterior STEMI
ST segment elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL).
Reciprocal ST depression in the inferior leads (mainly III and aVF).
The magnitude of the reciprocal change in the inferior leads is determined by the magnitude of the ST elevation in I and aVL (as these leads are electrically opposite to III and aVF), hence may be minimal or absent in anterior STEMIs that do not involve the high lateral leads.
Patterns of anterior infarction
The nomenclature of anterior infarction can be confusing, with multiple different terms used for the various infarction patterns. The following is a simplified approach to naming the different types of anterior MI.
The precordial leads can be classified as follows:
Septal leads = V1-2
Anterior leads = V3-4
Lateral leads = V5-6
The different infarct patterns are named according to the leads with maximal ST elevation:
Septal = V1-2
Anterior = V2-5
Anteroseptal = V1-4
Anterolateral = V3-6, I + aVL
Extensive anterior / anterolateral = V1-6, I + aVL
While these definitions are intuitive, there is often a poor correlation between ECG features and precise infarct location as determined by imaging or autopsy. For an alternative approach to the naming of myocardial infarctions, take a look at this 2006 article from Circulation)
Three other important ECG patterns to be aware of:
Anterior-inferior STEMI due to occlusion of a “wraparound” LAD: simultaneous ST elevation in the precordial and inferior leads due to occlusion of a variant (“type III”) LAD that wraps around the cardiac apex to supply both the anterior and inferior walls of the left ventricle.
Left main coronary artery occlusion: widespread ST depression with ST elevation in aVR ≥ V1
Wellens’ syndrome: deep precordial T wave inversions or biphasic T waves in V2-3, indicating critical proximal LAD stenosis (a warning sign of imminent anterior infarction)
Hyperacute Anteroseptal STEMI
ST elevation is maximal in the anteroseptal leads (V1-4).
Q waves are present in the septal leads (V1-2).
There is also some subtle STE in I, aVL and V5, with reciprocal ST depression in lead III.
There are hyperacute (peaked ) T waves in V2-4.
These features indicate a hyperacute anteroseptal STEMI
Anterior-inferior STEMI
ST elevation is present throughout the precordial and inferior leads.
There are hyperacute T waves, most prominent in V1-3.
Q waves are forming in V1-3, as well as leads III and aVF.
This pattern is suggestive of occlusion occurring in “type III” or “wraparound” LAD (i.e. one that wraps around the cardiac apex to supply the inferior wall)
On the left an overview of the coronary arteries in the anterior projection.
Left Main or left coronary artery (LCA)
Left anterior descending (LAD)
diagonal branches (D1, D2)
septal branches
Circumflex (Cx)
Marginal branches (M1,M2)
Right coronary artery
Acute marginal branch (AM)
AV node branch
Posterior descending artery (PDA
On the left an overview of the coronary arteries in the right anterior oblique projection.
Left Main or left coronary artery (LCA)
Left anterior descending (LAD)
diagonal branches (D1, D2)
septal branches
Circumflex (Cx)
Marginal branches (M1,M2)
Right coronary artery
Acute marginal branch (AM)
AV node branch
Posterior descending artery (PDA)
On the left an overview of the coronary arteries in the lateral projection.
Left Main or left coronary artery (LCA)
Left anterior descending (LAD)
diagonal branches (D1, D2)
septal branches
Circumflex (Cx)
Marginal branches (M1,M2)
Right coronary artery
Acute marginal branch (AM)
AV node branch
Posterior descending artery (PDA)
Prediction of the site of LAD occlusion
The site of LAD occlusion (proximal versus distal) predicts both infarct size and prognosis.
Proximal LAD / LMCA occlusion has a significantly worse prognosis due to larger infarct size and more severe haemodynamic disturbance.
The site of occlusion can be inferred from the pattern of ST changes in leads corresponding to the two most proximal branches of the LAD: the first septal branch (S1) and the first diagonal branch (D1).
Territories
S1 supplies the basal part of the interventricular septum, including the bundle branches (corresponding to leads aVR and V1)
D1 supplies the high lateral region of the heart (leads I and aVL).
Occlusion proximal to S1
Signs of basal septal involvement:
ST elevation in aVR
ST elevation in V1 >
Complete RBBB
ST depression in V5
Occlusion proximal to D1
Signs of high lateral involvement:
ST elevation / Q-wave formation in aVL
ST depression ≥
ST elevation in aVR of any magnitude is 43% sensitive and 95% specific for LAD occlusion proximal to S1. Right bundle branch block in anterior MI is an independent marker of poor prognosis; this is due to the extensive myocardial damage involved rather than the conduction disorder itself.
Ostial LAD occlusion (septal STEMI)
This patient’s ECG shows several signs of a very proximal LAD occlusion:
There is a septal STEMI with ST elevation maximal in V1-2 (extending out to V3).
There is a new RBBB with marked ST elevation (>
This patient came in post VF arrest and was taken straight to the cath lab where he was found to have a complete ostial occlusion of his LAD.
Inferior STEMI
Cinical Significance
Inferior MIs account for 40-50% of all myocardial infarctions.
Generally have a more favourable prognosis than anterior myocardial infarction (in-hospital mortality only 2-9%), however certain factors indicate a worse outcome.
Up to 40% of patients with an inferior STEMI will have a concomitant right ventricular infarction. These patients may develop severe hypotension in response to nitrates and generally have a worse prognosis.
Up to 20% of patients with inferior STEMI will develop significant bradycardia due to second- or third-degree AV block. These patients have an increased in-hospital mortality (>20%).
Inferior STEMI may also be associated with posterior infarction, which confers a worse prognosis due to increased area of myocardium at risk.
How to recognise an inferior STEMI
ST elevation in leads II, III and aVF
Progressive development of Q waves in II, III and aVF
Reciprocal ST depression in aVL (± lead I)
Which Artery Is the Culprit?
Inferior STEMI can result from occlusion of all three coronary arteries:
The vast majority (~80%) of inferior STEMIs are due to occlusion of the dominant right coronary artery (RCA).
Less commonly (around 18% of the time), the culprit vessel is a dominant left circumflex artery (LCx).
Occasionally, inferior STEMI may result from occlusion of a “type III” or “wraparound” left anterior descending artery (LAD). This produces the unusual pattern of concomitant inferior and anterior ST elevation.
While both RCA and circumflex occlusion may cause infarction of the inferior wall, the precise area of infarction in each case is slightly different:
The RCA territory covers the medial part of the inferior wall, including the inferior septum.
The LCx territory covers the lateral part of the inferior wall and the left posterobasal area.
This produces subtly different patterns on the ECG:
The injury current in RCA occlusion is directed inferiorly and rightward, producing ST elevation in lead III > lead II (as lead III is more rightward facing).
The injury current in LCx occlusion is directed inferiorly and leftward, producing ST elevation in the lateral leads I and V5-6.
These differences allow for electrocardiographic differentiation between RCA and LCx occlusion.
RCA occlusion is suggested by:
ST elevation in lead III > lead II
Presence of reciprocal ST depression in lead I
Signs of right ventricular infarction: STE in V1 and V4R
Circumflex occlusion is suggested by:
ST elevation in lead II = lead III
Absence of reciprocal ST depression in lead I
Signs of lateral infarction: ST elevation in the lateral leads I and aVL or V5-6
Relative Q-wave depth in leads II and III is not useful in determining the culprit artery. Both RCA and LCx occlusion produce a similar pattern of Q wave changes, often with deeper Q waves seen in lead III)
Early inferior STEMI:
Hyperacute (peaked) T waves in II, III and aVF with relative loss of R wave height.
Early ST elevation and Q-wave formation in lead III.
Reciprocal ST depression and T wave inversion in aVL.
ST elevation in lead III > lead II suggests an RCA occlusion; the subtle ST elevation in V4R would be consistent with this.
Note how the ST segment morphology in aVL is an exact mirror image of lead III. This reciprocal change occurs because these two leads are approximately opposite to one another (150 degrees apart).
The concept of reciprocal change can be further highlighted by taking lead aVL and inverting it… see how the ST morphology now looks identical to lead III.
Inferior STEMI:
ST elevation in II, III and aVF.
Q-wave formation in III and aVF.
Reciprocal ST depression and T wave inversion in aVL
ST elevation in lead II = lead III and absent reciprocal change in lead I (isoelectric ST segment) suggest a circumflex artery occlusion
Hyperacute inferior STEMI:
Hyperacute T waves in II, III and aVF.
Early ST elevation and loss of R wave height in II, III and aVF.
Reciprocal change in aVL and lead I.
Bradycardia and AV Block in Inferior STEMI
Up to 20% of patients with inferior STEMI will develop either second- or third degree heart block.
There are two presumed mechanisms for this:
Ischaemia of the AV node due to impaired blood flow via the AV nodal artery. This artery arises from the RCA 80% of the time, hence its involvement in inferior STEMI due to RCA occlusion.
Bezold-Jarisch reflex = increased vagal tone secondary to ischaemia.
The conduction block may develop either as a step-wise progression from 1st degree heart block via Wenckebach to complete heart block (in 50% of cases) or as abrupt onset of second or third-degree heart block (in the remaining 50%).
Patients may also manifest signs of sinus node dysfunction, such as sinus bradycardia, sinus pauses, sinoatrial exit block and sinus arrest. Similarly to AV node dysfunction, this may result from increased vagal tone or ischaemia of the SA node (the SA nodal artery is supplied by the RCA in 60% of people).
Bradyarrhythmias and AV block in the context of inferior STEMI are usually transient (lasting hours to days), respond well to atropine and do not require permanent pacing.
Inferior STEMI with third degree heart block and slow junctional escape rhythm.
Inferior STEMI with sinus node dysfunction (either sinus arrest or extreme sinus bradycardia) and a slow junctional escape rhythm.
Anteroseptal MI
Q, QS, or qrS complexes in leads V1-V3 (V4)
Evolving ST-T changes
Anterior MI
The next 12 lead is an example of an anterior septal wall MI.
Posterior MI
– Acute inferior myocardial infarction
Non-Q Wave MI
Recognized by evolving ST-T changes over time without the formation of pathologic Q waves (in a patient with typical chest pain symptoms and/or elevation in myocardial-specific enzymes)
Although it is tempting to localize the non-Q MI by the particular leads showing ST-T changes, this is probably only valid for the ST segment elevation pattern
Evolving ST-T changes may include any of the following patterns:
Convex downward ST segment depression only (common)
Convex upwards or straight ST segment elevation only (uncommon)
Symmetrical T wave inversion only (common)
Combinations of above changes
|
V1-V2 |
anteroseptal wall |
|
V3-V4 |
anterior wall |
|
V5-V6 |
anterolateral wall |
|
II, III, aVF |
inferior wall |
|
I, aVL |
lateral wall |
|
V1-V2 |
posterior wall (reciprocal) |
|
Infarct |
|
|
1. Ischemia |
Represented by symmetrical T wave inversion (upside down). The definitive leads for ischemia are: I, II, V2 – V6. |
|
2. Injury |
Acute damage – look for elevated ST segments. (Pericarditis and cardiac aneurysm can also cause ST elevation; remember to correlate it with the patient. |
|
3. Infarct |
Look for significant “patholgic” Q waves. To be significant, a Q wave must be at least one small box wide or one-third the entire QRS height. Remember, to be a Q wave, the initial deflection must be down; even a tiny initial upward deflection makes the apparent Q wave an R wave. |
Blood tests
Serum troponin I or T levels (or CK-MB if troponin is not available).
Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial necrosis occurs.
Troponin levels are now considered to be the criterion standard for defining and diagnosing myocardial infarction, according to the American College of Cardiology (ACC)/American Heart Association (AHA) consensus statement on myocardial infarction. Positive troponin levels are considered virtually diagnostic of myocardial infarction, according to a revised version of the ACC/AHA consensus statement, as they are without equal in combined specificity and sensitivity in this diagnosis. Reichlan et al suggest that absolute changes in troponin levels have a significantly higher diagnostic accuracy for acute myocardial infarction than relative changes. Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days. Improved cardiac troponin assays offer even greater diagnostic accuracy than the standard assays do, according to a study by Reichlin et al. This is especially true for the early diagnosis of acute myocardial infarction, particularly in patients with a recent onset of chest pain, according to the investigators.
Serum creatinine and electrolyte levels, particularly potassium concentration, as hypokalaemia is associated with an increased risk of arrhythmias, especially ventricular fibrillation (grade B recommendation). Knowledge of kidney function (expressed as estimated glomerular filtration rate) is strongly encouraged (grade B recommendation) given the association between renal impairment and adverse outcomes (evidence level III).
Serum creatine kinase (CK) level.
Creatine Kinase Levels: The 3 CK isoenzymes are as follows:
CK with muscle subunits (CK-MM), which is found mainly in skeletal muscle
CK with brain subunits (CK-BB), which is found predominantly in the brain
CK-MB, which is found mainly in the heart
Serial measurements of CK-MB isoenzyme levels were previously the standard criterion for the diagnosis of myocardial infarction. CK-MB levels increase within 3-12 hours of the onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours. levels peak earlier (wash out) if reperfusion occurs. Sensitivity is approximately 95%, with high specificity. However, sensitivity and specificity are not as high as they are for troponin levels, and, as mentioned above, the trend has favored using troponins for the diagnosis of myocardial infarction.
Serum lipid levels (fasting levels of total cholesterol, low-density-lipoprotein cholesterol, high-density-lipoprotein cholesterol and triglycerides) within 24 hours.
Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal muscle, is released more rapidly from infarcted myocardium than is troponin. Urine myoglobin levels rise within 1-4 hours from the onset of chest pain. Myoglobin levels are highly sensitive but not specific; they may be useful within the context of other studies and in the early detection of myocardial infarction in the emergency department (ED)
Patients without ST-segment elevation on the initial ECG should be further observed and investigated to promptly identify patients suitable for an emergency reperfusion strategy (based on ECG changes) and/or determine the best management protocol for NSTEACS based on risk stratification
Reperfusion may be obtained with fibrinolytic therapy or PCI. A combination of fibrinolysis and PCI may also be used (facilitated or rescue PCI). Coronary artery bypass graft (CABG) surgery may occasionally be more appropriate — particularly in patients who have suitable anatomy and are not candidates for fibrinolysis or PCI. CABG surgery may also be considered in patients with cardiogenic shock or in association with mechanical repair.
Aspirin (300 mg) should be given to all patients with STEMI unless contraindicated and, in the absence of significant side effects, low-dose therapy should be continued in the long term (grade A recommendation).
There is evidence that clopidogrel (300–600 mg loading dose) should be prescribed in addition to aspirin for patients undergoing PCI with a stent. In patients selected for fibrinolytic therapy, clopidogrel (300 mg) should be given in addition to aspirin, unless contraindicated (grade B recommendation). Note, however, that if it is thought that the patient is likely to require CABG acutely, clopidogrel should be withheld.
Clopidogrel (75 mg daily) should be continued for at least a month after fibrinolytic therapy, and for up to 12 months after stent implantation, depending on the type of stent and circumstances of implantation (level II evidence; grade B recommendation).
Antithrombin therapy. Antithrombin therapy should be used The aim should be to obtain an activated clotting time (ACT) between 200 and 300 seconds if using GP IIb/IIIa inhibitors, or between 300 and 350 seconds if these drugs are not used (grade B recommendation). It may be advisable to give a bolus of heparin while the patient is in transit to the catheterisation laboratory (grade D recommendation).
Antithrombin therapy should be used with fibrin-specific fibrinolytic agents (grade A recommendation).
Enoxaparin may be used in conjunction with fibrin-specific fibrinolytic agents
Morbidity and mortality from myocardial infarction are significantly reduced if patients and bystanders recognize symptoms early, activate the emergency medical service (EMS) system, and thereby shorten the time to definitive treatment. Trained prehospital personnel can provide life-saving interventions if the patient develops cardiac arrest. The key to improved survival is the availability of early defibrillation. Approximately
The first goal for healthcare professionals is to diagnose in a very rapid manner whether the patient is having an STEMI or NSTEMI because therapy differs between the 2 types of myocardial infarction. Particular considerations and differences involve the urgency of therapy and degree of evidence regarding different pharmacological options. As a general rule, initial therapy for acute myocardial infarction is directed toward restoration of perfusion as soon as possible to salvage as much of the jeopardized myocardium as possible. This may be accomplished through medical or mechanical means, such as PCI or CABG.
Further treatment is based on the following:
Restoration of the balance between the oxygen supply and demand to prevent further ischemia
Pain relief
Prevention and treatment of any complications that may arise
Coronary collateral circulation
The coronary collateral circulation is an important factor in terms of the amount of damage to the myocardium that results from coronary occlusion. Well-developed collaterals may greatly limit or even completely eliminate myocardial infarction despite complete occlusion of a coronary artery. Reports vary as to the number of patients who have collaterals at the time of a myocardial infarction; many patients develop collaterals in the hours and days after an occlusion occurs. When the patient is at rest, blood flow through collaterals is normal, a fact that accounts for the absence of resting ischemia. However, blood flow through collaterals does not increase with exercise; this inability accounts for the occurrence of ischemia during periods of stress.[
Prehospital notification by Emergency Medical Services (EMS) personnel should alert ED staff to the possibility of a patient with myocardial infarction. EMS personnel should receive online medical advice for a patient with high-risk presentation.
The AHA protocol can be adopted for use by prehospital emergency personnel. This protocol recommends empiric treatment of patients with suspected STEMI with morphine, oxygen, nitroglycerin, and aspirin.
Specific prehospital care includes the following:
Intravenous access, supplemental oxygen, pulse oximetry
Immediate administration of aspirin en route
Nitroglycerin for active chest pain, given sublingually or by spray
Telemetry and prehospital ECG, if available
Most deaths caused by myocardial infarction occur early and are attributable to primary ventricular fibrillation (VF). Therefore, initial objectives are immediate electrocardiographic monitoring; electric cardioversion of VF, should it occur; and rapid transfer of the patient to facilitate prompt coronary recanalization. The effectiveness of rapid response by rescuers (eg, police and firefighters) trained in defibrillation have been conclusively documented in community-based systems in Belfast, Ireland; Columbus, Ohio; Los Angeles, California; and Seattle, Washington.
Approximately 65% of deaths caused by myocardial infarction occur in the first hour. More than 60% of these deaths (ie, 39% of patients who would otherwise die) may be prevented with defibrillation by a bystander or a first-responding rescuer.
Additional objectives of prehospital care by paramedical and emergency personnel include adequate analgesia (generally achieved with morphine); pharmacologic reduction of excessive sympathoadrenal and vagal stimulation; treatment of hemodynamically significant or symptomatic ventricular arrhythmias (generally with lidocaine); and support of cardiac output, systemic blood pressure, and respiration.
The AHA published a statement on integrating prehospital ECGs into care for patients with ACS Prehospital integration of ECG interpretation has been shown to decrease “door to balloon time,” to allow paramedics to bypass non-PCI hospitals in favor of better-equipped facilities and to expedite care by allowing an emergency physician to activate the catheterization laboratory before patient arrival.
Prehospital administration of tissue-type plasminogen activator (t-PA), aspirin, and heparin may be given to patients with bona fide myocardial infarction by paramedics, as guided by electrocardiographic findings, within 90 minutes of the onset of symptoms. This treatment improves outcomes, as compared with thrombolysis begun after the patient arrives at the hospital.
Atropine, 0.5 mg given intravenously at 5-minute intervals to a maximum of 2-4 mg, is useful to counteract excessive vagal tone that often underlies bradyarrhythmias and hypotension. If bradycardia persists, transthoracic pacing may be life saving.
Timely reperfusion therapy has shown that the long-term mortality rate in patients with STEMI is 15.4% when the system delay (time from first contact with health care system to the initiation of reperfusion therapy) is 60 minutes or less. The long-term mortality doubles to a rate of 30.8% when the system delay is more than 180 minutes.
In experimental models of MI, erythropoietin reduces infarct size and improves left ventricular (LV) function. However, the Reduction of Infarct Expansion and Ventricular Remodeling With Erythropoietin After Large Myocardial Infarction (REVEAL) trial evaluated the safety and efficacy of a single intravenous bolus of epoetin alfa in patients with STEMI who had successful reperfusion with primary or rescue PCI. A single intravenous bolus of epoetin alfa within 4 hours of PCI did not reduce infarct size and was associated with higher rates of adverse cardiovascular events.
Treatment is aimed at the following:
Restoration of the balance between the oxygen supply and demand to prevent further ischemia
Pain relief
Prevention and treatment of complications
Treatment in the ED begins with focused cardiovascular history–taking and physical examination, the establishment of intravenous (IV) access, the use of 12-lead ECG (see the image below), and continuous rhythm monitoring. All patients with suspected myocardial infarction should be given chewable aspirin, 160-325 mg, unless they have a documented allergy to aspirin
A 53-year-old patient who had experienced 3 hours of chest pain had a 12-lead electrocardiogram performed, and the results are as shown. He was given sublingual nitroglycerin and developed severe symptomatic hypotension. His blood pressure normalized with volume resuscitation.
Pulse oximetry should be performed, and appropriate supplemental oxygen should be given (maintain oxygen saturation >90%) to prevent hypoxemia. High concentrations may be counterproductive because of vasoconstriction and the lack of augmented myocardial oxygen delivery in normoxemic patients.
A chest radiograph should be obtained soon after arrival, to screen for alternative causes of chest pain and to identify possible contraindications to thrombolysis (eg, aortic dissection).
Initial stabilization of patients with suspected myocardial infarction and ongoing acute chest pain should include administration of sublingual nitroglycerin; if pain persists, 2 additional doses of nitroglycerin may be administered at 5-minute intervals. Patients should be free of contraindications, such as hypotension (systolic blood pressure <
Refractory or severe pain should be treated symptomatically with IV morphine, meperidine, or pentazocine. Doses of morphine, 4-8 mg IV, may be repeated every 5-15 minutes with relative impunity until the pain is relieved or toxicity is manifested by hypotension, vomiting, or depressed respiration. Should toxicity occur, a morphine antagonist, such as naloxone, may reverse it. The patient’s blood pressure and pulse must be monitored; the systolic blood pressure must be maintained above
Relative hypotension may be treated by elevating the lower extremities or by giving fluids, except in patients with concomitant pulmonary congestion, in whom treatment for cardiogenic shock may be required. Atropine, in doses similar to those given in the prehospital phase, may increase blood pressure if hypotension reflects bradycardia or excess vagal tone.
Some EDs practice ambulance diversion, wherein the ED is temporarily closed to ambulance traffic. This practice has been associated with increased 30-day, 90-day, 9-month, and 1-year mortality among patients using Medicare who experienced acute myocardial infarction. Although confined to California, this study by Shen et al shows the importance between ED care and the survival of patients experiencing acute myocardial infarction.
Treatment of patients with STEMI
The initial focus in the ED should be on identifying patients with STEMI. An ECG should be performed and shown to an experienced emergency medicine physician within 10 minutes of ED arrival.
If STEMI is present, the decision as to whether the patient will be treated with thrombolysis or primary PCI should be made within the next 10 minutes. Treatment options include the immediate start of IV thrombolysis in the ED or the immediate transfer of the patient to the cardiac catheterization laboratory for primary percutaneous transluminal coronary angioplasty (PTCA). The goal for patients with STEMI should be to achieve a door-to-drug time of within 30 minutes and a door-to-balloon time of within 90 minutes.
In patients with STEMI who are to be treated with primary PCI, delays in administering the procedure are associated with higher mortality in these patients, according to a study by Rathore et al. In a prospective cohort study of 43,801 patients enrolled in the American College of Cardiology National Cardiovascular Data Registry, 2005-2006, longer door-to-balloon times were associated with a higher adjusted risk of in-hospital mortality, in a continuous, nonlinear fashion (30 min = 3%, 60 min = 3.5%, 90 min = 4.3%, 120 min = 5.6%, 150 min = 7%, 180 min = 8.4%). A reduction in door-to-balloon time from 90 minutes to 60 minutes was associated with 0.8% lower mortality, and a reduction from 60 minutes to 30 minutes was associated with a 0.5% lower mortality.
Delays in the administration of thrombolysis often occur because of the following factors:
Delay in obtaining an ECG
Interpretation
Lack of immediate availability of thrombolytic agents
Outdated protocols requiring cardiology consultation before thrombolytic treatment
The American Heart Association (AHA) recommends the initiation of beta-blockers to all patients with STEMI (unless beta-blockers are contraindicated). Sinert et al reviewed records from 1966 to August 2009 to determine the efficacy of treating STEMI patients with beta-blockers within the first 24 hours. They found a single randomized trial that met inclusion criteria. This trial demonstrated that beta-blocker treatment within 24 hours in patients presenting with STEMI followed by standardized care on day 2 or 3 did not reduce mortality or reinfarction when compared with placebo or no immediate treatment followed by standardized care.
A separate study by Brinkman et al also suggests that although a rationale for the use of beta-blockers prior to surgery has been reported, the use of these drugs should be considered on an individual basis. Because no differences in mortality or morbidity were found, the findings did not support preoperative beta-blockade as a useful quality indicator for coronary artery bypass graft surgery.
Treatment of patients with NSTEMI
If STEMI is not present, then the workup should proceed looking for unstable angina or NSTEMI and for alternative diagnoses. Confirmation of the diagnosis of NSTEMI requires waiting for the results of cardiac markers.
Point-of-care (POC) assays are common in the ED setting but have lower negative predictive values compared with laboratory assays. The current POC cardiac troponin I (cTnI) assays are less sensitive for outcome prediction among patients with myocardial injury. Clinical judgment and decision-making for the patient with suspected acute coronary syndrome (ACS) should not rely solely on POC assay results. If a clinical suspicion of myocardial infarction remains despite negative cTnI results with the POC assays, those results should be complemented by results from more sensitive laboratory assays.
In the case of unstable angina, diagnosis may await further diagnostic studies, such as coronary angiography or imaging studies, to confirm the diagnosis and to distinguish it from noncoronary causes of chest pain. Although patients presenting with no ST-segment elevation are not candidates for immediate thrombolytics, they should receive anti-ischemic therapy and may be candidates for PCI urgently or during admission.
Low-risk patients
Low-risk patients without obvious ischemia should be observed and monitored in either a step-down care unit or an intermediate care unit to evaluate or observe for chest pain.
Concordance of ED management of AMI
A study by Tsai et al determined that overall ED concordance with ACC/AHA guideline recommendations for management of AMI is low to moderate. Emergency physicians should continue to develop strategies with emergency medical services and cardiologists to improve the care process
In-Hospital Treatment
Critical care units (CCUs) have reduced early mortality rates from acute myocardial infarction by approximately 50% by providing immediate defibrillation and by facilitating the implementation of beneficial interventions. These interventions include the administration of IV medications and therapy designed to do the following:
Limit the extent of myocardial infarction
To salvage jeopardized ischemic myocardium
Recanalize infarct-related arteries.
The diagnose and treatment of other conditions is useful as well. Alternatives for coronary recanalization include the IV administration of thrombolytic agents and catheter-based approaches.
General measures commonly include the use of stool softeners to prevent constipation, straining, and consequent circulatory derangements.
Prophylaxis for stress ulcers with oral sucralfate,
Antipyretics (eg, acetaminophen) should be used to prevent or suppress the fever that is typically seen in the first 24-48 hours and its consequent tachycardia. Patients with uncomplicated myocardial infarctioeed be confined to bed for only 1 day.
Physical activity should be limited (bed-chair regimen) throughout the patient’s CCU stay, with gradual and carefully monitored resumption of ambulatory activity in the late hospital phase. Educational programs targeting smoking cessation, lipid lowering, and treatment of hypertension, as indicated, in addition to phased rehabilitation programs, should be started early during the hospital course for patients with uncomplicated myocardial infarction. Use of sedative, anxiolytic, and hypnotic drugs at night may be helpful. Also important are optimal communication with compassionate physicians and nurses and the reassurance it provides.
Preventive therapy in the acute hospital phase
Beta-adrenergic blockers are of benefit when given intravenously within 4 hours of the onset of pain and continued on a long-term basis. Mortality, sudden death, and infarct size are reduced in patients with Q-wave myocardial infarction when beta-blockers are given early. Patients with unstable angina also benefit through a reduction in the incidence or severity of myocardial infarction. Metoprolol or atenolol are commonly used.
Chewing an aspirin shortly after onset of chest pain is a ready means to inhibit thrombosis. In the hospital, small trials indicate benefits (decreased size of infarcts and mortality) from insulin infusion, along with glucose and potassium, presumably through an anti-apoptotic effect.
Patients with insulin-dependent diabetes mellitus and peripheral vascular disease may be treated with caution; the benefit of angioplasty is decreased in these patients.
ACE inhibitors are useful for long-term therapy and also appear to benefit patients who have no evidence of hypotension if administration is begun within the first 24 hours after the onset of myocardial infarction. Alternatives include captopril, 12.5-50 mg given orally twice a day; enalapril, 5-40 mg given orally daily or twice a day; or any of the newer agents (eg, lisinopril, quinapril, or ramipril), given in pharmacologically equivalent doses.
Treatment with both beta-adrenergic blockers and ACE inhibitors may improve the balance between myocardial oxygen supply and demand, and it may limit infarct size. Appropriate treatment of fluid status to optimize left ventricular filling pressures, maintain oxygen saturation, and control heart rate by avoiding reflex sympathoadrenal stimulation is also beneficial.
Calcium channel blockers have not been beneficial in acute myocardial infarction, and they may exert deleterious adverse effects alone or when given with other medications. Therefore, they should generally be avoided. Diltiazem may be useful for rate control in patients with atrial fibrillation. Verapamil may be useful in patients with obstructive hypertrophy.
Continuing chest pain suggestive of ischemia is an indication for cardiac catheterization and revascularization (PTCA or surgery). The decision to proceed and the choice of modality are largely made on the basis of the results of angiography and an assessment of ventricular function. IV nitroglycerin, titrated to 10-200 mcg/min to prevent hypotension, may alleviate coronary artery spasm and postinfarct angina by reducing arterial resistance and ventricular afterload. Dosages higher than this diminish systemic venous tone and blood pressure, potentially (paradoxically) exacerbating ischemia.
Diminished afterload and preload and decreased LVEDP probably mediate the favorable effects, facilitating myocardial perfusion. Tolerance to continuously administered IV nitrates occurs rapidly, often within hours.
Thrombolytic Therapy
Thrombolytic therapy has been shown to improve survival rates in ST-segment elevation myocardial infarction but is not indicated in the treatment for non–ST-segment elevation myocardial infarction. Door-to-drug time should be no more than 30 minutes. Thrombolytic therapy administered within the first 2 hours can occasionally abort myocardial infarction and dramatically reduce the mortality rate.
Thrombolysis is generally preferred to PCI in cases where the time from symptom onset is less than 3 hours and if there would be a delay to PCI, greater than 1-2 additional hours to door-to-balloon time.
Thrombolytic treatment may be helpful in some patients, particularly those with stuttering infarcts, who are first seen 6-12 hours after the onset of symptoms (see the image below). It has not been demonstrated to be effective in patients with non-Q-wave myocardial infarction or unstable angina. The clinical effectiveness of coronary thrombolysis depends on the frequency, rapidity, and persistence of recanalization. All of these factors depend not only on the intensity of fibrinolysis but also on the inhibition of coagulation and platelet-induced thrombosis, which undoubtedly occur concomitantly.
This patient has a symptom duration of fewer than 12 hours. In the setting of active chest pain and electrocardiographic changes showing acute myocardial infarction, he would still benefit from thrombolysis. His history of surgery is not a contraindication and his blood pressure can be controlled with nitrates and beta-blockers.
In general, use of thrombolytic agents has been well demonstrated to be effective in patients aged 75 years or younger who present with suspected Q-wave myocardial infarction within 6 hours after the onset of symptoms and in whom contraindications are not present. Although the absolute risk of complications is greatest in the elderly, overall mortality reduction is at least as great in this group as in others, because the prognosis for patients with myocardial infarction that is managed conservatively is also worse for elderly patients than it is for younger patients.
Fibrinolytic agents
The first generation of fibrinolytic drugs (eg, streptokinase, urokinase, acetylated plasminogen streptokinase activator complexes [APSACs], reteplase, and novel plasminogen activator [n-PA]) indiscriminately induce activation of circulating plasminogen and clot-associated plasminogen. First-generation drugs invariably elicit a systemic lytic state characterized by depletion of circulating fibrinogen, plasminogen, and hemostatic proteins and by marked elevation of concentrations of fibrinogen degradation products in plasma.
Second-generation drugs (eg, t-PA, single-chain urokinase plasminogen activator), including agents such as tenecteplase, preferentially activate plasminogen in the fibrin domain, rather than in the circulation, as with free plasminogen. Therefore, these drugs have clot selectivity. Tenecteplase should be initiated as soon as possible after the onset of acute myocardial infarction (AMI) symptoms. In AMI patients, tenecteplase administered as a single bolus exhibits a biphasic disposition from the plasma.
Pitfalls of coronary thrombolysis
The risks of coronary thrombolysis include bleeding, much of which is confined to sites of vascular access. Marked depletion of fibrinogen or prolongation of the bleeding time may be markers of pharmacologic effects that lead to bleeding. With thrombolysis, the incidence of hemorrhagic stroke is increased, but the risk of thrombotic or embolic stroke is somewhat reduced; overall, any small increase in fatal cerebrovascular accidents is more than offset by the favorable effect on survival.
Even optimally effective coronary thrombolysis is compromised by early thrombotic reocclusion in 6-20% of patients with initial recanalization, unless vigorous conjunctive anticoagulation is started immediately.
Thrombolytic agents and mechanical revascularization
Use of thrombolytic medications and mechanical revascularization may be required. In individuals in whom fibrinolytic therapy fails to successfully recanalize the infarct-related artery (defined by ST-segment resolution < 50% at 90 min), a rescue PCI can be performed. Rescue PCI should be performed in individuals who are younger than 75 years and suitable for revascularization, if, after thrombolysis, they have evidence of acute pulmonary edema, cardiogenic shock, or hemodynamically unstable ventricular arrhythmias. Diagnostic coronary angiography post thrombolysis may be performed; however, further studies are needed to clarify the role and benefit of routine PCI to the infarct-related
Antithrombotic Agents
At present, IV unfractionated heparin (UFH) is routinely administered, in addition to orally administered aspirin. Alternatives include low-molecular-weight heparin (LMWH or enoxaparin), other inhibitors of coagulation (eg, hirudin, fondaparinux, bivalirudin), and antagonists of binding of fibrinogen to the platelet surface glycoprotein IIb/IIIa (GPIIb/IIIa) receptor (eg, abciximab, eptifibatide, tirofiban, orbofiban). Thienopyridines (eg, ticlopidine, clopidogrel) similarly inhibit platelet aggregation by binding to platelet adenosine diphosphate receptors, which block activation of the IIb/IIIa pathway.
Anticoagulation therapy
In the management of all patients with ACS or suspected ACS, anticoagulation therapy is the standard of care. In patients with or suspected unstable angina (UA)/NSTEMI, anticoagulation therapy should be added to antiplatelet therapy as soon as possible. In patients who have been selected to undergo an early invasive strategy for UA/NSTEMI, proven effective anticoagulant therapy includes UFH, enoxaparin, fondaparinux, and bivalirudin.
Anticoagulation and Thrombolytic Therapy in STEMI
In the previous 2004 guidelines on STEMI management, patients treated with fibrinolytic therapy were recommended for heparin therapy depending on the fibrinolytic agent used. In the 2007 STEMI-focused update, heparin has an established role as an adjunctive agent in patients receiving both selective and nonselective fibrinolytic therapy, with a class I indication.
Additional Medical Therapy
Morphine sulfate
Morphine sulfate may be administered to relieve pain and anxiety. This is the analgesic of choice for anginal pain relief in STEMI. For unstable angina and NSTEMI, barring contraindications, it is reasonable to administer morphine sulfate if the patient has refractory chest discomfort despite nitroglycerin use.
Nitrates
Nitrates are useful for preload reduction and symptomatic relief but have no apparent impact on mortality rate in myocardial infarction. Systolic BP < 90, HR < 60 or >100, and right ventricular infarction are contraindications to nitrate use. IV nitroglycerin is indicated for relief of ongoing ischemic discomfort, control of hypertension, or management of pulmonary congestion. Nitrates should not be administered to patients who have taken any phosphodiesterase inhibitor for erectile dysfunction within the last 24 hours (extend timeframe to 48 h for tadalafil). Their use is in symptomatic relief and preload reduction. Administer to all patients with acute myocardial infarction within the first 48 hours of presentation, unless contraindicated (ie, in right ventricular infarction).
Angiotensin-converting enzyme inhibitors
ACE inhibitors reduce mortality rates after myocardial infarction. Administer ACE inhibitors as soon as possible as long as the patient has no contraindications and remains in stable condition. An ACE inhibitor (Captopril) should be given orally within the first 24 hours of an acute coronary syndrome to patients with pulmonary congestion or LVEF less than 40% in the absence of hypotension. ACE inhibitors have the greatest benefit in patients with ventricular dysfunction. Continue ACE inhibitors indefinitely after myocardial infarction.
Angiotensin-receptor blockers
Angiotensin-receptor blockers may be used as an alternative to ACE inhibitors in patients who develop adverse effects, such as a persistent cough. An angiotensin-receptor blocker (valsartan or candesartan) should be administered to patients with ACS who are intolerant of ACE inhibitors and who have either clinical or radiologic signs of heart failure or an LVEF of less than 40%.
Beta-blockers
Beta-blockers are believed to reduce the rates of reinfarction and recurrent ischemia and should be administered to all patients with myocardial infarction unless a noteworthy contraindication exists. Both ACC/AHA 2007 guidelines for STEMI and UA/NSTEMI give oral beta-blocker usage a class I indication within the first 24 hours. Specific contraindications to usage of this therapy include: (1) signs of heart failure, ( 2) evidence of a low output state, (3) increased risk for cardiogenic shock, (4) PR interval greater than 0.24 seconds (second- or third-degree heart block, and (5) active asthma or reactive airway disease.Metoprolol is the standard of care and is a selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. Intravenous beta-blockers have a class IIa recommendation, meaning that they may also be used in ACS if the patient is hypertensive and does not have a contraindication.
Lidocaine
Note that routine use of lidocaine as prophylaxis for ventricular arrhythmias in patients who have experienced a myocardial infarction has been shown to increase mortality rates; its use is class indeterminate.
Calcium channel blockers
The use of calcium channel blockers in the acute setting has come into question, with some randomized, controlled trials and retrospective studies showing increased adverse effects. However, in patients with continuing/frequently recurring ischemia and in whom beta-blockers are contraindicated, nondihydropyridine calcium channel blockers such as diltiazem and verapamil can be used only in the absence of pulmonary edema, AV block, and severe left ventricular dysfunction.
NSAIDs
With the exception of aspirin, both selective and nonselective cyclooxygenase (COX) inhibitors should not be used during the hospitalization of patients with ACS. An increased risk in mortality may result. NSAID use in this setting is associated with an increased risk of reinfarction, hypertension, heart failure, and myocardial rupture. Therefore, patients routinely taking NSAIDs should have these discontinued at the time of presentation.
Percutaneous Coronary Intervention
PCIs are a group of catheter-based technologies used to establish coronary reperfusion. Angiography, which provides essential knowledge of the extent of coronary disease, is performed prior to PCI. In regard to STEMI, PCI may then be performed as a primary intervention or as an intervention after thrombolysis failure. In patients presenting with unstable angina or NSTEMI, PCI is an appropriate revascularization strategy for individuals with a favorable risk factors and coronary anatomy.
Percutaneous coronary intervention versus thrombolysis
Evidence suggests that primary PCI is more effective than thrombolysis and should be performed for confirmed STEMI, new or presumably new left bundle-branch block (LBBB), severe congestive heart failure, or pulmonary edema if it can be performed within 12 hours of symptom onset. Door-to-balloon time should be 90 minutes or less. PCI is the treatment of choice in most patients with STEMI.
Considerations in percutaneous coronary intervention
Elective PCI should be considered for most patients receiving thrombolytic therapy in whom ischemia develops at rest, during ambulation in the hospital, or during a prehospital discharge exercise test. Complete revascularization within 3 months of myocardial infarction appears to offer outcomes better than those of repair of the infarct-related lesion alone.
A study by Vlaar et al supports existing guidelines in that multivessel PCI in patients with STEMI is associated with higher mortality. Staged PCI (for those with significant nonculprit lesions) is associated with better outcomes.
Only an experienced operator should perform primary PTCA, and PTCA should be performed only where the appropriate facilities are available. Operators should have at least 75 cases per year, while the center should perform at least 200 cases per year as per the recommendations of the ACC.
The 2009 focused updates to the ACC/AHA STEMI and PCI guidelines include recommendations for interventions and supportive measures for PCI:
Prasugrel is a reasonable alternative to clopidogrel for antiplatelet therapy during PCI, unless the patient has a history of stroke or transient ischemic attack.
Thrombus aspiration is reasonable for primary PCI.
Fractional flow reserve can be useful to determine whether a specific lesion should be stented.
Percutaneous coronary intervention in high-risk patients
Primary PCI appears to have a particular advantage over thrombolysis for the management of high-risk myocardial infarction patients, such as those with diabetes and the elderly. In an analysis of patients who were receiving Medicare in the Cooperative Cardiovascular Project database, primary PCI improved 30-day and 1-year survival. The benefits of primary PCI in the elderly persisted after stratification by the number of myocardial infarction patients cared for at individual hospitals and the presence of on-site angiography. When the transit time to such a facility is 90 minutes or more, facilitated half-dose thrombolysis followed by PCI may be effective. The risk of this approach may be lower than that of full-dose thrombolysis, and patency rates are greater than that of late PCI without lysis.
Coronary Artery Bypass Graft Surgery
Emergent or urgent CABG surgery is indicated in patients in whom angioplasty fails and in patients who develop mechanical complications, such as a ventricular septal defect, LV, or papillary muscle rupture.
Description of a venous “bridge” between the aorta and the heart arteries (coronary arteries).
New Treatment Strategies
Interventionalists have begun to embrace new treatment strategies, such as the use of stenting and IV platelet GPIIb/IIIa inhibitors, to improve results of PTCA in acute myocardial infarction. Stents that elute drugs such as sirolimus and paclitaxel may inhibit endothelial proliferation, prevent early closure, and improve results. This stenting appears to be more effective than brachytherapy (irradiation).
Patients with evolving chest pain and ST-segment elevations that persist for 90 minutes after the administration of a thrombolytic agent may be candidates for emergency catheterization, and, if the infarct-related vessel is occluded, for “rescue” PCI.
Local injection of progenitor cells, growth factors, or genes may stimulate vascular development. Investigators in a double-blinded study, the Reinfusion of Enriched Progenitor Cells And Infarct Remodeling in Acute Myocardial Infarction (REPAIR-AMI) study, examined 204 patients with acute STEMI; they reported demonstrated greater improvement in LVEF among patients receiving intracoronary progenitor cell infusion than among patients given placebo.
Some clinical trial results suggest that intracoronary delivery of autologous bone marrow mononuclear cells (BMCs) have improved LV function when administered within the first week following myocardial infarction. The LateTIME Randomized Trial tested whether intracoronary delivery of autologous BMCs improved global and regional LV function compared with placebo when delivered 2-3 weeks following first myocardial infarction. The results suggest that those patients with myocardial infarction and LV dysfunction following reperfusion with PCI show little improvement from this therapy.
