Atherosclerosis. Ischemic heart disease. Classification of WHPO. Angina pectoris. Classification. Emergency care. Cardiopulmonary resuscitation.
Ischemic Heart Disease
Ischemic heart disease, also known as myocardial ischemia, is a condition of the heart where the heart muscles are damaged or do not work as efficiently due to a reduced blood supply to the heart. The decreased blood flow is most often caused by narrowing of the coronary arteries, a condition called atherosclerosis. The risk of getting this disease increases with age, and is more prevalent among smokers thaon-smokers. Also at risk are people with diabetes, high blood cholesterol levels, high blood pressure (people suffering from hypertension), and individuals who have family history of the disease.
The symptoms of ischemic heart disease
The most serious symptom is chest pain, which can indicate a heart attack (also known as cardiac arrest). This is felt as a tightening or weighing down of the chest and upper body parts including the neck, jaws, and shoulders. Chest pains might also be the result of various other causes such as anxiety or panic attacks, or even something milder such as heartburn or angina. Angina pectoris is a generic term for any type of chest pains, and sadly sometimes the cause of angina is attributed to milder reasons such as heartburn through indigestion whereas it may be indicative of ischemic heart disease. If you are experiencing chronic chest pains it is imperative to stop smoking (if you are a smoker) and consult a physician for a full and thorough diagnostic of the heart and blood vessels to check for constriction of blood supply to major vital organs.
Related to the chest pain symptom is the feeling of discomfort in upper body parts similar to that resulting from a flatulent stomach. It may or may not be accompanied by a choking feeling or breathlessness, which might indicate not enough blood flowing to the lungs or a restricted blood supply to and from the pulmonary arteries (the blood vessels that carry blood to the lungs) causing fluids to be accumulated in the lungs.
Lack of ease in breathing can be confused with other symptoms, not all of which are indicative of severe heart diseases but might be serious illnesses in their own regard. This might be caused by pneumonia (a lung disease caused by certain bacteria and fungi) or pulmonary embolism (a blocked lung blood vein often resulting from a blood clot). For smokers emphysema is also a major cause, which is a chronic and progressive degeneration of the lower respiratory tracts from the constant inhalation of tobacco smoke and deposit of a layer of tar (hydrocarbons present in tobacco) on the lungs inner walls.
Orthopnea is another symptom, whereby the patient has difficulty of breathing lying down or sleeping (dyspnea) unless propped up by pillows from the waist up. This is common in victims of asthma or bronchitis, and might also show up as pulmonary oedema (fluid build-up in the lungs). If the other causes can be ruled out than most likely these symptoms indicate a presence of ischemic heart disease.
Cardiomegaly, or the condition of heart enlargement, can also be a possible consequence of ischemic heart disease. This is where the muscular walls of the heart increase in thickness resulting in an abnormally large size of the heart. Other possible causes include general heart failure, hypertension, obesity, diabetes, high cholesterol and high fat diet, and smoking. Sometimes the reason could be a congenital heart block, which is a genetic condition whereby few unlucky children are born with a block in their hurt and as they grow older in leads to cardiomegaly. Some viral infections and autoimmune diseases need to be ruled out as potential causes too before concluding that the condition is a direct result of ischemic heart disease.
Peripheral oedema, which is a specific type of oedema whereby fluids build up in the extremities of the body, i.e. limbs (arms and legs) and belly, is another symptom of the disease. The cause is again related to the fact of not enough blood being supplied to various peripheral tissues and organs of the body, hence the fluids retention leading to gain in body weight. Watch for sudden increases in weight in a short span of time, for example about 2kgs in 2 days. Apart from heart failure, peripheral oedema might also result from various kidney malfunctions, a thyroid condition, a liver failure, or lymphydema (swelling caused by lymphatic fluid retention, a close relative of the blood fluids). Also ieed of elimination are obvious hormonal conditions such as pregnancy and premenstrual syndrome, which can also cause peripheral oedema.
Cardiac arrhythmia, or the occurrence of an abnormal rhythm of the heart, is another symptom. Other causes include excessive alcohol consumption, some specific diet pills side effect, excessive caffeine intake, tobacco use, and inordinate and persistent stress in daily life. Sometime the blood sugar levels imbalance, a type of hypoglycaemia where blood sugar falls below normal levels, can also result in cardiac arrhythmia. The best way to eliminate the other causes in to ensure there is no family genetic disorder of diabetes, and to moderate or eliminate consumption of tobacco, alcohol, and caffeine. If in doubt if this symptom is the direct result of ischemic heart disease please consult your physician for an immediate diagnosis.
Diagnosis of Ischemic heart disease
Due to the various symptoms listed above and their innumerable possible causes other than ischemic heart disease, it is always recommended to get a thorough diagnosis from a reliable physician or hospital. There are some home diagnosis tools and methods available, but they should only be used to verify and monitor an existing condition as per the doctor’s prescription, or to eliminate certain sources as the cause of some symptoms.
The most important assessment is that of physical chest pains, and to ensure they are not the result of mild conditions such as heartburn. Other home diagnosis involves testing blood pressure through sphygmomanometers or home blood pressure monitors. Also available are home testing equipment for irregular heart beat detection via heart rate monitors and heart electrocardiogram (ECG) machines
Angina pectoris
Angina pectoris–commonly known as angina–is chest pain due to ischemia of the heart muscle, generally due to obstruction or spasm of the coronary arteries. The main cause of Angina pectoris is Coronary Artery Disease, due to atherosclerosis of the arteries feeding the heart. The term derives from the Latin angina (“infection of the throat”) from the Greek ἀγχόνη ankhonē (“strangling”), and the Latin pectus (“chest”), and can therefore be translated as “a strangling feeling in the chest”.
There is a weak relationship between severity of pain and degree of oxygen deprivation in the heart muscle (i.e., there can be severe pain with little or no risk of a heart attack, and a heart attack can occur without pain). In some cases Angina can be extremely serious and has been known to cause death. People that suffer from average to severe cases of Angina have an increased percentage of death before the age of 55, usually around 60%.
Worsening (“crescendo”) angina attacks, sudden-onset angina at rest, and angina lasting more than 15 minutes are symptoms of unstable angina (usually grouped with similar conditions as the acute coronary syndrome). As these may herald myocardial infarction (a heart attack), they require urgent medical attention and are generally treated as a presumed heart attack.
Classification
Stable angina
Also known as effort angina, this refers to the more common understanding of angina related to myocardial ischemia. Typical presentations of stable angina is that of chest discomfort and associated symptoms precipitated by some activity (running, walking, etc.) with minimal or non-existent symptoms at rest or with administration of sublingual nitroglycerin. Symptoms typically abate several minutes following cessation of precipitating activities and reoccur when activity resumes. In this way, stable angina may be thought of as being similar to claudication symptoms.
Unstable angina
Unstable angina (UA) (also “crescendo angina;” this is a form of acute coronary syndrome) is defined as angina pectoris that changes or worsens.
It has at least one of these three features:
1. it occurs at rest (or with minimal exertion), usually lasting >10 min;
2. it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or
3. it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than before).
UA may occur unpredictably at rest which may be a serious indicator of an impending heart attack. What differentiates stable angina from unstable angina (other than symptoms) is the pathophysiology of the atherosclerosis. The pathophysiology of unstable angina is the reduction of coronary flow due to transient platelet aggregation on apparently normal endothelium, coronary artery spasms or coronary thrombosis. The process starts with atherosclerosis, and when inflamed leads to an active plaque, which undergoes thrombosis and results in acute ischemia, which finally results in cell necrosis after calcium entryStudies show that 64% of all unstable anginas occur between 10 PM and 8 AM when patients are at rest.
In stable angina, the developing atheroma is protected with a fibrous cap. This cap (atherosclerotic plaque) may rupture in unstable angina, allowing blood clots to precipitate and further decrease the lumen of the coronary vessel. This explains why an unstable angina appears to be independent of activity.
Microvascular angina
Microvascular Angina or Angina Syndrome X is characterized by angina-like chest pain, but has different causes. The cause of Microvascular Angina is unknown, but it appears to be the result of poor function in the tiny blood vessels of the heart, arms and legs. Since microvascular angina isn’t characterized by arterial blockages, it’s harder to recognize and diagnose, but its prognosis is excellent.
Signs and symptoms
Most patients with angina complain of chest discomfort rather than actual pain: the discomfort is usually described as a pressure, heaviness, tightness, squeezing, burning, or choking sensation. Apart from chest discomfort, anginal pains may also be experienced in the epigastrium (upper central abdomen), back, neck area, jaw, or shoulders. This is explained by the concept of referred pain, and is due to the spinal level that receives visceral sensation from the heart simultaneously receiving cutaneous sensation from parts of the skin specified by that spinal nerve’s dermatome, without an ability to discriminate the two. Typical locations for referred pain are arms (often inner left arm), shoulders, and neck into the jaw. Angina is typically precipitated by exertion or emotional stress. It is exacerbated by having a full stomach and by cold temperatures. Pain may be accompanied by breathlessness, sweating and nausea in some cases. In this case, the pulse rate and the blood pressure increases. Chest pain lasting only a few seconds is normally not angina (such as Precordial catch syndrome).
Myocardial ischemia comes about when the myocardia (the heart muscles) receive insufficient blood and oxygen to functioormally either because of increased oxygen demand by the myocardia or by decreased supply to the myocardia. This inadequate perfusion of blood and the resulting reduced delivery of oxygen and nutrients is directly correlated to blocked or narrowed blood vessels.
Some experience “autonomic symptoms” (related to increased activity of the autonomic nervous system) such as nausea, vomiting and pallor.
Major risk factors for angina include cigarette smoking, diabetes, high cholesterol, high blood pressure, sedentary lifestyle and family history of premature heart disease.
A variant form of angina (Prinzmetal’s angina) occurs in patients with normal coronary arteries or insignificant atherosclerosis. It is thought to be caused by spasms of the artery. It occurs more in younger women.
Cause
Major risk factors
• Age (≥ 55 years for men, ≥ 65 for women)
• Cigarette smoking
• Diabetes mellitus (DM)
• Dyslipidemia
• Family history of premature cardiovascular disease (men <55 years, female <65 years old)
• Hypertension (HTN)
• Kidney disease (microalbuminuria or GFR<60 mL/min)
• Obesity (BMI ≥ 30 kg/m2)
• Physical inactivity
• prolonged psychosocial stress.
Routine counselling of adults to advise them to improve their diet and increase their physical activity has not been found to significantly alter behaviour, and thus is not recommended.
Conditions that exacerbate or provoke angina
• Medications
• vasodilators
• excessive thyroid replacement
• vasoconstrictors
• polycythemia which thickens the blood causing it to slow its flow through the heart muscle
One study found that smokers with coronary artery disease had a significantly increased level of sympathetic nerve activity when compared to those without. This is in addition to increases in blood pressure, heart rate and peripheral vascular resistance associated with nicotine which may lead to recurrent angina attacks. Additionally, CDC reports that the risk of CHD (Coronary heart disease), stroke, and PVD (Peripheral vascular disease) is reduced within 1–2 years of smoking cessation. In another study, it was found that after one year, the prevalence of angina in smoking men under 60 after an initial attack was 40% less in those who had quit smoking compared to those who continued. Studies have found that there are short term and long term benefits to smoking cessationOther medical problems
• profound anemia
• uncontrolled HTN
• hyperthyroidism
• hypoxemia
Other cardiac problems
• tachyarrhythmia
• bradyarrhythmia
• valvular heart disease
• hypertrophic cardiomyopathy
Myocardial ischemia can result from:
1. a reduction of blood flow to the heart that can be caused by stenosis, spasm, or acute occlusion (by an embolus) of the heart’s arteries.
2. resistance of the blood vessels. This can be caused by narrowing of the blood vessels; a decrease in radius. Blood flow is inversely proportional to the radius of the artery to the fourth power
3. reduced oxygen-carrying capacity of the blood, due to several factors such as a decrease in oxygen tension and hemoglobin concentration This decreases the ability to of hemoglobin to carry oxygen to myocardial tissue.
Atherosclerosis is the most common cause of stenosis (narrowing of the blood vessels) of the heart’s arteries and, hence, angina pectoris. Some people with chest pain have normal or minimal narrowing of heart arteries; in these patients, vasospasm is a more likely cause for the pain, sometimes in the context of Prinzmetal’s angina and syndrome X.
Myocardial ischemia also can be the result of factors affecting blood composition, such as reduced oxygen-carrying capacity of blood, as seen with severe anemia (low number of red blood cells), or long-term smoking.
Pathophysiology
Angina results when there is an imbalance between the heart’s oxygen demand and supply. This imbalance can result from an increase in demand (e.g. during exercise) without a proportional increase in supply (e.g. due to obstruction or atherosclerosis of the coronary arteries).
Diagnosis
Suspect angina in people presenting with tight, dull, or heavy chest discomfort which is
1. Retrosternal or left-sided, radiating to the left arm, neck, jaw, or back.
2. Associated with exertion or emotional stress and relieved within several minutes by rest.
3. Precipitated by cold weather or a meal.
Some people present with atypical symptoms, including breathlessness, nausea, or epigastric discomfort or burping. These atypical symptoms are particularly likely in older people, women, and those with diabetes.
Angina pain is not usually sharp or stabbing or influenced by respiration. Anti-acids and simple analgesia do not usually relieve the pain. If chest discomfort (of whatever site) is precipitated by exertion, relieved by rest, and relieved by glyceryl trinitrate, the likelihood of angina is increased.
In angina patients who are momentarily not feeling any one chest pain, an electrocardiogram (ECG) is typically normal, unless there have been other cardiac problems in the past. During periods of pain, depression or elevation of the ST segment may be observed. To elicit these changes, an exercise ECG test (“treadmill test”) may be performed, during which the patient exercises to their maximum ability before fatigue, breathlessness or, importantly, pain intervenes; if characteristic ECG changes are documented (typically more than 1 mm of flat or downsloping ST depression), the test is considered diagnostic for angina. Even constant monitoring of the blood pressure and the pulse rate can lead us to some conclusion regarding the angina. The exercise test is also useful in looking for other markers of myocardial ischaemia: blood pressure response (or lack thereof, particularly a drop in systolic pressure), dysrhythmia and chronotropic response. Other alternatives to a standard exercise test include a thallium scintigram or sestamibi scintigram (in patients who cannot exercise enough for the purposes of the treadmill tests, e.g., due to asthma or arthritis or in whom the ECG is too abnormal at rest) or Stress Echocardiography.
In patients in whom such noninvasive testing is diagnostic, a coronary angiogram is typically performed to identify the nature of the coronary lesion, and whether this would be a candidate for angioplasty, coronary artery bypass graft (CABG), treatment only with medication, or other treatments. There has been research which concludes that a frequency is attained when there is increase in the blood pressure and the pulse rate. This frequency varies normally but the range is 45–50 kHz for the cardiac arrest or for the heart failure] In patients who are in hospital with unstable angina (or the newer term of “high risk acute coronary syndromes”), those with resting ischaemic ECG changes or those with raised cardiac enzymes such as troponin may undergo coronary angiography directly.
Treatment
The most specific medicine to treat angina is nitroglycerin. It is a potent vasodilator that makes more oxygen available to the heart muscle. Beta-blockers and calcium channel blockers act to decrease the heart’s workload, and thus its requirement for oxygen. Nitroglycerin should not be given if certain inhibitors such as Sildenafil (Viagra), Tadalafil (Cialis), or Vardenafil (Levitra) have been taken within the previous 12 hours as the combination of the two could cause a serious drop in blood pressure. Treatments are balloon angioplasty, in which the balloon is inserted at the end of a catheter and inflated to widen the arterial lumen. Stents to maintain the arterial widening are often used at the same time. Coronary bypass surgery involves bypassing constricted arteries with venous grafts. This is much more invasive than angioplasty.
The main goals of treatment in angina pectoris are relief of symptoms, slowing progression of the disease, and reduction of future events, especially heart attacks and death. Beta blockers (e.g., carvedilol, propranolol, atenolol) have a large body of evidence in morbidity and mortality benefits (fewer symptoms, less disability and longer life) and short-acting nitroglycerin medications have been used since 1879 for symptomatic relief of angina.[(such as nifedipine (Adalat) and amlodipine), isosorbide mononitrate and nicorandil are vasodilators commonly used in chronic stable angina[citatioeeded]. A new therapeutic class, called If inhibitor, has recently been made available: ivabradine provides pure heart rate reduction[26] leading to major anti-ischemic and antianginal efficacy. ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit and, lastly, statins are the most frequently used lipid/cholesterol modifiers which probably also stabilize existing atheromatous plaque[citatioeeded]. Low-dose aspirin decreases the risk of heart attack in patients with chronic stable angina, and was previously part of standard treatment; however, it has since been discovered that the increase in haemorrhagic stroke and gastrointestinal bleeding offsets this gain so they are no longer advised unless the risk of myocardial infarction is very high.
Exercise is also a very good long term treatment for the angina (but only particular regimens – gentle and sustained exercise rather than intense short bursts), probably working by complex mechanisms such as improving blood pressure and promoting coronary artery collateralisation.
Identifying and treating risk factors for further coronary heart disease is a priority in patients with angina. This means testing for elevated cholesterol and other fats in the blood, diabetes and hypertension (high blood pressure), and encouraging smoking cessation and weight optimisation.
The calcium channel blocker nifedipine prolongs cardiovascular event- and procedure-free survival in patients with coronary artery disease. New overt heart failures were reduced by 29% compared to placebo; however, the mortality rate difference between the two groups was statistically insignificant
The fatty acid oxidation inhibitor mildronate is a clinically used anti-ischemic drug for the treatment of angina and myocardial infarction. Mildronate shifts the myocardial energy metabolism from fatty acid oxidation to the more oxygen sparing glucose oxidation under ischemic conditions, by inhibiting enzymes in the carnitine biosynthesis pathway including gamma-butyrobetaine dioxygenase. Mildronate also inhibits carnitine acetyltransferase and therefore acts as a myocardial energy metabolism regulator.
Suspected angina
Hospital admission for people with the following symptoms, as they may have unstable angina: Pain at rest (which may occur at night), pain on minimal exertion, angina that seems to be progressing rapidly despite increasing medical treatment. Refer urgently all people with suspected angina to a chest pain evaluation service, for confirmation of the diagnosis and assessment of the severity of coronary heart disease.
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. Previous Clinical Practice articles in the Journal have focused on noninvasive testing for coronary artery 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., 1 mm or more of ST-segment depression); ischemia at a low workload (below 5 to 6 metabolic equivalents); large, inducible single or multiple wall-motion abnormalities; and substantial nuclear-perfusion defects. 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 braiatriuretic 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.2 Diet therapy has been shown to lower total serum cholesterol between 5% and 10%.18 NCEP diet therapy is broken down into Step I and Step II diets (TABLE 4). 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.18 TABLE 5 lists common sources of these fats. TABLE 6 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 (100 cm) in men and 35 inches (88 cm) in women. However, these numbers may be too high when applied to, for example, Asians, Hispanics, Native Americans, and South Asians. Thus the definition of abdominal obesity is population specific
Regular exercise reduces the frequency of anginal symptoms, increases functional capacity, and improves endothelial function.24,33 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.35 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.
