Main symptoms and syndromes in ischemic heart disease
Ishaemic heart disease is a chronic condition by insufficient (or completely blocked) blood supply to the myocardium due to pathology in the coronary vessels (atherosclerotic their changes).
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.
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.
The medical history distinguishes between various alternative causes for chest pain (such as dyspepsia, musculoskeletal pain, pulmonary embolism). As part of an assessment of the three main presentations of IHD, risk factors are addressed. These are the main causes of atherosclerosis (the disease process underlying IHD): age, male sex, hyperlipidaemia (high cholesterol and high fats in the blood), smoking, hypertension (high blood pressure), diabetes, and the family history.
The term ischaemic heart disease includes many diseases, such as angina pectoris, myocardial infarction, and coronary cardiosclerosis. The pathology is based on insufficient blood supply to the heart. The disproportion between the heart’s demand for blood and the actual blood supply may arise when the heart’s demands increase significantly, or when the actual blood supply diminishes for some reasons.
The most frequent cause of angina pectoris is atherosclerosis of the coronary arteries of the heart. Much less frequently it develops in infectious and infectious-allergic vascular diseases, such as syphilitic aortitis, panarteritis, periarteritis nodosa, rheumatic vasculitis, and obliterating endarteritis. Arigina pectoris often concurs with essential hypertension. Paroxysms of angina pectoris may develop due to upset nervous regulation of the coronary arteries as a reflex or in cholelithiasis, hiatus hernia, diseases of the stomach, etc. by reflex. Spasms of the coronary arteries (without their anatomical changes) can sometimes provoke angina pectoris. The spasm may develop in heavy smokers or as a result of a strong emotional stress.
Hypoxaemia (ischaemia) of the myocardium provokes the attack. Ischaemia develops in conditions when the insufficient amount of blood is delivered to the heart muscle through the coronary arteries, and the myocardium does not receive the necessary amount of oxygen. Transient oxygen hunger causes a reversible disorder in the oxidation-reduction processes in the myocardium. Stimulation of the interoceptors of the myocardium or the vascular adventitia by the products of upset metabolism produces a current of impulses via the centripetal pathways to the cerebral cortex to cause the specific symptom of the disease, retrosternal pain. High activation of the sympatheticoadrenal system is also very important for the onset of angina pectoris.
1. Risk-factors of IHD.
The most important risk-factor of IHD if essential hypertension, which accelerates development of atherosclerosis and coronary spasm. Diabetes mellitus is another predisposing factor, it also stimulates development of atherosclerosis, leads to microangiopathy. Another factors are: smoking tobacco (provokes coronarospasm), hereditary, hyperholesterolaemia, psychic overstrains.
2. The classification of IHD, angina pectoris.
In according with classification of World Health Protection Organisation (WHPO) the following pathological onditions belong th IHD:
1. Sudden death.
2. Angina pectoris.
3. Myocardial infarction.
4. Postinfarctic cardiosclerosis.
5. Arrythmias.
6. Heart failure.
Angina pectoris is a frequently occurring disease. Its main clinical symptoms are attacks of retrosternal pain due to acute but transient disorder in the coronary circulation. The disease develops mainly in people over 40, and predominantly in men. Mental workers would mostly suffer from this disease.
There are some types of angina pectoris:
I. Exertional angina (pectoris):
1. First appeared angina (pectoris).
2. Stable angina (pectoris) . 4 funtional classes of angina pectoris are distinguished depending on the gravity of the course. The first class is characterized by rare attacks and they occur only during physical exertion; in the second and third classes tolerance to exercise decreases progressively, while patients with the fourth class develop attacks of angina pectoris during slight exercise or even at rest.
3. Progressive (instable) angina (pectoris).
II. Rest angina (pectoris), Prinzmetal’s angina (pectoris).
3. Main complaints and anamneis of patients with angina pectris and cardiosclerosis.
The main clinical symptom of the disease is pain in the centre of the sternum (retrosternal pain). Less frequently the pain originates in the heart region. The character of pain varies: the patient may feel constriction, compression, heaviness, burning, and sometimes sharp or stabbing pain. Pain is usually severe and the patient develops morbid fear of death. Pain radiates into the left shoulder, left arm, left side of the neck and the head, the mandible, the interscapular space, and sometimes to the upper abdomen. Pain arises under certain conditions: during walking (especially fast walking) and other exercises (angina pectoris of effort).
During physical exertion, the heart muscle requires more nutrition from blood. Atherosclerotic vessels cannot deliver the appropriate amount of blood and the patient has to stop exercise (walking) for a few minutes until pain subsides. Specific sign of angina pectoris is development of pain when the patient leaves a warm room and walks in the open during cold seasons. The symptom is even more pronounced if atmospheric pressure changes. Under emotional stress, the patient develops an attack of angina pectoris without any exercise. Attacks of pain may occur during sleep (angina pectoris at rest), after meals, in abdominal distention, and in high diaphragm.
Pain may last from few seconds to 20—30 min. Quick removal of pain after taking nitroglycerin suggests angina pectoris. The strength of attacks differs. In rare cases attacks end lethally.
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
Diagnosis
The diagnosis of ischaemic heart disease underlying particular symptoms depends largely on the nature of the symptoms. The first investigation is an electrocardiogram (ECG/EKG), both for “stable” angina and acute coronary syndrome. An X-ray of the chest and blood tests may be performed.
Myeloperoxidase has been proposed as a biomarker.
Stable angina
Angina pectoris
In “stable” angina, chest pain with typical features occurring at predictable levels of exertion, various forms of cardiac stress tests may be used to induce both symptoms and detect changes by way of electrocardiography (using an ECG), echocardiography (using ultrasound of the heart) or scintigraphy (using uptake of radionuclide by the heart muscle). If part of the heart seems to receive an insufficient blood supply, coronary angiography may be used to identify stenosis of the coronary arteries and suitability for angioplasty or bypass surgery.
Acute chest pain
Acute coronary syndrome and myocardial infarction
Diagnosis of acute coronary syndrome generally takes place in the emergency department, where ECGs may be performed sequentially to identify “evolving changes” (indicating ongoing damage to the heart muscle). Diagnosis is clear-cut if ECGs show elevation of the “ST segment”, which in the context of severe typical chest pain is strongly indicative of an acute myocardial infarction (MI); this is termed a STEMI (ST-elevation MI), and is treated as an emergency with either urgent coronary angiography and percutaneous coronary intervention (angioplasty with or without stent insertion) or with thrombolysis (“clot buster” medication), whichever is available. In the absence of ST-segment elevation, heart damage is detected by cardiac markers (blood tests that identify heart muscle damage). If there is evidence of damage (infarction), the chest pain is attributed to a “non-ST elevation MI” (NSTEMI). If there is no evidence of damage, the term “unstable angina” is used. This process usually necessitates admission to hospital, and close observation on a coronary care unit for possible complications (such as cardiac arrhythmias – irregularities in the heart rate).
Depending on the risk assessment, stress testing or angiography may be used to identify and treat coronary artery disease in patients who have had an NSTEMI or unstable angina.
4.Data of physical examination.
During an attack, the pulse is usually slow and rhythmical, but tachycardia, extrasystole, and increased arterial pressure are sometimes observed. Percussion and auscultation of the heart sometimes cannot reveal any abnormality, provided pronounced atherosclerotic cardioslecrosis is absent. The body temperature remains normal. Usually there are no changes in the peripheral blood.
Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, results from the interruption of blood supply to a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (cholesterol and fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and ensuing oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).
Typical symptoms of acute myocardial infarction include sudden retrosternal chest pain (typically radiating to the left arm or left side of the neck), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety (often described as a sense of impending doom).[1] Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue A sizeable proportion of myocardial infarctions (22–64%) are “silent”, that is without chest pain or other symptoms.
Among the diagnostic tests available to detect heart muscle damage are an electrocardiogram (ECG), echocardiography, cardiac MRI and various blood tests. The most often used blood markers are the creatine kinase-MB (CK-MB) fraction and the troponin levels. Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, and sublingual nitroglycerin.
Most cases of myocardial infarction with ST elevation on ECG (STEMI) are treated with reperfusion therapy, such as percutaneous coronary intervention (PCI) or thrombolysis. Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although PCI may be required if the patient’s risk warrants it People who have multiple blockages of their coronary arteries, particularly if they also have diabetes mellitus, may benefit from bypass surgery (CABG) The European Society of Cardiology guidelines in 2011 proposed treating the blockage causing the myocardial infarction by PCI and performing CABG later when the patient is more stable Rarely CABG may be preferred in te acute phase of myocardial infarction, for example when PCI has failed or is contraindicated
Ischemic heart disease (which includes myocardial infarction, angina pectoris and heart failure when preceded by myocardial infarction) was the leading cause of death for both men and women worldwide in 2004 Important risk factors are previous cardiovascular disease, older age, tobacco smoking, high blood levels of certain lipids (low-density lipoprotein cholesterol, triglycerides) and low levels of high density lipoprotein (HDL) cholesterol, diabetes, high blood pressure, lack of physical activity and obesity, chronic kidney disease, excessive alcohol consumption, the abuse of illicit drugs (such as cocaine and amphetamines), and chronic high stress levels.
Classification
There are two basic types of acute myocardial infarction based on pathology:
Transmural: associated with atherosclerosis involving a major coronary artery. It can be subclassified into anterior, posterior, inferior, lateral or septal. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area’s blood supply. In addition, on ECG, ST elevation and Q waves are seen.
Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. The subendocardial area is particularly susceptible to ischemia. In addition, ST depression is seen on ECG.
In the clinical context, a myocardial infarction can be further subclassified into a ST elevation MI (STEMI) versus a non-ST elevation MI (non-STEMI) based on ECG changes The phrase heart attack is sometimes used incorrectly to describe sudden cardiac death, which may or may not be the result of acute myocardial infarction. A heart attack is different from, but can be the cause of cardiac arrest, which is the stopping of the heartbeat, and cardiac arrhythmia, an abnormal heartbeat. It is also distinct from heart failure, in which the pumping action of the heart is impaired; however severe myocardial infarction may lead to heart failure. A 2007 consensus document classifies myocardial infarction into five main types
Type 1 – Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
Type 2 – Myocardial infarction secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension
Type 3 – Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
Type 4 – Associated with coronary angioplasty or stents:
Type 4a – Myocardial infarction associated with PCI
Type 4b – Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy
Type 5 – Myocardial infarction associated with CABG
Signs and symptoms
Rough diagram of pain zones in myocardial infarction; dark red: most typical area, light red: other possible areas; view of the chest
The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous. Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium where it may mimic heartburn. Levine’s sign, in which the patient localizes the chest pain by clenching their fist over the sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value
Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating) weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.
Women and older patients report atypical symptoms more frequently than their male and younger counterparts. Women also report more numerous symptoms compared with men (2.6 on average vs 1.8 symptoms in men). The most common symptoms of MI in women include dyspnea (shortness of breath), weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms that may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men.
At least one-fourth of all myocardial infarctions are silent, without chest pain or other symptoms. These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. Estimates of the prevalence of silent myocardial infarctions vary between 22 and 64% A silent course is more common in the elderly in patients with diabetes mellitus[ and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms
Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome
The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax, and esophageal rupture. Other non-catastrophic differentials include gastroesophageal reflux and Tietze’s syndrome
Risk factors for myocardial infarction include:
Age
Gender: At any given age men are more at risk than women, particularly before menopause,[35] but because in general women live longer than men ischemic heart disease causes slightly more total deaths in women
Diabetes mellitus (type 1 or 2)
High blood pressure
Dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides[37]
Tobacco smoking, including secondhand smoke
Short term exposure to air pollution including: carbon monoxide, nitrogen dioxide, and sulfur dioxide but not ozone
Family history of ischaemic heart disease or myocardial infarction particularly if one has a first-degree relative (father, brother, mother, sister) who suffered a ‘premature’ myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women)
Obesity (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).
Lack of physical activity
Psychosocial factors including, low socio-economic status, social isolation, negative emotions and stress increase the risk of myocardial infarction and are associated with worse outcomes after myocardial infarction. Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation are also correlated with a higher risk of MI.
Alcohol — Studies show that prolonged exposure to high quantities of alcohol can increase the risk of heart attack.
Oral contraceptive pill – women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.
Hyperhomocysteinemia (high homocysteine) in homocysteinuria is associated with premature atherosclerosis whether elevated homocysteine in the normal range is causal is contentious
