Coronary heart disease is the abbreviation of coronary atherosclerotic heart disease. The incidence is high in all the countries especially in the developed countries. Recently, the incidence in
Anaina Pectoris
The term "angina pectoris", derived from the Greek ankhein (to choke), was coined by William Heberden in 1768 to describe a clinical syndrome of exertional chest discomfort, but the cardiac origin of the syndrome was not fully appreciat-ed until Caleb Parry proposed in 1799 that angina was due to insufficient delivery of blood to the heart muscle, particularly during exercise.
Today angina pectoris is generally defined as a discomfort within or adjacent to the chest, typically provoked by exertion or anxiety, usually lasting for several minutes, alleviated by rest, and not resulting in myocardial necrosis. Besides this common syndrome of what is often termed classic exertional angina, there are a variety of other clinical presentations of angina pectoris described below, including unstable angina, variant (Prinzmetal's) angina, mixed angina, and an asymp-tomatic syndrome known as silent ischemia
Although incapacitating recurrent chest pain, myocardial infarction, and death are potential sequelae of angina, the past 25 years has witnessed the emergence and refinement of a re-markable armamentarium of pharmacologic and mechanical in-terventions which, if properly utilized, can considerably allevi-ate the symptomatic manifestations and extend the duration of survival of most patients with this common condition.
Pathophysiology and Classification
Angina pectoris is a symptom of myocardial ischemia, oc-curring when the requirement for oxygen by either ventricle exceeds its supply. The most common underlying disease is atherosclerotic coronary artery disease, although occasionally angina occurs secondary to other entities, such as hypertrophic cardiomyopathy, aortic stenosis, and coronary arteritis.
The major determinants of myocardial oxygen demand in-elude heart rate, contractility, and ventricular wall tension, a function of ventricular volume and intraventricular pressure. An increase in one or more of these determinants--as might occur with exercise, emotional stress, or other states of heightened adrenergic activity--triggers an increase in myocar-dial oxygen demand, and myocardial ischemia results unless myocardial oxygen supply rises proportionately.
Myocardial oxygen supply is governed by coronary blood flow and the ability of the myocardium to extract oxygen from the blood delivered to it. Unlike other organs, the heart al-ways extracts oxygen with near maximal efficiency from the blood, even under situations of minimal demand, so there is little potential for enhanced oxygen extraction to counter in-creased oxygen demands. Coronary blood flow, on the other hand, can increase several-fold in normal subjects as a result of coronary arterial vasodilation, most importantly at the arterio-lar level, triggered by the local build-up of lactate, adenosine, and other vasoactive substances as myocardial oxygen demands increase.
In the presence of obstructive coronary artery disease, myocardial ischemia may result when the coronary arterial stenosis prevents autoregulatory vasodilation so that coronary blood flow can no longer increase proportional to rising oxygen demands. In other situations, myocardial ischemia may occur when oxygen demands are constant but there is a primary de-crease in coronary blood flow mediated via ①coronary artery spasm, ② rapid evolution of the underlying atherosclerotic plaque (plaque disruption) leading to a reduced coronary arte-rial lumen caliber, and/or ③intermittent microvascular plug-ging by platelet aggregates.
In some patients with exertional angina, ischemia is pri-marily a manifestation of increased oxygen demands in the face of fixed coronary blood flow, whereas in patients with primary vasospastic angina, ischemia results when coronary artery spasm causes blood flow to diminish in the face of stable oxy-gen demands. However, many, if not most, patients fall be-tween these two extremes, experiencing angina as a result of both heightened oxygen demands and diminished supply, and are said to have mixed angina.
Angina is but one manifestation of myocardial ischemia. Ischemia typically begins in the subendocardium, where wall tension is high and compressive forces limit coronary microvas-cular flow, and then spreads like a wavefront toward the epi-cardium. The electrocardiogram often depicts ST-segment de-pression or T-wave inversion as manifestations of subendocar-dial ischemia but may show ST-segment elevation (injury cur-rent) if ischemia is prolonged and extends transmurally. These electrocardiographic changes may occur without typical anginal symptoms, a condition termed silent ischemia.
Segmental left ventricular contraction abnormalities occur in the region of the myocardium served by the coronary arterial branches distal to the stenosis responsible for the ischemia (the culpirt lesion), and, if about 10 per cent or more of the my-0cardium is rendered ischemic, a reduction in global function of the left ventricle may be detectable. In addition to abnormal systolic function during ischemia, increased diastolic stiffness of the left ventricle manifests by a rising left ventricular end-diastolic pressure and rising pulmonary venous pressure. Con-sequently, transient clinical evidence of left ventricular failure may occur during episodic ischemia and may explain why many patients describe their angina not as pain but as a feeling of "breathlessness" or "chest tightness".
It is prognostically and clinically useful to classify anginal syndromes into stable and unstable categories. Unstable angina refers to angina of recent onset (within 2 months) or angina that has begun to intensify or to occur at rest or with a lower level of exertion within the previous 2 months. Stable angina, as the name implies, describes a relatively constant pattern of pain with regard to its severity and precipitating factors within the recent months. Some authorities classify angina of recent onset as "stable angina" if it is precipitated by moderate or se-vere levels of exertion and maintains a constant threshold over time, because "stable angina" has to begin at some point in time.
Of patients with unstable angina, up to 20 per cent progress to acute myocardial infarction within the next 3 months. Coronary angiography and angioscopy reveal that more than 50 per cent of patients with unstable angina have multivessel disease with eccentric, irregular, or ulcerated atherosclerotic lesions associated with endothelial disruption and adherent thrombus. Left main coronary artery disease oc-curs in about 10 per cent of patients with unstable angina; It is likely that unstable angina represents a point on a continuum between stable exertional angina and acute myocardial infarc-tion.
Variant angina, originally described by Printzmetal, is characterized by rest pain accompanied by transient ST-seg-ment changes (often ST elevation resembling acute myocardial infarction, although ST depression can also occur) and ventric-ular arrhythmias. Variant angina is a form of unstable angina caused by coronary arterial spasm, usually within a coronary artery narrowed by plaque, but occasionally within an angio-graphically normal appearing artery.
History and Physical Examination
The diagnosis of angina pectoris often requires consider-able clinical skill because there is no totally specific symptom, physical finding, or laboratory examination to confirm its pres-ence. The history is probably the most powerful tool for diag-nosing angina and provides the skilled interviewer an assess-ment of both the stability (or instability) of the syndrome as well as its severity. The patient should be instructed to de-scribe the chest discomfort according to its character, location, radiation, duration, precipitating and alleviating factors, ac-companying symptoms, and change in pattern over the past few weeks or days.
As indicated above, the typical history is that of exertion-al chest discomfort of several minutes duration alleviated by rest. The discomfort typically involves the region of the ster-num (substernal or, more properly, retrosternat location) but may instead manifest itself in any region between the jaw and epigastrium. Commonly the discomfort radiates to the shoul-ders or arms, especially the left, to the neck or jaw, and less commonly to the back or epigastrium. Most patients perceive angina as a deep or visceral (rather than superficial) sensation and describe it as a "tightness heaviness", or "choking sen-sation" rather than as a definite pain. The discomfort is usually of several minutes duration; discomfort of less than 1 minutes' s duration is rarely angina, and discomfort at full intensity ex-ceeding 20 minutes in duration should arouse suspicion of my-ocardial infarction or discomfort unrelated to myocardial is-chemia. The pain of unstable angina, however, may wax and wane repeatedly over several hours.
Typically angina is provoked by exertion, especially walk-ing uphill, climbing stairs, vigorous arm work, coitus, or ex-ercising in cold weather (when peripheral vascular resistance is great). Discomfort may also be provoked by emotion (fear, anger, anxiety), may follow a meal, or may occur on lying down (angina decubitus) owing to increased ventricular filling pressure, or may occur during sleep (nocturnal angina), per-haps owing to increased adrenergic output related to dreams. Typically, exertional angina is relieved promptly (within 5 minutes) by rest; emotionally triggered angina may last longer; both usually are alleviated within 3 to 5 minutes with sublingual nitroglycerin. For patients with exertional angina, quantitation of the severity of the discomfort by a scale such as that of the Canadian Cardiovascular Society can be useful (Table 10).
During an episode of angina, the physical examination may be normal or may disclose one or more of the following: an increased heart rate and blood pressure; paradoxical split-ting of the second heart sound; a precordial presystolic bulge or fourth heart sound ($4), both due to enhanced atrial contrac-tion into a ventricle rendered stiff by ischemia; a systolic bulge due to left ventricular dyskinesis; a diastolic bulge or $3 gallop as evidence of significant left ventricular failure; a mid-to late-systolic murmur of mitral regurgitation related to ischemia-in-duced mitral papillary muscle dysfunction; or transient rales or other evidence of pulmonary venous congestion.
Other conditions that should be considered in the differen-tial diagnosis of angina include the following: gastrointestinal disease-especially disordered esophageal motility, gastroe-sophageal reflux, peptic ulcer disease, and cholecystitis; exer-tional bronchospasm related to asthmatic bronchitis; chest wall discomfort related to costochondritis, muscle spasm, herpes zoster, or anxiety states, the last often presenting as submam-mary sharp pain of a few seconds' duration; and other cardiac and vascular diseases such as pericarditis, myocardial infarc-tion, aortic dissection, or pulmonary embolism. These should be readily distinguished from angina in mast cases by a detailed histo-ry, physical examination, and appropriate laboratory tests.
General Management
Patients diagnosed with angina pectoris should be coun-seled concerning the potential serious and unpredictable nature of the condition but also advised that powerful new pharmaco-logic and mechanical interventions are available that may ame-li0rate symptoms and in many cases, extend survival. Patients with unstable angina should undergo hospital admission to rule out myocardial infarction, to receive intensive pharmacologic therapy, and, in most cases, to undergo coronary arteriogra-phy. All patients with angina should be thoroughly instructed in risk factor modification, particularly dietary management of cholesterol and saturated fat intake, smoking cessation, and blood pressure control. A search should be made for potentially correctable conditions such as aortic stenosis, severe anemia, thyrotoxicosis, and tachyarrhythmias that might be contribut-ing to the myocardial oxygen supply demand imbalance causing angina.
Pharmacologic Therapy
The goals of pharmacologic therapy of angina pectoris are to restore the imbalance between myocardial oxygen demand and supply by reducing oxygen demands, increasing coronary blood flow, or both. The most important categories of an-tianginal drugs are the nitrates, blockers, and calcium chan-nel blockers. Additionally, patients with unstable angina bene-fit from heparin and aspirin.
Acute Myocardial Infarction
Literally, acute myocardial infarction is a focus of necrosis resulting from inadequate perfusion of the tissue. What is gen-erally implied by the term, however, is the clinical syndrome resulting from such ischemia and manifested by sudden cardiac death; "typical" signs and symptoms of infarction such as crushing chest pain and diaphoresis, malignant ventricular ar-rhythmia, and congestive heart failure or shock; or atypical presentations that can be clinically silent or subtle with new-onset or accelerated angina, atypical chest pain mimicking "in-digestion”, impaired cerebral perfusion with syncope, or signs simulating, those of a cerebrovascular accident or psychosis. Coronary thrombosis was recognized as a potential cause as er-aly as
thrombosis with "status anginous" and respiratory embarrass-mennt, and in 1912 by Herrick, who described clinical fea-tures typical of sudden coronary occlusion. Although dimmu-tion of perfusion has not been questioned, the contribution of thrombotic occlusion at sites of severe atherosclerosis as a pri-mary phenomenon rather than as an epiphenomenon was re-solved only recently. Its pivotal role was established unequivo-cally by early angiograhic study of afflicted patients. Early catastrophic complication of infarction include ventricular fib-rillation, rupture of the ventricular free wall, ventricular septalrupture (with shock and left to right shunting), or papillary muscle rupture (with profound mitral or tricuspid regurgita-tion), Later complications include ventricular mural thrombus with peripheral embolization and cerebrovascular accident, congestive heart failure with or without ventricular true or pseudoaneurysm, ventricular dilatation and infarct expansion, and sudden cardiac death. Progression of underlying coronary artery disease in survivors of acute myocardial infarction may result in unstable, angina pectoris, "silent ischemia" [with electrocardiograrhic (ECG) changes without symptoms], re-current infarction, or sudden death.
Etiology Although most infarcts result from thrombotic occlusion superimposed on severe coronary atherosclerosis, se-vere atherosclerotic disease may exist for years with no change in severity of effort-induced angina. Occurrence of angina with progressively less effort or at rest, protracted angina simulating the pain of infarction, and acceleration of angina despite in-tense medical management and the absence exacerbating fac-tors such as anemia, arrhythmia, hypertension, congestive heart failure, thyrotoxicosis, or obesity often reflect dynamic changes in obstructing plaques with consequent intermittent thrombosis. Q-wave infarct (previously called transmural) ap-pear to result when occlusive thrombi persist, as documented angiographically in more than 90 per cent of patients with in-farction. Non-Q-wave infarcts (previously called subendocar-dial) result often from incomplete or spontaneously recanalized thrombotic occlusions after ischemia sufficiently persistent to elicit necrosis,. Reocclusion with early recurrent infarction is common. A common denominator of all actue coronary syn-dromes (sudden cardiac death, new-onset angina, unstable angina, acute myocardial infarction) appears to be instability of atherosclerotic plaques with intramural hemorrhage, fissur-ing, and plaque rupture, all of which may precipitate acute thrombotic occlusion.
Risk factors for infarction parallel those for atherosclerosis in general. Diabetes mellitus, hypertension, truncal obesity, smoking, increased concentrations of low density lipoprotein (LDL) cholesterol and decreased concentrations of high densi-ty lipoprotein (HDL) cholesterol in plasma, increased concen-trations of lipoprotein (a), elevated plasma homocysteine, and genetic predisposition to atherosclerosis manifested by a strong family history apply to both. Changes such as hyperglycemia and elevation of triglycerides in plasma early after infarction may be inappropriately interpreted as indicative of diabetes or
hyperlipidemia when in fact they reflect transiently impaired insulin release because of reduced pancreatic blood flow, aug-mented glycogenolysis secondary to catecholamines, increased gluconeogenesis secondary to 17-OH corticosteroids, increased concentrations of plasma free fatty acids, and augmented hep-atic synthesis of triglycerides. Conversely, plasma cholesterol may be diminished because of hepatic dysfunction and may be misinterpreted as the absence of hypercholesterolemia that would otherwise be evident. The fall in HDL cholesterol is greater than that of total cholesterol and may persist for 6 to 8 weeks.
Several causes of acute myocardial infarction other than atherosclerosis merit particular consideration. Embolization of coronary arteries secondary to infective or marantic endocardi-tis (associated with drug abuse or collagen vascular disease), calciom deposites or thrombi from prosthetic or calcified valves, ventricular mural thrombi, or atrial thrombi or myxo-mas may be responsible. Coronary thrombosis caused by trauma or by oral contraceptives in women, perhaps attributable to di-minished antithrombin III or increased plasminogen activator inhibitor type I (PAI-I) in plasma; vasculitis ; vasospasm (id-iopathic or associated with cocaine or amphetamine abuse); coronary vascular degeneration ( including accelerated atherosclerosis) after cardiac transplantation; or inflammatory small vessel coronary disease (0.1 to
Occasionally, acute myocardial infarction may occur in as-sociation with syndrome X (angina with "normal" coronary ar-teries) or variant angina. Diminished elaboration of endothelial cellderived relaxing factor or release of vasoconstrictors such as endothelin may contribute (Table 11).
