Historical Perspective
Angina pectoris literally translates as “strangling in the chest.” William Heberden presented one of the earliest descriptions of angina pectoris in 1768 in a lecture to the Royal College of Physicians. In it, he described the classic symptoms of angina :
This is a disorder of the breast, marked with strong and peculiar symptoms, considerable for the kind of danger belonging to it …. The seat of it, and sense of strangling and anxiety with which it is attended, may make it not improperly called angina pectoris …. Those who are afflicted with it are seized …with a painful and most disagreeable sensation in the breast, which seems as if it would take their life away, if it were to increase or continue …. When a fit of this sort comes on by walking, its duration is very short, as it goes off almost immediately upon stopping. If it comes on in the night, it will last an hour or two.
The clinical syndrome accompanying acute myocardial infarction was described by two Russian physicians, Obrastzov and Strazhesko in 1910, and then by William Herrick in 1912.
In 1937, Sampson and Eliaser and Feil published separate but remarkably similar case series describing a syndrome intermediate between chronic stable angina and acute myocardial infarction, which they termed impending acute coronary occlusion . Sampson and Eliaser wrote that “The character of the premonitory attack of precordial pain observed in these patients … rarely differed from their former pain either in its nature—i.e. squeezing, crushing—or in radiation. The effect of nitroglycerin on the premonitory attack was definitely transient, with failure of complete relief even on repeated doses ….”
Multiple terms for this syndrome proliferated in the literature, including preinfarction angina , accelerated angina , acute coronary insufficiency , and intermediate coronary syndrome . In 1971, Fowler first used the term unstable angina , which he defined as the
… sudden onset of one or more anginal attacks a day from a previous background of good health or … a dramatic change in the symptomatic pattern of previously recognized coronary disease …. In patients with unstable angina, the attacks, in addition to being more frequent, are also often of longer duration and may occur at rest without an apparent precipitating event …. The electrocardiogram shows no evidence of recent infarction, and such serum enzymes as the glutamic oxaloacetic transaminase or the creatine phosphokinase show no diagnostic alterations.
The term acute coronary syndrome was introduced by Fuster and colleagues in 1985 to highlight the common pathophysiologic link that distinguishes unstable angina (UA) and acute myocardial infarction from chronic stable angina. An important distinction was made between the fact that
… the early and some of the advanced coronary atherosclerotic lesions progress very slowly, … [while] some of the advanced coronary atherosclerotic lesions progress very rapidly, probably by means of complicating anatomic events, one of which is related to a thrombogenic process …. These complicated processes appear to be of paramount importance in the pathogenesis of some of the acute coronary syndromes including unstable angina, myocardial infarction, and sudden coronary death.
In 1989, I proposed a clinical classification of UA to “separate patients with unstable angina into a manageable number of meaningful and easily understood subgroups based on the severity, the presumed precipitating cause, and the presence of electrocardiographic changes ….” According to this classification, patients are divided into three groups (I to III) based on the severity of angina and three groups according to the clinical circumstances in which the acute ischemic episode occurs (A to C). This classification has been shown to correlate both with the severity of coronary disease as assessed by arteriography as well as with early mortality ( Table 11-1 ). From this classification, three principal presentations of unstable angina are recognized ( Table 11-2 ). ,
| Class | Definition | Death or MI to 1 Yr (%) * |
|---|---|---|
| Severity | ||
| Class I | New onset of severe angina or accelerated angina; no rest pain | 7.3 |
| Class II | Angina at rest within past month but not within preceding 48 hr (angina at rest, subacute) | 10.3 |
| Class III | Angina at rest within 48 hr (angina at rest, subacute) | 10.8 † |
| Clinical Circumstances | ||
| A (secondary angina) | Develops in the presence of extracardiac condition that intensifies myocardial ischemia | 14.1 |
| B (primary angina) | Develops in the absence of extracardiac condition | 8.5 |
| C (postinfarction angina) | Develops within 2 wk after acute myocardial infarction | 18.5 ‡ |
| Intensity of treatment | Patients with unstable angina may also be divided into three groups, depending on whether unstable angina occurs: (1) in the absence of treatment for chronic stable angina; (2) during treatment for chronic stable angina; or (3) despite maximal anti-ischemic drug therapy. These three groups may be designated with subscripts 1, 2, and 3, respectively. | |
| ECG changes | Patients with unstable angina may be further divided into those with or without transient ST-T wave changes during pain. | |
* Data from Scirica BM, Cannon CP, McCabe CH, et al; Thrombolysis in Myocardial Ischemia III Registry Investigators: Prognosis in the thrombolysis in myocardial ischemia III registry according to the Braunwald unstable angina pectoris classification. Am J Cardiol 2002;90:821-826.
| Class | Presentation |
|---|---|
| Rest angina * | Angina occurring at rest and prolonged, usually greater than 20 min |
| New-onset angina | New-onset angina of at least CCS class III severity |
| Increasing angina | Previously diagnosed angina that has become distinctly more frequent, longer in duration, or lower in threshold (i.e., increased by 1 or more Canadian Cardiovascular Society (CCS) class to at least CCS class III severity) |
The acute coronary syndromes comprise a wide spectrum of conditions that includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI; Fig. 11-1 ). Acute coronary syndromes are heterogeneous; their clinical severity ranges from an asymptomatic condition, recognizable only by a change in the electrocardiogram (ECG), to an explosive, life-threatening event. The most common pathophysiologic process that underlies the acute coronary syndromes is rupture or erosion of an unstable atherosclerotic plaque, with subsequent formation of a platelet-fibrin thrombus. Coronary vasospasm and vasoconstriction, progression of atherosclerosis, and increased myocardial oxygen demand in the presence of a fixed, limited supply may also play pathogenetic roles. The degree to which coronary blood flow is impaired, the level of myocardial oxygen demand, the presence or absence of collateral flow, and other patient-specific factors combine to determine the clinical presentation.
Clinical Setting
Most patients who present with an acute coronary syndrome have an antecedent history of angina pectoris, and approximately 80% have a prior history of coronary artery disease. Three fourths of patients with NSTEMI and slightly more than half of patients with UA are male. However, women predominate among the rapidly expanding older population with unstable angina.
Acute coronary syndrome has been found to have a circadian periodicity, with the peak incidence occurring between midnight and 6 am . Acute coronary syndromes can be precipitated by vigorous exercise, particularly in previously sedentary persons. Emotional stress, including that created by natural disasters, may lead to plaque rupture, acute coronary syndrome, and sudden cardiac death. However, most cases of acute coronary syndrome occur in patients with no identifiable trigger.
History
The hallmark of an acute coronary syndrome is ischemic chest pain ( Table 11-3 ). In unstable angina and NSTEMI, the ischemic pain is typically gradual in onset, and may not reach its peak intensity for several minutes. In myocardial infarction, this pain characteristically begins abruptly, is steady, and lasts for more than 30 minutes. In contrast, in unstable angina, the pain frequently waxes and wanes, lasting from a few minutes to as long as but usually less than 20 minutes. Patients frequently describe the pain using terms such as pressure , burning , gnawing , tightness , heaviness and when severe, crushing . These descriptions suggest a visceral rather than a superficial origin. The discomfort ranges from mild to very severe, depending on patient perception and the mass of myocardium that is ischemic or necrotic. Pain caused by ischemia is exacerbated by exertion and may diminish with rest. Chest pain that is fleeting, stabbing in nature, positional, pleuritic, reproduced by palpation, or that persists for days is rarely caused by an acute coronary syndrome.
