Acute coronary syndrome
Acute coronary syndrome is a spectrum of conditions involving chest discomfort or other symptoms caused by lack of oxygen to the heart muscle (the myocardium). The unification of these manifestations of coronary artery disease under a single term reflects the understanding that these are caused by a similar pathophysiology (sequence of pathologic events) characterized by erosion, fissuring, or rupture of a pre-existing plaque, leading to thrombosis (clotting) within the coronary arteries and
impaired blood supply to the heart muscle.
The clinical spectrum of Acute Coronary Syndromes results from varying degrees of coronary artery occlusion. Studies have shown that nearly everyone has some evidence of atherosclerotic plaque formation. However, as a result of life style, environment and/or genetics, this process is more pronounced in some individuals. An atherosclerotic plaque is characterized by a lipid rich core with one side embedded within the coronary intima and the other side, the luminal surface, covered by a fibrous cap. This fibrous cap is a dense extracellular matrix of collagen, elastin and proteoglycans and its integrity is essential for the maintenance of plaque stability. The fibrous cap is most vulnerable at its shoulder, where it meets the normal vessel intima. It is at this site where a combination of enzymatic processes and inflammation (thus the potential of cardiac specific C-reactive protein as an important marker of cardiac risk) begin to degrade the stability of the plaque. This susceptible plaque will erode, fissure and ultimately rupture, providing a site for platelet adhesion. As platelets begin to gather, they are further activated by the binding of vonWillibrand factor and the expression of glycoprotein IIb/IIIa, resulting in platelet aggregation. Thrombosis will continue, eventually leading to symptomatic coronary vessel occlusion.
Initial diagnosis of acute coronary syndrome is based almost entirely on history, risk factors, and, to a lesser extent, ECG. The symptoms are due to myocardial ischemia, which has an underlying cause of an imbalance between supply and demand for myocardial oxygen. Myocardial ischemia most often develops as a result of reduced blood supply, due to atherosclerotic plaques, to a portion of the myocardium. The plaques initially allow sufficient blood flow to match myocardial demand. These areas of narrowing may become clinically significant and precipitate angina when myocardial demand increases. Angina that is reproduced by exercise, eating, and/or stress and is subsequently relieved with rest and without recent change in frequency or severity of activity necessary to produce symptoms is called chronic stable angina. Over time, the plaques may thicken and rupture, exposing a thrombogenic surface upon which platelets aggregate and thrombi form. The patient may note a change in symptoms of cardiac ischemia with a change in severity or of duration of symptoms. This condition is referred to as unstable angina.
A less common cause of angina is dynamic obstruction, which may be caused by intense focal spasm of a segment of an epicardial artery (Prinzmetal angina). Two other causes include arterial inflammation and secondary unstable angina. Arterial inflammation may be caused by or related to infection. Secondary unstable angina occurs when the precipitating cause is extrinsic to the coronary arterial bed, such as fever, tachycardia, thyrotoxicosis, hypotension, anemia, or hypoxemia. Most patients who experience secondary unstable angina have chronic stable angina. Irrespective of the cause of unstable angina, the result of persistent ischemia is myocardial infarction (MI).
Acute coronary syndrome thus covers the spectrum of clinical conditions ranging from unstable angina to non-Q-wave myocardial infarction and Q-wave myocardial infarction. These life-threatening disorders are a major cause of emergency medical care and hospitalization in the United States. Coronary heart disease is the leading cause of death in the United States. Unstable angina and non-ST-segment elevation myocardial infarction are very common manifestations of this disease.
The treatment of Acute Coronary Syndromes is time sensitive and definitive treatment should be initiated within 30 minutes of presentation. Initial treatment strategies have remained largely unchanged and should be employed immediately. Patients who have symptoms of acute myocardial ischemia and are given an electrocardiogram (ECG or EKG) may or may not have an ST elevation. (An ECG provides a graph of the heartbeat. Portions of the graph are labeled P, Q, R, S and T. An ST elevation describes a rise in a particular portion of this graph.) Most patients who have ST-segment elevation will ultimately develop a Q-wave acute myocardial infarction (heart attack). (The Q-wave describes another part of an ECG graph.) Patients who have ischemic discomfort without an ST-segment elevation are having either unstable angina, or a non-ST-segment elevation myocardial infarction that usually leads to a non-Q-wave myocardial infarction.
While acute coronary syndromes can be readily identified and treated, routine health care maintenance that focuses on healthy lifestyles and prevention remains the most effective way to avoid the potential morbidity and mortality associated with cardiovascular disease. Numerous studies have confirmed the benefits of regular cardiovascular exercise on blood pressure, lipids, diabetes and weight. Similarly, the DASH (Dietary Approaches to Stop Hypertension) diet has been evaluated in well-designed trials and been shown to be an effective method for weight reduction that lowers blood pressure and lipids. With increasing concerns about obesity and metabolic syndrome and their associations with cardiovascular disease, routine screening has also taken on increased importance. This is best accomplished with a primary care continuity provider who can assess risk factors and make informed recommendations about patient-specific screening tests and the best strategies for cardiac risk factor reduction.