Chapter 21 Marini Acute Coronary Syndromes

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CHAPTER 21 • Acute Coronary Syndromes

metabolic demands for cardiac output, (2) height- ened LV afterload causing increased transmural wall tension (e.g., hypertension, LV cavity dilation, aortic stenosis), (3) increased LV mass (hypertrophy), and (4) increased contractility. Despite the predisposi- tion of the LV to ischemia, conditions that cause hypertrophy, dilation, or increased afterloading of the right ventricle (RV) also can put its muscle mass at risk. For example, pulmonary embolism may pre- cipitate RV ischemia—a phenomenon that is most common in patients with underlying right coronary artery (RCA) narrowing or cor pulmonale . Instability of a coronary atherosclerotic plaque is the key to the pathophysiology of ACS and infarc- tion. Degree of coronary narrowing plays a second- ary role. Histologic studies of coronary vessels have shown that atherosclerotic plaques are intimomedial in location. In general, there are two types of coro- nary plaques: (1) stable plaque with small lipid core and thick fibrous cap and (2) unstable plaque with large lipid core and thin cap. The former generally causes stable angina pectoris if it causes significant obstruction of the vessel (>50% to 70% of the ves- sel lumen diameter). Soft, lipid-laden plaques with thin caps are more prone to rupture, promote local clotting, and provoke ACS. Many of these plaques do not cause significant obstruction of the lumen of coronary vessels before the onset of the ACS. Hence, the patient may not have experienced any cardiac symptoms prior to the onset of ACS even with exercise, and stress tests may be negative. Acute instability and rupture of one or more coronary plaques with superimposed thrombosis are central to the pathophysiology of ACS. This clot, composed of platelets and thrombin, not only produces a fixed vessel occlusion but also stimu- lates reversible vasoconstriction. The resulting sudden coronary artery occlusion, which may be total or subtotal, causes acute myocardial ischemia or infarction. UA represents a high-risk transition period during which most patients undergo accel- erated myocardial ischemia. If unchecked, this transition culminates in acute myocardial infarc- tion (AMI) or sudden cardiac death (SCD) in up to 15% of patients within just a few weeks. Coronary angiography in many of these patients demonstrates complex coronary plaque lesions with varying degrees of superimposed thrombosis. Intravascular ultrasonic examination of coronary vessels (IVUS) is another useful tool that has helped shed consid- erable light, not only on the pathophysiology but

also on the management of coronary artery disease (CAD), particularly in the setting of ACS. The key role of platelets in the pathophysiology of ACS has undergone considerable review in the past decades. Platelet activation and aggregation encourage formation and propagation of a platelet- rich or “white” clot over a ruptured atherosclerotic plaque in patients with UA and NSTEMI. This contrasts with the fibrin-rich or “red” clot seen in the coronaries of patients with STEMI. The current recommendations on the use of antithrombin and antiplatelet therapies in NSTEMI and that of fibri- nolytic therapy in patients with STEMI derive not only from the pathophysiology of these conditions but also from the results of informative clinical trials performed within the last two decades. The term UA denotes new pain or a departure from a previous anginal pattern. UA occurs at rest or with less provocation than stable angina. Pain lasting longer than 15 minutes also suggests UA. Angina occurring in the early post-MI period or within weeks of an interventional coronary pro- cedure also is best termed “unstable.” Commonly, the pain is described as a “tightness,” “heaviness,” or “squeezing” in the substernal region. UA may awaken patients from sleep or present as pain at a new site such as the jaw or arm. Elderly, female, and diabetic patients are more likely to experience atypical symptoms, pain intensity, and distribution. Although the classical description is one of heavy central chest pressure radiating to the jaw and left arm, it is rational to raise suspicion of UA or evolv- ing MI in patients reporting acute pain from “nose to navel.” Autonomic manifestations (nausea, vom- iting, tachycardia, or sweating) also favor “instabil- ity.” Blood pressure frequently rises before the onset of pain, even in resting patients. Rising blood pres- sure boosts afterload, increasing wall tension and myocardial O 2 consumption. Less commonly, the abrupt onset of dyspnea and congestive heart failure (CHF) may be the only manifestation of UA. Diagnosis History and Physical Examination

Data Profile Electrocardiographic Changes

Electrocardiographic patterns are invaluable in deter- mining the presence of coronary occlusion and in