Chapter 21 Marini Acute Coronary Syndromes

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CHAPTER 21 • Acute Coronary Syndromes

patients with hypotension, CHF, and LV dysfunc- tion. However, with the ever-expanding capabilities of interventional cardiology, many of the patients who previously would have been offered bypass sur- gery are now receiving DES. The debate of which is better (bypass surgery or stenting) in patients with complex coronary disease (multivessel CAD, total occlusions, left main CAD, etc.) continues. The SYNTAX trial has compared the use of DES (paclitaxel-eluting) to CABG surgery in patients with over 1,800 patients with complex CAD who were randomized to either bypass surgery or multivessel stenting. The combined endpoint of death, repeat revascularization, stroke, and MI at 1 year favored bypass surgery. The differences were driven mainly by higher repeat revascularization rates in the stent arm of the trial. The risk of death or MI was no dif- ferent in the two arms. The risk of stroke was more than three times higher in the surgical group. This trial, although providing some clear insights, has by no means put to rest the raging debate. The recom- mendation therefore is to individualize therapy after taking into considerations the following factors: (1) coronary anatomy, (2) LV function, (3) comorbid conditions, (4) age of the patient, and (5) patient’s wishes. Intra-aortic Balloon Pump An IABP may occasionally prove needed for hemody- namic stabilization while awaiting PTCA or CABG, particularly for patients with LV dysfunction, CHF, hypotension, or acute mechanical defects (e.g., mitral regurgitation [MR] or ventricular septal defect [VSD]). Balloon inflation during diastole augments coronary perfusion and deflation during systole decreases LV afterload. Unless a rapidly correct- able mechanical defect is present, IABP does not improve outcomes. Risk Factor Modification For the patient who has been stabilized medically or following revascularization procedures, risk fac- tor modification is essential in preventing recur- rent ischemia, infarction, and sudden death from progression of CAD. Smoking cessation, control of diabetes mellitus and hypertension, correction of abnormal lipid patterns, and weight reduction are critical elements in risk factor modification. Most should remain on aspirin, β -blockers, high- dose statins, and angiotensin-converting enzyme inhibitors (ACEI). Establishing a regular program

of exercise is pivotal in achieving these goals and improving activity tolerance. Patients with good exercise capacity are known to have fewer cardio- vascular events and seem to tolerate them better. ACUTE CORONARY SYNDROMES: ST ELEVATION MYOCARDIAL INFARCTION (ACS-STEMI) Mechanisms STEMI results from plaque rupture and formation of superimposed thrombus. The thrombus that causes complete occlusion of a major coronary artery is usually rich in fibrin and red blood cells (red clot). This is in contrast to the thrombus seen with NSTE- ACS, which is characterized by formation of a plate- let-rich thrombus (white clot). Following complete coronary occlusion, a wave of myocardial necrosis spreads from the endocardium to the epicardium. The process of infarction is usually completed in 24 hours, and it is called a “full-thickness” or com- pleted infarction. Q waves are typically seen in the ECG with a completed or full-thickness infarction, but their presence does not always indicate a final- ized pathogenic process. If angiography is performed promptly, a fresh occlusive coronary thrombus may be demonstrated in most cases (approx. 90%). Nonthrombotic spasm of the coronary arteries in an area of atherosclerosis is responsible for a small fraction of AMIs. Rarely, coronary flow may be inter- rupted by embolism in patients with endocarditis, prosthetic valves, or rheumatic valvular disease. Only 5% to 10% of patients sustaining an MI have anatomically normal coronary arteries. (Although spontaneous thrombolysis of clot is suspected, the mechanism of infarction in these cases usually remains unknown.) Cocaine is responsible for an alarming number of MIs. Because cocaine enhances platelet aggregation, causes vasoconstriction, and increases heart rate through catecholamine-medi- ated mechanisms, it can produce infarction even in patients with normal coronary arteries.

Diagnosis History

1. Classical Presentation: The typical presen- tation is one characterized by the abrupt onset of left-sided or retrosternal chest, neck, and jaw