Tobacco use, dyslipidemia, hypertension, and diabetes are the major modifiable risk factors for atherosclerosis, which can manifest itself in the coronary circulation, the cerebral circulation, or the peripheral circulation. Not surprising, there is considerable overlap in the involved vascular bed, such that approximately 10% of patients suffer from atherosclerotic occlusive disease affecting all three systems and over 25% of patients have two or more vascular beds involved.

Mr. Sternbergh is suffering from angina pectoris. Usually substernal or centered in the left chest, the feeling has been described as crushing, pressure, or heaviness, occasionally radiating to the neck, left shoulder, or left arm. Typical anginal symptoms come on slowly, reach maximal intensity within minutes, and reside with rest and nitrates within minutes. Noncardiac causes of chest pain should be considered in patients with a sharp or stabbing pain, pain that lasts seconds only, or pain associated with specific movements of the arms or shoulders. Changes in position or posture usually do not affect anginal chest pain. It is important to note, however, that symptoms of breathlessness, fatigue, belching, or epigastric discomfort may also represent anginal equivalents. Also, some patients (e.g., diabetics) may be asymptomatic. The New York Heart Association Functional Classification of angina pectoris is useful to quantitate and compare anginal symptoms (Table 24.1).

The differential diagnosis of chest pain includes esophageal disorders, biliary disease, costochondritis, musculoskeletal pain or cervical radiculopathy, pericarditis, pulmonary hypertension, pulmonary embolism, and acute aortic dissection. Acute myocardial infarction (MI) must be excluded in any patient with a prolonged episode of chest pain.

Myocardial oxygen consumption is determined by the tension developed within the wall of the heart, the contractile state of the heart, the heart rate, and the energy costs of maintaining the integrity of the myocardial cells. Heart rate is of particular importance because conditions that increase heart rate, such as exercise, stress, hyperthyroidism, and sepsis, significantly increase myocardial oxygen consumption.

Unstable angina and acute MI are two manifestations of acute ischemic syndromes distinct from stable angina. An anginal pattern of increasing intensity or frequency is considered unstable and puts the patient at risk for acute MI. Unstable angina occurs when existing atherosclerotic plaques rupture, exposing the thrombogenic subendothelial layer. This results in localized platelet activation and thrombin generation. The localized clot may lyse, resulting in an unstable angina pattern or non-ST elevation MI, or it may progress to completely occlude the artery, causing an ST-elevation MI. The change from a stable to an unstable anginal pattern is important to recognize because medical therapy directed at inhibition of platelet function and coagulation can reduce the risk of acute MI. Although warfarin is ineffective in preventing MI in patients with acute coronary syndromes, platelet inhibition with aspirin or the more potent inhibitor clopidogrel significantly reduces the risk of MI.

ST elevation MI represents complete occlusion of the coronary artery resulting in a transmural MI. Therapy for ST elevation MI relies on immediate reperfusion strategies, either with percutaneous coronary intervention (PCI) or with thrombolytic drugs. PCI has been demonstrated to be a superior reperfusion strategy both in terms of safety and efficacy, but it requires immediate, 24/7 catheter laboratory availability.

Non-ST elevation MI implies partial occlusion at the site of plaque rupture with ongoing thrombosis and localized lysis of the clot. Medical therapy with antiplatelet drugs and thrombin inhibitors is effective. Cardiac catheterization to assess coronary anatomy is indicated after stabilization.

Complete algorithms for the care of patients with ST elevation MI and non-ST elevation MI are beyond the scope of this chapter but are readily available.

To restrict flow, a 75% reduction in luminal area is required; because coronary arteriograms are displayed in cross-section, this translates into a 50% reduction in cross-sectional area and therefore a stenosis of greater than 50% is generally considered to be significant. Determination of the severity of stenosis is relatively subjective and, in general, coronary angiography tends to underestimate lesion severity.

Yes. The vulnerability to rupture of atherosclerotic plaque is not related to the degree of luminal obstruction. Plaque rupture and subsequent MI can occur wherever there is atherosclerotic plaque. The vast majority of MIs, in fact, occur in vessels with less than 50% luminal stenosis, highlighting the importance of plaque stabilization and antithrombotic therapies in the prevention of acute coronary syndromes.