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Mr. Sternbergh is a 62-year-old salesman who presents to the emergency room with chest pain that began 2 hours earlier. He has had occasional episodes of epigastric discomfort over the last several months that he has attributed to indigestion. He describes the feeling as a heaviness that occurs in the middle of his chest and that spreads to his neck and throat. He denies back pain, arm pain, or nausea. Although he has a rather sedentary lifestyle, the pain usually occurs when he walks uphill to his office, or occasionally after meals. He also has noticed that stress from work will bring on the symptoms. Mr. Sternbergh smokes cigarettes at work and when he feels stressed. He has never been told he has diabetes. He is being treated for hypertension and dyslipidemia.
What are the major risk factors for coronary artery disease (CAD)?
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.
What are the current recommendations for target goals for the treatment of hypertension and dyslipidemia?
The targets for both blood pressure control and lipid levels are evolving, and the trend for both is “lower is better.” Current recommendations from the Joint National Committee on Hypertension 7 define the blood pressure readings as follows:
The National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines for cholesterol management state a low-density lipoprotein (LDL) level of less than 100 mg per dL is optimal and 130 to 159 mg per dl is borderline. A total cholesterol level of less than 200 mg per dL is desirable. A high-density lipoprotein (HDL) level of less than 40 mg per dL is recognized as an independent risk factor for CAD. Many lipid specialists state that more aggressive LDL lowering to below 70 mg per dL results in even greater reduction of risk.
Although these targets may change and become even more stringent, it is important to realize that a large number of patients fail to reach their targets, leaving significant room for improvement in the prevention of atherosclerotic disease.
What is your diagnosis of Mr. Sternbergh’s condition?
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
TABLE 24.1. New York Heart Association Functional Classification of Angina Pectoris
No limitations in physical activity. Ordinary activity does not precipitate symptoms.
Slight limitation in physical activity. Comfortable at rest. Ordinary activity may precipitate anginal symptoms.
Marked limitation in physical activity. Comfortable at rest. Less than ordinary activity precipitates anginal symptoms.
Severe limitation in physical activity. Symptoms occur even at rest. Any activity exacerbates anginal symptoms.
Name other causes of chest pain that may mimic angina.
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.
Angina is caused by myocardial ischemia, a mismatch between myocardial oxygen supply and demand. Typical angina is caused by an increase in myocardial oxygen demand brought about by physical activity. Patients with stable angina have fixed obstructive lesions in their coronary arteries and impaired vasodilatory capabilities. When the demands placed on the myocardium exceed the threshold at which the coronary arteries can supply oxygenated blood (due to the fixed obstruction), myocardial ischemia occurs and symptoms develop.
What are the determinants of myocardial oxygen consumption?
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.
Mr. Sternbergh is admitted to the emergency department. He is hypertensive and diaphoretic. An electrocardiogram demonstrates ST depression in the inferior leads. Cardiac enzymes are drawn. He is placed on oxygen, given 325 mg of aspirin, and treated with intravenous labetalol and unfractionated heparin. His blood pressure normalizes and his pain goes away. He is admitted to the hospital with a diagnosis of acute coronary syndrome and subsequently is diagnosed with a non-ST elevation MI. He remains pain free and is scheduled for cardiac catheterization.
What is the difference between an ST elevation MI and a non-ST elevation 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.
The next day, Mr. Sternbergh undergoes elective cardiac catheterization.
Describe the anatomy of the coronary arteries.
The first branches off the aorta are the right and left coronary arteries. The left coronary artery (or left main artery) quickly branches into two large vessels, the left anterior descending artery and the circumflex artery. The left anterior descending artery and its diagonal branches supply the anterolateral left ventricular wall as well as the interventricular septum. The obtuse marginal branches of the circumflex artery supply the posterolateral wall of the left ventricle. The right coronary artery and its branches supply the right ventricular free wall and, in 85% to 90% of patients, provide blood to the posterior left ventricular wall and posterior septum through the posterior descending artery. The origin of the posterior descending artery determines the dominance of the coronary circulation: 10% to 15% of the population have a left dominant coronary circulation in which the posterior descending artery arises from the circumflex system.
An understanding of the blood supply of several vital cardiac structures is important. The artery to the sinus node usually arises from the right coronary artery but in up to 40% of patients it may arise from the left system. The atrioventricular node is usually supplied by a branch of the right coronary artery. The anterolateral papillary muscle of the left ventricle is usually supplied by branches of the left anterior descending artery, whereas the posteromedial papillary muscle may arise from either the right or left systems, depending on which is dominant.
Mr. Sternbergh’s catheterization reveals a 90% stenotic lesion of the proximal right coronary artery and a 50% lesion in the proximal left anterior descending artery. The first obtuse marginal of the circumflex has a 20% to 30% stenosis. Left ventricular function is normal.
Which lesions are hemodynamically significant?
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.
Are stenoses of less than 50% physiologically significant?
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.
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