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Chronic Ischemic Heart Disease

General Considerations

For clinical purposes, patients with chronic ischemic heart disease fall into two general categories: those with symptoms related to the disease, and those who are asymptomatic. Although the latter are probably more common than the former, physicians typically see symptomatic patients more frequently. The issue of asymptomatic patients becomes important clinically when physicians are faced with estimating the risk to a particular patient who is undergoing some stressful intervention, such as major noncardiac surgery. Another issue is the patient with known coronary artery disease who is currently asymptomatic. Such individuals, especially if they have objective evidence of myocardial ischemia, are known to have a higher incidence of future cardiovascular morbidity and mortality. There is, understandably, a strong temptation to treat such patients, despite the fact that it is difficult to make an asymptomatic patient feel better, and some of the treatment modalities have their own risks. In such cases, strong evidence that longevity will be positively influenced by the treatment must be present in order for its benefits to outweigh its risks.
 

Pathophysiology & Etiology
In the industrialized nations, most patients with chronic ischemic heart disease have coronary atherosclerosis. Consequently, it is easy to become complacent and ignore the fact that other diseases can cause lesions in the coronary arteries. In young people, coronary artery anomalies should be kept in mind; in older individuals, systemic vasculitides are not uncommon. Today, collagen vascular diseases are the most common vasculitides leading to coronary artery disease, but in the past, infections such as syphilis were a common cause of coronary vasculitis. Diseases of the ascending aorta, such as aortic dissection, can lead to coronary ostial occlusion. Coronary artery emboli may occur as a result of infectious endocarditis or of atrial fibrillation with left atrial thrombus formation. Infiltrative diseases of the heart, such as tumor metastases, may also compromise coronary flow. It is therefore essential to keep in mind diagnostic possibilities other than atherosclerosis when managing chronic ischemic heart disease.
 

Clinical Findings


Coronary atherosclerosis is more likely to occur in patients with certain risk factors for this disease  These include advanced age, male gender or the postmenopausal state in females, a family history of coronary atherosclerosis, diabetes mellitus, systemic hypertension, high serum cholesterol and other associated lipoprotein abnormalities, and tobacco smoking. Additional minor risk factors include a sedentary lifestyle, obesity, high psychologic stress levels, and such phenotypic characteristics as earlobe creases, auricular hirsutism, and a mesomorphic body type. The presence of other systemic diseases—hypothyroidism, pseudoxanthoma elasticum, and acromegaly, for example—can accelerate a propensity to coronary atherosclerosis. In the case of nonatherosclerotic coronary artery disease, evidence of such systemic vasculitides as lupus erythematosus, rheumatoid arthritis, and polyarthritis nodosa should be sought. Although none of these risk factors is in itself diagnostic of coronary artery disease, the more of them are present, the greater the likelihood of the diagnosis.
 

Treatment
A. GENERAL APPROACH

Because myocardial ischemia is produced by an imbalance between myocardial oxygen supply and demand, in general, treatment consists of increasing supply or reducing demand—or both. Heart rate is a major determinant of myocardial oxygen demand, and attention to its control is imperative. Any treatment that accelerates heart rate is generally not going to be efficacious in preventing myocardial ischemia. Therefore, care must be taken with potent vasodilator drugs, which may lower blood pressure and induce reflex tachycardia. Furthermore, because most coronary blood flow occurs during diastole, the longer the diastole, the greater the coronary blood flow; and the faster the heart rate, the shorter the diastole.
Blood pressure is another important factor: Increases in blood pressure raise myocardial oxygen demand by elevating left ventricular wall tension, and blood pressure is the driving pressure for coronary perfusion. A critical blood pressure is required that does not excessively increase demand, yet keeps coronary perfusion pressure across stenotic lesions optimal. Unfortunately, it is difficult to tell in any given patient what this level of blood pressure should be, and a trial-and-error approach is often needed to achieve the right balance. Consequently, it is prudent to reduce blood pressure when it is very high, and it may be important to allow it to increase when it is very low. It is not uncommon to encounter patients whose myocardial ischemia has been so vigorously treated with a combination of pharmacologic agents that their blood pressure is too low to be compatible with adequate coronary perfusion. In such patients, withholding some of their medications may actually improve their symptoms. Although myocardial contractility and left ventricular volume also contribute to myocardial oxygen demand, they are less important than heart rate and blood pressure. Myocardial contractility usually parallels heart rate. Attention should be paid to reducing left ventricular volume in anyone with a dilated heart, but not at the expense of excessive hypotension or tachycardia because these factors are more important than volume for determining myocardial oxygen demand.
It is important to eliminate any aggravating factors that could increase myocardial oxygen demand or reduce coronary artery flow (Table 3–3). Hypertension and tachyarrhythmias are obvious factors that need to be controlled. Thyrotoxicosis leads to tachycardia and increases in myocardial oxygen demand. Anemia is a common problem that increases myocardial oxygen demand because of reflex tachycardia; it reduces oxygen supply by decreasing the oxygen-carrying capacity of the blood. Similarly, hypoxia from pulmonary disease reduces oxygen delivery to the heart. Heart failure increases angina because it often results in left ventricular dilatation, which increases wall stress, and in excess catecholamine tone, which increases contractility and produces tachycardia.
 

Prognosis
There are two major determinants of prognosis in patients with chronic ischemic heart disease. The first is the clinical status of the patient, which can be semiquantitated by the Canadian Cardiovascular Society's angina functional class system. In this system, class I is asymptomatic, II is angina with heavy exertion, III is angina with mild-to-moderate exertion, and class IV comprises patients who cannot perform their daily activities without getting angina or who are actually experiencing angina decubitus. The higher the Canadian class, the worse the prognosis. Prognosis can also be determined by exercise testing. If patients can exercise more than 9 min or into stage IV of the modified Bruce protocol, their prognosis is excellent. The presence of either angina or significant ischemic ST depression on the exercise test indicates a poor prognosis. In addition, when using perfusion scanning, the more extensive the perfusion abnormalities with exercise, the worse the prognosis. Left ventricular dysfunction with exercise, evidenced by a decrease or a failure to increase the ejection fraction on left ventricular imaging, or by significant lung uptake of thallium during stress perfusion imaging, also connotes a worse prognosis. Perhaps the most powerful predictor for future mortality is the resting left ventricular ejection fraction; values of less than 50% are associated with an exponential increase in mortality.
A second prognostic system is based solely on coronary anatomy. The more vessels involved, and the more severely they are involved, the worse the prognosis. This observation has formed the anatomic basis for revascularization in patients with coronary artery disease. Although this approach has some appeal, it has never been proven that revascularization in asymptomatic patients improves their prognosis. Even in patients with left main and severe three-vessel disease, proof is lacking that prophylactic revascularization is of any value if the patients are asymptomatic. Theoretical considerations suggest that ischemia—even in the absence of angina—that can be demonstrated by stress testing or ambulatory ECG recordings would support a decision to revascularize based on anatomy and the presence of ischemia. Although this seems like a much stronger case for revascularization in an asymptomatic patient, such treatment has not been proven efficacious in clinical trials.
The simplicity of the coronary anatomy approach to prognosis has resulted in considerable clinical data on the longevity of patients with chronic ischemic heart disease. Patients with one-vessel coronary artery disease have about a 3% per year mortality rate, less if the vessel is the right or circumflex coronary artery and somewhat more if it is the left anterior descending artery. Patients with two-vessel disease have a 5% or 6% mortality rate per year; in patients with three-vessel disease, this increases to 6–8% a year. Patients with left main disease, with or without other coronary occlusions, have about an 8–12% yearly mortality rate. Similar data do not exist for the clinical classification of patients because of the complexities of determining risk by this approach. A positive treadmill exercise test, at a low workload, for either angina or ischemic ST changes connotes a yearly mortality rate of 5%. This is less if the patient exercised a long time and had good left ventricular function and no previous myocardial infarction. It is worse if the patient exercised only a very short time on the treadmill and had evidence of left ventricular dysfunction or a prior myocardial infarction. How much modern pharmacologic and revascularization therapy can influence these prognostic figures is unclear at present.