Ischemic Heart Disease

Introduction

Ischemic heart disease (IHD) is defined as lack of oxygen and decreased or no blood flow to the myocardium resulting from coronary artery narrowing or obstruction. It may present as acute coronary syndrome (ACS), which includes unstable angina and non–ST-segment elevation (NSTE) or ST-segment elevation (STE) myocardial infarction (MI), chronic stable exertional angina, ischemia without symptoms, or ischemia due to coronary artery vasospasm (variant or Prinzmetal angina).

CLINICAL PRESENTATION

Many ischemic episodes are asymptomatic (silent ischemia). Patients often have a reproducible pattern of pain or other symptoms that appear after a specific amount of exertion. Increased symptom frequency, severity, or duration, and symptoms at rest suggest an unstable pattern that requires immediate medical evaluation.

• Symptoms may include a sensation of pressure or burning over the sternum or near it, which often radiates to the left jaw, shoulder, and arm. Chest tightness and shortness of breath may also occur. The sensation usually lasts from 30 seconds to 30 minutes.
• Precipitating factors include exercise, cold environment, walking after a meal, emotional upset, fright, anger, and coitus. Relief occurs with rest and within 45 seconds to 5 minutes of taking nitroglycerin.
• Patients with variant (Prinzmetal) angina secondary to coronary spasm are more likely to experience pain at rest and in the early morning hours. Pain is not usually brought on by exertion or emotional stress or relieved by rest; the electrocardiogram (ECG) pattern demonstrates current injury with ST-segment elevation rather than depression.
• Unstable angina is stratified into categories of low, intermediate, or high risk for short-term death or nonfatal MI. Features of high-risk unstable angina include: (1) accelerating tempo of ischemic symptoms in the preceding 48 hours; (2) pain at rest lasting more than 20 minutes; (3) age older than 75 years; (4) ST-segment changes; and (5) clinical findings of pulmonary edema, mitral regurgitation, S3 , rales, hypotension, bradycardia, or tachycardia.
• Episodes of ischemia may also be painless, or “silent,” perhaps due to a higher threshold and tolerance for pain than in patients who have pain more frequently

DIAGNOSIS

Obtain medical history to identify the nature or quality of chest pain, precipitating factors, duration, pain radiation, and response to nitroglycerin or rest. Ischemic chest pain may resemble pain from noncardiac sources, and diagnosis of anginal pain may be difficult based on history alone.

• Ask the patient about personal risk factors for coronary heart disease (CHD), including smoking, hypertension, and diabetes mellitus.
• Obtain family history that includes information about premature CHD, hypertension, lipid disorders, and diabetes mellitus.
• Findings on cardiac examination may include abnormal precordial systolic bulge, decreased intensity of S1 , paradoxical splitting of S2 , presence of S3 or S4 , apical systolic murmur, and diastolic murmur.
• Laboratory tests: hemoglobin, fasting glucose (to exclude diabetes), and fasting lipid panel. High-sensitivity C-reactive protein (hsCRP); homocysteine level; evidence of Chlamydia infection; and elevations in lipoprotein (a), fibrinogen, and plasminogen activator inhibitor may be helpful. Cardiac enzymes are normal instable angina. Troponin T or I, myoglobin, and creatinine kinase myocardial band (CK-MB) may be elevated in unstable angina.
• Resting ECG is normal in about half of patients with angina who are not experiencing acute ischemia. Typical ST–T-wave changes include depression, T-wave inversion, and ST-segment elevation. Variant angina is associated with ST-segment elevation, whereas silent ischemia may produce elevation or depression. Significant ischemia is associated with ST-segment depression greater than 2 mm, exertional hypotension, and reduced exercise tolerance.
• Exercise tolerance (stress) testing (ETT), thallium myocardial perfusion scintigraphy, radionuclide angiocardiography, ultrarapid computed tomography, and coronary angiography may be performed in certain circumstances. Obtain a chest radiograph if the patient has HF symptoms.

TREATMENT

Goals of Treatment: Short-term goals are to reduce or prevent anginal symptoms that limit exercise capability and impair quality of life. Long-term goals are to prevent CHD events such as MI, arrhythmias, and HF and to extend the patient’s life

PHARMACOLOGIC THERAPY

β-Adrenergic Blockers

• Decreased HR, contractility, and blood pressure reduce MVo2 and oxygen demand in patients with effort-induced angina. β-Blockers do not improve oxygen supply, and, in certain instances, unopposed α-adrenergic stimulation may lead to coronary vasoconstriction.

Nitrates

The half-life of nitroglycerin is 1 to 5 minutes regardless of the route, hence the potential advantage of sustained-release and transdermal products. Isosorbide dinitrate (ISDN) is metabolized to ISMN. ISMN has a half-life of approximately 5 hours and may be given once or twice daily, depending on the product chosen.

Calcium Channel Blockers

• Direct actions include vasodilation of systemic arterioles and coronary arteries, leading to reduced arterial pressure and coronary vascular resistance, as well as depression of myocardial contractility and conduction velocity of the sinoatrial (SA) and atrioventricular (AV) nodes.

Ranolazine

• Ranolazine reduces calcium overload in ischemic myocytes through inhibition of the late sodium current
• Ranolazine is indicated for treatment of chronic angina. In controlled trials, it modestly improved exercise time by 15 to approximately 45 seconds compared with placebo