Angina pectoris

The cardinal symptom in patients with CHD is angina pectoris. It is usually manifested as precordial chest pain or tightness that is often triggered by physical exertion, emotional distress, or eating. Angina pectoris is usually due to atherosclerotic heart disease. Coronary vasospasm may occur at the site of a lesion or even in otherwise normal coronary arteries. Angina typically lasts 5–10 minutes and is usually relieved by rest, nitroglycerin, or both. Patients may present with pain radiating into other areas, including the jaw, arm, neck, shoulder, back, chest wall, or abdomen.

Often, angina is misinterpreted as indigestion or musculoskeletal pain. The level of physical activity that results in angina pectoris is clinically significant and is useful in determining the severity of CHD, as well as its treatment and prognosis. Because myocardial ischemia may be painless in diabetic patients and in women, the diagnosis is often delayed in these patients until the disease is more advanced. The pain associated with myocardial infarction is similar to that of angina but is usually more severe and more prolonged.

Stable angina pectoris Angina is considered stable if it responds to rest or nitroglycerin and if the patterns of frequency, ease of onset, duration, and response to medication have not changed substantially over 3 months.

Variant (Prinzmetal) angina Variant angina occurs at rest and is not related to physical exertion. The ST segment is elevated on electrocardiography during the anginal episodes, which are caused by coronary artery spasm. Underlying atherosclerosis is present in 60%–80% of cases, and thrombosis and occlusion may result during the episodes of coronary artery spasm.

Acute coronary syndrome

Acute coronary syndrome (ACS) comprises the spectrum of unstable cardiac ischemia, from unstable angina to acute MI. Plaque rupture is considered the common underlying event. Unstable angina and acute MI should be considered closely related events, clinically differentiated by the presence or absence of markers of myocardial injury. In 2007, a task force representing groups from the United States and Europe established a definition of MI; it includes the detection of cardiac biomarkers (eg, troponin), ischemia symptoms, electrocardiogram (ECG) changes indicating new ischemia, pathologic Q waves on ECG, and evidence of loss of viable myocardium or wall-motion abnormalities on imaging.

If an occlusive coronary thrombus persists, MI can result. The location and extent of the infarction depend on the anatomical distribution of the occluded vessel, the presence of additional stenotic lesions, and the adequacy of collateral circulation. If the patient has chest pain at rest, unstable angina is the diagnosis. If the ischemia is severe enough to cause myocardial necrosis, infarction results. Acute MI is further differentiated into non–ST-segment elevation MI (NSTEMI) and ST-segment elevation MI (STEMI). Typical findings used to differentiate between these include the following:

• Unstable angina (chest pain at rest). The ECG shows ST-segment depression and/or T-wave inversion. No cardiac biomarkers are detected, indicating the absence of myocardial necrosis.

• NSTEMI (subendocardial, nontransmural). The ECG shows ST-segment depression and/or T-wave inversion. Cardiac biomarkers are present. The MI may be considered incomplete; thus, patients may be more susceptible to reinfarction or extension. Aggressive workup and treatment are required to prevent progression to STEMI.

• STEMI. The ECG shows early ST-segment elevation (Figs 5-1, 5-2) and later Q waves. This condition involves full-thickness or nearly full-thickness necrosis of the ventricular wall. If the necrosis has not yet involved the full thickness of the ventricular wall, early reperfusion therapy is required to avoid progression to full-thickness necrosis.

Myocardial infarction may occur suddenly, without warning, in a previously asymptomatic patient or in a patient with stable or variant angina; MI may also follow a period of unstable angina. Patients commonly experience chest pain, nausea, vomiting, diaphoresis, weakness, anxiety, dyspnea, lightheadedness, and palpitations. However, nearly 25% of myocardial infarcts are painless. Symptoms may begin during or after exertion or at rest.

The clinical findings in MI vary and depend on the location and severity of the ischemia or injury. Approximately half of all infarctions involve the inferior myocardial wall, and most of the remaining half involve the anterior regions. Examination may reveal pallor, coolness of the extremities, low-grade fever, signs of pulmonary congestion and increased central venous pressure (if left ventricular dysfunction is present), an S3 or S4 gallop, an apical systolic murmur (caused by papillary muscle dysfunction), hypertension, or hypotension. The ECG may demonstrate a variety of ST-segment and T-wave changes and arrhythmias.

Approximately 60% of patients who die of cardiac disease die suddenly, before reaching the hospital. However, the prognosis for patients hospitalized with MI has become remarkably good. Some studies in which thrombolytic therapy or PCI was used reported a mortality rate in the range of 5%–8%. Mortality is affected by a wide variety of factors, such as the degree of heart failure, extent of myocardial damage, severity of the underlying atherosclerotic process, heart size, and previous ischemia.

Figure 5-1 Nomenclature of the deflections, intervals, and segments of the normal electrocardiogram (ECG).

(Courtesy of Petr Heřman.)

Figure 5-2 ST segment and T-wave abnormalities. The changes in an ECG during myocardial infarction (ie, ST elevation, QRS reduction, and inverted T waves) occur in specific leads that determine its site. In the meantime, reciprocal changes can be observed in the opposite site.

(Reproduced with permission from Fuster V, Walsh RA, Harrington RA, eds. Hurst’s The Heart. 13th ed. New York: McGraw-Hill; 2011.)

Immediate coronary angiography and primary PCI (including stenting) of the infarct-involved artery have been shown to be superior to thrombolysis when done promptly by experienced operators in high-volume centers. If the time from first medical contact to intervention (“door to balloon” time) is kept under 90 minutes, the outcome is improved and is superior to that of thrombolysis. This intervention, in conjunction with antiplatelet and anticoagulant therapy, is widely used in patients with acute MI.

The complications of MI depend on its severity and may include CHF (see the section Congestive Heart Failure), rupture of the ventricular wall, pericarditis, and arrhythmias. Regional and global ventricular contractile dysfunction may result in CHF or pulmonary edema. Mild to moderate heart failure occurs in nearly 50% of patients following MI. Some patients experience post-MI pericarditis, characterized by a pericardial friction rub 2–3 days after infarction. Injury along the conduction pathways of the atria or ventricles may lead to bradycardia, heart block, supraventricular tachycardias, or ventricular arrhythmias. Arrhythmias often exacerbate ischemic injury by reducing the perfusion pressure in the coronary arteries. Most acute deaths from MI are caused by arrhythmia.

• Thygesen K, Alpert JS, Jaffe AS, et al; Executive Group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018;72(18):2231–2264.

Sudden cardiac death

Sudden cardiac death (SCD) is defined as unexpected, nontraumatic death that occurs within 1 hour after onset of symptoms in clinically stable individuals. A disproportionate number of SCDs take place in the early morning hours. SCD is usually caused by a severe arrhythmia, such as ventricular tachycardia, ventricular fibrillation, profound bradycardia, or asystole. SCD may result from MI, occur during an episode of angina, or strike without warning in a patient with frequent arrhythmias secondary to underlying IHD or ventricular dysfunction. Other causes of SCD are Wolff-Parkinson-White syndrome, long QT syndrome, torsades de pointes, atrioventricular block, aortic stenosis, myocarditis, cardiomyopathy, ruptured or dissecting aortic aneurysm, and pulmonary embolism. An implantable cardioverter-defibrillator (ICD) is recommended for patients who have survived a cardiac arrest or an episode of hemodynamically unstable ventricular tachycardia and for patients with severe left ventricular dysfunction after MI.

Asymptomatic ischemic heart disease

Asymptomatic patients with CHD are at particular risk for unexpected MI, life-threatening arrhythmias, and SCD. Advanced CHD may develop in these patients, and they may experience multiple infarcts before the correct diagnosis is made and appropriate treatment is initiated. Older adults, women, and individuals with diabetes mellitus are more likely to have painless ischemia. Approximately 25% of MIs are asymptomatic, but they may be detected on a subsequent ECG. A patient who has unexplained dyspnea, weakness, arrhythmias, or poor exercise tolerance requires cardiac testing to evaluate for the presence of undiagnosed CHD.

Excerpted from BCSC 2020-2021 series: Section 1 - Update on General Medicine. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.