CLINICAL FORMS OF CAD

Many people who have atherosclerosis of the coronary arteries live their lives symptom-free. Other people develop symptoms and heart damage from atherosclerosis. The ischemic heart problems of atherosclerotic coronary artery disease fall into two general classes: chronic coronary syndromes and acute coronary syndromes.

Chronic Coronary Syndromes

Coronary artery disease is a chronic, progressive disease that is punctuated by sudden medical emergencies, the acute coronary syndromes. The long, chronic phases of the disease have two forms: stable angina and stable ischemic heart disease. When oxygen demand exceeds the ability of the coronary arteries to supply a sufficient amount of blood flow, myocardial ischemia is the result (Lewis et al., 2020).

STABLE ANGINA

Insufficient blood flow to the myocardium through coronary arteries whose internal diameter is narrowed or blocked causes chest pain. This may be brought about by exertion or stress. Such pain that occurs in a recognizable pattern and ceases upon rest or after anti-anginal medication is taken is known as stable angina (NHLBI, 2021b).

The occurrence of angina is influenced by the general tone of the sympathetic nervous system (which tends to be higher in the mornings) and by the demands of blood flow by the gastrointestinal tract after a meal. Although the symptoms of chronic stable angina are predictable, the amount of exercise or stress that will produce these symptoms varies during the course of a day.

The chest pain of chronic stable angina can also be brought on by any medical condition that increases the work of the heart, such as hypertension, aortic stenosis, systemic infections, or thyrotoxicosis. Likewise, conditions that reduce the oxygenation of the blood, such as COPD, anemia, or intolerance to high altitudes, can also cause angina.

STABLE ISCHEMIC HEART DISEASE

A second chronic syndrome is stable ischemic heart disease (or ischemic cardiomyopathy), in which years of damage from ischemia have weakened the heart muscle or myocardium sufficiently that it gradually fails. Stable ischemic heart disease is a major cause of heart failure in older adults.

Most patients with this condition have had acute myocardial infarctions in the past, although not all infarctions may have been symptomatic. In people who have had “silent” myocardial infarctions, heart failure from stable ischemic heart disease can be the first evidence of their coronary artery disease.

PROGNOSIS

A patient with any form of coronary artery disease has a higher chance of dying when the left ventricle of the heart has been weakened. Signs of a failing left ventricle include an enlarged heart, pulmonary edema, leg and ankle edema, jugular venous distension, or a third heart sound (S₃). Previous myocardial infarctions weaken the heart, so a history of past heart attacks also worsens a patient’s prognosis.

The CHA₂DS₂-VASc score stands for congestive heart failure, hypertension, age (>65 years = 1 point, >75 years = 2 points), diabetes, previous stroke/transient ischemic attack (2 points). VASc stands for vascular disease (peripheral arterial disease, previous myocardial infarction, aortic atheroma), and sex category (female gender) is also included in this scoring system. It was initially used for the assessment of the risk of thromboembolic events in patients with atrial fibrillation. Now it can be used to predict adverse outcomes in various cardiovascular diseases. When used to predict the occurrence of mortality in patients who have chronic stable angina with no history of myocardial infarction, the score has predicted a significant increase in the possibility in deaths specifically with diabetes, hypertension, and cardiac dysrhythmias (Healio.com, 2021).

Acute Coronary Syndromes

Sudden, unpredictable episodes of severe heart ischemia are called acute coronary syndromes. The ischemia is prolonged and not immediately reversible. The syndromes include sudden cardiac death, myocardial infarction, and unstable angina. Acute coronary syndromes result from a disruption of a formerly stable plaque that then causes ischemia severe enough to injure or kill muscle cells in the heart, infarction, or necrosis. This transpires when the ruptured plaque causes platelet aggregation (clumping) and thrombus (blood clot) formation, leading to partial or complete blockage of a blood vessel, possibly one of the coronary arteries. This condition is exacerbated by inflammation in the arteries (Lewis et al., 2020; Sole et al., 2021).

An acute coronary syndrome needs immediate treatment in a prepared emergency room. People with the highest risk of developing an acute coronary syndrome are those who already have serious cardiovascular disease or diabetes.

Similar to other types of heart disease, risk factors for acute coronary syndromes include:

• Older age (above 45 years for men and above 55 years for women)
• High blood pressure
• High blood cholesterol
• Cigarette smoking
• Physical inactivity
• Unhealthy diet
• Obesity or overweight
• Diabetes
• Family history of chest pain, heart disease, or stroke
• For women, a history of high blood pressure, preeclampsia, or diabetes during pregnancy
  (Mayo Clinic, 2021a)

SUDDEN CARDIAC DEATH

The most catastrophic of the acute coronary syndromes is sudden cardiac death (SCD), an unexpected death from cardiac causes that happens quickly, usually within an hour of the first symptoms. In adults SCD is usually associated with coronary artery disease (in 80% of all cases). The cause may also be due to such diverse diseases such as cardiac dysrhythmias, congenital coronary artery anomalies, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, dilated cardiomyopathy, and aortic valve stenosis.

One possible etiology involves considerable stimulation of the sympathetic nervous system’s stress response, leading to elevation of circulating catecholamines. This is a theoretical foundation for the SCD of young athletes in the absence of abnormal cardiac physiology or drug use (Yow et al., 2021).

The direct cause of these deaths is often fatal dysrhythmias, such as ventricular fibrillation. The dysrhythmias develop in cardiac cells that have been made overly excitable because of sudden ischemia from a blood clot or a vasospasm.

MYOCARDIAL INFARCTION

Myocardial infarctions are a type of acute coronary syndrome. MIs are caused by ruptured plaques, blood clots dislodged from atherosclerotic plaques, blunt trauma, or vasospasms. These cause an imbalance between oxygen demand and oxygen supply.

Myocardial infarctions occur when the plaque, blood clot, vasospasm, or some combination of these partially or completely obstruct a coronary artery or one of its major branches. If the obstruction persists for more than 20–30 minutes, some of the cell injury will be permanent. Contractility of the injured (infarcted) tissue becomes impaired, resulting in weakness of the cardiac pump; eventually, poor cardiac contractility becomes pump failure.

The area of infarction determines the portion of the cardiac pump that fails. The most damaging area of infarction is the left ventricle. The left ventricle is responsible for supplying the body with reoxygenated blood. An infarction in the myocardium of this ventricle is the most likely to cause pump or cardiac failure.

A myocardial infarction produces distinctive ECG changes. On a 12-lead ECG, an elevated ST segment indicates the corresponding coronary artery is completely obstructed, causing an MI. The ST segment elevation occurs only in the leads facing the area of infarction. This is referred to as an ST-segment elevated MI (STEMI). An MI caused by an incompletely blocked coronary artery does not cause the ST segment to be elevated on the ECG. This is referred to as a non-ST-segment elevated MI (NSTEMI).

The area of infarction is electrically unstable, causing dysrhythmias particular to that area. Infarcted ventricular tissue will cause ventricular dysrhythmias, which may be the most life-threatening. The area surrounding the infarcted tissue may still be ischemic. This ischemic tissue post infarction is referred to as the corona (crown). If the blocked coronary artery that caused the infarction continues to supply an inadequate amount of oxygenated blood to the area, the ischemic corona will quickly become infarcted. This can be prevented by reopening the blocked artery within 90 minutes of infarctions (see “Management of Acute CAD” later in this course). The larger the area of infarction, the more likely there will be dysrhythmias and ST segment changes (Ecgwaves, 2018; Lewis et al., 2020; Sole et al., 2021).

The symptoms of an MI may be different for women and therefore not as easy to assess. The American Heart Association stresses the importance of clinicians recognizing the difference in symptoms between the genders and the necessity of teaching these differences to patients and families.

UNSTABLE ANGINA

A third common acute coronary syndrome is unstable angina (UA). An episode of unstable angina includes symptoms of heart ischemia that do not go away after more than 10 minutes of rest or the use of nitrates, including sublingual nitroglycerin. Unstable angina occurs without a recognizable pattern. It is new in onset, unpredictable, and may also follow exercise or exertion (NHLBI, 2021b).

In unstable angina, the level of heart damage is much less than occurs in a myocardial infarction, but unstable angina often foreshadows a subsequent MI. Chronic stable angina may progress to UA. Women will see a physician more frequently than men for UA but may present with atypical symptoms such as fatigue, dyspnea, or indigestion rather than recognizable chest pain (Lewis et al., 2020).

PROGNOSIS

MIs are the cause of most deaths from coronary artery disease. The most common causes of mortality in the first 30 days are cardiogenic shock, sudden cardiac death, heart failure, mechanical cardiac complications, or another MI event.

In patients who survive to be admitted to the hospital, mortality rates have decreased from 5.3% to 3.8% due to recent developments in reperfusion techniques. Interventions such as reperfusion thrombolytic therapy, immediate use of aspirin, percutaneous intervention, statins, ACE inhibitors, and beta blockers account for the improvement in survival rates. Thirty-day post-MI mortality rates are 13% with medical therapy alone, including lifestyle changes such as smoking cessation, weight management, dietary changes, stress management, decreased alcohol consumption, exercise, and medications. The postmortality rates are 6%–7% with fibrinolytic therapy and 3%–5% with primary percutaneous coronary intervention within 2 hours of hospitalization (ACLS.com, 2020).

One method of predicting post-MI mortality is the TIMI score (see below).

Patients who survive an MI have a 14% chance of dying within one year. As a cause of death, MI mortality is 36% (Virani et al., 2021). Larger areas of heart injury lead to higher mortality rates. Approximately 50% of all patients with a myocardial infarction are rehospitalized within one year (ACLS.com, 2020).