- Clinical science
Coronary heart disease (CHD) refers to a mismatch between myocardial oxygen supply and demand. Atherosclerosis is the most important cause. Atherosclerotic changes in coronary vessel walls lead to a narrowing of the lumen and prevent vessels from dilating. As a result, an increase in oxygen demand (e.g., during physical activity) can no longer be satisfied and/or myocardial perfusion at rest is insufficient. Acute retrosternal chest pain (angina) is the cardinal symptom of CHD. Other symptoms include dyspnea, dizziness, anxiety and nausea. If ischemia is severe, myocardial infarction can occur. Coronary heart disease is diagnosed via a cardiac stress test (possibly provoking symptoms and instrumental findings) and/or coronary catheterization (e.g., measurement of coronary blood flow). Management of CHD involves primary and secondary prevention of atherosclerosis (e.g., weight reduction), antianginal treatment (e.g., beta blockers) and, in some cases, revascularization (e.g., PCTA).
- Lifetime risk of coronary heart disease
- Age 40: 49% in men and 32% in women
- Age 75: 35% in men and 24% in women
- Cardiovascular disease is the leading cause of death in the US and the world.
Epidemiological data refers to the US, unless otherwise specified.
Plaque formation and coronary artery stenosis
- For plaque formation, see .
- Stable atherosclerotic plaque → vascular stenosis → increased resistance to blood flow in the coronary arteries → decreased myocardial blood flow → oxygen supply-demand mismatch → myocardial ischemia
- The extent of coronary stenosis determines the severity of the oxygen supply-demand mismatch and, thus, the severity of myocardial ischemia.
- Severe ischemia results in myocardial infarction (see acute coronary syndrome for details).
Coronary flow reserve (CFR): the difference between maximum coronary blood flow and coronary flow at rest; a measure of the ability of the coronary capillaries to dilate and increase blood flow to the myocardium.
- In healthy individuals, the CFR can be up to 4 times higher on exertion than at rest.
- CFR is reduced in individuals with CAD due to vascular stenosis and reduced vascular compliance.
Myocardial oxygen supply-demand mismatch
- Definition: mismatch between the amount of oxygen the myocardium receives and the amount it requires
- Factors reducing oxygen supply
- Factors increasing oxygen demand
An increased heart rate reduces oxygen supply and increases oxygen demand!
Effect of vascular stenosis on resistance to blood flow
- The resistance to blood flow within the coronary arteries is calculated using the Poiseuille equation: R = 8Lη/(πr4), where R = resistance to flow, L = length of the vessel, η = viscosity of blood, and r = radius of the vessel.
- Provided the length of the vessel and viscosity of blood remain constant, the degree of resistance can be calculated using the simplified formula: R ≈ 1/r4
Reversible ischemia: Tissue is ischemic but not irreversibly dead and, therefore, still potentially salvageable.
- Myocardial stunning: acutely ischemic myocardial segments with transiently impaired but completely reversible contractility
- Hibernating myocardium: a state in which myocardial tissue has persistently impaired contractility due to repetitive or persistent ischemia
- Irreversible ischemia: tissue necrosis (myocardial scars)
- Definition: a phenomenon of vasodilator-induced alteration of coronary blood flow in patients with coronary atherosclerosis resulting in myocardial ischemia and symptoms of angina
- Long-standing CAD requires maximal coronary arterial dilation distal to the stenosis to maintain normal myocardial function.
- In CAD, the affected coronary artery is maximally dilated distal to the stenosis to compensate for the reduced blood flow
- If a vasodilator (e.g., dipyridamole) is administered, the subsequent vasodilation of healthy vessels causes these to “steal blood from the stenotic blood vessels, resulting in poststenotic myocardial ischemia
Clinical relevance: coronary steal is the underlying mechanism of
- Administration of vasodilators (e.g., dipyridamole) → coronary vasodilation → decreased hydrostatic pressure in the normal coronary arteries → blood shunting back to well-perfused myocardium → decreased flow to the ischemic myocardium → myocardial ischemia downstream to the pathologically dilated vessels → angina pectoris and/or ECG changes
- Typically retrosternal chest pain or pressure
- Dizziness, palpitations
- Restlessness, anxiety
- Autonomic symptoms (e.g., diaphoresis, nausea, vomiting, syncope)
- Symptoms are reproducible/predictable
- Complaints often subside within minutes; , with rest or after administration of nitroglycerin
- Mental or physical stress
- Exposure to cold
- Symptoms are not reproducible/predictable
- Usually occurs at rest or with minimal exertion and is usually not relieved by rest or nitroglycerin
- Every new-onset angina
- Severe, persistent, and/or worsening angina (crescendo angina)
- Increasing intensity, frequency, or duration in a patient with a known stable angina
- Angina caused by transient coronary spasms (usually occurring close to areas of coronary stenosis)
- Unrelated to exertion and may even occur at rest (classically at night)
- Etiology: e.g., cigarette smoking, use of stimulants (e.g., cocaine, amphetamines) or sumatriptan, alcohol, stress, hyperventilation, exposure to cold
- Epidemiology: average onset around 50 years
- The five-year survival rate is > 90% (with treatment).
- Persistence of symptoms is common.
- The five-year survival rate is > 90% (with treatment).
Patient history and physical exam
- History of recurrent angina episodes
- Signs of atherosclerotic vessel disease (e.g., absent foot pulses, carotid bruit) → see also
- Best initial test for both types of angina (and other types of chest pain)
- Usually normal in stable angina
- Treat as unstable angina if abnormalities (of the ST segment or the T wave) occur during an episode of chest pain
Choosing the most appropriate provocation and detection methods
- Able to exercise (and no contraindications for exercise testing): exercise stress test
- Unable to exercise (and no contraindications to pharmacologic testing): pharmacologic stress test
- Example: In a 75-year-old patient with acute aortic dissection, exercise testing would be contraindicated. If he also has atrial fibrillation, imaging would be indicated to monitor the test. Therefore, a pharmacologic stress test with either echocardiography or scintigraphy would be indicated.
Cardiac exercise stress test
- The patient exercises until the target heart rate is achieved (e.g., on a treadmill).
- Acute myocardial infarction with elevated troponin levels and/or ST elevations (in the past 2 days)
- Unstable angina pectoris or ST depressions at rest
- Decompensated heart failure or severe symptomatic stenosis of one or more heart valves
- Acute endocarditis, myocarditis, or pericarditis
- Hemodynamically significant arrhythmias
- Acute thromboembolic disease
- Acute aortic dissection
- Mental or physical impairment to exercise
Cardiac pharmacological stress test
- IV administration of positive inotropic/chronotropic substances (e.g., dobutamine) or vasodilators (e.g., dipyridamole or adenosine) to simulate the effect of exercise on the myocardium
- Adenosine, dipyridamole:
- If cardiac stress test is done for primary diagnosis, withhold the following:
- If cardiac stress test is done for treatment evaluation, medication can be continued.
Findings in stress-induced ischemia
- Clinical findings: If one of the following symptoms occurs, the exercise stress should be stopped.
- The goal is to distinguish between:
- Irreversible ischemia: necrosis (myocardial scars)
Reversible ischemia: tissue that is ischemic (but not yet irreversibly dead) and therefore still potentially salvageable
- Myocardial stunning: acutely ischemic myocardial segments that demonstrate transiently impaired contractility that is completely reversible
- Hibernating myocardium: persistently impaired myocardial contractility that is partially or completely reversible when adequate oxygen supply is restored (e.g., after angioplasty or CABG)
- Radionuclide myocardial perfusion imaging
- The goal is to distinguish between:
- Persistent symptoms of angina despite appropriate therapy or
- Pathological result of the non-invasive examination or
- Noninvasive procedure with ambiguous results and high clinical suspicion of CHD
- Gold standard of CHD diagnosis
- Holter monitoring: can detect silent ischemia and arrhythmias and be used to evaluate heart rate variability and pacemaker/ICD function
- Coronary magnetic resonance imaging (CMRI) or coronary computed tomography angiography (CCTA)
- See .
The differential diagnoses listed here are not exhaustive.
- All patients: risk factor reduction and antiplatelet drugs; see “Prevention” below
- Mild CHD: pharmacologic therapy
- Moderate CHD; : consider coronary angiography and percutaneous transluminal coronary angioplasty (PTCA)/percutaneous coronary intervention (PCI)
- Severe CHD: coronary angiography and revascularization or coronary artery bypass grafting
- Calcium channel blockers (CCBs): indicated if there are contraindications to beta-blockers or in addition to beta-blockers (if angina or hypertension persist)
Ranolazine: indicated in stable angina that is refractory to first-line treatment
- Two mechanisms of action to reduce myocardial oxygen demand: 1) inhibit late phase sodium influx into cardiac myocytes → reduced calcium flux (via sodium-calcium channel pump) → reduced wall stress and oxygen demand; and 2) decreased rate of fatty acid beta oxidation (aerobic process) with simultaneous increase in glycolysis (anaerobic process).
- Combination therapy: indicated if angina persists with monotherapy
- Prognostic factors
- Stable angina
Prevention of atherosclerosis
Special considerations in coronary heart disease
- Antiplatelet drugs indicated in all patients: aspirin; or clopidogrel (if aspirin/ASA is contraindicated) → ↓ risk of infarction, ↓ morbidity
- Treating arterial hypertension
- Reduce blood pressure to < 140/90 mm Hg in cases of low/moderate risk and to < 130/80 mm Hg in high-risk patients
- Beta-blockers are the first-line therapy for CHD combined with arterial hypertension.
- ACE-inhibitors patients post-MI, especially those with left ventricular systolic dysfunction.
- Calcium channel blockers (for indications, see “Antianginal therapy” above)
- HbA1c of 6.5–7%
- Risk-adjusted LDL values: see for details