Also called: CAD, Coronary arteriosclerosis, Coronary atherosclerosis, Coronary heart disease
Coronary artery disease (CAD) is the most common type of heart disease. It is the leading cause of death in the United States in both men and women. CAD happens when the arteries that supply blood to heart muscle become hardened and narrowed. This is due to the buildup of
cholesterol and other material, called plaque, on their inner walls. This buildup is called atherosclerosis. As it grows, less blood can flow through the arteries. As a result, the heart muscle can't get the blood or oxygen it needs. This can lead to chest pain (angina) or a
heart attack. Most heart attacks happen when a blood clot suddenly cuts off the hearts' blood supply, causing permanent heart damage. Over time, CAD can also weaken the heart muscle and contribute to heart failure and
arrhythmias. Heart failure means the heart can't pump blood well to the rest of the body. Arrhythmias are changes in the normal beating rhythm of the heart. NIH: National Heart, Lung, and Blood InstituteSummary
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- Coronary Artery Disease (American Academy of Family Physicians) Also in Spanish
- Coronary Artery Disease - Coronary Heart Disease (American Heart Association)
- What Is Coronary Heart Disease?
(National Heart, Lung, and Blood Institute) Also in Spanish
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Tests: MedlinePlus Health Topic (National Library of Medicine) Also in Spanish
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- Screening for Coronary Heart Disease with Electrocardiography (U.S. Preventive Services Task Force) - PDF
- Drug-Eluting Stents: Do They Increase Heart Attack Risk? (Mayo Foundation for Medical Education and Research) Also in Spanish
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Coronary artery disease (Medical Encyclopedia) Also in Spanish
- Coronary Arteries (Texas Heart Institute) Also in Spanish
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Works (National Heart, Lung, and Blood Institute) Also in Spanish
Coronary artery disease (CAD) involves impairment of blood flow through the coronary arteries, most commonly by atheromas. Clinical presentations include silent ischemia, angina
pectoris Angina Pectoris Angina pectoris is a clinical syndrome of precordial discomfort or pressure due to transient myocardial ischemia without infarction. It is typically precipitated by exertion or psychologic stress... read more ,
acute coronary syndromes
Overview of Acute Coronary Syndromes (ACS) Acute coronary syndromes result from acute obstruction of a coronary artery. Consequences depend on degree and location of obstruction and range from unstable angina to non–ST-segment elevation... read more
(unstable angina
Unstable Angina Unstable angina results from acute obstruction of a coronary artery without myocardial infarction. Symptoms include chest discomfort with or without dyspnea, nausea, and diaphoresis. Diagnosis... read more ,
myocardial infarction
Acute Myocardial Infarction (MI) Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. Symptoms include chest discomfort with or without dyspnea, nausea, and/or diaphoresis... read more
In high-income countries, coronary artery disease is the leading cause of death in both sexes, accounting for about one third of all deaths. Mortality rate among White men is about 1/10,000 at ages 25 to 34 and nearly 1/100 at ages 55 to 64. Mortality rate among White men aged 35 to 44 is 6.1 times that among age-matched White women. For unknown reasons, the sex difference is less marked in patients who are not White and in patients with diabetes mellitus. Mortality rate among women increases after menopause and, by age 75, equals or even exceeds that of men.
Usually, coronary artery disease is due to
Less often, coronary artery disease is due to
Rare causes include coronary artery embolism, dissection, aneurysm (eg, in
Kawasaki disease
Kawasaki Disease Kawasaki disease is a vasculitis, sometimes involving the coronary arteries, that tends to occur in infants and children between the ages of 1 year and 8 years. It is characterized by prolonged... read more
Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia. The consequences of acute ischemia, collectively
referred to as acute coronary syndromes
Overview of Acute Coronary Syndromes (ACS) Acute coronary syndromes result from acute obstruction of a coronary artery. Consequences depend on degree and location of obstruction and range from unstable angina to non–ST-segment elevation... read more (ACS), depend on the location
and degree of obstruction and range from unstable angina, non-ST elevation myocardial infarction (NSTEMI), to ST elevation myocardial infarction (STEMI), which can result in transmural infarction, and other
complications
Complications of Acute Coronary Syndromes Numerous complications can occur as a result of an acute coronary syndrome and increase morbidity and mortality. Complications can be roughly categorized as Electrical dysfunction (conduction... read more
In arteries without
atheroma, basal coronary artery tone is probably increased, and response to vasoconstricting stimuli is probably exaggerated. The exact mechanism is unclear but may involve endothelial cell abnormalities of nitric oxide production or an imbalance between endothelium-derived contracting and relaxing factors. In arteries with atheroma, the atheroma causes endothelial dysfunction, possibly resulting in local hypercontractility. Proposed
mechanisms include loss of sensitivity to intrinsic vasodilators (eg, acetylcholine) and increased production of vasoconstrictors (eg, angiotensin II, endothelin, leukotrienes, serotonin, thromboxane) in the area of the atheroma. Recurrent spasm may damage the intima, leading to atheroma formation.
Use of vasoconstricting drugs (eg, cocaine, nicotine) and emotional stress also can trigger coronary spasm.
Coronary artery dissection is a rare, non-traumatic tear in the coronary intima with creation of a false lumen. Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen sometimes causing coronary ischemia or infarction. Dissection may occur in atherosclerotic or non-atherosclerotic coronary arteries. Non-atherosclerotic dissection is more likely in pregnant or postpartum women and/or patients with fibromuscular dysplasia or other connective tissue disorders.
High blood levels of lipoprotein a
Low blood levels of high-density lipoprotein (HDL) cholesterol
Smoking
Obesity
Physical inactivity
High level of apoprotein B (apo B)
High blood levels of C-reactive protein (CRP)
Smoking may be a stronger predictor of myocardial infarction in women (especially those < 45). Genetic factors play a role, and several systemic disorders (eg, hypertension, hypothyroidism) and metabolic disorders (eg, hyperhomocysteinemia) contribute to risk. A high level of apo B may identify increased risk when total cholesterol or LDL level is normal.
High blood levels of C-reactive protein indicate plaque instability and inflammation and may be a stronger predictor of risk of ischemic events than high levels of LDL. High blood levels of triglycerides and insulin (reflecting insulin resistance) may be risk factors, but data are less clear. CAD risk is increased by smoking tobacco; by a diet high in fat and calories and low in phytochemicals (found in fruits and vegetables), fiber, and vitamins C, D, and E; by a diet relatively low in omega-3 (n-3) polyunsaturated fatty acids (PUFAs—at least in some people); and by poor stress management.
The right and left coronary arteries
arise from the right and left coronary sinuses in the root of the aorta just above the aortic valve orifice (see figure Arteries of the
heart Arteries of the heart
The left coronary artery begins as the left main artery and quickly divides into the left anterior descending (LAD), circumflex, and sometimes an intermediate artery (ramus intermedius). The LAD artery usually follows the anterior interventricular groove and, in some people, continues over the apex. This artery supplies the anterior septum (including the proximal conduction system) and the anterior free wall of the left ventricle (LV). The circumflex artery, which is usually smaller than the LAD artery, supplies the lateral LV free wall.
Most people have right dominance: The right coronary artery passes along the atrioventricular (AV) groove over the right side of the heart; it supplies the sinus node (in 55%), right ventricle, and usually the AV node and inferior myocardial wall. About 10 to 15% of people have left dominance: The circumflex artery is larger and continues along the posterior AV groove to supply the posterior wall and AV node.
Arteries of the heart
Medical therapy including antiplatelet drugs, lipid-lowering drugs (eg, statins), and beta-blockers
Percutaneous coronary intervention
For acute thrombosis, sometimes fibrinolytic drugs
Coronary artery bypass grafting
Medical management of patients with CAD depends on symptoms, cardiac function, and presence of other disorders. Recommended therapy includes .
Antiplatelet drugs to prevent clot formation
Statins to lower LDL cholesterol levels
Beta-blockers to reduce symptoms of angina
Antiplatelet drugs and statins improve short-term and long-term outcomes, probably by improving atheromatous plaque stability and endothelial function.
Beta-blockers reduce symptoms of angina by reducing heart rate and contractility and decreasing myocardial oxygen demand. Beta-blockers also reduce mortality post-infarction, especially in the presence of post-myocardial infarction (MI) LV dysfunction.
Calcium channel blockers are also helpful. They often are combined with beta-blockers in managing angina and hypertension but have not been proven to reduce mortality.
Nitrates modestly dilate coronary arteries and decrease venous return, decreasing cardiac work and relieving angina quickly. Longer acting nitrate formulations help decrease angina events but do not decrease mortality.
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are most effective at reducing mortality post MI in CAD patients with LV dysfunction.
Little evidence exists to guide therapy for patients with endothelial dysfunction. Treatment is generally similar to that for typical large-vessel atherosclerosis, but there is concern that use of beta-blockers may enhance endothelial dysfunction.
Drug-eluting stents, which release an antiproliferative drug (eg, everolimus, zotarolimus) over a period of several weeks, have reduced the rate of restenosis to < 10%.Most PCI is done with stents, and most stents used in the US are drug-eluting.
Patients without significant infarct or complications may quickly return to work and usual activities after stenting. However, cardiac rehabilitation is recommended for all patients.
In-stent thrombosis occurs because of the inherent thrombogenicity of metallic stents. Most cases occur within the first 24 to 48 hours. However, late stent thrombosis, occurring after 30 days and as late as ≥ 1 year (rarely), can occur with both bare-metal and drug-eluting stents, especially after cessation of antiplatelet therapy. Progressive endothelialization of
the bare-metal stent occurs within the first few months and reduces the risk of thrombosis. However, the antiproliferative drugs released by drug-eluting stents inhibit this process and prolong the risk of thrombosis. Thus, patients who undergo stent placement are treated with various
antiplatelet drugs
Antiplatelet Drugs Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications... read more . The current standard regimen for patients with
a bare-metal or drug-eluting stent consists of all of the following (2
Treatment references Coronary artery disease (CAD) involves impairment of blood flow through the coronary arteries, most commonly by atheromas. Clinical presentations include silent ischemia, angina pectoris, acute... read more
Intraprocedural anticoagulation with heparin or a similar agent (eg, bivalirudin, particularly for those at high risk of bleeding)
-
Aspirin given indefinitely
Clopidogrel, prasugrel, or ticagrelor for at least 6 to 12 months
The best results are obtained when the newer antiplatelet drugs are begun before the procedure.
Overall, risks of undergoing PCI are comparable to those of CABG. Mortality rate is < 1%; Q wave MI rate is < 2%. In < 1% of patients, intimal dissection causes obstruction requiring emergency CABG. Risk of stroke with PCI is clearly less than with CABG (0.34% vs 1.2%).
CABG uses arteries (eg, internal mammary, radial) whenever possible, and if necessary, sections of autologous veins (eg, saphenous) to bypass diseased segments of the coronary arteries. At 1 year, about 85% of venous bypass grafts are patent, and after 5 years, one third or more are completely blocked. However, after 10 years, as many as 97% of internal mammary artery grafts are patent. Arteries also hypertrophy to accommodate increased flow. CABG is superior to PCI in patients with diabetes and in patients with multivessel disease amenable to grafting.
Coronary artery bypass grafting is typically done during cardiopulmonary bypass with the heart stopped; a bypass machine pumps and oxygenates blood. Risks of the procedure include stroke and MI. For patients with a normal-sized heart, no history of MI, good ventricular function, and no additional risk factors, risk is < 5% for perioperative MI, 1 to 2% for stroke, and ≤ 1% for mortality; risk increases with age, poor LV function, and presence of underlying disease. Operative mortality rate is 3 to 5 times higher for a second bypass than for the first.
After cardiopulmonary bypass, about 25 to 30% of patients develop cognitive dysfunction or behavioral changes, possibly caused by microemboli originating in the bypass machine. Cognitive or behavioral changes are more prevalent in older patients, prompting suspicion that these changes are most likely due to diminished "neuronal reserve," making older patients more susceptible to minor injuries incurred during cardiopulmonary bypass. Dysfunction ranges from mild to severe and may persist for weeks to years. To minimize this risk, some centers use a beating heart technique (off-pump CABG, which uses no cardiopulmonary bypass), in which a device mechanically stabilizes the part of the heart upon which the surgeon is working. However, long-term studies have failed to demonstrate lasting benefits of this approach in comparison to conventional on-pump CABG.
CAD may progress despite bypass surgery. Postoperatively, the rate of proximal obstruction of bypassed vessels increases. Vein grafts become obstructed early if thrombi form and later (several years) if atherosclerosis causes slow degeneration of the intima and media. Aspirin prolongs vein graft patency. Continued smoking has a profound adverse effect on patency. After CABG, a statin should be started or continued at maximally tolerated doses.
1. Byrne RA, Joner M, and Kastrati A: Stent thrombosis and restenosis: what have we learned and where are we going? The Andreas Gruntzig Lecture ESC 2014. Eur Heart J 36(47):3320–3331, 2015. doi: 10.1093/eurheartj/ehv511
2. Lawton JS, Tamis-Holland JE, Bangalore S, et al: 2021 ACC/AHA/SCAI guideline for coronary artery revascularization: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol 79 (2): e21–e129, 2022. doi: 10.1016/j.jacc.2021.09.006
2. O'Gara PT, Kushner FG, Ascheim DD, et al: 2013 ACCF/AHA Guideline for the management of ST-elevation myocardial infarction. Circulation 127(4):e362–425, 2013. doi.org/10.1161/CIR.0b013e3182742cf6
3. Stone NJ, Robinson J, Lichtenstein AH, et al: 2013 ACC/AHA Guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults. Circulation 129: S1–S45, 2014. doi: 10.1161/01.cir.0000437738.63853.7a
Weight loss
Healthful diet
Regular exercise
Modification of serum lipid levels
Reduction of salt intake
Control of hypertension
Control of diabetes
Modification of serum lipid levels (particularly with statins) may slow or even partially reverse the progression of CAD. Treatment goals have been modified. Instead of trying to achieve specific target low density lipoprotein cholesterol (LDL) levels, patients are selected for treatment based on their risk of ASCVD. Lower risk patients with elevated LDL may not require statin treatment. Four higher risk patient groups have been identified in whom the benefit of statin therapy outweighs the risk of adverse events:
Patients with clinical ASCVD
Patients with LDL cholesterol ≥ 190 mg/dL (≥ 4.9 mmol/L)
Patients age 40 to 75 years with diabetes and LDL cholesterol levels of 70 to 189 mg/dL (1.8 to 4.9 mmol/L)
Patients age 40 to 75 years without diabetes and LDL cholesterol levels of 70 to 189 mg/dL (1.8 to 4.9 mmol/L) with ASCVD risk > 7.5%
Aspirin is not recommended for primary prevention of CAD in patients ≥ 60 years. It can be considered for patients aged 40 to 59 whose 10-year risk of cardiovascular disease exceeds 10%, but absolute benefit is likely to be small.
1. Arnett DK, Blumenthal RS, Albert MA, et al: 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol 74:1376–1414, 2019.
2. Whelton PB, Carey RM, Aronow WS, et al: ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol 71:e127–e248, 2018.
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