Overview of Coronary Artery Disease

Coronary atherosclerosis is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing 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 ). The degree of stenosis required to cause ischemia varies with oxygen demand.

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 including malignant ventricular arrhythmias, conduction defects, heart failure, and sudden death.

Coronary artery spasm is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow; symptomatic ischemia (variant angina Variant Angina Variant angina is angina pectoris secondary to epicardial coronary artery spasm. Symptoms include angina at rest and rarely with exertion. Diagnosis is by electrocardiography (ECG) and provocative... read more ) may result. Marked narrowing can trigger thrombus formation, causing infarction or life-threatening arrhythmia. Spasm can occur in arteries with or without atheroma.

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.

(See also Drugs for Acute Coronary Syndromes Drugs for Acute Coronary Syndromes 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 .)

Medical management of patients with CAD depends on symptoms, cardiac function, and presence of other disorders. Recommended therapy includes .

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.

PCI is indicated for patients with acute coronary syndrome 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) or with stable ischemic heart disease who have angina despite optimal medical therapy.

At first, PCI was done with balloon angioplasty alone. However, roughly 5 to 8% of patients developed abrupt vessel closure after balloon angioplasty, resulting in acute myocardial infarction and often requiring emergency bypass surgery (1 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 ). In addition, 30 to 40% of patients developed restenosis within 6 months, and 1 in 3 ultimately required repeat angioplasty or CABG. Insertion of a bare-metal stent after angioplasty reduced the rate of restenosis, but many patients still required repeat treatment.

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 ):

The best results are obtained when the newer antiplatelet drugs are begun before the procedure.

Glycoprotein IIb/IIIa inhibitors are no longer routinely used in stable patients (ie, no comorbidities, no acute coronary syndrome) having elective stent placement. They may be beneficial in some patients with an acute coronary syndrome but should not be considered routine. It is unclear whether it is beneficial to give glycoprotein IIb/IIIa inhibitors before arrival in the cardiac catheterization laboratory, but most national organizations do not recommend their use in this situation (3 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 ).

A statin is started after stent insertion, if one is not already being used because PCI by itself does not cure or prevent the progression of CAD. Statin therapy has been shown to improve long-term event-free survival (4 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 ). Patients who receive a statin before the procedure have a lower risk of periprocedural MI.

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.