Medical Care: The goals of management of myocardial ischemia are to relieve symptoms and to prevent future fatal and nonfatal acute coronary syndromes such as UA/NSTEMI, STEMI, and sudden cardiac death.
Current understanding of myocardial ischemia suggests that the favored management approach is to appropriately and aggressively pursue all causes of myocardial ischemia and to appropriately treat all reversible causes until clinical and/or perfusion studies confirm that the myocardial ischemia is maximally reduced or eliminated.
Risk-factor modification is extremely important in the reduction and alleviation of myocardial ischemia. Indeed, medical therapy for risk factor reduction—particularly the use of statins, angiotensin-converting enzyme (ACE) inhibitors, aspirin, and beta-blockers (see below)—may reduce the risk of future cardiac events to an even greater degree than revascularization approaches. Elimination of preventable risk factors of CAD, such as smoking, obesity, and sedentary lifestyle—as well as satisfactory control of risk factors such as hypertension, diabetes, and hyperlipidemia—are key to the management of myocardial ischemia. All evidence suggests that the antianginal medications used in treatment of angina pectoris are equally effective in treatment of both symptomatic and asymptomatic myocardial ischemia.
Pharmacologic treatment of CAD can be divided into agents that prolong survival (eg, aspirin, statin drugs, ACE inhibitors, beta-blockers) and those that treat symptoms (eg, calcium channel blockers, nitrates).
Hypertension
Treatment of hypertension to satisfactory endpoints of systolic blood pressure of less than 130 mm Hg and diastolic blood pressure of less than 85 mm Hg is strongly recommended.
In patients with angina pectoris, the first-line agents are beta-adrenergic blocking agents such as metoprolol (Toprol, Lopressor), atenolol (Tenormin), or propranolol (Inderal), since they also reduce myocardial oxygen demand by reducing heart rate, contractility, and wall stress, and/or ACE inhibitors, since they retard progression of CAD.
Other antihypertensive agents may be employed to achieve blood pressure goals in addition to beta-blockers or ACE inhibitors (or in place of beta-blockers or ACE inhibitors if contraindication or intolerance).
ACE inhibitors and beta-blockers are particularly useful in treating hypertension in patients with CAD, although guidelines from the Joint National Committee for the Treatment of Hypertension also advocate the use of diuretics and other agents (see Hypertension).
Hyperlipidemia
The statins, such as atorvastatin (Lipitor), simvastatin (Zocor), pravastatin (Pravachol), lovastatin (Mevacor, Altocor), and fluvastatin (Lescol) are the first-line (and most popular) agents in the treatment of hyperlipidemias. Their use has led to rapid and significant improvement in endothelium-dependent dilation of coronary and peripheral arteries in patients with hyperlipidemia.
The statins have the advantage of stabilizing atheromatous plaques in coronary arteries and reduce acute coronary syndromes by this mechanism. Growing evidence also indicates that they may contribute to regression of coronary atherosclerosis, thereby reducing the frequency of and/or propensity for myocardial ischemia in patients with CAD.
Numerous studies have demonstrated that statins are effective in both secondary and primary prevention of MI and cardiac death, even in individuals with only minimally elevated LDL cholesterol (>100 mg/dL).
Cholesterol-lowering agents markedly reduce evidence of myocardial ischemia on ambulatory ECG monitoring in patients with stable coronary disease and hypercholesterolemia over a period of 4-6 months.
Antianginal therapy is the cornerstone of medical treatment in both patients with symptomatic and those with asymptomatic myocardial ischemia. Beta-blockers, as a single agent, are the preferred agents, provided no absolute contraindication to their use exists. Calcium channel antagonists are suitable alternatives, as well as effective agents in combination with beta-blockers, particularly such dihydropyridine agents as nifedipine, felodipine, and amlodipine. Care must be taken in the use of nondihydropyridine calcium channel antagonists. Avoid their use in patients with depressed LV function. Long-acting nitrates are effective in treatment of myocardial ischemia and are frequently used in combination with both beta-blockers and calcium channel antagonists. Short-acting nitroglycerin is the agent of choice in treatment of acute symptomatic myocardial ischemia. For further details of the antianginals, see Medications.
Antiplatelet therapy, with aspirin, clopidogrel (Plavix), ticlopidine (Ticlid), or dipyridamole (Persantine), is useful in both prevention and treatment of acute coronary syndromes from ruptured coronary plaques and subsequent thrombus formation. Of these, aspirin is most effective in reducing risk for MI, stroke, and cardiac death, while combinations of aspirin and clopidogrel are useful after coronary stenting and in other circumstances. Intravenous glycoprotein IIb/IIIa inhibitors, such as abciximab (ReoPro) and eptifibatide (Integrillin), are useful in patients with recurrent UA/NSTEMI, particularly in the subset of patients who undergo immediate PCI such as coronary angioplasty.
Antithrombin therapy with standard or low molecular weight heparin is useful in patients with UA/NSTEMI as well.
Treatment of reversible noncardiac causes of myocardial ischemia is important in improving myocardial oxygen supply (eg, anemia) and in reducing myocardial oxygen demand (eg, thyrotoxicosis).
Surgical Care:
Percutaneous coronary interventions
Percutaneous transluminal coronary angioplasty (PTCA), with or without stenting
Brachytherapy - Intracoronary radiation therapy with either gamma- or beta-ray devices
Coronary atherectomy
Ablative laser-assisted angioplasty
Catheter-based thrombolysis and mechanical thrombectomy
Percutaneous valvuloplasty - For patients with mitral or aortic stenosis as the cause of myocardial ischemia/heart failure
Coronary artery bypass surgery
Open heart surgery with use of bypass pump
Beating heart surgery
Keyhole or minimal incision coronary bypass (MIDCAB)
Bypasses using arterial conduits
Surgical transmyocardial laser revascularization (TMLR)/percutaneous transmyocardial laser revascularization (PTMLR)
Ileal bypass surgery
Miscellaneous therapies - Chelation therapy, EDTA, hydrogen peroxide
Plethysmography/extracorporeal counterpulsation (ECCP) for angina pectoris
Intraaortic balloon counterpulsation
Since the 1980s, intraaortic balloon counterpulsation (IABCP) has been increasingly used in various clinical situations as a lifesaving intervention to attain hemodynamic stabilization prior to definite therapy.
Diastolic augmentation enhances perfusion of the coronary circulation and carotid arteries. The reduction in end-diastolic pressure decreases aortic impedance (afterload) and augments systole.
IABCP reduces aortic impedance and systolic pressure, leading to a 15-25% reduction in LV wall stress. This level of afterload reduction improves LV volume, LV emptying, and myocardial oxygen consumption.
Diastolic aortic pressure augmentation increases myocardial perfusion and coronary blood flow. The effects on coronary blood flow are variable, but the boost generally ranges from 10-20% in ischemic territories.
IABCP can decrease LV filling pressures by 20-25% and can improve cardiac output by 20% in patients with cardiogenic shock; therefore, IABCP reduces myocardial oxygen demand significantly, although the additional beneficial effect of increased oxygen supply to the myocardium may occur in some clinical situations.
Indications
IABCP is effective in providing temporary support to patients in cardiogenic shock while definitive therapies such as angioplasty or cardiac bypass surgery are undertaken. At most institutions, IABCP is considered to be a bridge to a definitive revascularization procedure or to implementation of an LV assist device.
IABCP is effective in hemodynamically stabilizing patients with UA refractory to medical therapy prior to a definitive revascularization procedure.
IABCP may be a lifesaving intervention in patients with acute mitral regurgitation secondary to papillary muscle ischemia, infarction, and other causes such as infectious endocarditis or myxomatous degeneration. IABCP reduces afterload (thereby reducing severity of mitral regurgitation), enhances forward cardiac output, reduces left atrial pressure, and improves pulmonary edema.
IABCP is used to stabilize patients who are hemodynamically unstable, which allows time to plan the definitive surgical procedure.
IABCP can provide hemodynamic support in the perioperative and postoperative periods.
Contraindications
The absolute contraindications for IABCP are aortic dissection, severe aortic regurgitation, presence of a large arteriovenous shunt, and severe coagulopathy.
The relative contraindications are severe peripheral vascular disease, recent thrombolytic therapy, and bleeding diathesis.
Complications
IABCP can cause several complications that should be monitored while the patient is maintained on IABCP support. Generally, platelet count is reduced mildly; however, it usually does not fall below 100 X 103/mL.
Complications may occur during cannulation of the femoral artery, including perforation, laceration, or dissection of the artery (1-6%). Thrombosis of the iliofemoral artery and distal emboli may occur (1-7%), and limb ischemia has been reported in as many as 40% of patients. The limb ischemia is reversible upon removal of the intraaortic balloon pump unless thrombosis develops, which requires embolectomy to save the limb.
Other complications are localized bleeding (3-5%), infection (2-4%), thrombocytopenia (<1%), and intestinal ischemia (<1%).
The risk of these complications can be lessened by avoiding long-term use of IABCP. In most patients with myocardial ischemia, limit use of IABCP to the time necessary to perform definitive (percutaneous or surgical) revascularization.