The Pharmacologic Treatment of Myocardial Infarction
- Page 1: The Pathophysiology of Myocardial Infarction - Causes and Effects
- THIS PAGE: Rationale for Drug Therapy in Myocardial Infarction
- Page 3: Classes of Drugs Used to Treat Myocardial Infarction
Rationale for Drug Therapy in Myocardial Infarction
Rationale for Pharmacologic Treatment
of Myocardial Infarction
Improve Myocardial Oxygen
- Restore coronary blood flow
- dilate coronaries (inhibit vasospasm)
- coronary thrombolysis
- inhibit coagulation and platelet function
- Decreased myocardial oxygen consumption
↓ heart rate
- Analgesic drugs
Control Heart Rhythm
- Suppress arrhythmias
Inhibit Cardiac Remodeling
- Inhibit sympathetic activity
- Inhibit cardiac effects of angiotensin II
The most important goal of drug therapy early in the course of acute myocardial infarction is to improve the oxygen supply/demand ratio for the heart. The reduction in this ratio that occurs when coronary flow is compromised is the primary reason cardiac function is impaired, which leads to the clinical signs associated with myocardial infarction (see above). There are two strategies to improve the coronary supply/demand ratio, 1) restore normal coronary blood flow, and 2) decrease myocardial oxygen consumption.
Restoring Normal Coronary Blood Flow
The two major approaches for restoring normal cardiac perfusion are 1) percutaneous transluminal angioplasty (PCTA), often coupled with the placement of an intracoronary stent, and 2) administering a thrombolytic drug to induce clot lysis. Both of these procedures include anticoagulant drugs to inhibit new clot formation. Patients are also treated with anti-platelet drugs, which helps to prevent recurrent thrombosis. Because coronary vasospasm can also contribute to the reduced perfusion, vasodilators such as nitroglycerine are often given to prevent or reverse vasospasm.
Decreasing Myocardial Oxygen Consumption
Myocardial oxygen demand can be decreased by decreasing 1) heart rate, 2) contractility (inotropy), 3) ventricular afterload, and 4) ventricular preload. Because the heart is being stimulated by increased sympathetic activity and circulating catecholamines during infarction, drugs such as beta-blockers that inhibit sympathetic activity (sympatholytics) are commonly given. Systemic vasodilators are sometimes given to reduce systemic vascular resistance; however, care must be taken not to cause hypotension because this would reduce coronary perfusion pressure and blood flow. Finally, venous dilator drugs such as nitroglycerin are used to reduce ventricular preload, which reduces oxygen demand.
Pain management is an important consideration because pain and associated anxiety stimulates sympathetic activity, which can be deleterious to the heart. Therefore, analgesic drugs such as morphine are often given in the acute setting to reduce pain. Morphine also has other beneficial effects as a vasodilator. Antiarrhythmic drugs are administered particularly when their are serious ventricular rhythm disturbances. Diuretics may also be given depending on the degree of heart failure and fluid retention.
Because myocardial infarctions usually occur because of coronary artery disease, most patients will be placed on long-term anti-platelet therapy. Additionally, most post-infarct patients are treated with a beta-blocker because they have been shown to reduce cardiac remodeling and reduce mortality following infarction. Angiotensin converting enzyme inhibitors have a similar beneficial effect.