Use of invasive hemodynamic monitoring should be reserved for those patients with clear indications, including diagnosis of suspected left or right ventricular failure with hypotension and pulmonary edema, acute mitral regurgitation, acute ventricular septal defects, or persistent oliguria and azotemia in the patient with unclear volume status. Invasive monitoring may also be useful when initiating treatment with inotropic or vasocactive agents.
What techniques are used to risk stratify patients with myocardial infarction?
Postinfarction risk stratification and assessment of prognosis are important in planning long-term therapy. In patients with postinfarction angina, heart failure, or late arrhythmias, urgent angiography should be performed to evaluate the need for PTCA or CABG. In patients with uncomplicated myocardial infarction, noninvasive means may be used to assess ventricular function and residual ischemia, including a symptom-limited exercise test and assessment of left ventricular function by echocardiography or gated blood pool scan.
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Other tests available for special problems include exercise thallium testing, stress echocardiography, dipyridamole thallium scanning, positron emission tomography, and ambulatory Holter monitoring. These tests can be performed in most patients 1^4 weeks after myocardial infarction to determine high and low risk groups. High-risk groups are identified by low exercise capacity, hypotension, ST-segment depression at low heart rates, and angina during traditional exercise testing. Evidence of ischemia in addition to the infarction visualized on echocardiography or radionuclide imaging may also be useful in assessing risk after myocardial infarction. These principles should be applied to those who have received thrombolytic therapy as well as those who have had a non-Q-wave myocardial infarction. There is controversy surrounding the use of noninvasive tests for risk stratification following non-Q-wave infarctions, and some recommend routine angiography in all these patients.
What agents or interventions are used in secondary prevention of myocardial infarction?
Secondary prevention of myocardial infarction should focus on modification of risk factors. In particular, smoking cessation should be encouraged. Lipid-lowering agents in combination with diet modification in certain subsets of patients can reduce mortality by 20% and should be instituted in the appropriate settings. Exercise should be encouraged and supplemented by a rehabilitation program. |3-blockers have been extensively studied and, in the postinfarction patient with moderate to high risk, have been shown to reduce mortality and risk of reinfarction by as much as 33%. Aspirin decreases the rates of reinfarction and should be used in all postinfarction patients. Calcium channel blockers may have a role in secondary prevention of non-Q-wave infarctions, particularly reinfarction, but no mortality benefit has been shown. Angiotensin-converting enzyme (ACE) inhibitors decrease reinfarction rates and incidence of sudden death and improve mortality, and they should be standard in postinfarction patients with ejection fractions 40%, especially those with symptoms of heart failure.
Is there a role for free radical scavengers?
In animal models, free radical scavengers have been shown to limit reperfusion injury in myocardial infarction. Such drugs may have a role in the future, although currently none are approved for clinical use. Most recently, the use of vitamin E has been suggested to benefit patients in primary prevention of myocardial infarction, but further study is necessary.
What is ventricular remodeling?
Remodeling of the heart is defined as a change in the mass and shape of the heart in response to damage caused by myocardial infarction and is characterized by hypertrophy and progressive dilatation. Depending on the extent of damage, subsequent wall stress, and local tissue environment, remodeling may result in late pump failure, instability of electrical activity, and reinfarction. Factors that favorably modify this process include prevention of reinfarction, reperfusion, afterload reduction, and possibly prevention of reperfusion injury by free radicals. Therapy should aim to prevent complications of ventricular remodeling by ventricular unloading with ACE inhibitors and resolving chronic ischemia by PTCA or CABG.