It is sufficient to identify the combination of left heart failure (by symptoms, physical examination, and chest x-ray) and normal systolic function (by echocardiogram or radionuclide ventriculogram). One should also look for the more specific findings for some of the disease states causing diastolic dysfunction, such as Kussmaul’s sign seen in restrictive cardiomyopathy or the characteristic decrease in murmur intensity during Valsalva maneuver in hypertrophic obstructive cardiomyopathy. More sophisticated tests of diastolic function using echocardiography or radionuclide ventriculography have been described in research studies but are of limited usefulness in individual patients and may not be well done in all laboratories.
What drugs are used in patients with heart failure?
In patients with systolic dysfunction, treatment with angiotensin-converting enzyme (ACE) inhibitors should receive first consideration, since these agents decrease mortality. It is important to use the maximum tolerated dose. These drugs are almost always used in combination with a diuretic. In patients with left ventricular enlargement, especially if an S3 is present, digoxin is added. Although there are no definitive studies to support their use, most specialized centers use anticoagulants in patients with severe systolic dysfunction to decrease the risk of stroke from left ventricular thrombi.
In patients with diastolic dysfunction, treatment is aimed at the underlying cause, such as valve replacement in aortic stenosis. In hypertensive or obstructive disease states, (3-blockers or verapamil should receive first consideration.
If a patient’s symptoms of heart failure persist despite appropriate use of these medications, what can be done?
Patients who have unacceptable symptoms despite use of adequate doses of ACE inhibitors, diuretics, and digitalis should be considered for admission. Further adjustment of drug dosing based on data obtained from a pulmonary artery catheter is often useful. Short-term infusion of dobutamine for 48-72 hours has benefit that may last up to a month. When drug treatment fails, heart transplantation is an option in selected patients.
Are beta blockers useful in the treatment of heart failure?
Because the negative inotropic properties of beta blockers are so well known, it seems odd to suggest that they might be useful in the treatment of heart failure. Yet, over the past 20 years, a number of small-scale studies have done exactly that. Both laboratory and clinical studies have shown that advancing heart failure is accompanied by increasing levels of activation of the sympathetic nervous system. Although this activation starts as a consequence of the physiologic abnormalities in heart failure, it leads to excessive peripheral vasoconstriction which increases afterload and to down-regulation of cardiac (3-receptors. These latter two actions contribute to a downward spiral of declining contractility. Some have speculated that this spiraling might be interrupted by blockading the peripheral effects of catecholamines with (3-blockers.
For: In one recent study, 383 patients with heart failure were randomized to receive either placebo or a carefully titrated dose of metoprolol. After 12 months, fewer patients in the metoprolol group required heart transplantation than in the placebo group, but there was no difference between the two groups in mortality or in the combined endpoint of death or need for transplantation.
Against: Although some argue that a decrease in need for heart transplantation (as in the above study) is reason enough to initiate (3-blockade in all patients with heart failure, others argue that such a recommendation must be based on a decrease in mortality.
Discuss the incidence and mortality rate of infective endocarditis (IE).
Although the mortality rate of IE has declined from almost 100% to 5-15% with the use of antibiotics, the incidence probably has increased. The reason for this increase is multifactorial: an aging population, increased number of patients with prosthetic valves, adults surviving with congenital heart disease, improved detection, recurrence in survivors of endocarditis, virulence of pathogens, poor compliance or inadequate prophylaxis, and intravenous drug use. The majority of cases involve patients with prosthetic cardiac valves, users of illicit intravenous drugs, and patients with mitral valve prolapse or other nonrheumatic abnormalities. Underlying anatomy, clinical situation, and infecting organism serve as the basis for prognosis and management.