(Circulation. 2001;104:4.)
© 2001 American Heart Association, Inc.
Editorials |
From the Section of Cardiology, Rush-Presbyterian-St Lukes Medical Center, Chicago, Ill.
Correspondence to Joseph E. Parrillo, MD, the Section of Cardiology, Rush-Presbyterian-St Lukes Medical Center, 1653 W. Congress Parkway, Chicago, IL 60612. E-mail jparrill@rush.edu
Key Words: Editorials inflammation cardiomyopathy myocarditis immunohistochemistry heart failure
In patients presenting with congestive heart failure in the United States, approximately one-quarter have idiopathic dilated cardiomyopathy (IDC). IDC is thought to result from a number of mechanisms that injure the myocardium and lead to a common pathway of cardiac dilatation and heart failure. Known mechanisms of myocardial injury include alcohol, toxins, infections, cytotoxic chemotherapy, and metabolic abnormalities.1 Recent studies have highlighted important genetic links, suggesting that familial transmission is important in a subgroup of IDC patients. However, in most IDC patients, a cause cannot be determined.
Substantial animal experimental data has demonstrated a strong pathogenetic link between infectious agents (usually viruses) and subsequent immune-mediated damage to the myocardium resulting in IDC.2 3 Human studies have demonstrated a high prevalence of viral genome in the hearts of patients with IDC. Enteroviruses, adenovirus, influenza, HIV, and hepatitis C have been implicated in the pathogenesis of dilated cardiomyopathy and myocarditis. Much of the data suggests cell-mediated immune damage, although cytokines and antibodies have also been hypothesized to play a role.3 4
Patients with heart failure due to IDC should be treated
with conventional heart failure regimens, including diuretics,
angiotensin-converting enzyme (ACE) inhibitors,
digitalis, ß-blockers, vasodilators, aldosterone
antagonists, and other effective medications and
technology. However, the specific question for patients with an
inflammatory cardiomyopathy is whether a regimen
designed to reduce or eliminate inflammation would provide added
clinical benefit compared with conventional heart failure therapy. This
has been a difficult question to answer for several reasons. First, the
clinical presentation of inflammatory
cardiomyopathy is very
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