Display Settings:


Send to:

Choose Destination
See comment in PubMed Commons below
Schweiz Med Wochenschr. 1994 Jul 30;124(30):1326-33.

[Heart and AIDS].

[Article in German]

Author information

  • 1Departement Pathologie, Universität Zürich.


Although pulmonary and central nervous symptoms prevail before death, autopsy often reveals marked myocardial alterations in AIDS patients. This discrepancy prompted us to systematically study cardiac alterations in 100 sequential autopsies of patients who died of AIDS. We appraised the results in relation to changes noted in other organ systems, and compared our data with the AIDS-associated cardiac alterations described in the literature. Cardiac lesions were present in more than 50% of our patients, predominantly in the myocardium (47%). 38 patients displayed signs of active myocarditis. The endocardium and epicardium were secondarily involved, although drug abuse (23 patients) was the most important risk factor for HIV infection, after homosexuality (44%). The prevailing opportunistic agents were identical to those generally seen in AIDS patients, i.e. toxoplasma, cytomegalovirus, mycobacteria and fungi, with the exception of Pneumocystis carinii. This microorganism spared the heart, although it was present in the lungs of 47 patients. Our results are in keeping with other published data. Toxoplasma, present in the myocardium of our patients more frequently than reported in other series, did not necessarily cause a concomitant myocarditis; Coxsackie viruses are deemed to be responsible for many cases of myocarditis in AIDS patients, perhaps even in cases in which we found toxoplasma pseudocysts to be present in the heart muscle. The study clearly shows that the heart is often the unrecognized target of AIDS-associated lesions, even in the initial phase of the AIDS outbreak (1981-1989). Thus, not every shortness of breath is necessarily of pulmonary origin.(ABSTRACT TRUNCATED AT 250 WORDS)

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Loading ...
    Write to the Help Desk