Type and extent of myocardial injury related to brain damage and its significance in heart transplantation: a morphometric study.
BACKGROUND
Focal myocardial necrosis reported in patients who died of brain lesions and in donor hearts soon after insertion has been attributed to catecholamine-related injury induced before operation, or in the perioperative period. Interpretation of the morphofunctional type of myocardial injury observed and its quantification may help understand both its pathophysiology and clinical relevance.


METHODS
In 27 patients without heart disease who died of intracranial brain hemorrhage after berry aneurysm rupture, terminal clinical signs were correlated with the presence of absence of myocardial injury. All hearts were systematically examined, and the total histologic area was measured in square millimeters, with both the number of foci and myocardial cells showing necrosis, normalized to 100 mm2. Forty-five cases of fatal head trauma (26 "instantaneous" and 19 "rapid" deaths) in normal subjects and 38 cases of acquired immunodeficiency syndrome with (14 cases) or without (24 cases) severe brain damage were used as control subjects.


RESULTS
Contraction band necrosis was the only form of myocardial necrosis found in 89% of patients with acute brain hemorrhage. Its extent was 26 +/- 34 foci and 67 +/- 104 necrotic myocardial cells x 100 mm2. In patients with acquired immunodeficiency syndrome, its frequency was 58% in those without and 78.5% with severe brain lesions, with foci and myocardial cell values of 1 +/- 1.5 and 10 +/- 22 and 7 +/- 16 and 17 +/- 32, respectively. In head trauma cases with instantaneous death, the frequency was 4% (one case only with foci 0.5 and myocardial cells 35), whereas with a rapid death it was 40% (foci 12 +/- 18 and myocardial cells 21 +/- 33).


CONCLUSIONS
The observed myocardial injury was present in all groups examined, being maximal in patients with intracranial brain hemorrhage with longer survival and minimal in patients with head trauma who died instantaneously. In this setting, this lesion is typical of catecholamine myotoxicity and may express a sympathetic overstimulation either in the agonal period and independent of therapy or be caused by brain injury, especially intracranial brain hemorrhage. However, the extent of myocardial injury observed was minimal and should not jeopardize cardiac function if hearts from such subjects are transplanted.
Baroldi
G
G
Department of Cardiology De Gasperis, Niguarda Hospital, University of Milan, Italy.
Di Pasquale
G
G
Silver
M D
MD
Pinelli
G
G
Lusa
A M
AM
Fineschi
V
V
D015526:AIDS Dementia Complex / Q000150:complications / Q000503:physiopathology; D000163:Acquired Immunodeficiency Syndrome / Q000150:complications / Q000503:physiopathology; D000328:Adult; D000367:Age Factors; D000368:Aged; D017542:Aneurysm, Ruptured / Q000150:complications / Q000503:physiopathology; D001922:Brain Abscess / Q000150:complications / Q000503:physiopathology; D001927:Brain Diseases / Q000150:complications* / Q000503:physiopathology; D002395:Catecholamines / Q000502:physiology; D002423:Cause of Death; D002543:Cerebral Hemorrhage / Q000150:complications / Q000503:physiopathology; D006259:Craniocerebral Trauma / Q000150:complications / Q000503:physiopathology; D005260:Female; D016027:Heart Transplantation / Q000473:pathology*; D006801:Humans; D002532:Intracranial Aneurysm / Q000150:complications / Q000503:physiopathology; D008297:Male; D008590:Meningoencephalitis / Q000150:complications / Q000503:physiopathology; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D009929:Organ Size; D012737:Sex Factors; D013566:Sympathomimetics / Q000494:pharmacology
D002395:Catecholamines; D013566:Sympathomimetics