Baroldi G, Di Pasquale G, Silver M D, Pinelli G, Lusa A M, Fineschi V
Department of Cardiology De Gasperis, Niguarda Hospital, University of Milan, Italy.
J Heart Lung Transplant. 1997 Oct;16(10):994-1000.
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.
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.
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).
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.
在死于脑部病变的患者以及植入后不久的供体心脏中报告的局灶性心肌坏死，被归因于手术前或围手术期诱导的儿茶酚胺相关损伤。对观察到的心肌损伤的形态功能类型及其量化进行解读，可能有助于理解其病理生理学和临床相关性。
在27例因浆果动脉瘤破裂后死于颅内脑出血的无心脏病患者中，将终末期临床体征与心肌损伤的有无进行关联。对所有心脏进行系统检查，以平方毫米为单位测量总组织学面积，同时记录坏死灶数量和显示坏死的心肌细胞数量，并将其标准化为100平方毫米。45例正常受试者的致命性头部创伤（26例“即刻”死亡和19例“快速”死亡）以及38例有（14例）或无（24例）严重脑损伤的获得性免疫缺陷综合征患者作为对照。
收缩带坏死是89%的急性脑出血患者中发现的唯一心肌坏死形式。其范围为每100平方毫米有26±34个病灶和67±104个坏死心肌细胞。在获得性免疫缺陷综合征患者中，无严重脑损伤者的发生率为58%，有严重脑损伤者为78.5%，病灶和心肌细胞值分别为1±1.5和10±22以及7±16和17±32。在即刻死亡的头部创伤病例中，发生率为4%（仅1例有0.5个病灶和35个心肌细胞），而快速死亡者为40%（病灶12±18和心肌细胞21±33）。
在所检查的所有组中均观察到心肌损伤，在存活时间较长的颅内脑出血患者中损伤最大，在即刻死亡的头部创伤患者中损伤最小。在这种情况下，这种病变是儿茶酚胺肌毒性的典型表现，可能在濒死期表示交感神经过度刺激且与治疗无关，或者由脑损伤尤其是颅内脑出血引起。然而，观察到的心肌损伤程度极小，如果移植来自此类受试者的心脏，不应危及心脏功能。
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