Myocardial damage from acute cerebral lesions.

Abstract

SUMMARY Autopsy findings in 58 patients with intracranlal lesions were compared with those in 50 control patients for myocardial damage, characterised by a change from a myofibrillar to a granular staining pattern, using a histochemical method for succinic dehydrogenase. Transmurally scattered foci of damaged myocardial fibres were significantly more common (p<0.01) in patients with intracranlal lesions (62%) compared to controls (26%). No victims of sudden violent deaths showed these cardiac lesions.Focal myocardial damage required at least six hours to develop after onset of the acute neurological event and was not observed after the second week. It was associated with lesions producing a rapid increase in intracranial pressure and was usually absent in patients with slowly enlarging or small cerebral lesions. Similar myocardial changes were seen in patients in the control group dying from prolonged shock or other forms of acute circulatory or metabolic failure.The postulated mechanism of cardiac damage in these patients is increased levels of plasma catecholamines secondary to rapidly increasing intracranial pressure, irrespective of the cerebral pathology.Stroke Vol 15, No 6, 1984ELECTROCARDIOGRAPHS (ECG) changes in patients with cerebral lesions were first described in 1938 1 and these findings were later confirmed by other workers.2 ' 3 In acute stroke patients, evidence of myocardial damage was also found, including increased serum levels of cardiac enzymes, 4 -5 the occurrence of cardiac arrhythmias 6 and high levels of plasma catecholamines.7 Focal myocytolysis was described at autopsy in 8-12% of patients dying from a variety of acute cerebral lesions.8 ' 9 Since this secondary myocardial damage may indicate more widespread and subtle reversible cardiac changes, we undertook the present study using a more sensitive histochemical method to determine the frequency and extent of myocardial injury in stroke and other forms of acute cerebral lesions. Materials and MethodsConsecutive complete autopsies supervised by the same pathologist in a general teaching hospital were performed within 36 hours of death. Death was due to an acute intracranial lesion in 58 patients and to noncerebral causes, including a variety of heart diseases, in 45 patients. In five other patients, death was instant and due to a sudden violent cause, such as suicide.The hearts were weighed, measured and transversely sliced through the ventricles. Transmural blocks of the left ventricular wall were obtained from the sites of attachment of the anterior and posterior papillary muscles and split horizontally for corresponding cryostat and paraffin blocks. If either of these sites was affected by necrosis or fibrosis, an additional transmural block was obtained from an apparently healthy segment of the ventricle. Cross-sections of the three major coronary artery trunks were collected for routine histology. Unfixed cryostat sections (8u) from each cardiac sample were stained with nitro-blue tetrazolium (NBT) to demonstrate succinic dehydroge...

Activation of the Heart by Donor Brain Death Accelerates Acute Rejection After Transplantation

“…20 These factors may produce localized coronary vasospasm with insufficient blood flow for adequate myocardial perfusion, resulting in necrosis of the subendocardium of the left ventricle, petechial hemorrhage, contraction bands, and coagulative myocytolysis with a mononuclear cell infiltrate. 4,8,21 Exhaustion of catecholamine stores after autonomic storm may be so profound that hypotension results. With gradualonset BD, catecholamine levels remain relatively low and the heart is less affected.…”

Serum Cardiac Troponin T Levels as an Indicator of Myocardial Injury in Ischemic and Hemorrhagic Stroke Patients

“…In acute coronary syndromes, there is a close relation between high troponin levels and mortality (Kolin and Norris 1984;Bhagat et al 1997). Other noncoronary related disorders resulting in elevation of cTnT are myocarditis, acute pulmonary edema, septic shock, cardiotoxic medication, cardioversion, ablation, percutaneous transcoronary angiography (PTCA) and renal insufficiency.…”

Reversible Left Ventricular Systolic Dysfunction-Reversibility of Coronary Microvascular Abnormality.

“…Transient left ventricular dysfunction with similar pathological changes has been described in patients with acute cerebral injury. [10][11][12] Left ventricular dysfunction in patients with severe acute brain injury is also a reversible phenomenon, as reported in rats 13) and humans. 14) Reversible left ventricular dysfunction in patients with a noncardiac illness may have the same pathogenesis as the disorder seen in patients with acute brain injury.…”