Myocardial damage in patients with SAH.pptVIP

Myocardial damage in patients with SAH Ri 劉品宏 After SAH··· 27-100% patient → EKG change 40% patient → CK-MB cardiac Troponin I ↑ 10% patient → lethal arrhythmia (ventricular tachycardia, ventricular fibrillation, torsades de pointes) 10% patient → left ventricular (LV) wall motion abnormalities by cardiac echo; a subset of these patients will have irreversible myocardial damage, but most regain LV function in several weeks History 1903, Cushing: cardiac effects of intracranial hemorrhage (alterations in blood pressure and cardiac rhythm) 1947, Byer et al: ECG changes in a patient with subarachnoid hemorrhage (SAH) 1954 :”cerebral T wave” in patient with SAH EKG change after SAH large and inverted T waves (cerebral T waves) prolonged QT intervals Marked QT prolongation, sometimes with deep, wide T-wave inversions, may occur with intracranial bleeds, particularly subarachnoid hemorrhage (CVA T-wave pattern) Others: ST segment alterations, Q waves Prolonged QT intervals most common stroke-related EKG abnormality (in 71% of patients with SAH ) QT prolonged →serious ventricular arrhythmias including sudden death torsade de pointes T wave abnormalities The suggestion that these abnormalities are neurally induced is supported by the observation that inverted T waves may normalize if brain death occurs. Furthermore, inverted or flat T waves have been reported in 55 percent of patients with subarachnoid hemorrhage, but autopsy studies of these patients have failed to reveal any underlying cardiac abnormality. Pathophysiology The pathophysiology of cardiac injury after SAH remains controversial. Coronary artery disease (CAD) and coronary vasospasm as possible mechanisms? 1. some SAH patients have ECG and echocardiographic findings → no angiographic evidence of CAD or vasospasm 2. myocardial ischemia secondary to excessive tachycardia and/or hypertension Catecholamine hypothesis? 1. A series of autopsy studies in patients with SAH (with/without EKG