TY - GEN
T1 - Cardiac damage after subarachnoid hemorrhage
AU - Wu, Bihua
AU - Wang, Xiaoming
AU - Zhang, John H.
N1 - Part of the Acta Neurochirurgica Supplements book series (NEUROCHIRURGICA, volume 110/1) Patients who had no heart disease had T-wave inversion and prolongation of the QT interval in electrocardiogram after Subarachnoid hemorrhage (SAH), which was reported 70years before. Cardiac complications, including focal myocytolysis, electrocardiographic changes, arrhythmias and left ventricular wall motion abnormalities and pulmonary edema.
PY - 2011
Y1 - 2011
N2 - Patients who had no heart disease had T-wave inversion and prolongation of the QT interval in electrocardiogram after Subarachnoid hemorrhage (SAH), which was reported 70years before. Cardiac complications, including focal myocytolysis, electrocardiographic changes, arrhythmias and left ventricular wall motion abnormalities and pulmonary edema. The autonomic and cardiovascular effects of SAH, however, are modulated by concomitant factors such as pre-existent cardiac diseases, electrolyte disorders and, probably, by genetic alterations in the ionic control of myocyte repolarization. Although beta-blockers have been reported to prevent myocardial damage following SAH, adequate clinical trials are lacking, and the widespread use of these drugs in acute cerebrovascular disease is not supported by evidence. Cardiac injury occurs frequently after SAH, and the most widely investigated form of neurocardiogenic injury.
AB - Patients who had no heart disease had T-wave inversion and prolongation of the QT interval in electrocardiogram after Subarachnoid hemorrhage (SAH), which was reported 70years before. Cardiac complications, including focal myocytolysis, electrocardiographic changes, arrhythmias and left ventricular wall motion abnormalities and pulmonary edema. The autonomic and cardiovascular effects of SAH, however, are modulated by concomitant factors such as pre-existent cardiac diseases, electrolyte disorders and, probably, by genetic alterations in the ionic control of myocyte repolarization. Although beta-blockers have been reported to prevent myocardial damage following SAH, adequate clinical trials are lacking, and the widespread use of these drugs in acute cerebrovascular disease is not supported by evidence. Cardiac injury occurs frequently after SAH, and the most widely investigated form of neurocardiogenic injury.
KW - Cardiac complications
KW - EKG
KW - SAH
UR - http://www.scopus.com/inward/record.url?scp=85052610344&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85052610344&partnerID=8YFLogxK
U2 - 10.1007/978-3-7091-0353-1_37
DO - 10.1007/978-3-7091-0353-1_37
M3 - Conference contribution
C2 - 21116942
SN - 9783709103524
T3 - Acta Neurochirurgica, Supplementum
SP - 215
EP - 218
BT - Early Brain Injury or Cerebral Vasospasm
PB - Springer-Verlag Wien
ER -