Clinical communicationElectrocardiographic and serum enzyme changes in subarachnoid hemorrhage
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Cited by (77)
Acute Cardiac Complications in Critical Brain Disease
2018, Neurosurgery Clinics of North AmericaCitation Excerpt :Last, Meaudre and colleagues112 revealed that BNP increases gradually over 2 days and returns to baseline within a week after SAH without echo-estimated LV filling pressure elevation, thus providing an additional argument that cardiac injury is catecholamine-induced during SAH. Plasma levels of CK-MB are elevated among 20% to 50% of patients with SAH.84,113 A retrospective study conducted in 72 patients with SAH showed that myocardial injury, as manifested by CK-MB levels, was associated with impaired LV performance.103
Acute Cardiac Complications in Critical Brain Disease
2017, Neurologic ClinicsCitation Excerpt :Last, Meaudre and colleagues112 revealed that BNP increases gradually over 2 days and returns to baseline within a week after SAH without echo-estimated LV filling pressure elevation, thus providing an additional argument that cardiac injury is catecholamine-induced during SAH. Plasma levels of CK-MB are elevated among 20% to 50% of patients with SAH.84,113 A retrospective study conducted in 72 patients with SAH showed that myocardial injury, as manifested by CK-MB levels, was associated with impaired LV performance.103
Neurocardiology
2017, Handbook of Clinical NeurologyCitation Excerpt :Stress-related CMO is perhaps most notably illustrated in neurogenic stunned myocardium associated with SAH. Nonspecific and transient ECG abnormalities occur in most SAH patients (50–100%) (Hunt et al., 1969; Brouwers et al., 1989; Mayer et al., 1995; Yoshikawa et al., 1999; Zaroff et al., 1999). ECG abnormalities are seen near universally in prospective SAH studies with serial monitoring (Brouwers et al., 1989; Mayer et al., 1995).
Unraveling of the Effect of Nodose Ganglion Degeneration on the Coronary Artery Vasospasm after Subarachnoid Hemorrhage: An Experimental Study
2016, World NeurosurgeryCitation Excerpt :Furthermore, the arrhythmias produced by stimulation of these nerves were eliminated by bilateral vagotomy or by extirpation of the stellate ganglia.28 Hunt et al30 suggest that ECG changes in patients with SAH are due to an autonomic imbalance resulting from irritation or depression of the vagus or sympathetic centers or their pathways. After SAH, massive sympathetic discharges after stimulation or lesion of sympathetic centers in the posterior diencephalon and upper midbrain alter the balance of autonomic outflow and result in myocardial necrosis.31
The role of ischemic neurodegeneration of the nodose ganglia on cardiac arrest after subarachnoid hemorrhage: An experimental study
2011, Experimental NeurologyCitation Excerpt :Furthermore, the arrhythmias produced by stimulation of these nerves were abolished by bilateral vagotomy or extirpation of the stellate ganglia (Manning and Cotton, 1962). Hunt et al. (1969) suggested that electrocardiographic changes in patients with subarachnoid hemorrhage are due to an autonomic imbalance resulting from irritation or depression of the vagus or sympathetic centers or their pathways. Following subarachnoid hemorrhage, massive sympathetic discharges after stimulation or lesion of sympathetic centers in the posterior diencephalon and upper midbrain alter the balance of autonomic outflow and result in myocardial necrosis (Greenhoot and Reichenbach, 1969).
Prolonged QTc as a Predictor of Mortality in Acute Ischemic Stroke
2009, Journal of Stroke and Cerebrovascular DiseasesCitation Excerpt :A population study by Elming et al16 consisting of 3455 subjects showed QTc greater than 440 milliseconds to be associated with a relative risk (RR) of almost 1.9 for mortality from all causes and RR of 3.31 for mortality from a cardiovascular event. Studies relating ECG findings to central nervous system events have focused mostly on subarachnoid hemorrhage.17-19 Few studies have examined the relationship of QTc and mortality exclusively in patients with acute ischemic stroke.
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National Heart Foundation Research Fellow in receipt of Grant in Aid No. G438.
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Assistant Physician, Cardiac Department.
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Biochemist.