Subarachnoid Hemorrhage and the Heart

Neurosurgery ◽  
1986 ◽  
Vol 18 (1) ◽  
pp. 101-106 ◽  
Author(s):  
Donald W. Marion ◽  
Ricardo Segal ◽  
Mark E. Thompson

Abstract Electrocardiographic abnormalities, both morphological and rhythmic, are frequently seen in association with spontaneous subarachnoid hemorrhage. These changes, which often reflect subendocardial damage, seem to be caused by hypothalamic stimulation leading to an acute increase in sympathetic tone. As a result, potentially life-threatening ventricular arrhythmias may develop in subarachnoid hemorrhage patients. These arrhythmias have responded to sympathetic blocking agents, which may also have a protective effect on subendocardial tissue in this setting. There is no evidence that the prophylactic administration of propranolol or other autonomic blockers significantly alters outcome in these patients. Ultimate morbidity and mortality are clearly related to the degree of intracerebral-intraventricular hemorrhage and vasospasm. This article reviews experimental and clinical evidence regarding the causes of cardiac abnormalities after subarachnoid hemorrhage, the types of abnormalities most frequently seen, their relationship with subendocardial lesions, and the role of autonomic blockers.

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
M. Jelinek ◽  
M. Jurajda ◽  
K. Duris

This review focuses on the problem of oxidative stress in early brain injury (EBI) after spontaneous subarachnoid hemorrhage (SAH). EBI involves complex pathophysiological mechanisms, including oxidative stress. In the first section, we describe the main sources of free radicals in EBI. There are several sources of excessive generation of free radicals from mitochondrial free radicals’ generation and endoplasmic reticulum stress, to hemoglobin and enzymatic free radicals’ generation. The second part focuses on the disruption of antioxidant mechanisms in EBI. The third section describes some newly found molecular mechanisms and pathway involved in oxidative stress after EBI. The last section is dedicated to the pathophysiological mechanisms through which free radicals mediate early brain injury.


2011 ◽  
Vol 153 (8) ◽  
pp. 1663-1668 ◽  
Author(s):  
Karl-Michael Schebesch ◽  
Alexander Brawanski ◽  
Simone Maria Kagerbauer ◽  
Jan Martin ◽  
Sylvia Bele ◽  
...  

Physiology ◽  
1997 ◽  
Vol 12 (4) ◽  
pp. 152-157 ◽  
Author(s):  
MC Sanguinetti ◽  
MT Keating

Cardiac action potentials are long because the magnitude of some potassium currents is reduced at depolarized potentials. The slow onset of repolarization is initiated by the opening of delayed rectifier potassium channels. A decrease in function of these channels resulting from gene mutations or pharmacological block increases risk of life-threatening ventricular arrhythmias.


Author(s):  
Brenda Gerull ◽  
Andreas Brodehl

Abstract Purpose of Review Arrhythmogenic cardiomyopathy (ACM) is a genetic disease characterized by life-threatening ventricular arrhythmias and sudden cardiac death (SCD) in apparently healthy young adults. Mutations in genes encoding for cellular junctions can be found in about half of the patients. However, disease onset and severity, risk of arrhythmias, and outcome are highly variable and drug-targeted treatment is currently unavailable. Recent Findings This review focuses on advances in clinical risk stratification, genetic etiology, and pathophysiological concepts. The desmosome is the central part of the disease, but other intercalated disc and associated structural proteins not only broaden the genetic spectrum but also provide novel molecular and cellular insights into the pathogenesis of ACM. Signaling pathways and the role of inflammation will be discussed and targets for novel therapeutic approaches outlined. Summary Genetic discoveries and experimental-driven preclinical research contributed significantly to the understanding of ACM towards mutation- and pathway-specific personalized medicine.


2007 ◽  
Vol 28 (14) ◽  
pp. 1746-1749 ◽  
Author(s):  
Jeffrey S. Healey ◽  
Al P. Hallstrom ◽  
Karl-Heinz Kuck ◽  
Girish Nair ◽  
Eleanor P. Schron ◽  
...  

Neurosurgery ◽  
1979 ◽  
Vol 5 (6) ◽  
pp. 675-680 ◽  
Author(s):  
Bruno Estañol Vidal ◽  
Elias Badui Dergal ◽  
Eduardo Cesarman ◽  
Oscar Marin San Martin ◽  
Mauro Loyo ◽  
...  

Abstract This is a prospective study of cardiac arrhythmias in patients with acute subarachnoid hemorrhage (SAH) secondary to ruptured aneurysm. Twenty per cent of the patients had serious, life-threatening arrhythmias. However, 100% of the patients had some kind of cardiac arrhythmia. The arrhythmias occurred during the first 48 hours after SAH. Such arrhythmias occur in patients without overt, pre-existing heart disease, hypoxemia, or electrolyte imbalance. A prolonged Q-T interval is frequently observed in patients with SAH who develop serious ventricular arrhythmias.


2021 ◽  
Vol 23 (5) ◽  
Author(s):  
Ronpichai Chokesuwattanaskul ◽  
Koonlawee Nademanee

Abstract Purpose of Review To discuss the role of catheter ablation in treating life-threatening ventricular arrhythmias associated with Brugada syndrome (BrS), by presenting recent findings of BrS arrhythmogenic substrate, mechanisms underlying ventricular arrhythmias, and how they can be treated with catheter ablation. Recent Findings Almost three decades ago when the clinical entity of Brugada syndrome (BrS) was described in patients who had abnormal coved-type ST elevation in the right precordial EKG leads in patients who had no apparent structural heart disease but died suddenly from ventricular fibrillation. Since its description, the syndrome has galvanized explosive research in this field over the past decades, driving major progress toward better understanding of BrS, gaining knowledge of the genetic pathophysiology and risk stratification of BrS, and creating significant advances in therapeutic modalities. One of such advances is the ability for electrophysiologists to map and identify the arrhythmogenic substrate sites of BrS, which serve as good target sites for catheter ablation. Subsequently, several studies have shown that catheter ablation of these substrates normalizes the Brugada ECG pattern and is very effective in eliminating these substrates and preventing recurrent VF episodes. Summary Catheter ablation has become an important addition for treatment of symptomatic BrS patients with recurrent VT/VF episodes.


2018 ◽  
Vol 60 (2) ◽  
pp. 247-259 ◽  
Author(s):  
Isabel Fragata ◽  
Patrícia Canhão

Spontaneous subarachnoid hemorrhage (SAH) accounts for about 5% of strokes, but has a very high morbidity and mortality. Many survivors are left with important cognitive impairment and are severely incapacitated. Prediction of complications such as vasospasm and delayed cerebral ischemia, and of clinical outcome after SAH, is challenging. Imaging studies are essential in the initial evaluation of SAH patients and are increasingly relevant in assessing for complications and prognosis. In this article, we reviewed the role of imaging studies in evaluating early brain injury and predicting complications as well as clinical and neuropsychological prognosis after acute SAH.


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