IMPACTS OF SYSTEMIC HYPERTENSION AND LEFT VENTRICULAR HYPERTROPHY ON OUTCOME OF CARDIOPULMONARY RESUSCITATION AND THERAPEUTIC HYPOTHERMIA IN A CARDIAC ARREST MODEL OF RAT

Shock ◽  
2016 ◽  
Vol 45 (4) ◽  
pp. 434-440 ◽  
Author(s):  
Pei Wang ◽  
Lei Zhang ◽  
Yushun Gong ◽  
Hehua Zhang ◽  
Xiang Wang ◽  
...  
Author(s):  
R. Nadarajah ◽  
P. A. Patel ◽  
M. H. Tayebjee

AbstractSudden cardiac death (SCD) is most commonly secondary to sustained ventricular arrhythmias (VAs). This review aimed to evaluate if left ventricular hypertrophy (LVH) secondary to systemic hypertension in humans is an isolated risk factor for ventricular arrhythmogenesis. Animal models of hypertensive LVH have shown changes in ion channel function and distribution, gap junction re-distribution and fibrotic deposition. Clinical data has consistently exhibited an increase in prevalence and complexity of non-sustained VAs on electrocardiographic monitoring. However, there is a dearth of trials suggesting progression to sustained VAs and SCD, with extrapolations being confounded by presence of co-existent asymptomatic coronary artery disease (CAD). Putatively, this lack of data may be due to the presence of more homogenous distribution of pathophysiological changes seen in those with hypertensive LVH versus known pro-arrhythmic conditions such as HCM and myocardial infarction. The overall impression is that sustained VAs in the context of hypertensive LVH are most likely to be precipitated by other causes such as CAD or electrolyte disturbance.


Heart Rhythm ◽  
2014 ◽  
Vol 11 (6) ◽  
pp. 1040-1046 ◽  
Author(s):  
Kumar Narayanan ◽  
Kyndaron Reinier ◽  
Carmen Teodorescu ◽  
Audrey Uy-Evanado ◽  
Harpriya Chugh ◽  
...  

1977 ◽  
Vol 232 (6) ◽  
pp. H639-H644 ◽  
Author(s):  
M. A. Pfeffer ◽  
J. M. Pfeffer ◽  
A. K. Weiss ◽  
E. D. Frohlich

Spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were treated with beta-adrenergic receptor inhibiting drugs (either propranolol or timolol) from conception until 12 weeks of age to determine if this therapy would alter the development of systemic hypertension or left ventricular hypertrophy. Therapy (propranolol or timolol, 500 mg/liter drinking water) was initiated with breeding parents and continued throughout the pregnancy, nursing, and postweaning periods. Although the heart rates of beta-adrenergic receptor inhibited WKY and SHR rats were consistently reduced with respect to their respective tap-water controls, this therapy did not alter body growth. Hemodynamic studies demonstrated reduced central venous pressure, cardiac index, and maximum acceleration of aortic flow in the beta-adrenergic inhibited rats. In spite of these findings, the arterial pressure of the treated rats and the degree of left ventricular hypertrophy of the SHR were unaltered by treatment. Thus, administration of the beta-adrenergic receptor blocking agents, propranolol or timolol, from conception through the developmental stage of SHR hypertension, failed to alter either the progressive rise in arterial pressure or the development of hypertensive vascular disease and left ventricular hypertrophy.


1983 ◽  
Vol 51 (6) ◽  
pp. 1044 ◽  
Author(s):  
Luigi Corea ◽  
Maurizio Bentivoglio ◽  
Paolo Verdecchia ◽  
Mario Motolese

1984 ◽  
Vol 53 (9) ◽  
pp. 1299-1303 ◽  
Author(s):  
Luigi Corea ◽  
Maurizio Bentivoglio ◽  
Paolo Verdecchia ◽  
Mario Motolese

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