Bretylium tosylate in patients with acute myocardial infarction

Torresani, J

doi:10.1016/0002-9149(84)90813-0

Cited by 10 publications

(10 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[7][8][9][10][11] James and Keyes 149 strongly challenged this assumption as untenable many years ago. Our study presented here confirms and expands on those of Torresani, 150 who showed that routine prophylactic administration of bretylium to AMI patients in the CCU virtually eliminates arrhythmias and VF, as well as other deleterious catecholamine actions, including ECG manifestations of ischemic myocardiopathy, as shown in more than 1500 AMI patients treated over a 10-year period. 141 and Selye, 10,11 in a brilliant series of experimental studies and well-documented reviews, books, and symposia, have pulled together a wealth of convincing clinical and experimental evidence, from many sources, highlighting the critical role that nonvascular neurohormonal activation of sympathetic hypothalamic actions with participation of sympathetic ganglia and nerve endings has in directly causing IsHD.…”

Section: The Concept Of Metabolic Neurohormonal Cardiovascular Diseasesupporting

confidence: 89%

“…The study to be presented provides strong evidence that immediate administration of bretylium (15 mg/kg/d for 5 days) to patients with an impending AMI prevents arrhythmias and lowers mortality, CHF, and cardiogenic shock, confirming prior reports by Torresani 150 and Day and Bacaner 183 showing the protective actions of bretylium during AMI. Bretylium is shown to be effective in blocking the major deleterious actions of ischemia and catecholamines on the human heart, which have been consistently observed in many experimental animal studies.…”

Section: Coronary Thrombosis and Thrombolysissupporting

confidence: 82%

“…150 In a series of studies similar to ours, Torresani reported a series of controlled studies on the prophylactic use of bretylium in more than 1500 consecutive patients over a 10-year period, giving them 10 mg/kg/24 h by IV infusion for 5-7 days in the CCU. His results were similar to ours in that all ventricular arrhythmias were significantly reduced, and VF was virtually eliminated.…”

Section: Discussionmentioning

confidence: 59%

“…93,140,141 It also suggests a need in vulnerable patients for total norepinephrine transmitter blockade as achieved with bretylium, which certainly reduces the risk of SCD from VF. 150,[153][154][155][156][157][158][159][160][161][162][163][164][165][166][167] This protective effect of adrenergic blockade against vascular disease is not surprising because catecholamines activate phospholipases that have an important impact on lipid metabolism. 96,[119][120][121][122][123][124] This further links the development of atherosclerotic disease to adrenergic actions 2,74,79 since it can be antagonized by adrenergic blockade.…”

Section: Connecting the Dots Leading To The Concept Of Adcvhd And Neumentioning

confidence: 99%

“…206 The positive inotropic effect has been erroneously attributed solely to release of catecholamines from sympathetic nerve endings, which might account for a transient inotropic effect often observed after initial IV administration, but this alone would not account for the sustained increase in contractility and augmented hemodynamics observed long after bretylium has been given. 206 We believe that coronary dilation with increased coronary flow and O 2 delivery also reduces peripheral resistance, 150 augments myocardial contractility, and may also be a major factor that improves hemodynamics depressed by ischemia. It has also been reported that bretylium has a digitalis-like inotropic action in inhibiting Na + -K + , ATPase.…”

Section: Bretylium Inotropicity 200-207mentioning

confidence: 99%

See 4 more Smart Citations

Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

Bacaner

Brietenbucher²,

LaBree³

2004

American Journal of Therapeutics

View full text Add to dashboard Cite

It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur in 15%-20% of patients with anatomically unobstructed and grossly normal coronaries. Moreover, severe obstructive coronary disease often occurs without associated pathologic myocardiopathy or prior symptoms, ie, unexpected sudden death, silent myocardial infarction, or the insidious appearance of congestive heart failure (CHF). The fact that catecholamines explosively augment oxidative metabolism much more than cardiac work is generally underappreciated. Thus, adrenergic actions alone are likely to be more prone to cause cardiac ischemia than reduced coronary blood flow per se. The autonomic etiology of IsHD raises contradictions to the traditional concept of anatomically obstructive CAD as the lone cause of cardiac ischemia and AMI. Actually, all the signs and symptoms of IsHD reflect autonomic nervous system imbalance, particularly adrenergic hyperactivity, which may by itself cause ischemia as in rest angina. Adrenergic activity causing ischemia signals cardiac pain to pain centers via sympathetic efferent pathways and tend to induce arrhythmogenic and necrotizing ischemic actions on the cardiovascular system. This may result in ischemia induced metabolic myocardiopathy not unlike that caused by anatomic or spasmogenic coronary obstruction. The clinical study and review presented herein suggest that adrenergic hyperactivity alone without CAD can be a primary cause of IsHD. Thus, adrenergic heart disease (AdHD), or actually adrenergic cardiovascular heart disease (ACVHD), appears to be a distinct entity, most commonly but not necessarily occurring in parallel with CAD. CAD certainly contributes to vulnerability as well as the progression of IsHD. This vicious cycle, which explains the frequent parallel occurrence of arteriosclerosis and IHD, an association that appears to be linked by the same cause, comprises a common vulnerability to deleterious adrenergic actions on the myocardium, lipid metabolism, and vascular system alike, rather than viewing CAD and IsHD as having a putative cause and effect relationship as commonly thought. Adrenergic actions can also cause the abnormal lipid metabolism that is associated with CAD and IsHD by catecholamine-induced metabolic actions on lipid mobilization by activation of phospholipases. This may also be part of toxic catecholamine hypermetabolic actions by enhancing deleterious cholesterol and lipid actions in damaging coronary vessels by plaque formation as well as inducing obstructive coronary spasm and platelet aggregation. This may also cause direct toxic necrosis on the myocardium as well as atherosclerosis in blood vessels. In fact, drugs that inhibit adrenergic actions like propranolol, reserpine, and guanethidine all inhibit arteriosclerosis induced by hypercholestero...

show abstract

Section: The Concept Of Metabolic Neurohormonal Cardiovascular Diseasesupporting

confidence: 89%

Section: Coronary Thrombosis and Thrombolysissupporting

confidence: 82%

Section: Discussionmentioning

confidence: 59%

Section: Connecting the Dots Leading To The Concept Of Adcvhd And Neumentioning

confidence: 99%

Section: Bretylium Inotropicity 200-207mentioning

confidence: 99%

See 3 more Smart Citations

Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

Bacaner

Brietenbucher²,

LaBree³

2004

American Journal of Therapeutics

View full text Add to dashboard Cite

show abstract

Prevention of ventricular fibrillation by dextrorotatory sotalol in a conscious canine model of sudden coronary death

Lynch

Coskey

Montgomery

et al. 1985

American Heart Journal

View full text Add to dashboard Cite

The antiarrhythmic and antifibrillatory actions of the dextrorotatory isomer of sotalol, administered in a multiple-dose regimen, were evaluated in conscious dogs 3 to 5 days after anterior myocardial infarction. The intravenous administration of d-sotalol, four 8 mg/kg doses over a 24-hour treatment period, suppressed the induction of ventricular tachycardia by programmed electrical stimulation in six of nine dogs tested, slowed the rate of the induced tachyarrhythmia in two of the remaining three dogs, and provided significant protection (5 of 8 d-sotalol vs 0 of 8 vehicle control) against the development of ventricular fibrillation in response to ischemia at a site distant to a previous myocardial infarction. Increases in ventricular myocardial refractoriness and in QTc and paced QT intervals suggest that class III electrophysiologic actions contribute to the antiarrhythmic properties of dextrorotatory sotalol in this animal model. The degree of beta-adrenergic receptor blockade produced by d-sotalol in this dose regimen was negligible. These findings suggest the potential utility of d-sotalol in the prevention of ventricular tachycardia and ventricular fibrillation in the setting of myocardial infarction, particularly when beta-adrenergic receptor blockade is undesirable or contraindicated.

show abstract