Neural Factors and Ventricular Electrical Instability

Verrier, Richard L.

doi:10.1007/978-94-009-8834-7_8

Cited by 26 publications

(7 citation statements)

References 76 publications

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“…Enhanced adrenergic nervous activity is well known to predispose to ventricular arrhythmias (Verrier et al ., 1980; Schwartz & Vanoli, 1981). Correspondingly, use of β‐adrenergic receptor blocking agents protects against malignant arrhythmias after acute myocardial infarction (Yusuf et al ., 1985; Viscoli et al ., 1993).…”

Section: Discussionsupporting

confidence: 92%

Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction

Simula

Lakka

Kuikka

et al. 2000

Clinical Physiology

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It is widely accepted that myocardial infarction results in adrenergic denervation of the infarcted and peri-infarcted myocardium. On the contrary, the concept of re-innervation of adrenergic nerve fibres is less well established. Although there is evidence of partial re-innervation occuring several months after myocardial infarction, the extent and time scale of re-innervation are only poorly known. In this study we investigated changes in cardiac adrenergic innervation and myocardial perfusion during the early convalescence period (the first 3 months) after an acute myocardial infarction. Single-photon emission computed tomographic imaging was conducted in 15 men 1 week and 3 months after an acute myocardial infarction with I123-metaiodobentzylguanidine (MIBG) and Tc99m-sestamibi (MIBI) to determine the extent of adrenergic denervation and impaired perfusion, respectively. A MIBG and MIBI defect was determined as regional uptake

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Section: Discussionsupporting

confidence: 92%

Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction

Simula

Lakka

Kuikka

et al. 2000

Clinical Physiology

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“…[1][2][3][4][5][41][42][43][44] In the present study, sympathetic hyperactivity is deleterious not only because of its direct electrophysiological effects but also because it produces a further increase in an already physiologically elevated heart rate. This, in turn, increases the severity of ischemia and precipitates ventricular fibrillation.…”

Section: Discussionmentioning

confidence: 99%

Autonomic mechanisms and sudden death. New insights from analysis of baroreceptor reflexes in conscious dogs with and without a myocardial infarction.

et al. 1988

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“…The importance of high vagal CIRCULATION LABORATORY INVESTIGATION-VENTRICULAR ARRHYTHMIA activity to oppose high sympathetic activity is consistent with recent concepts on the susceptibility to VF24' 35 and particularly the concept that the vagi exert their protective action by antagonizing elevated sympathetic activity in the heart. 38 The importance of heart rate in the occurrence of life-threatening arrhythmias seems to be primarily related to the underlying autonomic state, which is partially reflected by the changes that occur in heart rate.…”

Section: Discussionmentioning

confidence: 99%

Autonomic mechanisms in ventricular fibrillation induced by myocardial ischemia during exercise in dogs with healed myocardial infarction. An experimental preparation for sudden cardiac death.

Schwartz¹,

Billman²,

Stone³

1984

Circulation

429

186

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The relationship between activity of the autonomic nervous system, myocardial ischemia, and malignant arrhythmias has been investigated in a new experimental preparation for sudden death. Fifty-seven dogs were chronically instrumented and studied under control conditions (n = 15) and 1 month after production of an anterior myocardial infarction (n = 42). The protocol consisted in occluding the left circumflex coronary artery for 2 min, commencing at the last minute of an exercise stress test and extending through the first minute after cessation of exercise. With this protocol, ventricular fibrillation was observed in 40% of normal dogs and 66% of dogs with infarction. In 14 dogs.with infarction, left stellectomy reduced the incidence of ventricular fibrillation to zero (p < .001). The reflex changes in heart rate elicited within the first minute of ischemia during exercise in the animals that survived (from 204 ± 14 to 198 ± 31 beats/min, -6) were opposite those in animals that had ventricular fibrillation (from 208 24 to 229 30 beats/min, + 21) (p < .05). The ischemiainduced reduction in heart rate despite continuation of exercise suggests the presence in the dogs that survived of active vagal reflexes that may have played an important role in the maintenance of cardiac electrical stability. This preparation has the potential to induce ventricular fibrillation consistently in conscious animals by the interaction of a few clinically relevant factors (acute myocardial ischemia, submaximal exercise and its cessation, sympathetic and vagal reflexes, and heart rate) and offers the possibility of acquiring further insights into the mechanisms of malignant arrhythmias and evaluating novel strategies for targeted prevention. Circulation 69, No. 4, 790-800, 1984. TARGETED prevention of sudden cardiac death depends on an adequate understanding of the mechanisms of and the factors leading to ventricular fibrillation, as well as an understanding of their relative roles. Basic electrophysiologic experiments, usually performed in isolated hearts or in open-chest preparations, are designed to identify these factors and their probable modes of action, but comprehension of their relative roles in the clinical setting requires experiments in unanesthetized animals.Necessary to achieve this goal are the identification of the most critical factors, the capability of controlling

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Neural Factors and Ventricular Electrical Instability

Cited by 26 publications

References 76 publications

Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction

Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction

Autonomic mechanisms and sudden death. New insights from analysis of baroreceptor reflexes in conscious dogs with and without a myocardial infarction.

Autonomic mechanisms in ventricular fibrillation induced by myocardial ischemia during exercise in dogs with healed myocardial infarction. An experimental preparation for sudden cardiac death.

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