1,720,965 research outputs found
Vagal reflexes and survival during acute myocardial ischemia in conscious dogs with healed myocardial infarction
No full textThe role of vagal tone and reflexes in the genesis of life-threatening arrhythmias was investigated in a clinically relevant animal model for sudden cardiac death. Forty-five dogs with a healed anterior myocardial infarction in which transient myocardial ischemia during exercise did not induce malignant arrhythmias were utilized for the study. They underwent a further exercise and ischemia test in which atropine (75 micrograms/kg) was injected before coronary artery occlusion. Novel occurrence of ventricular arrhythmia, or worsening of the type of arrhythmia present in the control test, occurred in 23 of 45 dogs (51%) and ventricular fibrillation occurred in 11 of 45 (24%, P = 0.001). Analysis of heart rate response to acute ischemia in the control test indicates that these 11 animals had powerful vagal reflexes during coronary artery occlusion, compared with the 34 survivors (-32 +/- 35 vs. +2 +/- 27 beats/min, P = 0.003). This study indicates that approximately 75% of animals resistant to ventricular fibrillation are characterized by weak sympathetic reflexes in response to acute myocardial ischemia. In the remaining 25% powerful vagal reflexes counteract concomitant reflex sympathetic hyperactivity, decrease heart rate, and are essential for survival
Do increases in markers of vagal activity imply protection from sudden death? The case of scopolamine.
No full textScopolamine increases vagal tone and vagal reflexes in patients after myocardial infarction.
No full textThe effects of transdermal administration of scopolamine on heart rate variability and baroreceptor reflex sensitivity were assessed in 20 patients (mean age 59 +/- 11 years) by pharmacologic washout 14 +/- 3 days after myocardial infarction. Heart rate variability and baroreceptor reflex sensitivity were measured 24 h after application of the scopolamine patch and compared with the values measured before scopolamine and after application of a placebo patch. The following variables were derived from a 15-min electrocardiographic recording: the mean RR interval and its standard deviation, the mean square successive difference, the percent of intervals differing > 50 ms from the preceding RR interval and the low and high frequency areas resulting from power spectral analysis.
RESULTS:
The placebo patch had no effect on the variables measured. Scopolamine increased both heart rate variability and baroreceptor reflex sensitivity significantly. Specifically, the mean RR interval and its standard deviation increased by 7.1% (p = 0.01) and 25% (p = 0.004), respectively. The mean square successive difference increased by 38% (p = 0.0003) and the percent of intervals differing > 50 ms from the preceding interval by 100% (p = 0.001). The ratio of low to high frequency areas of the power spectrum decreased by 24% (p = 0.02), and baroreceptor reflex sensitivity increased by 42% (p = 0.0006). These effects were also evident in patients with very low initial values. Side effects were minimal.
CONCLUSIONS:
Transdermal scopolamine increased measures of heart rate variability and baroreceptor reflex sensitivity in patients with a recent myocardial infarction toward values associated with a better prognosis. Pharmacologic modulation of the autonomic balance by scopolamine or related drugs deserves evaluation as a new and promising approach to reduce risk after myocardial infarction
Unexpected interaction between beta-adrenergic blockade and heart rate variability before and after myocardial infarction. A longitudinal study in dogs at high and low risk for sudden death.
No full textVagal stimulation and prevention of sudden death in conscious dogs with a healed myocardial infarction
No full textK+ channel blockade in the prevention of ventricular fibrillation in dogs with acute ischemia and enhanced sympathetic activity.
No full textThe value of K+ channel blockade in preventing lethal arrhythmias, and specifically those triggered by acute myocardial ischemia and sympathetic hyperactivity, remains unproven. To address this issue, we tested the antifibrillatory effect of d-sotalol, and Ikr blocker, d,l-sotalol, its racemic compound which blocks Ikr, and beta-adrenoreceptors, and propranolol. Ten dogs with a healed anterior myocardial infarction (MI) had ventricular fibrillation (VF) during a 2-min occlusion of the circumflex coronary artery performed toward the end of a submaximal exercise stress test. In successive trials in the same animals, d-sotalol (three injections of 8 mg/kg, one every 12 h), d,l-sotalol (8 mg/kg), and propranolol (1 mg/kg) were tested. All three interventions significantly reduced heart rate (HR) response to exercise, but only d,l-sotalol and propranolol also blunted the reflex HR increase during acute myocardial ischemia. With d-sotalol, HR at 30 s of coronary occlusion was similar (253 +/- 28 beats/min) to that observed in the control tests (259 +/- 35 beats/min). d-Sotalol prevented recurrence of VF in only 1 of 10 dogs tested. One dog was lost to the continuation of the study after occurrence of VF with d-sotalol. Six of 9 dogs (67%) tested with d,l-sotalol and 5 (56%) of the same 9 dogs tested with propranolol were protected from VF. d-Sotalol does not reduce risk of VF during acute myocardial ischemia associated with sympathetic hyperactivity, and lethal events can be prevented by antiadrenergic interventions
Vagal stimulation and prevention of sudden death in conscious dogs with a healed myocardial infarction.
Full text linkExercise training confers anticipatory protection from sudden death during acute myocardial ischemia.
No full textSeven conscious dogs documented to be at high risk by the occurrence of ventricular fibrillation (VF) during acute myocardial ischemia were randomly assigned to 6 weeks of either daily exercise training or cage rest followed by exercise training. After 6 weeks of daily treadmill training, heart rate variability, a marker of vagal tone, increased by 74% (P < .001); baroreflex sensitivity, a marker of the capability to reflexly augment vagal activity, increased by 69% (P < .01); the repetitive extrasystole threshold, a marker of ventricular electrical stability, increased by 44% (P < .05). After exercise training, the incidence of ventricular fibrillation during acute myocardial ischemia decreased by 100%, as all animals survived. Neither passage of time nor heart rate level during ischemia contributed to the outcome. The most likely mechanism to explain the striking change in risk status is the shift in autonomic balance characterized by increased cardiac vagal activity, which was previously shown to have an antifibrillatory effect. These results suggest that exercise training in healthy individuals may decrease their likelihood of developing lethal arrhythmias during acute myocardial ischemia
Tocainide and mortality after myocardial infarction: a prospective study in conscious dogs.
Full text link- …
