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Early autonomic and repolarization abnormalities contribute to lethal arrhythmias in chronic ischemic heart failure. Characteristics of a novel heart failure model in conscious dogs with post-myocardial infarction left ventricular dysfunction
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Hemodynamic effects of a new inotropic compound, PST-2744, in dogs with chronic ischemic heart failure.
Full text linkDietary Omega-3 Fatty Acids and Susceptibility to Ventricular Fibrillation: Lack of Protection and A Proarrhythmic Effect.
Full text linkBackground-Recent clinical studies that evaluated the effects of supplemental omega-3 polyunsaturated fatty acids (n-3 PUFAs) on sudden cardiac death have yielded conflicting results. Our aim was to clarify this issue using an established and clinical relevant canine model of sudden cardiac death.
Methods and Results-Susceptibility to ventricular fibrillation (VF) was evaluated using a 2-minute left circumflex artery occlusion during the last minute of an exercise test in 76 dogs (from 2 independent studies) with healed myocardial infarctions (MI); 44 developed VF (susceptible, VF+), whereas 32 did not (resistant, VF-). These dogs were then randomly assigned to either placebo (1 g/d, corn oil; 15 VF+, 11 VF-) or n-3 PUFA (1-4 g/d, docosahexaenoic acid+eicosapentaenoic acid ethyl esters, 29 VF+, 21 VF-) groups. Seven sham (no-MI) dogs were also treated with n-3 PUFA (4 g/d). After treatment (3 months), the exercise+ischemia test was repeated. Dietary n-3 PUFAs produced significant (P<0.01) increases in red blood cell and left ventricular n-3 PUFA levels. Nine post-MI (5 placebo versus 4 n-3 PUFA) and 2 sham dogs died suddenly during the 3-month treatment period. The n-3 PUFA treatment failed to prevent arrhythmias in VF+ dogs (decreased in 27% placebo versus 24% n-3 PUFA, P=0.5646) but induced VT/VF in VF-animals (n-3 PUFA 33% versus placebo 0%, P=0.0442).
Conclusions-Despite large increases in cardiac tissue n-3 PUFA content, dietary n-3 PUFAs did not prevent ischemia-induced VF and actually increased arrhythmia susceptibility in both noninfarcted and low-risk post-MI dogs
Ephedrine Increases Ventricular Arrhythmias in Conscious Dogs After Myocardial Infarction
No full textThe sympathomimetic amine, ephedrine, is used to augment physical performance and as a weight loss aid, but little is known about the cardiovascular consequences in individuals with ischemic heart disease.To assess the effects of ephedrine on cardiac autonomic control, baroreceptor reflex sensitivity (BRS), heart rate (HR) variability, HR response to acute myocardial ischemia, and resting catecholamines were measured before and after ephedrine in dogs with a prior myocardial infarction at low risk for sudden death. Nine of 15 animals had increased ventricular arrhythmias during ephedrine treatment (p = 0.01) and four had VF. Three dogs that had VF could not be resuscitated. Ephedrine increases ischemia-dependent arrhythmias at doses recommended in over-the-counter preparations. Increased arrhythmia risk was associated with augmented ischemia-dependent sympathetic reflex activation
Prediction of unexpected sudden death among healthy dogs by a novel marker of autonomic neural activity.
No full textWetestedthehypothesisthataparametercombining BRS and HRV could predict risk for ventricular fibrillation (VF) during a first ischemic episode in otherwise healthy dogs.
METHODS In 43 fully instrumented dogs, BRS and frequency do- main analysis of HRV were determined, as well as the occurrence (n 10, high-risk) or absence (n 33, low-risk) of VF during 2 minutes of myocardial ischemia superimposed on submaximal ex- ercise. TARVA (Tonic and Reflex Vagal Activity), expressed in units, is the parameter resulting from the multiplication of BRS by HF/LF (an index of tonic vagal activity).High-risk dogs had markedly lower TARVA values, re- flecting lower cardiac vagal activity, than low-risk animals (12 5 versus 56 43 units, P .001). The area under the receiver- operator characteristic curve for TARVA was 0.96 (95% confidence interval 0.86 to 0.99); its optimal cutoff had a 100% sensitivity and a 88% specificity with positive and negative predictive values of 71% and 100%, respectively.
CONCLUSION Differencesincardiacautonomicactivity,presentin healthy dogs, allow prediction of arrhythmic risk during a first isch- emic episode. Increased risk is associated with reduced vagal activity. If confirmed in humans, this finding would open the way to the identification of those apparently healthy subjects at risk for sudden cardiac death during their first episode of myocardial ischemia
Autonomic modulation during acute myocardial ischemia by low-dose pirenzepine in conscious dogs with a healed myocardial infarction: a comparison with beta-adrenergic blockade.
Full text linkExperimental and clinical evidence documents the ben- eficial effects of blocking sympathetic activity and modulating heart rate to reduce risk for lethal events in ischemic heart disease. Beside -adrenergic receptor blockade, vagal activation is a meaningful ap- proach but not yet easily attainable. Promising results were shown with low-dose atropine and scopolamine, but no follow-up was done because of significant adverse side effects. Pirenzepine is an atropine analogue approved to treat peptic ulcer disease in Europe that is de- void of central actions, which are mostly responsible for anti- muscarinic agents side effects. The vagomimetic action of IV low- dose pirenzepine was studied at rest under control conditions, at rest during acute coronary artery occlusion, and during exercise in con- scious dogs with a healed anterior myocardial infarction (MI). The effects of pirenzepine were then compared, by internal control analy- sis, with those of atenolol (1 mg/kg). Increasing doses of pirenzepine (from 0.01 to 1 mg/kg) were tested in 11 dogs at rest by measuring time and frequency domain heart rate variability (HRV). The most effective dose (0.1 mg/kg) was used in the study. At the most effective dose, pirenzepine increased all measures of time domain HRV by 40–50%. However, the vagomimetic action of pirenzepine was lost during exercise and brief ischemia and no anti-arrhythmic action was observed. Conversely, pirenzepine effectively modulated the heart rate increase during acute ischemia at rest with an effect comparable to that of atenolol. The vagomimetic action of pirenzepine in the acutely ischemic heart supports the possibility that this intervention may be helpful for chronic autonomic modulation in post-MI patients
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