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Biomedical subjects

T Peter

Publications and source records attributed to T Peter.

At least 109 records · Page 6Linked to original sources
PubMed1983

The electrophysiologic basis for the use of amiodarone for treatment of cardiac arrhythmias.

The electrophysiologic basis for the use of amiodarone in the treatment of cardiac arrhythmias is outlined, with reference to studies in isolated cardiac tissues, whole animal, and human studies. Amiodarone appears to have the distinctive property of directly prolonging action potential duration (and hence refractory periods) in nearly all cardiac tissues. Independent of its effects on refractory periods, conduction may also be impaired in the His-Purkinje system, possibly due to depression of phase 0 of the action potential. Sinus node and atrial automaticity, as well as that arising from diseased Purkinje fibers, may be depressed. Normal ventricular escape pacemakers appear relatively unaffected, however. A nonspecific anti-adrenergic action may contribute to its observed effects. These electrophysiological effects are more obvious and predictable after several weeks of oral treatment than after intravenous administration, suggesting a time-dependent mechanism of action. The drug appears well suited to the prevention of enhanced automaticity in the ventricle and re-entry throughout the heart, and its frequent clinical success in a broad spectrum of cardiac arrhythmias attests to this. Unwanted side effects include sinus node depression, His-Purkinje conduction delay or block, and ventricular arrhythmias enhanced by QT prolongation. However, the frequency of clinically significant examples of unwanted arrhythmic effects appears to be acceptably low.

Action Potentials↗
PubMed1982

Comparison of clinical signs and hemodynamic state in the early hours of transmural myocardial infarction.

The initial PCW, Killip-Scheidt classification, presence of third heart sound, and mortality were compared in 90 patients presenting with acute transmural myocardial infarction. Clinical and hemodynamic assessment was performed within 12 hours (time to clinical classification = 4.7 +/- 2.7 hours (mean +/- SD), time to hemodynamic assessment = 5.8 +/- 2.4) of the sentinel event. A poor correlation was observed between early Killip-Scheidt clinical classification and early hemodynamic state when measured as percent correct classification (66%) or as a Kappa statistic (36% for the total population, 9% for nonsurvivors). Increased initial LVFP (greater than 18 mm Hg) was associated with increased mortality (p less than 0.01) and early clinical classification was not. Addition of third heart sound information did not alter this observation.

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PubMed1982

Electrophysiologic effects of chronic amiodarone therapy in patients with ventricular arrhythmias.

Detailed electrophysiologic studies were performed in nine patients with chronic refractory ventricular arrhythmias before and after 7 to 20 weeks (mean 11 weeks) of amiodarone therapy. The amiodarone dose at the time of the repeat study ranged from 400 to 800 mg/day. The drug reduced the sinus rate (p less than 0.001) and prolonged the sinoatrial conduction time (p less than 0.05) with some prolongation of the corrected sinus node recovery time. Intra-atrial conduction was slightly prolonged both in sinus rhythm and during atrial pacing. Anterograde conduction through the AV node was significantly prolonged both in sinus rhythm (p = 0.001) and during atrial pacing (p less than 0.005), and Wenckebach AV block was seen at significantly lower atrial pacing rates after the drug (p less than 0.005). The HV interval was prolonged both in sinus rhythm (p less than 0.05) and during atrial pacing (p = 0.001), and so was the QRS width during atrial pacing (p less than 0.005) and the QT interval in sinus rhythm (p less than 0.005) and during atrial pacing (p less than 0.005). Significant prolongation of the refractory periods in the atrium, AV node, and ventricular muscle were also seen following the drug. We concluded that the significant electrophysiologic effects of this drug throughout the heart during chronic oral use attest to its clinical effectiveness in patients with atrial and ventricular arrhythmias. With due care and despite its effects on the HV interval and QRS width, it can be used in patients with intraventricular conduction defects complicating severe organic heart disease.

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PubMed1982

The potentiation of warfarin anticoagulation by amiodarone.

The potentiation of the anticoagulant effect of sodium warfarin by amiodarone is reported in 10 patients. Amiodarone appears to augment the depression of vitamin K-dependent coagulation factors caused by warfarin by an uncertain mechanism, and may lead to serious bleeding. The maintenance dose of warfarin should be halved when amiodarone and warfarin are prescribed together.

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PubMed1981

Electrophysiologic and hemodynamic actions of diltiazem: disparate temporal effects shown by experimental dose-response studies.

Diltiazem (DT), a potent slow channel blocker, has been found to be clinically useful for treatment of coronary vasospasm, hypertension, and tachyarrhythmias. Nevertheless, only limited data are available on the hemodynamic and electrophysiologic effects of DT. Atrial, His, right ventricular apex, aortic, and Swan-Ganz thermodilution catheters were used in 10 anesthetized dogs, and recordings were made during control period and after each of four infusions of DT (0.01, 0.02, 0.04, and 0.08 mg/kg/min) each lasting 30 minutes. Results showed that heart rate, pulmonary capillary wedge pressure, stroke volume, and HV interval did not change significantly. However, two dogs had second-degree AV block and a third had escape junctional rhythm during DT 0.08 mg/kg/min. Mean aortic pressure (AP), corrected sinus node (SN) recovery time, and systemic vascular resistance (SVR) were significantly reduced, whereas AH interval, AV functional and effective refractory periods were prolonged by DT. AV nodal refractory periods and AH interval were the only parameters significantly affected at DT 0.02 mg/kg/min. SN recovery time was significantly shortened at DT 0.04 mg/kg/min, whereas AP and SVR tell significantly at DT 0.08 mg/kg/min. DT had significant electrophysiologic effects at low doses, whereas hemodynamics were significantly altered only at high doses. Further, major electrophysiologic effects were on the AV node with lesser effects on SN function. Therefore, at a dose when antiarrhythmic effects are evident, the safety of diltiazem is corroborated by lack of adverse hemodynamic effects.

Animals↗
PubMed1981

Effects of verapamil on supraventricular tachycardia in patients with overt and concealed Wolff-Parkinson-White syndrome.

Verapamil (0.15 mg/kg) intravenously, was administered to 19 patients with recurrent supraventricular tachycardia (SVT) undergoing electrophysiological evaluation. Twelve patients had overt Wolff-Parkinson-White (WPW) syndrome and seven patients had concealed accessory pathways conducting in the retrograde direction only. Verapamil had a significant effect in delaying conduction and prolonging refractoriness in the atrioventricular (AV) node, but no significant actions on any of the other cardiac tissues that formed the tachycardia circuit in these patients. In particular, it had no significant effects on anterograde or retrograde bypass conduction or refractoriness. Sustained SVT was initiated in 15 patients, and was terminated within 60 to 105 seconds of a 30-second injection of verapamil in 13 patients. Cycle length alternation during SVT was seen in six patients prior to reversion, and spontaneous ventricular complexes (VPCs) were observed following verapamil administration in five patients. Two patients with apparently normal sinus node function showed prolongation of their sinus node recovery times immediately following reversion of SVT by verapamil. Echo zones were assessed before and after verapamil, and sustained or self-terminating SVT could still be induced after the drug in 13 of the 15 patients who had sustained SVT beforehand. It was concluded that intravenous verapamil was effective in terminating sustained SVT in the majority of patients with overt or concealed WPW and that, despite a potential for sinus node depression and the initiation of VPCs, it had no clinically significant side effects. The ability to reinitiate SVT following its administration suggests the need for immediate follow-up with maintenance drug therapy.

Adult↗
PubMed1981

Prognostic implications of reduction of left ventricular filling pressure in early transmural acute myocardial infarction.

The left ventricular filling pressure (LVFP) was measured within 12 hours of onset of acute myocardial infarction (AMI) in 99 patients, including 21 nonsurvivors. Initial LVFP for survivors was 18 +/- 6 mm Hg (mean +/- SD) and for nonsurvivors was 24 +/- 8 mm Hg (p less than 0.005). Of the total population, 87% had initial LVFP of 12 mm Hg or greater and all nonsurvivors were in this group. Life table analysis was employed to determine LVFP related mortality rates. If initial LVFP was less than or equal to 18 mm Hg, 72-hour mortality rate was 4% and 30-day mortality rate was 10%. For initial LVFP greater than 18 mm Hg, 72-hour mortality rate was 21% and 30-day mortality rate was 33% (p less than 0.005 for both 72 hours and 30 days). When final LVFP was analyzed 30-day mortality rate for final LVFP less than or equal to 18 mm Hg was 5%. Mortality rate of 60% was observed for final LVFP greater than 18 mm Hg. We compared sequential measurements of LVFP in a subset of survivors and nonsurvivors and observed that long-term average trend was for survivors to decrease their LVFP. We conclude that AMI mortality rate is related to LVFP and that LVFP greater than 18 mm Hg is associated with very high mortality rate when compared to LVFP less than or equal to 18 mm Hg. Thus reduction of LVFP either spontaneously or as result of therapy may lower AMI mortality rate.

Actuarial Analysis↗
PubMed1981

Effect of verapamil on conduction delay produced by myocardial ischemia and reperfusion.

Changes in conduction times induced by ischemia (delta CT) have been shown to be quantitatively related to genesis of spontaneous ischemic ventricular fibrillation (VF). We studied conduction delay encountered by premature impulses in epicardium and endocardium in both anterograde and retrograde directions during ischemia and reperfusion in eight control and in eight verapamil treated dogs. Acute myocardial ischemia was produced by single-stage ligation of left anterior descending artery below second diagonal initially, and 30 minutes later below first diagonal branch. In treated dogs, verapamil was given, 0.15 mg/kg intravenous bolus, immediately after first ligation and was followed by an infusion of 7.5 micrograms/kg/min. Thus post-treated segment and pretreated segment were obtained in the same animal. delta CT was compared between control and treated dogs in four myocardial zones: (1) normal, (2) ischemic including pre- and post-treated segments, (3) reperfused, and (4) border of reperfusion or ischemia. Results showed that ischemia-induced conduction delay was significantly less in verapamil treated dogs throughout period of ischemia and reperfusion, both in epicardium and endocardium. In addition, in the border of ischemia retrograded conduction showed significantly less depression during ischemia and reperfusion. The protective effect of verapamil was impressive both in pretreated and post-treated segments of ischemic myocardium. We conclude that verapamil offers significant protective action with regard to ischemia-induced conduction delay. Since delta CT is quantitatively related to ischemic VF, verapamil can be antiventricular fibrillatory in myocardial ischemia.

Animals↗
PubMed1981

Verapamil therapy in variant angina pectoris refractory to nitrates.

Conventional therapy including nitrates, beta blockers, and surgical bypass has proved to be generally unsatisfactory in patients with variant angina of suspected vasospastic etiology. Recent evidence regarding the role of calcium in the pathogenesis of vascular smooth muscle spasm prompted an open study of the clinical effects of verapamil in seven patients with recurrent rest angina refractory to nitrates. The patients studied met strict clinical ECG and angiographic criteria for vasospastic angina. All patients had rapid (within 24 hours) and complete (without recurrence of symptoms) chronic response to oral verapamil therapy. The pharmacology of verapamil relating to the pathogenesis of vasospastic angina is delineated and guidelines for the clinical application of the agent are presented.

Adult↗
PubMed1981

Effects of nifedipine on conduction delay during ventricular myocardial ischemia and reperfusion.

Nifedipine has been suggested to have more potent slow channel blocking action than other agents of this type. However, its use in the treatment of cardiac arrhythmias has been limited. Electrophysiologic studies on AV conduction have shown that nifedipine lacks any significant effect. However, the action of the drug on intraventricular conduction has not been investigated with regard to its potential in the treatment of ventricular arrhythmias especially during ischemia. Therefore, the effects of nifedipine on conduction delay during ischemia and reperfusion were assessed in the present study. Sixteen dogs (eight control and eight nifedipine-treated dogs) were used. Transmural electrodes were positioned in normal, ischemic, and reperfused tissue, and at the border of these segments. The left anterior descending artery was initially ligated below the second diagonal branch (first ligation) and 30 minutes later below the first diagonal branch (second ligation); the second ligation was released 30 minutes later. Conduction of electrically induced premature impulses from the midwall of the left ventricle was recorded at epicardial and endocardial sites. Conduction delay was measured from the stimulus artifact to the first high-frequency deflection in each zone in the anterograde (base to apex) and retrograde (apex to base) directions. Intravenous nifedipine 0.1 mg/kg was given over 10 minutes immediately after the first ligation. Nifedipine slightly decreased the magnitude of conduction delay in the ischemic myocardium at 15 minutes of ischemia, which corresponded with the peak plasma nifedipine level. However, conduction delay throughout the remainder of the study was essentially unaltered by nifedipine. In conclusion, though nifedipine may improve ischemic myocardial metabolism, infarct size, and hemodynamics, the effect on the electrophysiologic parameters affecting conduction was insignificant. This lack of any further deterioration in conduction in the ischemic and reperfused tissue by the drug further attests to its safety during acute myocardial ischemia.

Animals↗
PubMed1981

Disparity between the clinical and electrophysiologic effects of amiodarone in the treatment of recurrent ventricular tachyarrhythmias.

Nine patients with life-threatening ventricular arrhythmias were administered oral amiodarone over a period of months. Sustained ventricular tachycardia (VT) was induced during programmed stimulation in seven of the nine patients prior to their receiving amiodarone therapy. Despite an excellent clinical response to the drug over a period of 10 to 24 months (median 15 months), sustained VT was still able to be initiated in seven patients after 7 to 20 weeks of therapy, with multiform VT induced in several patients both before and after amiodarone. Some effects of the drug were noted, however, in that the induced VT was often slower with an increased QRS width, and right ventricular refractory periods were prolonged. Repeated ambulatory ECG monitoring in six patients showed a reduction in the frequency and complexity of spontaneous ventricular arrhythmias, but there was no consistent effect on the prematurity of the ventricular complexes. The reason for the disparity in some patients between the effects of amiodarone on the electrical initiation of VT and its clinical recurrence is unclear, but the findings suggest that the clinical efficacy of amiodarone in patients with ventricular arrhythmias may not be reliably predicted by electrophysiologic studies (EPS).

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PubMed1981

Characterization of left ventricular mechanical function during arrhythmias with two dimensional echocardiography. I. Premature ventricular contractions.

Two dimensional echocardiography was applied experimentally in the closed chest dog to quantitate left ventricular function during and immediately after single premature ventricular contractions induced through threshold stimulation at the apex. Coupling intervals were varied over a range from 35 to 85 percent of the R-R interval during normal sinus rhythm (920 to 980 ms). The quality of tomographic echocardiographic images during premature as well as postextrasystolic beats was found to be satisfactory for quantitating short axis section areas at end-diastole and end-systole. A systolic fractional area change was computed from two dimensional echocardiographic measurements to characterize mid ventricular cardiac function, which correlated significantly with peak left ventricular pressure and maximal first derivative of left ventricular pressure (dP/dt). Marked shortening of coupling intervals reduced fractional shortening during premature systole and enhanced the degree of potentiation during the postextrasystolic beat. By contrast, premature beats with relatively long coupling intervals caused less reduction in contraction and only minor postextrasystolic potentiation. Systolic shortening of left ventricular length as well as transverse diameters were studied in a two dimensional echocardiographic long axis cross section. During long coupling intervals contraction was normal except for distinct regional systolic outward "bulging" in the apical region. In contrast, short coupling intervals were associated with a more significant generalized derangement of ventricular wall motion during systole. It is concluded that the two dimensional echocardiographic method can be used to portray and quantitate global as well as regional left ventricular function during disturbances of cardiac rhythm.

Animals↗
PubMed1981

Effects of diltiazem on conduction of premature impulses during acute myocardial ischemia and reperfusion.

The effect of diltiazem on conduction of cardiac impulses was studied using premature impulses. Conduction times were measured in the epicardium and endocardium in both anterograde and retrograde directions during ischemia and reperfusion of the left ventricular anterior wall. In 16 dogs (8 control and 8 treated with diltiazem), the left anterior descending artery was occluded initially below the second diagonal branch and 30 minutes later below the first diagonal branch. Infusion of diltiazem (0.02 mg/kg per min) was begun at the time of the first ligation in the treated dogs. Conduction delay in normal, ischemic and reperfused myocardium and at the border of ischemia or reperfusion was compared in the two groups. In addition, treated and nontreated ischemic zones were analyzed in the diltiazem-treated group. Results show significantly less ischemia-induced conduction delay in the diltiazem-treated group in both ischemic myocardium and at the border of ischemia. This beneficial effect was seen in the ischemic segment in the treated dogs whether or not the medication was given before or after coronary ligation. Further, the effect of the drug on epicardial and endocardial conduction did not differ significantly. These data suggest that diltiazem may have potential value in the treatment of ventricular reentrant arrhythmias associated with acute ischemia over and above the well recognized hemodynamic and metabolic effects of calcium channel blocking agents.

Animals↗
PubMed1981

Relation between conduction delay and ventricular fibrillation: characteristics of conduction of premature impulses during acute myocardial ischemia.

Critical conduction delay has been shown to be the important factor in reentrant arrhythmias. To determine the causal relation between conduction delay and spontaneous ischemic ventricular fibrillation, conduction delay of induced premature ventricular impulses in the ischemic and the border zones of ventricular myocardium was investigated in 23 dogs. There were 8 control dogs, 9 dogs that manifested ventricular fibrillation within 30 minutes of ligation of the distal left anterior descending coronary artery (group I), and 6 dogs that manifested ventricular fibrillation between 30 and 60 minutes of ligation of the proximal left anterior descending coronary artery (group II). Conduction delay was measured as the change of conduction time from preligation levels to postligation levels in epicardial and endocardial sites in both base to apex (anterograde) and apex to base (retrograde) directions. Conduction delay in all four directions was compared in the control group and groups I and II (ventricular fibrillation). By means of continuous recordings on tape, the origin of ventricular fibrillation was determined to be in the ischemic zone (13 of 15 dogs) or in the border zone (2 of 15 dogs). Conduction delay in all directions was greater in the group with ventricular fibrillation whether the fibrillation occurred after the first or second ligation. Specifically, epicardial anterograde conduction (in the border zone) and retrograde conduction (in the ischemic zone) were significantly delayed in group I. Conduction in group II was significantly delayed in both the ischemic and the border zones in three of four directions at 35 minutes. The rate of change of conduction time in all four directions was significantly greater in the group with ventricular fibrillation than in the control group. Pending further work, this model may provide a reliable marker for the development of spontaneous ventricular fibrillation during acute myocardial ischemia and may permit assessment of various interventions as specific therapy for acute reentrant ischemic tachyarrhythmias leading to ventricular fibrillation.

Acute Disease↗
PubMed1981

Effects of thiopentone on cardiac performance, coronary hemodynamics and myocardial oxygen consumption in chronic ischemic heart disease.

Thiopentone was administered as induction agent for general anesthesia to eight patients with stable ischemic heart disease; 6 mg/kg of the drug induced decrease in arterial blood pressure (-27%), systematic vascular resistance (-20%), stroke volume index (-14%), mean pulmonary arteriolar occlusion pressure (-15%) and left ventricular stroke work index (-38%), while heart rate increased by 10% and cardiac output remained unchanged. Total body oxygen consumption decreased by 30%. Myocardial oxygen consumption decreased by 39% with unchanged or decreased myocardial oxygen extraction and myocardial lactate uptake decreased by 40%. Arterial and coronary sinus hypoxanthine levels were unchanged and no ST-T-segment changes or dysrhythmias were recorded. In the present experimental setting, the results indicate that thiopentone substantially decreased myocardial oxygen requirements. In spite of the marked reduction in coronary perfusion, myocardial oxygen demand was matched by supply, myocardial dysoxia was not induced and cardiodepression was clinically negligible. Rate pressure product was a poor indicator of changes in myocardial oxygen consumption after thiopentone administration.

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