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Biomedical subjects

T Peter

Publications and source records attributed to T Peter.

At least 91 records · Page 5Linked to original sources
PubMed1985

Sinus node electrogram in patients with the hypersensitive carotid sinus syndrome.

Sinus node electrograms were obtained in two patients with unexplained syncope and the cardioinhibitory form of the hypersensitive carotid sinus syndrome. Direct recordings of sinus node potentials were obtained using a transvenous electrode catheter. Sinus node function was normal in both patients during standard electrophysiologic evaluation. Carotid sinus massage was performed in both patients and the sinus node electrogram was continuously recorded. After the onset of carotid sinus massage, prolongation of sinoatrial time, slowing of sinus rate of depolarization, sinoatrial exit block and finally sinus node arrest were recorded. After termination of carotid sinus massage, sinus node potentials did not precede the first atrial impulse; subsequent beats showed markedly prolonged sinoatrial times as well as changes in the P wave on the surface electrocardiogram. Sinus rate and sinoatrial time returned to control values gradually, as did the P wave configuration. Intravenous atropine (1.0 mg) abolished the abnormal response to carotid sinus massage. It is concluded that the application of carotid sinus massage in patients with the hypersensitive carotid sinus syndrome produces profound changes in sinoatrial conduction including sinoatrial exit block, as well as shifts in primary pacemaker site and sinus node arrest. These alterations in conduction and automaticity are reversible with atropine and may be secondary to denervation sensitivity to acetylcholine.

Aged↗
PubMed1985

Evaluation of amiodarone therapy in the treatment of drug-resistant cardiac arrhythmias: long term follow-up.

The clinical efficacy of amiodarone in the management of patients with complex cardiac arrhythmias refractory to therapy with two or more conventional or other investigational anti-arrhythmic agents was studied by long-term follow-up of patients who had received the drug for a period of at least three months. A total of 181 patients, classified into four groups (Group 1--supraventricular arrhythmias, n = 42; Group 2--frequent VPBs, n = 46; Group 3--nonsustained V-tach, n = 16; and Group 4--sustained V-tach, n = 77) received a daily maintenance dose of 200-800 mg of Amiodarone for a period of up to 30 months. There were a total of 26 deaths (14%). Ten of these were classified as probable arrhythmic deaths; however, all had either good or excellent response to therapy over a mean follow-up period of 14.9 months prior to death. The drug had to be permanently discontinued due to side effects only in three patients and in the majority of patients with side effects symptoms could be alleviated with adjustment of dosage, thyroid replacement therapy or transient cessation of therapy. We conclude that amiodarone is highly effective in the management of high-risk patients with complex refractory cardiac arrhythmias and that close monitoring and prompt recognition of side effects and appropriate adjustment of dosage or institution of supplemental or replacement therapy (in less than 5% of patients) will allow continuation of amiodarone. The benefit of suppression of symptomatic arrhythmias and the potential of prevention of sudden death, far outweighs the incidence of severe side effects.

Adolescent↗
PubMed1984

Electrophysiologic and hemodynamic effects of propafenone, a new antiarrhythmic agent, on the anesthetized, closed-chest dog: comparative study with lidocaine.

The relative hemodynamic and electrophysiologic effects of a new antiarrhythmic drug, propafenone, and lidocaine were evaluated in eight closed-chest, anesthetized dogs. Propafenone (4 mg/kg intravenously) significantly (p less than 0.05) lowered aortic and pulmonary systolic pressures and caused a rise in heart rate (p less than 0.05). Cardiac output decreased from 4.5 +/- 1 to 3.8 +/- 0.7 L/min (p less than 0.05) during atrial pacing at 400 msec cycle length. Propafenone had no effect on pulmonary and aortic diastolic pressures. Lidocaine (5 mg/kg intravenously) caused a significant (p less than 0.05) decrease in aortic systolic pressure and a rise in heart rate. Lidocaine had no significant effect on the other measured hemodynamic parameters. Propafenone, unlike lidocaine, significantly (p less than 0.05) increased atrioventricular nodal functional refractory period and right ventricular endocardial (apex) cathodal (0.5 +/- 0.1 mA to 1.9 +/- 0.3 mA) and bipolar (1.4 +/- 0.3 to 2.2 +/- 0.4 mA) diastolic excitability threshold. Propafenone, unlike lidocaine, also caused a significant (p = 0.05) intraatrial conduction delay; however, neither drug caused conduction slowing in the His-Purkinje system. Both drugs had no effect on sinus nodal recovery time and on the effective refractory period of the right ventricular endocardium (apex). Mean plasma propafenone levels during hemodynamic and electrophysiologic measurement ranged between 3.2 +/- 1.8 micrograms/ml and 1.7 +/- 1.1 micrograms/ml. All of the propafenone-induced effects were reversible within 90 minutes. We conclude that propafenone differs from lidocaine in its atrial, AV nodal, and ventricular electrophysiologic properties, and thus these may explain propafenone's greater efficacy over lidocaine against both certain atrial and ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1984

Verapamil effects in AV node reentry tachycardia with intermittent supra-Hisian AV block.

The electrophysiologic details of two patients with atrioventricular (AV) node reentry tachycardia with intermittent 2:1 supra-Hisian block are presented. Both patients had clear evidence for atrial arrhythmias as well, emphasizing the need for a careful diagnostic analysis. Evidence supporting a diagnosis of AV node reentry tachycardia included: (1) short ventriculoatrial (VA) coupling intervals, (2) normal retrograde sequence of atrial activation, (3) dependence on critical AV node conduction times for initiation of tachycardia by atrial pacing, (4) ability to pace and capture the atria or ventricles without interrupting the tachycardia, and (5) fixed VA coupling intervals despite changes in tachycardia cycle length. Ten milligrams of verapamil was administered during sustained supraventricular tachycardia with 1:1 AV conduction, but despite prompt termination of tachycardia in both cases, 2:1 AV block was not induced. Atrial echoes could still be induced after verapamil, and diagnostic features (3) and (5) were particularly evident after the drug. Further analysis confirmed that verapamil did not have any observable effects on the likely site for supra-Hisian block--that is, the "final common pathway" of the AV node. This would support a contention that verapamil may have a selective effect on tissues within the confines of the AV node.

Adult↗
PubMed1984

The relationship between ventricular arrhythmias and ischemia-induced conduction delay in closed-chest animals within 24 hours of myocardial infarction.

To investigate the myocardial conduction characteristics of premature impulses during the first 24 hours following coronary ligation and its relationship to late infarction ventricular arrhythmias, transmural electrodes were positioned in the normal and ischemic myocardium in nine dogs. Cardiac conduction in ischemic myocardium was delayed 15 minutes post coronary occlusion both in the epicardium and endocardium, both in the anterograde (base to apex) and retrograde (apex to base) direction, and was maintained at the same level throughout the experiment. Conduction across the border of ischemic myocardium from ischemic to the normal segment was also delayed, especially in the endocardium. Spontaneous ventricular arrhythmias recorded on Holter tapes showed significant increase in the number of premature ventricular complexes and ventricular tachyarrhythmias 9 hours after infarction. Thus our findings suggest that spontaneous arrhythmias occurring in the late phase of acute myocardial infarction (AMI) are independent of the ischemia-induced conduction delay and an alternate mechanism such as abnormal automaticity may be responsible for late ventricular arrhythmias.

Animals↗
PubMed1984

Prognosis after sudden cardiac death without associated myocardial infarction: one year follow-up of empiric therapy with amiodarone.

Thirty-three consecutively referred patients with cardiac arrest from ventricular arrhythmias unassociated with a new acute myocardial infarction (AMI) were commenced on amiodarone therapy and followed for a minimum of 12 months. The dose of amiodarone was adjusted to maximum tolerance and not according to the incidence of asymptomatic ventricular premature complex activity. Eight patients died including five sudden deaths. Five out of the eight deaths occurred either within 3 months of therapy or when the dose of amiodarone was less than 400 mg/day. The majority of patients were found to have corneal microdeposits or either thyroid or liver function abnormalities, although none had any clinical manifestation. Ten patients had neurologic side effects. In summary, although the overall cardiac mortality seemed to be reduced by amiodarone therapy and the drug appears to be well tolerated by patients, its role in the prophylaxis against recurrent ventricular fibrillation may be enhanced by a regimen of higher loading and maintenance doses.

Adult↗
PubMed1984

Factors related to the induction of ventricular fibrillation in the normal canine heart by programmed electrical stimulation.

Programmed electrical stimulation was performed in eight normal dogs using a stimulator and endocardial electrode catheters identical to those used in human studies. The right and left ventricular apex were paced at a drive cycle length of 400 ms and, in some cases, 500 ms, with a pacing sequence of single (S1S2), double (S1S2S3) and triple (S1S2S3S4) premature impulses introduced after eight paced complexes. Pacing sequences were performed using combinations of pulse width (1, 2 and 4 ms) and current strengths of 2, 5 and 10 times diastolic threshold, and in three dogs, 15 times diastolic threshold. Twenty-two episodes of ventricular fibrillation were initiated in five dogs in 170 pacing sequences using current strengths up to 10 times diastolic threshold, and six episodes of ventricular fibrillation in the two of three remaining dogs tested at 15 times diastolic threshold. Ventricular fibrillation was reproducible on seven of nine occasions. Ventricular fibrillation was never induced by S1S2 at up to 15 times diastolic threshold; it was induced by S1S2S3 in 3 (1.8%) of 170 sequences, but only at 10 times diastolic threshold. It was induced by S1S2S3S4 in 19 (11.4%) of 167 sequences using 2 to 10 times diastolic threshold, although 20 of 28 episodes only occurred with S1S2S3S4 at 10 or more times diastolic threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Evaluation of amiodarone therapy in the treatment of drug-resistant cardiac arrhythmias: long-term follow-up.

The clinical efficacy of amiodarone in the management of complex cardiac arrhythmias refractory to therapy with two or more conventional or other investigational antiarrhythmic agents was determined by long-term follow-up in patients who had received the drug for at least 3 months. A total of 181 patients, classified into four groups (group 1, supraventricular arrhythmias, n = 42; group 2, frequent ventricular premature complexes, n = 46; group 3, nonsustained ventricular tachycardia, n = 16; and group 4, sustained ventricular tachycardia, n = 77) received a daily maintenance dose of 200 to 800 mg amiodarone for up to 30 months. There was a total of 26 deaths (14%). Ten of these were probably attributable to arrhythmia, although all patients had either good or excellent response to therapy over a mean follow-up of 14.9 months prior to death. The drug had to be permanently discontinued because of side effects in only three patients, and in the majority of patients with side effects, symptoms could be alleviated with adjustment of dosage, thyroid replacement therapy, or temporary cessation of therapy. We conclude that amiodarone is highly effective in high-risk patients with complex refractory cardiac arrhythmias, and that close monitoring and prompt recognition of side effects and appropriate adjustment of dosage or institution of supplemental or replacement therapy (in less than 5% of patients) will allow continuation of amiodarone. The benefit of suppression of symptomatic arrhythmias and the potential of prevention of sudden death clearly outweigh the modest incidence of severe side effects.

Aged↗
PubMed1983

Electrophysiologic effects of bretylium on canine ventricular muscle during acute ischemia and reperfusion.

Electrophysiologic effects of bretylium were assessed on a recently developed animal model for analysis of conduction of premature impulses and excitation threshold. Bretylium was administered intravenously 10 mg/kg over 10 minutes followed by 2 mg/min of infusion immediately after coronary ligation. Conduction of the premature impulse was recorded in the epicardial and endocardial sites both in the base-to-apex and apex-to-base directions, in the normal, in the center, and across the border of ischemic myocardium. Compared to the control group of animals, bretylium did not cause any significant change in the conduction characteristics in the ischemic myocardium; however, it delayed the conduction of premature impulses in the normal myocardium. Thus the disparity in conduction times between the normal and the ischemic myocardium was lessened by bretylium. Further, conduction of impulses from normal tissue across the border of ischemia was also delayed. Bretylium also decreased the excitability threshold in the ischemic myocardium, although the normal myocardial excitation threshold was unaffected. These unique effects of bretylium on conduction and excitability in the normal, in the center, and across the border of ischemic myocardium, when a therapeutic dosage of the drug is used, further validate its antiarrhythmic potential and offer an insight into its mechanism of action in the setting of acute myocardial ischemia.

Animals↗
PubMed1983

Atrioventricular node reentry: intravenous verapamil as a method of defining multiple electrophysiologic types.

Fourteen patients with recurrent supraventricular tachycardia (SVT) underwent electrophysiological evaluation. Each patient was shown to have reentry confined to the region of the atrioventricular (AV) node. Verapamil, 0.075 to 0.15 mg/kg was administered intravenously to each patient during a stable episode of SVT, resulting in termination in each instance. There was more than one mechanism for termination of SVT. Nine patients showed termination by anterograde AV node block preceded by an increase in conduction time in the anterograde limb of the tachycardia circuit (Ae-H intervals) with no change in the conduction time in the retrograde limb (H-Ae intervals). Three patients showed termination by block in the retrograde limb of the circuit preceded by increases in both Ae-H and H-Ae intervals. An additional example of termination by spontaneous ventricular premature complexes and usurpation by sinus rhythm were also seen. Common features were that verapamil had significant effects on anterograde and retrograde conduction and refractoriness in the AV node. It prolonged the refractory periods of both fast and slow pathways in patients with dual anterograde AV node pathways, and observable effects on retrograde conduction and refractoriness were seen even in patients with constant ventriculoatrial conduction times during incremental ventricular pacing in a control study. However, three distinct groups of patients were identified on the basis of their response to ventricular pacing in a control study and upon verapamil effects recorded during their SVT. An explanation for these latter findings may be that there is a normal variation in the retrograde response of parts of the AV node to ventricular pacing, and a variability in some of the patients' responses to verapamil.

Adult↗
PubMed1983

Electrophysiologic observations during the spontaneous initiation of ischemia-induced ventricular fibrillation.

Electrophysiologic features of spontaneous, ischemia-induced ventricular fibrillation were studied in 17 dogs using multiple endocardial bipoles positioned in normal and ischemic zones and at the border of ischemic myocardium. All dogs showed ventricular tachyarrhythmias prior to the initiation of ventricular fibrillation. The heart rate prior to the fatal arrhythmia in the ventricular fibrillation dogs was significantly faster than that of nonventricular fibrillation dogs. There was no difference in the coupling intervals of the initial premature complex between episodic and sustained ventricular arrhythmia in most dogs. However, shorter coupling intervals initiated sustained arrhythmia in some dogs. Sites of initiation of arrhythmia were mostly in the ischemic zone. Furthermore, diastolic electrical activity was consistently observed in the ischemic zone during fatal arrhythmia in dogs showing diastolic activity. Cycle length during the fatal arrhythmia prior to ventricular fibrillation gradually shortened, whereas cycle length of episodic ventricular tachycardia remained approximately 200 msec followed by lengthening prior to restoration of sinus rhythm. The disparity of local activation (time differences between the earliest and latest onset of the activation in the five recording sites) increased during the fatal arrhythmia. Examples of progressive intraventricular block (Wenckebach-like) between the border and the center of ischemic myocardium leading to ventricular fibrillation are resynchronization of this disparity leading to the termination of ventricular tachycardia are shown. The recording of continuous electrical activity using bipolar electrodes with an interelectrode distance of 1 mm suggests a smaller reentrant pathway during fatal arrhythmia. Our observations confirm the importance of endocardial recordings within ischemic myocardium, and adds new insight into the events leading to both episodic and sustained ventricular tachycardia.

Animals↗
PubMed1983

Electrophysiologic observations on ventricular tachyarrhythmias following reperfusion.

The threat of reperfusion fibrillation could potentially deter attempts of reperfusion in patients with acute myocardial infarction. Delineation of the mechanisms of this arrhythmia could pave the way to newer interventions designed as prevention or definitive treatment. Therefore the purpose of the present study was to investigate the features of initiation of reperfusion-induced ventricular fibrillation, and further to distinguish between episodic and sustained ventricular arrhythmias following reperfusion. Nine instances of reperfusion ventricular fibrillation and five instances of episodic tachyarrhythmia were analyzed in the study utilizing endocardial bipolar electrograms from normal, ischemic, reperfused, and border of these myocardial segments. In 11 of 14 instances, the site of initiation of the tachyarrhythmias was in the reperfused myocardium; however, maintenance of the arrhythmia defined as diastolic and or continuous electrical activity suggestive of reentry was not seen in the reperfused myocardium in any of these instances. Diastolic electrical activity was observed in 8 of 14 instances, and was seen either in the center or border of ischemic myocardium. Neither heart rate or mean aortic pressure was different between episodic and sustained arrhythmia groups; however, the initial beat of the fatal arrhythmia was significantly more premature than that of episodic arrhythmia. In addition, shorter cycle length, greater variations in the cycle length, and greater disparity in local activation during the tachyarrhythmia were seen in the sustained arrhythmia group compared to the episodic group; cycle length increased and the disparity in local activation improved gradually prior to the termination of the arrhythmia. There was no particular difference in conduction delay immediately prior to reperfusion between control and reperfusion ventricular fibrillation groups. We conclude that different mechanisms exist for the initiation and maintenance of reperfusion-induced arrhythmias. Further, several features seem to distinguish episodic from fatal arrhythmias following reperfusion.

Animals↗
PubMed1983

Wall motion abnormalities and electrocardiographic changes in acute transmural myocardial infarction: implications of reciprocal ST segment depression.

Left ventricular ejection fraction and regional wall motion were assessed by multigated equilibrium radionuclide ventriculography within 24 hours of onset of first acute transmural myocardial infarction (MI) in 32 patients. Abnormal left ventricular wall motion was noted in all 16 patients with anterior infarction and in 14 of 16 (87.5%) patients with inferior infarction. Regional wall motion abnormalities frequently included areas adjacent to and remote from those predicted by the ECG location of ST elevation and pathologic Q waves. Such remote wall motion abnormalities were associated with reciprocal ST segment depression in 17 of 18 (94%) patients, and conversely reciprocal ST segment depressions were associated with remote wall motion abnormalities in 17 of 24 (71%) patients. The left ventricular ejection fraction was lower in patients with a reciprocal ST segment depression compared to those without (anterior MI 0.29 +/- 0.07 vs 0.43 +/- 0.08, p less than 0.01; inferior MI 0.45 +/- 0.11 vs 0.63 +/- 0.06, p less than 0.001). In addition, the peak MB-CK levels were higher in patients with compared to those without reciprocal ST segment depression (anterior MI 268 +/- 183 vs 102 +/- 60, p less than 0.05; inferior MI 186 +/- 120 vs 67 +/- 20, p less than 0.05). Thirteen of 18 (72%) patients with reciprocal ST segment depression compared to 4 of 13 (31%) patients without reciprocal ST segment depression had a complicated clinical course during their hospital stay. These observation suggest that global left ventricular dysfunction in first acute transmural MI is greater when reciprocal ST segment depression is present on the 12-lead ECG.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Comparative study of the effect of slow channel inhibiting agents on ischemia-induced conduction delay as relevant to the genesis of ventricular fibrillation.

Conduction delay has been shown to be an important factor in the genesis of ventricular fibrillation (VF). We evaluated the relationship between conduction delay and (1) initiation of VF and (2) the effects of Ca++ blockers on conduction delay in 41 dogs: eight control (nontreated, non-VF); nine ischemic VF; eight verapamil-treated (0.15 mg/kg bolus followed by 7.5 micrograms/kg/min); eight diltiazem-treated (20 micrograms/kg/min); and eight nifedipine-treated (0.1 mg/kg bolus). Propagation of electrically-induced premature impulses from the midmyocardial bipole of one transmural electrode was recorded at epicardial and endocardial bipoles of other electrodes before and 5, 15, and 30 minutes after coronary ligation. Conduction delay (i.e., conduction times compared to preligation levels) of VF, verapamil, diltiazem, and nifedipine groups were compared to control group in normal and in the center and border of ischemic zones in both base to apex (anterograde) and apex to base (retrograde) directions. Results showed that there was no change in conduction delay in the normal zone between control and VF groups or the treated groups, but both in the center and border of ischemic zone VF was quantitatively related to conduction delay and Ca++ blockers, except that nifedipine significantly reduced conduction delay. We conclude that our model provides a new approach to the assessment of anti-VF intervention. Further, verapamil and diltiazem appear to be useful agents in reducing the risk of ischemia-induced reentrant ventricular tachyarrhythmias.

Animals↗
PubMed1983

Characterization of left ventricular mechanical function during arrhythmias by two-dimensional echocardiography. II. Location of the site of onset of premature ventricular systoles.

Two-dimensional echocardiography was applied experimentally in a closed chest dog model with intact pericardium to determine the location, magnitude and extent of contractile response during pacing from discrete ventricular sites. Midventricular short-axis tomographic images obtained during regular sinus rhythm and subsequent premature ventricular beats provided comparative measurements of global and segmental systolic changes of cross-sectional luminal areas and myocardial wall thickness. Computer-assisted standardized analysis of segmental systolic fractional area change and wall thickening was used to map left ventricular contraction during normal rhythm and premature beats of 70% coupling interval, induced alternately from anterior and lateral aspects of the mid-left ventricular short-axis cross-sectional plane. A characteristic pattern consisting of early systolic contraction and wall thickening was followed by paradoxical motion and wall thinning in late systole in segments corresponding to the region of direct electrical stimulation. Statistical analysis of segment by segment function indicated a maximal amount of premature beat contractile derangement at the site of the stimuli. Pacing from a right ventricular wall site in the midventricular plane caused a similar premature beat response at the anterior aspect of the interventricular septum. It is concluded that two-dimensional echographic analysis of segmental ventricular function can identify the location of electrical stimuli, and thus might noninvasively characterize regional patterns of contraction associated with ectopic foci during arrhythmias.

Animals↗