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Biomedical subjects

T Peter

Publications and source records attributed to T Peter.

At least 73 records · Page 4Linked to original sources
PubMed1986

Hemodynamic influences on sinus node recovery time: effects of autonomic blockade.

Ten patients with normal sinus node function were evaluated prospectively, to determine whether the decrease in blood pressure during rapid atrial pacing shortens the corrected sinus node recovery time. All patients had 30 seconds of atrial pacing at cycle lengths from 600 to 300 ms, with continuous arterial pressure monitoring, before and after intravenous administration of propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg). In the control state, a decrease in corrected sinus node recovery time was recorded with faster atrial pacing rates, which was significantly related to the initial drop in systolic blood pressure at the onset of atrial pacing. Specifically, as the initial pressure drop increased from 15 mm Hg or less to 16 to 45 and 45 to 100 mm Hg, corrected sinus node recovery time decreased from 272 +/- 79 to 205 +/- 70 ms (p less than 0.04) and to 134 +/- 120 ms (p less than 0.04), respectively. In contrast, after autonomic blockade, the corrected sinus node recovery time was prolonged, in a near linear fashion, as atrial pacing rates increased. The magnitude of blood pressure drop with atrial pacing did not differ significantly from that in the control state at similar pacing rates. These findings suggest that hypotension during rapid atrial pacing activates autonomic reflexes that significantly shorten the corrected sinus node recovery time. Autonomic blockade negates this effect and the corrected sinus node recovery time prolongs with faster atrial pacing.

Adult↗
PubMed1986

Inducible sustained ventricular tachycardia and ventricular fibrillation in conscious dogs with isolated right ventricular infarction: relation to infarct structure.

The susceptibility of infarcted right ventricular myocardium to inducible ventricular tachyarrhythmias was serially evaluated in 18 conscious dogs during the first 2 weeks after permanent right coronary artery occlusion. Properly timed double premature stimuli applied to the right ventricular outflow tract induced sustained (longer than 1 minute) ventricular tachycardia at rates of 190 to 400 beats/min in nine dogs, and ventricular fibrillation in six dogs. No ventricular arrhythmias could be induced in the remaining three dogs. The zone of premature coupling intervals within which ventricular tachyarrhythmias could be induced decreased in each dog as the infarct aged, and by day 12 after occlusion, no ventricular arrhythmias could be induced in any of the dogs studied. Both the size and the degree of patchiness (graded from 0 for no patchiness to +4 for patchiness throughout the infarct) of the infarct appear to be related to the nature of the induced rhythm. Infarcts with greater heterogeneity and those that were larger than 8% of the right ventricular volume were associated with a higher incidence of ventricular fibrillation, and infarcts with a lesser degree of patchiness were more suitable for sustained ventricular tachycardia (3.4 +/- 1.2 versus 1.4 +/- 0.4, p less than 0.05). These findings indicate that the infarcted right ventricular myocardium, independent of left ventricular involvement, can be associated with malignant ventricular tachyarrhythmias, ventricular tachyarrhythmias can be induced only during a well defined postinfarction period; and both the size and geometry of the right ventricular infarct determine the nature of the induced ventricular rhythm.

Animals↗
PubMed1986

Coronary venous retroinfusion of procainamide: a new approach for the management of spontaneous and inducible sustained ventricular tachycardia during myocardial infarction.

The efficacy of retrograde coronary venous delivery of procainamide for the management of spontaneous and inducible sustained ventricular tachycardia was evaluated and compared with systemic intravenous procainamide administration in 22 conscious dogs with permanent left anterior descending coronary artery occlusion. Selective retrograde injection of procainamide was achieved through an autoinflatable balloon catheter placed in the great cardiac vein, with the tip positioned in the vicinity of the site of left anterior descending coronary occlusion. Great cardiac vein retroinfusion of procainamide was significantly (p less than 0.05) more effective than systemic intravenous injection against spontaneous ventricular tachycardia 1 day after coronary artery occlusion (13 dogs) and against electrically induced sustained ventricular tachycardia in the 3 to 12 day postocclusion period (9 dogs). Significantly lower doses of procainamide were used with retroinfusion as compared with systemic administration, that is, 19.6 +/- 8.8 versus 35 +/- 0 mg/kg body weight during spontaneous tachycardia and 13.4 +/- 4.1 versus 32.1 +/- 2 mg/kg during induced tachycardia (p less than 0.01). Retroinfusion of saline solution through the great cardiac vein had no effect on either type of tachycardia. Myocardial tissue procainamide levels measured in infarcted and ischemic zones of the left anterior ventricular wall were 9 to 100 times higher after great cardiac vein retroinfusion than after systemic injection. Great cardiac vein dye injection studies demonstrated a preferential distribution in left ventricular regions supplied by the occluded coronary artery. It is concluded that regional coronary venous procainamide retroinfusion in dogs with myocardial infarction is more effective than systemic intravenous injection against both spontaneous and inducible sustained ventricular tachycardia. The greater efficacy of great cardiac vein treatment appears to be primarily related to selectively increased delivery of procainamide to ischemic myocardial sites.

Animals↗
PubMed1986

Wide QRS tachycardia due to AV nodal reentry and a "bystander" bypass tract with slow conduction properties.

An unusual mechanism for recurrent, wide QRS complex supraventricular tachycardia is described in this report. A 25-year-old man with normal PR and QRS intervals during sinus rhythm was shown to have preexcitation with a left bundle branch block pattern during tachycardia and during atrial pacing. Electrophysiologic studies demonstrated slow and decremental conduction properties in an accessory "bystander" AV pathway utilized for antegrade conduction during AV nodal reciprocating tachycardia. The differential diagnosis of this tachycardia is discussed in detail.

Adult↗
PubMed1985

Electropharmacologic testing in sustained ventricular tachycardia associated with coronary heart disease: value of the response to intravenous procainamide in predicting the response to oral procainamide and oral quinidine treatment.

Twenty patients with inducible, sustained ventricular tachycardia (VT) were prospectively evaluated to determine whether the response to intravenous procainamide administration, as assessed by programmed ventricular stimulation, predicted the response to oral procainamide and oral quinidine treatment. Six patients (30%) responded to intravenous procainamide (fewer than 10 beats of inducible VT). Ten of 20 patients (50%) responded to oral quinidine and 5 (25%) responded to oral procainamide. Mean drug serum levels were 11.3 +/- 2.1 micrograms/ml for intravenous procainamide, 5.4 +/- 0.8 micrograms/ml for oral quinidine and 11.7 +/- 3.4 micrograms/ml for oral procainamide. There was no significant difference in serum levels between those who responded and those who did not. Fifteen patients (75%) had a concordant drug response for intravenous and oral procainamide. Ten patients (50%) had a concordant response for intravenous procainamide and oral quinidine. Fifteen patients (75%) had a concordant drug response for oral procainamide and oral quinidine. Thus, in patients with sustained VT, the response to intravenous procainamide does not reliably predict the response to oral quinidine or oral procainamide, and serial day drug testing with these agents is necessary. Furthermore, high-dose quinidine therapy may be more effective in controlling VT in these patients than procainamide.

Administration, Oral↗
PubMed1985

Rate-dependent effects of procainamide on His-Purkinje conduction in man.

Microelectrode studies in isolated cardiac tissues have shown that the depressant effect of several antiarrhythmic drugs on the maximal upstroke velocity of the cardiac action potential is rate-dependent. To determine whether this effect of antiarrhythmic drugs is seen in humans, 14 patients undergoing atrial pacing at several rates were prospectively studied before and after the infusion of procainamide (15 mg/kg). The HV interval (His-Purkinje conduction rate) and the QRS duration (intraventricular conduction rate) were measured. Before procainamide infusion, atrial pacing did not significantly prolong the maximal HV interval (from 54 +/- 15 to 58 +/- 13 ms). After procainamide infusion (mean serum level 10.0 +/- 3 micrograms/ml) atrial pacing at an average of 5 pacing rates significantly prolonged the HV interval (from 67 +/- 18 to 80 +/- 20 ms, p less than 0.001). The extent of HV prolongation with atrial pacing after procainamide infusion was independent of the HV interval at rest before procainamide. The duration of the QRS complex also tended to prolong with atrial pacing after procainamide infusion, but this prolongation was not statistically significant. Thus, procainamide produces a rate-dependent depressant effect on His-Purkinje and intraventricular conduction, confirming observations made in isolated tissue preparations.

Adult↗
PubMed1985

Factors that determine the direction and magnitude of precordial ST-segment deviations during inferior wall acute myocardial infarction.

Sixty-one patients with inferior acute myocardial infarction (AMI) and no evidence of prior AMI were studied to determine which factors influence the magnitude of precordial ST-segment depression. In the total study group, there was a significant but weak correlation between the magnitude of precordial ST-segment depression and the magnitude of inferior ST-segment elevation (r = -0.46, p less than 0.001). In the 29 patients with evidence of concomitant right ventricular (RV) involvement, precordial ST-segment depression was significantly smaller both in absolute terms (-1.3 +/- 1.8 vs -2.8 +/- 1.9 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -0.2 +/- 1.0 vs -1.1 +/- 0.5, p less than 0.01), whereas in the 15 patients with lateral ST-segment elevation (greater than or equal to 1 mm in lead V6), precordial ST-segment depression was significantly greater both in absolute terms (-3.5 +/- 2.3 vs -1.6 +/- 1.7 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -1.1 +/- 0.8 vs -0.5 +/- 0.9, p less than 0.02). Consistent with these findings, the correlation between the magnitudes of precordial and inferior ST-segment deviations was considerably improved when only the 24 patients with neither evidence of RV involvement nor lateral ST-segment elevation were analyzed (r = 0.89, p less than 0.001, n = 24). These data suggest that in patients with inferior AMI, there is a reciprocal relation between precordial and inferior ST-segment deviations, which is distorted by concomitant RV involvement and by concomitant lateral left ventricular wall involvement.

Aged↗
PubMed1985

Hemodynamic benefits of synchronized 1:1 atrial pacing during sustained ventricular tachycardia with severely depressed ventricular function in coronary heart disease.

The hemodynamic effects of atrial pacing were studied in 8 patients who had ventricular tachycardia (VT) during electrophysiologic testing. These patients had chronic recurrent VT associated with organic heart disease and depression of left ventricular function (ejection fraction = 0.23 to 0.35). Hemodynamic variables were recorded during sinus rhythm (58 to 103 beats/min), pacing-induced VT (133 to 214 beats/min) and synchronized 1:1 triggered atrial pacing (atrium paced, ventricle sensed and triggered mode) during VT. For the latter, the ventriculoatrial coupling interval was adjusted to produce a maximal blood pressure response; the optimal interval was observed to be between 60% and 73% of the RR interval. Mean arterial blood pressure decreased after the onset of VT (90 +/- 11 to 79 +/- 14 mm Hg, p less than 0.05) but increased again when atrial pacing was added, to 98 +/- 12 mm Hg. Cardiac index decreased during VT (2.2 +/- 0.5 to 1.8 +/- 0.5 liters/min/m2 p less than 0.05), but in each case improved by the addition of atrial pacing, to 1.9 +/- 0.5 liters/min/m2. Evidence from pressure recordings suggested that optimal atrial pacing resulted in atrial contraction in early left ventricular diastole. Thus, appropriately timed atrial pacing during VT can result in significant increases in blood pressure and a consistent increase in cardiac index. In addition to offering insight into the mechanisms of hemodynamic compromise during VT, the clinical use of this technique may be to improve hemodynamic values in patients with hemodynamically unstable VT.

Aged↗
PubMed1985

Mode of stimulation versus response: validation of a protocol for induction of ventricular tachycardia.

Electrophysiologic studies were prospectively performed in 91 consecutive patients referred for evaluation of sustained ventricular tachycardia or sudden cardiac death. Fifty-two patients had a history of sustained ventricular tachycardia and 39 patients had a history of sudden cardiac death. The identical stimulation protocol was used in all patients. The stepwise protocol involved atrial pacing, burst ventricular pacing, single, double, and triple extrastimuli during ventricular pacing. Stimulation was performed at the right ventricular apex at two and five times diastolic threshold. Using this protocol, ventricular tachycardia was inducible in 48 (92%) of the 52 patients with a history of sustained ventricular tachycardia and in 28 (72%) of 39 patients with a history of sudden cardiac death (p less than 0.02). The use of a third extrastimulus increased the yield of inducible ventricular tachycardia by 37% in patients with a history of sustained ventricular tachycardia and by 25% in patients with a history of sudden cardiac death. Stimulation at five times diastolic threshold and stimulation from the right ventricular outflow tract added a 15% increment in overall yield of inducible ventricular tachycardia in patients with a history of sustained ventricular tachycardia, and a 26% increment in yield in patients with a history of sudden cardiac death. Forty-four (92%) of the 48 inducible patients in the sustained ventricular tachycardia group had inducible monomorphic ventricular tachycardia as compared to 19 (68%) of 28 patients in the sudden cardiac death group (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

The yield of programmed ventricular stimulation in mitral valve prolapse patients with ventricular arrhythmias.

A high-risk subset of patients with mitral valve prolapse (MVP) and a predisposition to sudden cardiac death (SCD) has been proposed. We analyzed the results of programmed ventricular stimulation (PVS) in 20 patients with MVP and ventricular arrhythmias (ventricular premature depolarization in 6, ventricular couplets in 2, nonsustained ventricular tachycardia [VT] in 7, ventricular fibrillation [VF] in 5) and in 12 "normal" control subjects. With the use of an identical stimulation protocol from the right ventricular apex (twice diastolic threshold, three extrastimuli), 9 of 20 MVP patients and 1 of 12 normal subjects had inducible ventricular arrhythmias (p less than 0.05). When more aggressive attempts at ventricular stimulation were used, an additional five MVP patients had positive responses to PVS while no normal subjects did. In the MVP group, the following arrhythmias were induced: nonsustained polymorphic VT in 10, VF in three, and ventricular flutter in one. In all but two patients, triple ventricular extrastimuli were required to elicit this response. Two of the 10 MVP patients undergoing electropharmacologic testing had a successful antiarrhythmic regimen identified, while 13 patients were discharged on empiric antiarrhythmic therapy. At a follow-up of 19.8 +/- 13.1 months, all 19 MVP patients who could be contacted were alive. Five patients had symptomatic recurrences at follow-up including two SCD survivors (VT in one and VF in one). In conclusion, it was found that the majority of MVP patients with ventricular arrhythmias have inducible ventricular tachyarrhythmias during PVS and are more susceptible to this than patients without structural heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Spontaneous ventricular tachycardia associated with isolated right ventricular infarction, one day after right coronary artery occlusion in the dog: studies on the site of origin and mechanism.

The electrophysiologic and arrhythmic properties of isolated infarcted right ventricle (RV) were studied in 17 dogs during the first 24 hours after complete occlusion of the right coronary artery (RCA). During the 16-to-20-hour post occlusion period, spontaneously occurring sustained monomorphic ventricular tachycardia (VT) was present in all 17 dogs. Overdrive ventricular pacing (cycle lengths 200 to 250 msec) caused significant suppression of the VT when the rate of the VT was slower than 150 bpm (range 120 to 145 bpm) (n = 9), but had negligible effect when VT rate was higher than 150 bpm (range 160 to 245 bpm (n = 8). Overdrive pacing could not terminate either the slow or the fast type of VT. Bipolar intramural electrograms have showed electrical activity in the infarcted RV zone to precede Q wave of the VT by 15.4 +/- 5.8 msec regardless of VT rate. Microelectrode studies on isolated RV endocardial infarcted tissues 24 hours after RCA occlusions have shown the presence of spontaneous repetitive activity at a rate of 87 +/- 47 bpm, which was overdrive suppressed in dogs with slow VT, and spontaneous activity at a rate of 115.2 +/- 36 bpm (p less than 0.05) which was not overdrive suppressed in dogs with fast VT. Maximum diastolic potential, action potential amplitude, and Vmax of surviving subendocardial Purkinje fibers (SEPF) in the infarct zone were slightly but significantly depressed (p less than 0.05), and they manifested enhanced phase 4 depolarization, giving rise to automatic impulse initiation. Although action potential duration of these fibers was somewhat prolonged (p less than 0.05), no conduction delay occurred. Histopathologic examinations have shown necrosis of the basal two thirds of the RV, with no left ventricular involvement. Electron microscopy revealed lipid accumulation in the surviving SEPF as the sole abnormality. We conclude (1) that occlusion of the RCA in the dog is associated with high survival rate despite extensive necrosis involving exclusively the RV and (2) that VT seen during the 20 to 24 hours after occlusion arise in the infarcted zone of the RV, by an enhanced automatic mechanism in the surviving SEPF, possibly caused by cytoplasmic lipid accumulation. This model, by virtue of its high survival rate and frequency of late VTs, should be useful in providing clues to determine factors involved in the genesis of early VT/VF and for the evaluation of new pharmacologic agents during the 20- to 24-hour VT period.

Animals↗
PubMed1985

Precordial ST segment depression during acute inferior myocardial infarction: early thallium-201 scintigraphic evidence of adjacent posterolateral or inferoseptal involvement.

To investigate the myocardial perfusion correlates of precordial ST segment depression during acute inferior myocardial infarction, a rest thallium-201 scintigram and a closely timed 12 lead electrocardiogram were obtained within 6 hours of the onset of infarction in 44 patients admitted with their first acute inferior myocardial infarction. Thirty-six patients demonstrated precordial ST segment depression (group 1) and eight did not (group 2). A perfusion defect involving the inferior wall was present in all 44 patients. Additional perfusion defects of the adjacent posterolateral wall (n = 20), the ventricular septum (n = 9) or both (n = 6) were present in 35 of 36 patients from group 1 compared with only 1 of 8 patients from group 2 (p less than 0.001). There was no significant difference in the frequency of multivessel coronary artery disease or disease of the left anterior descending artery between group 1 and group 2 or between patients with and those without a thallium-201 perfusion defect involving the ventricular septum. Thus, precordial ST segment depression during an acute inferior myocardial infarction is associated with thallium-201 scintigraphic evidence of more extensive involvement of the adjacent posterolateral or inferoseptal myocardial segments, which probably reflects the extent and pattern of distribution of the artery of infarction, rather than the presence of coexistent multivessel coronary artery disease or disease of the left anterior descending artery.

Aged↗
PubMed1985

Closed chest catheter ablation of an accessory pathway in a patient with permanent junctional reciprocating tachycardia.

This report describes a 23 year old woman with a lifelong history of permanent junctional reciprocating tachycardia refractory to conventional antiarrhythmic medications who was successfully treated with closed chest, transvenous selective ablation of a posteroseptal bypass tract. Two 100 J (stored) direct-current shocks were delivered to the region of the os of the coronary sinus using a quadripolar catheter positioned in the coronary sinus. At a 2 month follow-up interval, the patient is asymptomatic without recurrence of the tachycardia. It is concluded that in patients with permanent junctional reciprocating tachycardia, selective catheter ablation of a posteroseptal accessory pathway is a feasible alternative to a difficult pharmacologic regimen or to ablative surgery.

Adult↗
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↗