QT prolongation and torsades de pointes after administration of trimethoprim-sulfamethoxazole.
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Aged↗
Biomedical subjects
T Peter
Publications and source records attributed to T Peter.
Atropine resistant post infarction complete AV block: possible role of adenosine and improvement with aminophylline.
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Aged↗
Effects of propafenone on sinus nodal and ventricular automaticity: in vitro and in vivo correlation.
The electrophysiologic effects of the new antiarrhythmic drug, propafenone, were evaluated in anesthetized closed-chest dogs and on isolated cardiac tissues with the microelectrode technique. Propafenone (2 to 4 mg/kg intravenously) had no effect on sinus rate or on sinus nodal recovery time, but caused a dose-dependent significant decrease in the rate of idioventricular rhythm and increased the duration of ventricular overdrive suppression in dogs (n = 8) with complete atrioventricular block. On isolated canine Purkinje fibers (n = 8) manifesting automaticity with resting membrane potential less negative than -70 mV, propafenone reduced the slope of phase 4 depolarization and reduced the rate of automatic impulse initiation in a concentration-dependent manner (10(-6) M-4.10(-5) M). At these concentrations, propafenone had no effect on rabbit sinus nodal automaticity (n = 8) or on sinoatrial conduction. However, significant depression of sinus nodal automaticity occurred with propafenone concentrations above 5.10(-6) M in the presence of cholinergic or complete autonomic blockade with atropine (10(-6) M) and propranolol (5.10(-5) M). Propafenone caused a concentration-dependent decrease in the disparity of Purkinje fiber-ventricular muscle action potential duration (APD), mainly by shortening Purkinje fiber APD. We conclude: that propafenone suppresses idioventricular rhythm in the intact dog, most likely by depressing Purkinje fiber automaticity; the depressant effect of propafenone on sinus nodal automaticity is evident only during cholinergic receptor blockade; and the antiarrhythmic properties of propafenone may include removal of APD disparity by selective shortening of Purkinje fiber and not of ventricular muscle APD.
Animals↗
Acute and chronic effects of amiodarone on delayed afterdepolarization and triggered automaticity in rabbit ventricular myocardium.
The effects of amiodarone on delayed afterdepolarization (DAD) and triggered automaticity induced by low potassium (0.5 mEq/L) were evaluated on isolated rabbit right ventricular muscles, by means of standard microelectrode techniques. Triggered automaticity was induced in 6 of 10 muscles in the control group, in four of eight in the amiodarone-superfused group, and in three of four in the Tween 80-pretreated group. In contrast, triggered automaticity could be induced in only 2 of 10 of amiodarone-pretreated muscles (n = 10) (20 mg/kg intraperitoneally, daily for 4 weeks; p less than 0.05 compared to control and amiodarone-superfused groups). The amplitude of DAD was significantly lower in muscles isolated from rabbits pretreated with amiodarone compared to those from nontreated control rabbits (n = 17). The degree of reduction was significant during all three cycle lengths of stimulation tested (800, 600, and 400 msec), that is, 2.5 +/- 1.8 vs 5.1 +/- 1.8, 2.4 +/- 2.1 vs 5.5 +/- 2.3, and 3.3 +/- 3.4 vs 9.3 +/- 4.3, respectively (values are in millivolts of mean +/- SD). Superfusion with amiodarone (3 micrograms/ml; n = 8) significantly (p less than 0.05) reduced the amplitude of DAD at 800 msec cycle length, but had no significant effect at cycle lengths of 600 and 400 msec. Tissue concentrations of amiodarone in the pretreated group were significantly (p less than 0.05) lower than those in the superfused group (10 +/- 6.8 vs 21 +/- 3.1 micrograms/gm).(ABSTRACT TRUNCATED AT 250 WORDS)
Action Potentials↗
Failure of episodic high-dose oral verapamil therapy to convert supraventricular tachycardia: a study of plasma verapamil levels and gastric motility.
The practicality of administering large oral doses of verapamil tablets to terminate supraventricular tachycardia (SVT) was investigated in 10 patients. A pilot study in four patients showed that unexpectedly low plasma levels (less than 40 ng/ml) were obtained 60 minutes after administering 160 mg or 240 mg of verapamil during SVT. Nuclear studies in the six other patients showed that fractional liquid gastric emptying times (T) were significantly prolonged in SVT compared to sinus rhythm (SR), p less than 0.05 from T 1/3 onward. Further verapamil absorption studies (200 to 360 mg) performed during SVT and SR in five of six patients showed that peak verapamil levels in four patients in SVT were 23% to 71% lower than in sinus rhythm, where they had peaked at greater than 250 ng/ml 60 minutes post verapamil ingestion, and areas under the plasma concentration time curves were 26% to 100% (mean 67%) less in SVT than in SR for all five patients. SVT was terminated by verapamil in one patient after 40 minutes and the rate of SVT was slowed after 90 minutes in two other patients. Thus plasma verapamil levels are considerably reduced during SVT as compared to SR, and changes in gastric emptying are likely a contributing cause. Since SVT was converted to sinus rhythm in only 1 of 10 patients within 1 hour, large oral doses of verapamil tablets appear unsatisfactory for the episodic treatment of SVT.
Administration, Oral↗
Progression of complete heart block to isolated infra-Hisian block following penetrating cardiac trauma.
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Adult↗
Cellular electrophysiologic characteristics of surviving subendocardial fibers in chronically infarcted right ventricular myocardium susceptible to inducible sustained ventricular tachycardia.
Permanent occlusion of the right coronary artery (RCA) is associated with inducible sustained ventricular tachyarrhythmias (VT) during days 3 to 10 post RCA occlusion period in the conscious dog; VT could no longer be induced beyond this post occlusion period. The aims of the present study were to determine if subendocardial (SE) fibers in the infarcted right ventricle (RVI) during both inducible and noninducible phases of VT remain viable, and if so, to characterize their transmembrane potential properties with the microelectrode and to assess their morphologic features. The RCA was occluded in 13 closed-chest anesthetized dogs with intracoronary balloon inflation. In one group (N = 7), the infarcted tissues were isolated during the VT inducible phase and in another group (N = 6) these tissues were isolated during the VT noninducible phase. Resting membrane potential, action potential amplitude, maximum upstroke velocity, and action potential duration of the surviving SE Purkinje fibers (PF) and ventricular muscle (VM) in the IZ (first layer) were not significantly different in the two groups. Conduction velocity for both basic and premature stimuli from the base to the apex were similar in the two groups. Rapid stimulation at cycle lengths of 300 to 200 msec failed to induce triggering of automatic activity in the two groups. Electron microscopy of SEPF in the IZ showed a drastic reduction in cytosolic lipid droplet accumulation when compared to 24-hour-old infarct. We conclude that: (1) SEPF and VM network in the infarct zone remain electrically viable during the chronic phase of RVI; (2) transmembrane potential properties of this fiber network remain constant and independent of temporal changes of VT inductibility; and (3) ultrastructural improvement of this fiber network suggests an evolution toward normalcy.
Action Potentials↗
The signal-averaged electrocardiogram as a screening test for inducibility of sustained ventricular tachycardia in high risk patients: a prospective study.
The role of the signal-averaged electrocardiogram in predicting the induction of sustained monomorphic ventricular tachycardia in high risk patients was assessed prospectively in 100 consecutive patients. Presenting diagnoses were syncope (38 patients), nonsustained ventricular tachycardia (24 patients), sustained ventricular tachycardia (25 patients) and sudden cardiac arrest (13 patients). Using programmed ventricular stimulation, 71 patients (group I) did not have and 29 patients (group II) did have inducible sustained monomorphic ventricular tachycardia. Using the signal-averaged electrocardiogram with filtering (6 dB/octave) at high pass corner frequencies of 67 and 100 Hz, the two groups were compared. The signal-averaged electrocardiogram was considered abnormal if all of the following criteria were satisfied: 1) the total filtered QRS complex duration was greater than 120 ms, 2) the duration of the terminal QRS complex of less than or equal to 20 microV was greater than or equal to 30 ms, and 3) at least one deflection (late potential) was present in this region. Differences between groups I and II in these three measures were highly significant (p less than or equal to 0.001). The sensitivity and specificity of signal averaging for predicting the induction of sustained ventricular tachycardia were 93 and 94%, respectively. Stepwise logistic regression analysis identified the signal-averaged electrocardiogram as the best predictor of induction of sustained monomorphic ventricular tachycardia, independent of left ventricular ejection fraction, presence of ventricular aneurysm, myocardial infarction and other clinical variables (chi-square = 93.2, p less than 0.0001). The signal-averaged electrocardiogram is a sensitive and specific test for the induction of sustained monomorphic ventricular tachycardia, having independent predictive value.
Coronary Disease↗
Selective perfusion of ischemic myocardium during coronary venous retroinjection: a study of the causative role of venoarterial and venoventricular pressure gradients.
Coronary venous retroinjection is often associated with preferential distribution of flow to ischemic myocardium. The purpose of this study was to define the mechanism of such retrodistribution of flow. In 24 anesthetized open chest dogs, Monastral blue dye (10 ml) was injected by way of a balloon catheter in the distal great cardiac vein as a marker for retrograde flow distribution. The injection rate (0.6 to 2.4 ml/s) was adjusted such that systolic pressure in the anterior interventricular vein ranged between 60 and 85 mm Hg. In 11 dogs with no ischemia and normal myocardial perfusion pressure (96 +/- 8 mm Hg), no myocardial staining occurred despite retrograde filling of epicardial veins. One minute after occlusion of the left anterior descending coronary artery, dye injections caused selective staining of the cyanotic area in 15 of 18 episodes, sparing the normal myocardium within the zone of retroperfused veins. In five dogs, with the arterial pressure less than 55 mm Hg, retroinjection resulted in homogeneous staining of all the myocardium drained by the retroperfused veins. Selective staining of the ischemic myocardium caused by retroinjection was associated with the following pressure gradients: during systole from the anterior interventricular vein to the occluded coronary artery, 31 to 58 mm Hg, and during diastole from the retroperfused veins to the left ventricular chamber, 9 to 28 mm Hg. There was no diastolic venoarterial gradient in the ischemic myocardium. In normal myocardium, retroinjection did not reverse the arteriovenous pressure gradient. In conclusion, retrograde flow is primarily directed to myocardium with low anterograde perfusion pressure. Selective retrograde penetration of acutely ischemic myocardium can thus be achieved by a mechanism consistent with the development of venoarterial and venoventricular pressure gradients.
Animals↗
Decline in ventricular fibrillation threshold after successive premature extrastimuli: a possible explantation for the induction of ventricular fibrillation during programmed stimulation with multiple extrastimuli.
To examine the relation between the ventricular fibrillation threshold and the number of premature extrastimuli delivered to the right ventricle during programmed ventricular stimulation, a clinical stimulation protocol was performed in nine normal, anaesthetised, closed chest dogs. In addition, the ventricular fibrillation threshold was measured in each dog after a train of eight paced (S1) beats (VFT-S2), after a single premature extrastimulus (VFT-S3), and after two extrastimuli (VFT-S4). The VFT-V3 was 32% lower than the VFT-S2 (16(7) mA vs 24(9) mA, p less than 0.001). The VFT-S4, or the current required by the S4 extrastimulus to induce ventricular fibrillation, was 25% lower than the VFT-S3 (12(8) mA vs 16(7) mA, p less than 0.05). The cumulative reduction in the ventricular fibrillation threshold measured by the S1S2S3S4 stimulation protocol was approximately 50%. Although in most dogs the VFT-S4 was still considerably higher than twice threshold current intensity, the results of the study suggest that a possible mechanism for the induction of non-clinical ventricular fibrillation in the clinical electrophysiology laboratory may be the progressive lowering of the ventricular fibrillation threshold caused by the addition of multiple extrastimuli. This may be particularly relevant in patients with an already reduced fibrillation threshold.
Action Potentials↗
Intermittent fascicular extrasystoles producing pseudo AV block: electrophysiologic effects of beta agonists and antagonists.
This report describes a patient with pseudo-type II second-degree AV block due to an intermittent parasystolic focus located in the left bundle branch. A paradoxical increase in the fascicular rate was seen following intravenous propranolol, and fascicular extrasystoles were suppressed after intravenous isoproterenol treatment. All propagated fascicular extrasystoles were conducted to the ventricle with incomplete or complete right bundle branch block and a decrease in the H'-V interval compared to the H-V interval during sinus rhythm. Treatment with oral quinidine abolished fascicular extrasystoles without worsening of AV conduction.
Bundle-Branch Block↗
Orthodromic tachycardia initiation dependent on 1:2 atrioventricular conduction in the presence of a left lateral bypass tract.
This report describes a patient who presented with atrial fibrillation associated with a rapid ventricular response (270 bpm) and wide QRS complexes. At the time of electrophysiology study, a left lateral bypass tract with both anterograde and retrograde conduction was demonstrated. Orthodromic tachycardia with atrial premature impulses was initiated and was dependent on two ventricular responses to one atrial impulse. Intravenous procainamide administration had little effect on anterograde or retrograde conduction in the accessory pathway; however, it prevented orthodromic tachycardia initiation with atrial premature impulses by prolonging atrial muscle refractoriness.
Adult↗
Life-threatening postoperative pulmonary complications in patients with previous amiodarone pulmonary toxicity undergoing cardiothoracic operations.
Amiodarone therapy for cardiac arrhythmias is increasingly being recognized to be associated with pulmonary toxicity. In this report, we describe the case histories of four patients with previously diagnosed amiodarone pulmonary toxicity in whom the adult respiratory distress syndrome developed after cardiothoracic operations for malignant ventricular arrhythmias. Three patients underwent endocardial resection (two died), and a fourth patient had implantation of an automatic defibrillator unit. Radiographic changes and results of pulmonary function testing are evaluated during initial toxicity and preoperatively. These four patients (mean amiodarone dosage of 420 mg/day for 20 months) are compared to 13 other patients undergoing cardiothoracic operations with prior amiodarone treatment (one patient with preoperative pulmonary toxicity) in whom life-threatening postoperative pulmonary complications did not develop (mean dosage of 550 mg/day for 10 months). Mean preoperative serum amiodarone levels for the four patients were 1.5 micrograms/ml. In the two patients who died, desethylamiodarone levels were 510 and 4,400 micrograms/gm in pulmonary tissue. Histologic examination showed "honeycomb" appearance of the lung with prominent septae, alveolar foamy macrophages, and hyperplasia of alveolar lining cells, consistent with amiodarone pulmonary toxicity. Causes including pump-oxygenator time, oxygen toxicity, anesthetic agents, congestive heart failure, and pulmonary infection superimposed on amiodarone pulmonary toxicity are discussed with a review of the literature.
Aged↗
Detection of late potentials on the surface electrocardiogram in unexplained syncope.
To assess the usefulness of signal averaging of the surface electrocardiogram for detecting hitherto undocumented ventricular tachycardia (VT) in patients with unexplained syncope, 24 such patients were evaluated by electrocardiography and programmed ventricular stimulation. The surface electrocardiograms of 15 normal volunteers and 22 patients with documented sustained VT were also examined. No study subject had a bundle branch block or a QRS duration longer than 120 ms. Sustained VT was recorded in 9 of the 24 patients with syncope (8 patients with inducible VT and 1 with a spontaneous episode of recorded sustained VT). The signal-processed electrocardiogram contained late potentials and a filtered QRS duration longer than 120 ms in 8 of these 9 patients (89% sensitivity). None of the remaining 15 patients had these electrocardiographic abnormalities. Similar results were found in the patients with previously documented sustained VT (82% sensitivity) and in normal volunteers (no instances of abnormal recordings). In patients with unexplained syncope, signal processing of the surface electrocardiogram may be a sensitive and specific noninvasive test for detecting a high-risk subset of patients prone to lethal ventricular tachyarrhythmias.
Adult↗
Influence of dielectronic recombination on fast heavy-ion charge states in plasma.
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Journal Article↗
Ratio of ST-segment depression in lead V2 to ST-segment elevation in lead aVF in evolving inferior acute myocardial infarction: an aid to the early recognition of right ventricular ischemia.
The potential value of the ratio of precordial ST-segment depression to inferior ST-segment elevation as a sign of concomitant right ventricular (RV) ischemia was examined. The study group consisted of 68 patients, admitted within 3 hours of the onset of inferior acute myocardial infarction (AMI), in whom there was no evidence of prior AMI. In 27 of the 34 patients in whom inferior AMI was the result of right coronary artery occlusion proximal to the RV branch, the magnitude of ST-segment depression in lead V2 was 50% or less of the magnitude of ST-segment elevation in lead aVF, whereas in only 3 of the 34 patients in whom the site of occlusion was either distal to the RV branch (n = 23) or in the left circumflex artery (n = 11) was this ratio 50%; in no patient was it less than 50% (p less than 0.001). All 34 patients with occlusion of the right coronary artery proximal to the RV branch also had regional or global ischemic RV dysfunction by radionuclide ventriculography, with a mean RV ejection fraction of 30 +/- 10% compared with 42 +/- 6% in patients with occlusion distal to the RV branch or in the left circumflex artery (p less than 0.001). In conclusion, in patients with evolving inferior AMI, ST-segment depression in lead V2 of 50% or less of the magnitude of ST-segment elevation in lead aVF may be a useful sign (sensitivity 79%, specificity 91%, positive predictive value 90% and negative predictive value 82%) for identifying patients with concomitant RV ischemia.
Adult↗
The efficacy of lidocaine and verapamil alone and in combination on spontaneously occurring automatic ventricular tachycardia in conscious dogs one day after right coronary artery occlusion.
Occlusion of the right coronary artery (RCA) in the dog is associated with spontaneous sustained ventricular tachycardia (VT) during the 18 to 26 hours post occlusion period. Electrophysiologic studies suggest that these tachycardias are caused mainly by an automatic mechanism. In the present study we evaluated in 16 conscious dogs with VT 1 day after RCA occlusion the efficacy of (1) lidocaine (L), which depresses primarily the mechanism of enhanced normal automaticity; (2) verapamil (V), which depresses the mechanism of abnormal and triggered automaticity; and (3) combination of both L and V on these VTs. The RCA was occluded in 16 anesthetized closed-chest dogs by intracoronary balloon inflation. All 16 dogs had spontaneous VT while in the conscious state during the 18 to 26 hours post occlusion study period. L (5 mg/kg intravenously) bolus restored within 1 minute normal sinus rhythm (NSR), with a mean rate of 118 +/- 14 bpm, in dogs (n = 7) which had their VTs overdrive suppressed and had a mean rate of 145 +/- 14 bpm (range 110 to 150 bpm). L was ineffective in dogs (n = 9) which did not have their VTs overdrive suppressed and had a mean VT rate of 192 +/- 24 bpm (range 175 to 250 bpm). In contrast, however, V (0.15 mg/kg intravenously) was ineffective in all seven dogs with the slower VT rates, but was effective in restoring NSR with a mean rate of 140 +/- 14 bpm in six out of nine dogs with the faster VT rates.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
The efficacy of cibenzoline and propafenone against inducible sustained and nonsustained ventricular tachycardias in conscious dogs with isolated chronic right ventricular infarction: a comparative study with procainamide.
The efficacy of intravenous cibenzoline (3 mg/kg), propafenone (4 mg/kg), and procainamide (20 mg/kg) against inducible sustained and nonsustained ventricular tachycardias (VT) was evaluated in 12 conscious dogs with chronic isolated right ventricular (RV) infarction. RV infarct was caused by permanent occlusion of the right coronary artery in the closed-chest dog by intracoronary balloon inflation. Three to 10 days following the occlusion period, programmed electrical stimulation reproducibly induced sustained and/or nonsustained VT, allowing evaluation of antiarrhythmic drug efficacy. Propafenone was effective in preventing the induction of sustained VT in only one out of six dogs tested, but caused a significant (p less than 0.05) slowing of VT rate (269 +/- 13 to 230 +/- 10 bpm). Procainamide had effects similar to those seen with propafenone. Propafenone and procainamide were ineffective against nonsustained VT, and on established sustained VT once induced. Cibenzoline was effective in preventing the induction of sustained VT in two out of seven dogs, an effect which was not significantly different from either propafenone or procainamide. However, cibenzoline was significantly (p less than 0.05) more effective than either procainamide or propafenone in terminating an established induced sustained VT (four out of six dogs). Furthermore, cibenzoline converted nonsustained to sustained VT in four out of seven dogs tested. Histopathologic studies have shown infarction of the basal two thirds of the RV (38.5 +/- 7.8% of the RV) with no left ventricular involvement. It is concluded that the isolated RV infarction model is highly suitable for serial drug testing against inducible VT in conscious dogs, and this model of VT appears to be fairly resistant to standard and newer antiarrhythmic drug therapy.
Animals↗