Biomedical subjects

M J Reiter

Publications and source records attributed to M J Reiter.

At least 55 records · Page 3Linked to original sources

PubMed1994

Implantation of an automatic defibrillator using a new nonthoracotomy approach.

Most current nonthoracotomy systems for defibrillator implantation use monophasic devices. To determine the safety and efficacy of a new nonthoracotomy lead configuration when used in conjunction with a device that used biphasic waveforms, 38 consecutive patients were taken to the operating room for implantation of a Cadence tiered therapy defibrillator system. The lead system consisted of a transvenous coil electrode positioned at the right atrial-superior vena caval junction, a bipolar endocardial right ventricular lead, and a large patch placed subcutaneously near the cardiac apex. Of the 38 nonthoracotomy defibrillator implantations attempted, 36 (95%) were completed with adequate defibrillation thresholds. The mean defibrillation threshold in these 36 patients was < or = 563 +/- 10 V (< or = 20 +/- 1 J). There was no perioperative mortality. Complications included coil lead migration (5), sensing lead migration (1), infection (3), pneumothorax (2), arterial embolism (1), and folding of the subcutaneous patch with an increase in defibrillation threshold (1). No patient died during a median follow-up period of 22 weeks. Fourteen patients (39%) had spontaneous sustained ventricular tachyarrhythmias, which were all successfully terminated by the implanted device. Shocks for nonsustained arrhythmias were aborted in eight patients (22%). Spurious discharges for sinus tachycardia or atrial fibrillation occurred in six patients (17%) and were readily diagnosed by examination of the stored electrograms. Thus, implantation of a biphasic tiered therapy defibrillator system using this nonthoracotomy approach is feasible in the majority of patients. The major complication associated with this procedure is lead dislodgment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

Low dose disopyramide often fails to prevent neurogenic syncope during head-up tilt testing.

Low dose disopyramide has been used to prevent neurally-mediated syncope during head-up tilt testing but a correlation between blood levels and efficacy has not been described. We measured disopyramide levels in 15 patients with recurrent syncope and positive 70 degrees head-up tilt tests who underwent one or more repeat tests on the drug. There were 9 males and 6 females, age range 15-78 years. Fourteen of the 15 patients had structurally normal hearts. The daily disopyramide dose was 645 +/- 165 mg (mean +/- SD). Patients developed syncope during 9 tests and had no syncope during 12 tests. The mean disopyramide level in patients with positive tests was significantly lower than the level in patients with negative tests (2.4 +/- 0.15 mu/mL vs 3.2 +/- 0.22 mu/mL, P = 0.018). Six patients were tested twice on different disopyramide doses. Five of these six patients had syncope during head-up tilt testing on the lower dose and negative tests on the higher dose (disopyramide levels 2.2 +/- 0.17 mu/mL vs 3.2 +/- 0.17 mu/mL, P = 0.004). Thus, disopyramide is effective in preventing neurogenic syncope during head-up tilt testing, but higher blood levels are often necessary for efficacy. In a given patient, failure to respond to low dose disopyramide does not preclude success on higher doses.

Adolescent↗

PubMed1994

Interaction of acute ventricular dilatation and d-sotalol during sustained reentrant ventricular tachycardia around a fixed obstacle.

BACKGROUND: Antiarrhythmic therapy of ventricular tachycardia is associated with decreased efficacy and increased proarrhythmia in patients with congestive heart failure, but the explanation for these observations is not known. This study examined the interaction of ventricular dilatation and d-sotalol in a model of reentry ventricular tachycardia. METHODS AND RESULTS: Thin epicardial layers of anisotropic myocardium were created in Langendorff-perfused rabbit left ventricles by a cryo procedure. A fluid-filled, latex balloon was secured within the left ventricle to change ventricular volume. Sustained reentrant ventricular tachycardia, around a central cryolesion, was induced by rapid pacing in all preparations (n = 7). Epicardial mapping was performed through 248 electrodes. Single premature beats introduced within the reentry circuit were used to define the excitable gap. Dilatation did not influence ventricular tachycardia cycle length or conduction velocity. A 1.25-mL increase in left ventricular volume widened the excitable gap by 12% (range, 5% to 29%) (P < .001) because of a decrease in myocardial refractoriness. d-Sotalol (final concentration, 10 mg/L) narrowed the excitable gap 18% (range, 7% to 29%) (P = .002) in the undilated left ventricle. d-Sotalol was less effective in the dilated left ventricle, narrowing the excitable gap only 9%, a difference that was not statistically significant. During pacing to induce or terminate tachycardia, tachycardia acceleration was observed significantly more frequently in the dilated than in the undilated ventricle. Ventricular tachycardia acceleration was due to the development of double-wave reentry (two successive waves traveling in the same circuit in the same direction). d-Sotalol, which narrowed the excitable gap, prevented tachycardia acceleration and double-wave reentry. CONCLUSIONS: Antiarrhythmic efficacy may be decreased by dilatation because of widening of the initial excitable gap and a decrease in the gap-narrowing effect of these agents. Double-wave reentry, more likely with a widening of excitable gap, may partially explain tachycardia acceleration in the dilated ventricle.

Animals↗

PubMed1993

Mechanical correlates of contraction-excitation feedback during acute ventricular dilatation.

OBJECTIVE: The purpose was to examine the mechanical correlates of the electrophysiological changes that occur during acute left ventricular dilatation. METHODS: Ten isolated, retrogradely perfused, ejecting rabbit hearts were studied. Left ventricular volume was adjusted by varying left atrial perfusion pressure. Left ventricular pressure was measured directly. Changes in left ventricular chamber dimensions at the level of an epicardial electrode were evaluated with two dimensional echocardiography and wall stress was calculated from these measures. Regional left ventricular electrophysiological properties were measured at two left atrial perfusing pressures. RESULTS: Increases in left atrial perfusion pressure resulted in significant increases in left ventricular end diastolic and end systolic pressures, epicardial and endocardial circumference, and wall stress. Only changes in diastolic wall stress correlated with changes in ventricular refractoriness (r = 0.69, p = 0.027). CONCLUSIONS: Left ventricular dilatation results in shortening of ventricular refractoriness in the isolated, ejecting rabbit heart. Regional changes in refractoriness are best correlated with changes in wall stress.

Acute Disease↗

PubMed1993

Influence of a third extrastimulus in defining effective drug therapy during serial electrophysiological testing.

Many electrophysiology laboratories use three extrastimuli in all patients with ventricular tachyarrhythmias during antiarrhythmic drug testing, regardless of the mode of arrhythmia induction in the baseline state. The purpose of this study was to compare this pacing protocol (full protocol) with a protocol in which three extrastimuli were only used during drug tests, if they were required in the baseline state for arrhythmia induction (limited protocol). There were 181 electrophysiology tests performed on 69 patients with ventricular tachyarrhythmias that were retrospectively analyzed. In all studies the full protocol was used, but the results of stimulation were also analyzed assuming the limited protocol had been used. In the baseline state, sustained ventricular tachyarrhythmias were reproducibly inducible with one or two extrastimuli in 38 (55%) patients. Of these patients, six (16%) achieved a drug efficacy prediction using the full protocol versus 15 (39%) patients using the limited protocol (P < 0.001). In all 69 patients, the drug response rate increased from 25% to 38% (P < 0.01) using the limited protocol.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1993

Palpitations occur frequently following radiofrequency catheter ablation for supraventricular tachycardia, but do not predict pathway recurrence.

Radiofrequency ablation of extranodal pathways is an effective treatment for supraventricular tachycardia, but late recurrences of pathway conduction do occur. To determine if recurrence of palpitations following ablation predicts pathway recurrence, we interviewed 77 patients who were at least 4 weeks status-post successful ablation of an accessory pathway (43 overt, 11 concealed) or slow pathway (23) for AV nodal reentrant tachycardia. Palpitations were reported by 45 (58%) patients postablation, and 28 (36%) patients reported palpitations lasting > or = 10 seconds and/or felt their symptoms represented recurrent tachycardia (major palpitations). Repeat electrophysiological testing was performed 3 months postablation in 53 patients, including 34 patients with palpitations (22 with major symptoms). Eight (10%) patients had recurrent pathway conduction demonstrated on repeat testing: two had no symptoms prior to restudy and six had major symptoms. One patient had major symptoms, but was found to have inducible atrial tachycardia and not pathway recurrence on restudy. Thus, 15 (68%) of 22 patients with major symptoms who were restudied had no pathway recurrence or inducible arrhythmia to explain their symptoms. Of the 24 patients not restudied, none has had documented recurrent tachycardia or overt pathway conduction by electrocardiogram over a mean follow-up of 335 +/- 138 (range 132-616) days. Thus, palpitations, including palpitations reminiscent of preablation symptoms, are common following radiofrequency ablation and often do not predict pathway recurrence. Repeat electrophysiological testing is frequently required to document long-term success of radiofrequency ablation for supraventricular tachycardia in patients with recurrence of major symptoms.

Adult↗

PubMed1993

Interaction of hypokalemia and ventricular dilatation in isolated rabbit hearts.

Potassium depletion has been implicated in the genesis of ventricular arrhythmias, especially in patients with congestive heart failure, but the nature of this interaction is unknown. We studied the electrophysiological effects of varying concentrations of extracellular K+ in 24 isolated, retrogradely perfused rabbit hearts. The left ventricular cavity was dilated with a fluid-filled balloon. Left ventricular effective refractory period decreased significantly (from 119 +/- 3 to 105 +/- 3 ms) with ventricular dilatation but was not influenced by K+ concentration. Conduction velocity was not changed by dilatation but was decreased by hypokalemia (81 +/- 2 cm/s, K+ = 4.9 mM; 75 +/- 2 cm/s, K+ = 3.5 mM; 70 +/- 2 cm/s, K+ = 2.5 mM; P < 0.05). No ventricular arrhythmias were induced in undilated hearts at a K+ concentration of 4.9 mM. Induced ventricular fibrillation was more frequent (38%; P < 0.01) in the dilated heart and increased markedly (92%; P < 0.01) with coexisting hypokalemia. The incidence of induced fibrillation was highly correlated with the wavelength of the ventricular impulse (wavelength = refractory period x conduction velocity). Thus dilatation and hypokalemia have very different electrophysiological effects that can interact synergistically to predispose the heart to reentrant arrhythmias in this model.

Animals↗

PubMed1992

Inhibition of murine tumor growth by an interferon-inducing imidazoquinolinamine.

The low-molecular-weight imidazoquinolinamine derivative, 1-(2-methylpropyl)-1H-imidazo[4,5-c]quinolin-4-amine (imiquimod, previously described as R-837), induced alpha-interferon (IFN-alpha) in mice. IFN induction was identified at oral doses as low as 3 mg/kg. The 10% lethal dose for daily treatment with imiquimod was 200 mg/kg. Oral treatment with 30 mg/kg imiquimod once every three days significantly inhibited MC-26 colon carcinoma. Delay of treatment from day 1 to day 5, when tumors were easily palpable, did not reduce benefits. Ten daily treatments were slightly more effective than five. However, delivery of the same total dose of imiquimod either once every day for 20 days, once every 4 days, once every 7 days, or once every 10 days inhibited tumor growth to the same level. The antitumor effects of imiquimod were significantly abrogated by an antiserum to murine IFN-alpha, suggesting that the antitumor effect was to a substantial extent mediated by IFN induction. Imiquimod also significantly reduced the number of lung colonies in mice inoculated i.v. with MC-26 tumor cells. Combination of treatment with imiquimod and cyclophosphamide was significantly (P less than 0.01) better than treatment with either drug alone. Combination treatment with cyclophosphamide led to cures in some of the mice inoculated either s.c. or i.v. with MC-26 cells. Treatment with imiquimod also inhibited the growth of RIF-1 sarcoma and Lewis lung carcinoma but was ineffective for P388 leukemia. Imiquimod is an oral IFN-alpha inducer with antitumor effectiveness for transplantable murine tumors.

Aminoquinolines↗

PubMed1992

Effect of pacing drive cycle length on induction of sustained monomorphic ventricular tachycardia.

To assess the effect of pacing drive cycle length on induction of sustained monomorphic ventricular tachycardia, 40 patients were prospectively studied in the drug-free state. Ventricular extrastimuli were sequentially delivered at the same coupling interval at each of three drive cycle lengths (600, 500, and 400 ms) before the coupling interval was shortened and the process repeated. This protocol was continued until sustained monomorphic ventricular tachycardia was induced at all three drive cycle lengths or until pacing was completed through three extrastimuli. Of the 27 patients in whom sustained monomorphic ventricular tachycardia was induced, tachycardia was induced at all 3 drive cycle lengths in 12 (44%), only 2 drive cycle lengths in 11 (41%), and only 1 drive cycle length in 4 (15%) patients. Although the yield of inducible ventricular tachycardia increased with each additional extrastimulus, this yield increased even further with the use of multiple drive cycle lengths. In 10 of 11 patients, failure to induce ventricular tachycardia at any drive cycle length was not due to failure to achieve at that drive cycle length the critical extrastimulus coupling interval required to induce tachycardia at other drive cycle lengths. Induction of sustained monomorphic ventricular tachycardia is often drive cycle length specific, and failure to induce tachycardia cannot be explained by failure to achieve critically short coupling intervals. Pacing at multiple drive cycle lengths increases the yield of induced ventricular tachycardia.

Cardiac Pacing, Artificial↗

PubMed1992

Effect of acute ventricular dilatation on fibrillation thresholds in the isolated rabbit heart.

We examined the effects of ventricular dilatation on epicardial refractoriness and ventricular fibrillation threshold (VFT) in the isolated, retrograde-perfused rabbit heart. Ventricular size was modified by acutely changing the volume of a fluid-filled balloon secured within either the left or right ventricle. Left ventricular dilatation (to an end-diastolic pressure of 30-38 mmHg) significantly decreased left ventricular effective refractory period (ERP) and myocardial wavelength (calculated as ERP x conduction velocity). Left VFT (determined by scanning the vulnerable period with a train of pulses) decreased from 6.4 +/- 0.9 to 4.4 +/- 0.5 mA; P < 0.01) with left but not right ventricular dilatation. Right ventricular dilatation was associated with a decrease in the right ventricular ERP and myocardial wavelength, and right VFT decreased from 13.6 +/- 1.8 to 4.1 +/- 0.3 mA (P < 0.01). Changes in VFT correlated with the decrease in local refractoriness and shortening of local excitation wavelength.

Animals↗

PubMed1991

Atrioventricular nodal reentrant tachycardia initiated by catecholamine-induced ventricular tachycardia. A case report.

The authors describe a patient who experienced recurrent wide-complex and narrow-complex tachycardias during exercise. Electrophysiologic testing in the resting state revealed dual atrioventricular (AV) nodal pathways. AV nodal reentrant tachycardia was inducible by ventricular premature stimulation but was always nonsustained, terminating with block in the anterograde slow pathway. During isoproterenol infusion, runs of ventricular tachycardia occurred frequently, and spontaneously initiated sustained AV nodal reentrant tachycardia. Exercise testing also provoked ventricular tachycardia and sustained AV nodal reentrant tachycardia. The patient was effectively treated with a combination of atenolol and verapamil. This case is an unusual example of a catecholamine-induced arrhythmia, possibly due to triggered activity (exercise-induced ventricular tachycardia), initiating an arrhythmia due to reentry (AV nodal reentrant tachycardia).

Catecholamines↗

PubMed1991

Electrophysiologic evaluation of cardiovascular agents in the isolated intact rabbit heart.

A modification of the Langendorff perfused rabbit heart is described. This model can be used to perform electrophysiologic studies in the isolated heart and is ideally suited for acute pharmacologic evaluation. His bundle electrograms were measured with a plunge electrode and allowed atrioventricular (AV) nodal physiology to be directly and precisely evaluated. Atrial conduction and refractoriness, atrioventricular node conduction and refractoriness, His-Purkinje conduction, and ventricular conduction and refractoriness could be accurately measured. Verapamil had a depressant effect on AV nodal conduction and refractoriness without affecting His--Purkinje conduction or myocardial refractoriness. Flecainide prolonged atrial conduction and His-Purkinje conduction with less effect on AV nodal physiology. The use of this isolated perfused rabbit heart model is an inexpensive and reliable technique for the evaluation of the electrophysiologic effects of pharmacologic agents on the conduction system of the heart. A major advantage of the isolated heart model is the absence of autonomic reflexes, which can confound studies performed in intact animals.

Animals↗

PubMed1991

Hydrogen peroxide decreases effective refractory period in the isolated heart.

Although previous investigations have concluded that reactive oxygen metabolites contribute to reperfusion arrhythmias, the experimental models employed also had a significant amount of tissue injury, which may have contributed to the observed electrophysiologic effects. We studied whether exposure of the intact heart to a reactive oxygen metabolite at doses that are not associated with histologic evidence of cell necrosis would alter myocardial refractoriness, suggesting that subtle and reversible oxidative stress could alter myocardial electrophysiologic properties and perhaps contribute to ventricular arrhythmias. Isolated rabbit hearts were perfused for 30 min with low doses of hydrogen peroxide (H2O2), either 10(-5), 5 x 10(-6), or 10(-6)-M H2O2 versus vehicle alone; followed by a 30-min washout period without H2O2. Infusion of H2O2 for 30 min decreased ventricular epicardial effective refractory period (ERP) in a dose-dependent manner compared to saline controls (delta ERP). The delta ERP versus time curves during the last 10 min of H2O2 infusion were different (p less than 0.01) for each of the three H2O2 doses. Creatine phosphokinase and reversible oxidized glutathione release occurred during 10(-5)-M H2O2 infusion, but not with lower H2O2 doses. Exposure of the intact heart to low concentrations of H2O2, in a range that caused subtle oxidative injury, decreased ventricular ERP in a dose-dependent manner. Thus, H2O2 generation could contribute to ventricular arrhythmias, even in settings of sublethal and potentially reversible oxidative injury.

Animals↗

PubMed1991

Electrophysiologic effects of verapamil metabolites in the isolated heart.

The electrophysiologic effects of the metabolites of verapamil are unknown and may contribute to the observed differences between intravenous and oral verapamil. We examined the electrophysiologic effects of verapamil and its metabolites (norverapamil, N-dealkylverapamil (D617), and N-dealkylnorverapamil (D620)) at estimated, free therapeutic concentrations, in the retrogradely perfused, isolated rabbit heart. Verapamil at 5 and 10 ng/ml significantly prolonged anterograde (11 and 27%, respectively) and retrograde (10 and 25%, respectively) atrioventricular (AV) nodal block cycle lengths. Anterograde and retrograde AV nodal conduction times and refractory periods were also prolonged. Norverapamil at 100 ng/ml had qualitatively similar effects equivalent to 20-50% that observed with verapamil at 10 ng/ml. D620 had small but statistically significant effects on some AV nodal parameters. D617 had no effect. The combination of verapamil plus its principal metabolite, norverapamil, had additive effects. None of the compounds had any measurable effect on atrial conduction, His-Purkinje conduction, or atrial refractoriness. Ventricular refractoriness was significantly prolonged only by norverapamil. In conclusion, some of the metabolites of verapamil have important electrophysiologic AV nodal effects and may contribute to the clinical effects observed during chronic oral verapamil dosing.

Animals↗

PubMed1990

Effects of upright posture on atrioventricular accessory pathway conduction.

The electrophysiologic effects of 45 degrees head-up tilt were studied in 19 patients with atrioventricular accessory pathways. Upright posture enhanced both anterograde and retrograde accessory pathway conduction when compared to the supine position: the anterograde block cycle length decreased from 374 +/- 52 ms (mean +/- standard error) (supine) to 303 +/- 33 ms (tilt) (p less than 0.05); anterograde effective refractory period decreased from 286 +/- 17 to 249 +/- 10 ms (p less than 0.05); retrograde block cycle length shortened from 331 +/- 36 to 291 +/- 35 ms (p less than 0.05); retrograde effective refractory period decreased from 312 +/- 26 ms to 274 +/- 15 ms (p less than 0.05). During induced atrial fibrillation the mean RR interval and the shortest RR interval between preexcited beats decreased approximately 10% with head-up tilt. During orthodromic reciprocating tachycardia, tachycardia cycle length shortened 15%. Tachycardia rate during electrophysiologic study in the head-up position more closely approximated the rate of clinical tachycardia than did the rate in the supine position. Head-up tilt significantly enhances anterograde and retrograde accessory pathway conduction, increases the rate of arrhythmias using an accessory pathway and may be clinically useful in the assessment of patients with an accessory pathway.

Adult↗

PubMed1990

Electrocardiographic abnormalities in patients with myotonic dystrophy.

In examining the incidence and progression of electrocardiographic abnormalities in 45 patients with myotonic dystrophy, 26 (58%) of whom at entry had at least 1 electrocardiographic abnormality, we found conduction abnormalities in 17 (38%). In 21 patients (47%), new abnormalities developed during follow-up (mean, 4.6 years). The overall incidence of electrocardiographic abnormalities increased to 78%, and the incidence of conduction defects increased to 62%. Second-degree or complete atrioventricular block did not develop in any of the patients. Pseudoinfarction patterns were common at entry and during follow-up and were not correlated with evidence of clinical coronary artery disease. There was no correlation between the presence of electrocardiographic abnormalities and apparent disease severity.

Adolescent↗

PubMed1989

Effects of flecainide on defibrillation thresholds in the anesthetized dog.

The effects of flecainide on defibrillation thresholds in 21 open chest, anesthetized dogs were studied. Defibrillation was accomplished using nontruncated exponential pulses delivered through two epicardial patches. Multiple shocks of varying energy were administered after 10 s of ventricular fibrillation in random order. The percent success was plotted against the energy delivered for each dog. A sigmoidal curve was fit to the data and the energy associated with 50% success (E50) calculated. Flecainide (n = 16) or saline solution (n = 5) was then infused and E50 again determined. Flecainide infusion produced mean (+/- standard error of the mean) plasma levels of 610 +/- 111 ng/ml. Defibrillation thresholds were obtainable in 10 of 16 dogs that received flecainide infusion. Flecainide infusion increased E50 by 75% (from 6.5 +/- 1.9 to 11.4 +/- 2.6 J) (P less than 0.05). Infusion of saline solution did not significantly affect defibrillation energy. Of 16 dogs that received flecainide infusion, 12 had one or more complications: 6 had ventricular fibrillation resistant to defibrillation, 6 developed severe hypotension after successful defibrillation and 5 had spontaneous ventricular fibrillation after successful defibrillation. These effects were not seen in any control dogs. Flecainide infusion significantly increases defibrillation threshold and has important adverse arrhythmic and hemodynamic effects in this experimental preparation.

Animals↗

PubMed1989

Effects of ventricular fibrillation and defibrillation on pacing threshold in the anesthetized dog.

The effects of transthoracic and internal defibrillation on the bipolar ventricular pacing threshold in 20 anesthetized dogs were examined. Ventricular pacing was accomplished with a computer-controlled, constant voltage pacemaker that permitted rapid determination of pacing threshold. Defibrillation at various energy levels was administered during ventricular pacing and after ventricular fibrillation of 5, 15, 30, 45, 60 or 120 s duration in the 20 dogs. Defibrillation during pacing or within 15 s after initiation of ventricular fibrillation did not significantly increase threshold, regardless of defibrillation energy or mode of delivery. Defibrillation after ventricular fibrillation lasting greater than or equal to 30 s increased (p less than 0.05) threshold determined 6 s after defibrillation. The increase in threshold (in volts) determined 6 s after defibrillation was an exponential function of fibrillation duration (30 s = 0.30 +/- 0.09 V; 45 s = 0.53 +/- 0.13 V; 60 s = 2.24 +/- 1.05 V), but was independent of defibrillation energy or mode of delivery. Threshold returned to control values 15 to 30 s after defibrillation. Cardiopulmonary bypass to maintain coronary perfusion prevented the increase in pacing threshold even after ventricular fibrillation of up to 2 min duration. Pacing threshold is not increased by transthoracic or internal defibrillation, but is increased by ventricular fibrillation of sufficient duration to create substantial myocardial hypoxemia.

Anesthesia↗