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Biomedical subjects

H Garan

Publications and source records attributed to H Garan.

At least 55 records · Page 3Linked to original sources
PubMed1992

Electrophysiologic response to moricizine in patients with sustained ventricular arrhythmias.

OBJECTIVE: To assess the short-term efficacy and safety of moricizine in patients receiving electrophysiologically guided therapy for sustained ventricular arrhythmias refractory to treatment with class IA antiarrhythmic agents. DESIGN: Uncontrolled clinical trial. SETTING: Referral-based teaching medical center. PATIENTS: Twenty-one patients (18 of whom had coronary artery disease) with a mean left ventricular ejection fraction of 32% +/- 11% who presented with sustained ventricular tachycardia (13 patients), syncope (4 patients), or cardiac arrest (4 patients). INTERVENTIONS: Moricizine, 743 +/- 85 mg daily. MEASUREMENTS: Electrophysiologic testing in the drug-free state and after administration of moricizine unless sustained arrhythmias occurred. MAIN RESULTS: Sustained ventricular tachycardia was inducible in the absence of antiarrhythmic drugs in 20 patients and was not suppressed by moricizine in any patient. Four patients had six episodes of spontaneous ventricular tachycardia while receiving moricizine. A probable proarrhythmic response occurred in four patients. CONCLUSION: In patients with compromised left ventricular function caused by coronary artery disease in whom class IA antiarrhythmics were ineffective, moricizine was ineffective in suppressing sustained ventricular arrhythmias and resulted in proarrhythmic effects in some patients.

Adult↗
PubMed1992

Low energy conversion of atrial fibrillation in the sheep.

OBJECTIVES: In this study, the feasibility, efficacy and safety of low energy internal atrial cardioversion were investigated in a sheep model. The relation between the level of energy used for atrial defibrillation and the probability of successful cardioversion was examined. BACKGROUND: Atrial fibrillation is a common clinical arrhythmia that frequently recurs after termination with high energy external cardioversion. In some patients with drug-refractory and poorly tolerated atrial fibrillation, an automatic implantable cardioverter may prove useful by providing rapid restoration of sinus rhythm. METHODS: In 16 pentobarbital-anesthetized sheep, a right atrial spring electrode was implanted percutaneously and a left thoracic cutaneous patch electrode was placed on the thorax. Sustained atrial fibrillation was induced by rapid atrial pacing and terminated by biphasic cathodal shocks synchronized to the R wave of the surface electrocardiogram (ECG). RESULTS: During 768 defibrillation attempts in 16 sheep, the percent of successful cardioversion attempts increased in a dose-response manner, reaching a plateau at the average energy level of 5 J. With greater than or equal to 1.5 and greater than or equal to 2.5 J energy levels, cardioversion was achieved, respectively, in greater than 50% and greater than 80% of attempts. Ventricular fibrillation occurred in 18 (2.4%) of 768 cardioversion attempts; in all 18 cases, the shock was poorly synchronized with the ECG R wave. CONCLUSIONS: Low energy cardioversion of atrial fibrillation to sinus rhythm is feasible with use of a right atrial spring/cutaneous patch electrode configuration. The percent of successful cardioversion attempts depends on the level of energy output, and there is a risk of ventricular fibrillation if cardioversion is poorly synchronized with ventricular depolarization.

Animals↗
PubMed1992

Local activation variability during monomorphic ventricular tachycardia in the dog.

OBJECTIVE: The aim was to determine the beat to beat variability in local activation time during sustained monomorphic ventricular tachycardia in a canine model of experimental myocardial infarction. METHODS: A digital template matching algorithm was developed for detecting subtle beat to beat variability in local activation timing at each of multiple ventricular sites. Ten electrically induced sustained ventricular tachycardia episodes, mean cycle length 211 (SD 40) ms, were endocardially and epicardially mapped in mongrel dogs weighing 15-20 kg. Digitised data were analysed for beat to beat local activation time variability. Similar data recorded during ventricular pacing at comparable rates and during sinus rhythm served as controls. RESULTS: The overall mean variability of local activation time for all 10 ventricular tachycardias was 3.2(1.6) ms, range 1.8(1.1) ms to 4.7(2.8) ms, in contrast to the overall mean variability of 0.2(0.4) ms (p = 0.0001) for ventricular pacing and 0.7(0.6) ms (p = 0.0001) for sinus rhythm. Oscillations in local activation time manifested alternans type periodicity during seven of 10 ventricular tachycardias independent of any alternans in local electrogram morphology. CONCLUSIONS: During sustained, monomorphic ventricular tachycardia, beat to beat variability and alternans type oscillations in local activation time are common and may be an intrinsic property of re-entry since they are negligibly small during ventricular pacing.

Animals↗
PubMed1991

Sudden cardiac death: management of high-risk patients.

Sudden cardiac death remains a leading cause of death in the United States, accounting for more than 350,000 deaths each year, and the survival rate of victims remains low. Most survivors face a significant risk for recurrence. The typical substrate is chronic--abnormal myocardium with fibrosis (often from previous myocardial infarction) and left ventricular dysfunction. Acute triggers for sudden cardiac death are primarily electrical, ischemic, metabolic, neurohormonal, and pharmacologic. In most electrocardiographically documented cases of sudden cardiac death, the trigger-substrate interaction appears to result in ventricular tachycardia and fibrillation. After initial resuscitation, survivors need a thorough cardiovascular evaluation, including definition of coronary anatomy, left ventricular function, and wall-motion abnormalities, as well as an electrophysiologic evaluation. An attempt must be made to determine what each survivor's correctable triggers are. Management should address all reversible triggers, such as acute ischemia and electrolyte abnormalities, and should include modifying or correcting the arrhythmogenic substrate. Empiric antiarrhythmic therapy offers no advantage in such modification. Pharmacologic therapy with antiarrhythmic drugs should be guided by an objective therapeutic endpoint, which is best accomplished through the use of programmed ventricular stimulation and serial electrophysiologic studies. Other therapeutic options include surgical suppression of ventricular tachycardia and implantation of a cardioverter defibrillator.

Arrhythmias, Cardiac↗
PubMed1991

Current treatment of patients surviving out-of-hospital cardiac arrest.

Most out-of-hospital cardiac arrests result from the sudden onset of a sustained ventricular arrhythmia in the absence of a new myocardial infarction. Individuals who survive cardiac arrest are at high risk for recurrent arrhythmias and sudden unexpected death. To prevent recurrent cardiac arrest, effective treatment must be provided during hospitalization after the initial episode. Caring for the survivor of cardiac arrest requires a detailed clinical investigation to define the underlying cardiac anatomy and left ventricular function and to elucidate the mechanism and characteristics of the patient's arrhythmia. Appropriate antiarrhythmic therapy, such as drugs or a nonpharmacological intervention (eg, implantable cardioverter-defibrillator), is then selected based on these considerations. In addition, ischemia is treated aggressively with beta-adrenergic blocking agents and, when appropriate, with surgical coronary artery revascularization.

Arrhythmias, Cardiac↗
PubMed1991

Immediate reproducibility of electrically induced sustained monomorphic ventricular tachycardia before and during antiarrhythmic therapy.

The immediate reproducibility of sustained ventricular tachycardia induction was evaluated prospectively during 106 studies performed in 53 patients with clinical sustained monomorphic ventricular tachycardia. Programmed electrical stimulation was performed twice, using the same protocol during 53 drug-free studies and 53 subsequent studies on antiarrhythmic therapy. Sustained monomorphic ventricular tachycardia was reproduced in 104 (98%) of the 106 studies. There was no significant difference in the incidence of reproducible tachycardia in the drug-free state compared with that observed during treatment with different classes of antiarrhythmic drugs. An increase in the number of extrastimuli was required to reinitiate the tachycardia in 9 (11%) of 83 studies in which single or double extrastimuli were initially required to induce the tachycardia. In 39 (37%) of 104 studies with reproducible tachycardia induction, the two tachycardias significantly differed in electrocardiographic (ECG) configuration and cycle length. These observations suggest that the overall reproducibility of ventricular tachycardia induction is sufficiently high to provide a reliable marker for evaluating the efficacy of therapeutic interventions. However, specific tachycardia characteristics such as cycle length and ECG configuration are more variable even within the same study and may be less useful in assessing the effects of subsequent interventions.

Anti-Arrhythmia Agents↗
PubMed1991

Localization of breakthrough site of canine monomorphic ventricular tachycardia by pacemapping. A vectorial approach.

BACKGROUND: The precision and limitations of ventricular pacemapping as a method to localize the site of earliest breakthrough of ventricular tachycardia (VT) were investigated in a canine model of experimental myocardial infarction. METHODS AND RESULTS: Forty-one episodes of VT induced in 10 animals were mapped using a standard grid of 64 endocardial and epicardial bipolar electrodes to determine the site of earliest endocardial or epicardial breakthrough of activation during VT. Each of these 64 recording sites was also used for ventricular pacing during sinus rhythm at cycle lengths comparable to those of the VTs. Orthogonal X, Y, and Z Frank electrocardiographic (ECG) leads were recorded during all episodes of VT and ventricular pacing from all sites after the chest was closed in all animals. Surface ECG waveforms corresponding to each VT and each ventricular pacing were compared pairwise by measuring the Euclidean metric difference between the VT and ventricular pacing vectors with the orthogonal ECG leads as their X, Y, and Z components. The pacing site that generated the vector most similar to VT vector (smallest vectorial difference) was defined as the predicted breakthrough site. This predicted site of breakthrough was identical to the actual site of breakthrough determined by activation sequence mapping during VT for only nine VTs (22%). However, for an additional 27 VTs (66%), the observed and predicted breakthrough locations were at adjacent (1 cm or less apart) recording sites. For five VTs (12%), the two sites were remote, the distance between them exceeding 1 cm. CONCLUSIONS: In this model, locating the breakthrough site by pacemapping is exact in only a small minority of VTs. However, when orthogonal surface ECG leads are used for comparison, pacemapping can predict the site of earliest breakthrough during VT with a 1-cm resolution in the majority of VTs.

Animals↗
PubMed1991

Repolarization inhomogeneities in ventricular myocardium change dynamically with abrupt cycle length shortening.

BACKGROUND: In single heart cells, abrupt changes in stimulation rate elicit complex alterations in repolarization. The effects of rate change on dispersion of repolarization, however, have not been well characterized. METHODS AND RESULTS: To determine the effects of abrupt cycle length (CL) shortening on spatial inhomogeneity of repolarization in a syncytium of ventricular cells, 124 action potentials were simultaneously recorded from Langendorff-perfused guinea pig hearts using high-resolution optical mapping with voltage-sensitive dye. The distribution of ventricular action potential durations (APDs) mapped during each cardiac cycle was used to calculate mean APD and repolarization dispersion index (DI), defined as the variance of the distribution. After abruptly shortening CL from 500 to 300 msec, mean APD declined exponentially in normoxic controls (by 23 +/- 3 msec, p less than 0.0001). This response was characterized by beat-to-beat oscillations of APD that were synchronized at all ventricular sites. After 30 minutes of hypoxia, mean APD decreased from 175.0 +/- 13.3 to 76 +/- 25.7 msec. However, during hypoxia, abrupt CL shortening lowered mean APD by only an additional 6 +/- 6 msec, and APD oscillations were no longer synchronized throughout the ventricle. In controls, beat-to-beat DI decreased significantly (-51.0 +/- 6.8%, p less than 0.01) by the sixth post-CL shortening beat and then recovered (by 15-20 beats). In contrast, DI failed to decrease during hypoxia (+7.1 +/- 23%). Two mechanisms for the transient decline of DI in controls were identified: synchronous APD oscillations and transient diminution of the apical-to-basal ventricular APD gradient. CONCLUSIONS: These data demonstrate that inhomogeneity of ventricular repolarization, as measured by DI, changes dynamically with CL shortening. Furthermore, the hypoxic ventricle does not attenuate DI after abrupt CL shortening and thereby lacks a physiological response expected to diminish vulnerability to arrhythmias.

Action Potentials↗
PubMed1990

Late potentials on the signal-averaged electrocardiogram after canine myocardial infarction: correlation with induced ventricular arrhythmias during the healing phase.

Signal-averaged electrocardiograms (ECGs) and programmed ventricular stimulation were serially performed in 12 dogs (3 weeks of age) after experimental anteroapical myocardial infarction. At electrophysiologic study, sustained ventricular tachyarrhythmia was induced in seven dogs on at least one occasion. Of a total of 39 electrophysiologic studies, sustained monomorphic ventricular tachycardia was induced in seven studies and ventricular fibrillation in eight studies. In the remaining studies, no ventricular arrhythmia could be induced with triple ventricular extrastimuli. There was considerable day to day variability in the response to programmed stimulation and the results of the signal-averaged ECG. The signal-averaged QRS complex was significantly longer in dogs with inducible ventricular tachycardia or fibrillation (61 +/- 5 versus 57 +/- 3 ms, p = 0.02), had a lower terminal QRS amplitude (24 +/- 20 versus 46 +/- 33 microV, p = 0.04) and a longer late potential duration (19 +/- 4 versus 15 +/- 3 ms, p = 0.003) compared with that in animals with no inducible ventricular arrhythmia. Late potentials were defined as a total QRS duration greater than 58 ms, a terminal QRS amplitude less than 20 microV and a late potential duration greater than 18 ms. Using this definition, late potentials were seen in two distinct phases--immediately after coronary ligation and then beyond the first 72 h after infarction. The appearance of late potentials coincided with a change in arrhythmia inducibility from no ventricular arrhythmia to initiation of sustained monomorphic ventricular tachycardia. There is a close relation between inducibility of ventricular tachycardia in experimental canine myocardial infarction and the appearance of late potentials on the surface ECG.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Surgical coronary revascularization in survivors of prehospital cardiac arrest: its effect on inducible ventricular arrhythmias and long-term survival.

In a selected subgroup of 50 survivors of cardiac arrest, the impact of surgical myocardial revascularization on inducible arrhythmias, arrhythmia recurrence and long-term survival was examined. The effects of several clinical, angiographic and electrophysiologic variables on arrhythmia recurrence and survival were also analyzed. All patients had a prehospital cardiac arrest and severe operable coronary artery disease and underwent myocardial revascularization. Preoperative electrophysiologic study was performed in 41 patients; 33 (80%) had inducible ventricular arrhythmias. Of 42 patients studied off antiarrhythmic drugs postoperatively, 19 (45%) had inducible ventricular arrhythmias. Thirty patients with inducible arrhythmias preoperatively underwent postoperative testing off antiarrhythmic drugs; arrhythmia induction was suppressed in 14 (47%). By multivariate analysis, the induction of ventricular fibrillation at the preoperative electrophysiologic study was the only significant predictor of induced ventricular arrhythmia suppression by coronary surgery (p less than 0.001). Inducible ventricular fibrillation was not present postoperatively in any of the 11 patients who manifested this arrhythmia preoperatively. In contrast, inducible ventricular tachycardia persisted in 80% of patients in whom preoperative testing induced this arrhythmia. Patients were followed up for 39 +/- 29 months. There were four arrhythmia recurrences; one was fatal. There were three nonsudden cardiac deaths and three noncardiac deaths. By life-table analysis, 5 year survival, cardiac survival and arrhythmia-free survival rates were 88%, 98%, and 88%, respectively. Depressed left ventricular ejection fraction and advanced age were predictive of death (p = 0.015 and 0.026, respectively) and cardiac death (p = 0.037 and 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1990

Exercise electrophysiology testing: the effect of exercise on the induction of ventricular arrhythmias by programmed ventricular stimulation.

In order to assess the effect of acute, reversible myocardial ischemia on the outcome of programmed ventricular stimulation (PVS), ventricular stimulation was performed at rest, during exercise, and during recovery in 10 patients with coronary artery disease. Of these ten patients, four were tested while off antiarrhythmic drugs and six were tested on antiarrhythmic drug therapy. Nine of the ten patients developed acute myocardial ischemia during exercise PVS. However, in only two of these ten patients ventricular arrhythmia could be induced by PVS, one during exercise and one during recovery.

Aged↗
PubMed1989

Usefulness of sotalol in suppressing ventricular tachycardia or ventricular fibrillation in patients with healed myocardial infarcts.

The electrophysiologic effects and antiarrhythmic efficacy of oral sotalol were investigated in 42 patients with coronary artery disease and prior myocardial infarction who presented with ventricular tachycardia (VT), ventricular fibrillation (VF) or syncope. The mean left ventricular ejection fraction was 36 +/- 9%. Baseline programmed cardiac stimulation initiated sustained VT (26 patients) or VF (16). The induced arrhythmia was not suppressed by conventional antiarrhythmic drugs in any patient (3 +/- 2 trials/patient). The mean daily dosage of sotalol was 221 +/- 84 mg. The right ventricular effective refractory period increased from 247 +/- 25 to 273 +/- 26 ms with sotalol (p = 0.0001) and the corrected QT interval increased from 431 +/- 35 to 456 +/- 62 ms (p = 0.02). Arrhythmia suppression was defined as no sustained VT or VF in response to programmed cardiac stimulation using up to 3 extrastimuli. Induced VT or VF was suppressed by sotalol therapy in 10 (24%) patients (group 1). Group 1 patients had faster induced arrhythmias at the baseline study than patients whose induced ventricular arrhythmia was not suppressed (group 2). The mean left ventricular ejection fraction tended to be higher in group 1 patients (p = 0.07). Fourteen patients (including 9 group 1 patients) continued receiving sotalol after discharge. In 2 group 2 patients, sotalol was combined with a class IA antiarrhythmic drug. During a mean follow-up period of 7.9 +/- 4.9 months, 2 patients had recurrent VT and in 2 others sotalol was discontinued due to side effects.

Aged↗
PubMed1989

Electrocardiographic localization of the site of origin of ventricular tachycardia in patients with prior myocardial infarction.

The utility of the 12 lead electrocardiogram (ECG) in identifying the site of origin of sustained ventricular tachycardia in patients with previous myocardial infarction was studied. A new mapping grid, based on biplanar fluoroscopic imaging of the heart, was utilized for the definition of left ventricular endocardial sites. On the basis of QRS configurations resulting from left ventricular endocardial pacing at disparate sites in 22 patients (Group I), ECG features that were specific for particular sites were identified and used to construct an algorithm. Apical and basal sites were differentiated by the QRS configuration in leads V4 and aVR, anterior and inferior sites by that in leads II, III and V6 and septal and lateral sites were differentiated using leads I, aVL and V1. The algorithm was used to predict the site of earliest endocardial activation during 44 episodes of sustained ventricular tachycardia in a second group of 42 patients (Group II) in a blinded fashion. Anterior sites were correctly predicted in 83% of cases, inferior sites in 84%, septal sites in 90% and lateral sites in 82% of cases. Apical and basal sites were each correctly predicted in 70% of cases, whereas intermediate sites were less well predicted (29 to 55%) on the basis of QRS configuration. Precise localization of the site of origin of ventricular tachycardia (in all three planes) was achieved in 17 cases (39%), and in 16 cases (36%) the site of origin was immediately adjacent to the predicted site. Prediction of the site of origin of ventricular tachycardia from the 12 lead ECG may serve as a useful, time-saving adjunct to, but not a substitute for, activation sequence mapping during ventricular tachycardia.

Algorithms↗
PubMed1989

Therapeutic serum lidocaine and metabolite concentrations in patients undergoing electrophysiologic study after discontinuation of intravenous lidocaine infusion.

Serum concentrations of lidocaine and its metabolites monoethylglycinexylidide (MEGX) and glycinexylidide (GX) were measured in seven patients after discontinuation of intravenous lidocaine necessary for control of spontaneous arrhythmias prior to electrophysiologic study. Standard loading doses of lidocaine were given intravenously followed by 2 mg/min infusions for 79.5 +/- 6.5 hours. Electrophysiologic studies all started more than 5 half-lives or 7.5 hours after discontinuation of intravenous lidocaine. Local anesthesia with subcutaneous lidocaine (mean 162 +/- 96 mg) was administered in six patients. Plasma concentrations of lidocaine and its metabolites were determined at the termination of the infusion, 2 and 4 hours afterwards, at the start of the electrophysiologic study prior to local anesthesia, and at the end of the study. Levels were also determined at 12 and 24 hours after discontinuation of the infusion. Mean plasma concentrations of lidocaine, MEGX, and GX at the start of the study were 1.02, 0.86, and 0.62 micrograms/ml, respectively. These had increased to 2.78, 0.92, and 0.68 by the end of the electrophysiologic study. One patient with coronary artery disease and prior out-of-hospital ventricular fibrillation had a therapeutic lidocaine level and no inducible arrhythmia at the time of the initial study. At a subsequent electrophysiologic study, no lidocaine or metabolites were detected in the serum and ventricular fibrillation was induced. Thus using the reported half-life of 90 minutes and discontinuing lidocaine 5 half-lives prior to electrophysiologic evaluation does not ensure lack of electrophysiologic effects of the parent compound or its metabolites. Lidocaine given for local anesthesia further increases lidocaine and metabolite levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Programmed ventricular stimulation in patients with left ventricular dysfunction and ventricular tachycardia: effects of acute hemodynamic improvement due to nitroprusside.

To assess the electrophysiologic effects of acute hemodynamic improvement in patients with left ventricular systolic dysfunction, 12 patients with a left ventricular ejection fraction less than 0.40 and a history of sustained monomorphic ventricular tachycardia were studied. All patients had underlying coronary artery disease. Patients underwent programmed cardiac stimulation in random order during a baseline period and with nitroprusside infusion. Mean pulmonary capillary wedge pressure decreased from 20 +/- 8 mm Hg at baseline study to 8 +/- 3 mm Hg during nitroprusside infusion (p less than 0.0001). Pulmonary artery, right atrial and systemic arterial pressures also decreased with nitroprusside (p less than 0.01). Cardiac output did not change. Left ventricular dimensions, determined by two-dimensional echocardiography, decreased significantly during nitroprusside infusion. The right ventricular effective refractory period, measured during ventricular drive trains at cycle lengths of 400 and 600 ms, were similar during baseline and nitroprusside periods (271 +/- 30 versus 274 +/- 31 ms at 600 ms, and 249 +/- 25 versus 246 +/- 18 ms at 400 ms). In 2 patients no ventricular arrhythmias were induced during either study period; in the other 10, ventricular tachyarrhythmias were induced during both periods. The mean number of extrastimuli required to induce a ventricular tachyarrhythmia was similar during the baseline period (1.8 +/- 0.6) and during nitroprusside infusion (1.9 +/- 0.7). As well, the mean cycle length of ventricular tachycardia induced was similar during the baseline period (347 +/- 61 ms) and during nitroprusside infusion (342 +/- 70 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Modified magnet test for a reversed automatic implantable cardioverter defibrillator.

We present the case of a 55-year-old man with atrial septal defect and cardiomyopathy who underwent implantation of an automatic cardioverter defibrillator (AICD) for ventricular tachycardia resulting in collapse. This case demonstrates multiple unusual complications related to AICD, including rotation of the pulse generator unit about its long axis requiring a "left-handed" magnet test to determine the appropriate counts.

Cardiomyopathies↗