PubMed Health⌕ Search

Biomedical subjects

H Garan

Publications and source records attributed to H Garan.

At least 73 records · Page 4Linked to original sources

Cardiac conduction abnormalities during percutaneous balloon mitral or aortic valvotomy.

To evaluate the electrophysiologic changes in the cardiac conduction system that occur during percutaneous mitral or aortic balloon valvotomy, we prospectively studied the conduction system in 19 patients (10 mitral, 8 aortic, and 1 both) undergoing this procedure. A His bundle electrogram was recorded in all patients, and when sinus rhythm was present, the atrioventricular (AV) node effective refractory period was measured. Holter monitoring was performed during and for 24 hours after the procedure. Follow-up electrocardiograms (ECG) were available in 11 patients 2.3 +/- 1.5 months after the procedure. The AV node effective refractory period before (276 +/- 86 msec) and after valvotomy (298 +/- 85 msec) were not significantly different. The maximum His-Purkinje conduction time (HV interval) observed during valvotomy (66 +/- 20 msec) was significantly longer (p less than 0.01) than that measured before (57 +/- 10 msec) or after (60 +/- 18 msec) valvotomy. The mean HV intervals before and after valvotomy were not significantly different. The mean QRS complex duration increased from 95 +/- 28 to 112 +/- 28 msec during valvotomy and remained significantly prolonged (109 +/- 26 msec) 24 hours after the procedure (p less than 0.01). A new intraventricular conduction defect (QRS complex duration greater than 100 msec) or bundle branch block occurred in five of 13 patients who had normal QRS duration before the procedure. The change in HV interval did not correlate with the change in QRS complex duration. In four patients, the newly acquired intraventricular conduction defect was still present on follow-up ECG tracing. Complete heart block was not observed in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Electrophysiologic evaluation of antiarrhythmic therapy for ventricular tachyarrhythmias.

The use of electrophysiologic studies has contributed significantly to our understanding of the mechanisms of ventricular tachyarrhythmias and enhanced our ability to assess objectively the efficacy of various therapeutic interventions in modifying or preventing their recurrence. The basis on which electrophysiologic testing techniques is founded is the ability reproducibility to initiate ventricular arrhythmias by programmed electrical stimulation in patients with a history of recurrent ventricular tachycardia or fibrillation. Ventricular tachycardia can be initiated by electrophysiologic studies in approximately 90% of patients with clinically documented recurrent, sustained ventricular tachycardia related to coronary artery disease and in 60% of patients with nonsustained ventricular tachycardia. Reports indicate that electrophysiologic testing is highly specific as well (99% for sustained monomorphic ventricular tachycardia). Studies in patients with recurrent ventricular tachycardia demonstrate that prevention by antiarrhythmic drugs of the ability to initiate tachycardias that were previously inducible by comparable stimulation techniques in the absence of therapy is highly predictive of freedom from recurrent episodes of spontaneous ventricular tachycardia and ventricular fibrillation. This end point can be achieved in 35 to 75% of patients. This wide range of success rates results from differences in the patient populations studied, as well as major differences in the programmed stimulation and antiarrhythmic drug protocols used among laboratories. The positive predictive value of this technique (defined as the percentage of patients in whom complete suppression of inducible ventricular tachycardia or ventricular fibrillation is achieved during electrophysiologic testing with antiarrhythmic drugs and in whom no spontaneous arrhythmia occurs at 1- to 2-year follow-up) ranges between 80 and 95%.

Anti-Arrhythmia Agents↗

Electrically induced ventricular arrhythmias in acute myocardial infarction treated with thrombolytic agents.

Ninety-two patients underwent programmed ventricular stimulation 12 +/- 3 days after acute myocardial infarction (AMI) treated with thrombolytic agents (streptokinase, recombinant tissue plasminogen activator, or both). Cardiac catheterization was performed in all patients on admission to hospital and was repeated in 97% of them 13 +/- 5 days later. Sustained ventricular arrhythmias--either tachycardia (VT) or fibrillation--were induced in 20 (22%) patients, with nonsustained VT induced in another 12 (13%). Multivariate analysis was used to identify predictors of induction of sustained VT, with short right ventricular effective refractory period (p = 0.0061), site of AMI (inferior or posterior, p = 0.008), infarct-related artery (right or circumflex coronary artery, p = 0.018), multivessel coronary artery disease (p = 0.043) and male sex (p = 0.028) being significant predictors of sustained VT. Neither successful reperfusion, time to reperfusion, nor residual stenosis in the infarct-related artery was significant. All patients in whom VT was induced were treated with electrophysiologically guided antiarrhythmic therapy. Cardiac mortality after hospital discharge was 1% over 30 +/- 16 months.

Cardiac Catheterization↗

Predictors of automatic implantable cardioverter defibrillator discharge for life-threatening ventricular arrhythmias.

Data from 100 patients with life-threatening ventricular arrhythmias and automatic implantable cardioverter defibrillators (AICDs) were analyzed to determine if clinical, angiographic and electrophysiologic variables are predictive of AICD discharge. During a median follow-up period of 18 months, 45% of patients experienced greater than or equal to 1 device discharge during a documented ventricular arrhythmia or in association with presyncope or syncope ("appropriate" AICD discharge). Univariate predictors of appropriate AICD discharge included depressed left ventricular ejection fraction (p = 0.0007), inducible sustained ventricular arrhythmia at electrophysiologic study performed in the absence of antiarrhythmic drugs (p = 0.009), fewer number of extrastimuli required for induction at this study (p = 0.001), inducible sustained arrhythmia at electrophysiologic study performed on the discharge antiarrhythmic regimen (p = 0.0005) and fewer extrastimuli required for this induction (p less than 0.0001). Multivariate analysis identified the induction of a sustained ventricular arrhythmia by 1 or 2 extrastimuli during electrophysiologic study performed on the discharge regimen as the only independent predictor among the variables analyzed (p less than 0.0001). The probability of appropriate AICD discharge at 18 months was 86% for patients who had a sustained arrhythmia induced with 1 or 2 extrastimuli versus 15% for those requiring 3 extrastimuli for arrhythmia induction and 13% for patients without inducible sustained arrhythmias.

Arrhythmias, Cardiac↗

Early assessment of the effect of map-guided transcatheter intracardiac electric shock on sustained ventricular tachycardia secondary to coronary artery disease.

Short-term efficacy of transcatheter intracardiac electric shock was evaluated in 25 patients with recurrent sustained ventricular tachycardia (VT) secondary to coronary artery disease. Pace mapping and activation sequence mapping during VT were both used to direct intracardiac electric shocks applied between the distal electrode of the catheter (cathode) and a chest wall plate (anode) using a mean total energy of 588 +/- 209 J/patient. The short-term outcome of the procedure was considered successful in 3 patients (12%) who neither developed spontaneous VT nor had sustained VT in response to programmed electrical stimulation 1 week after the procedure. The short-term outcome in the remaining 22 patients (88%) was considered unsuccessful: 7 of the 22 patients developed spontaneous sustained VT and in 19 patients, including 15 with no spontaneous VT, sustained VT was still inducible by programmed electrical stimulation 7 +/- 2 days after the intracardiac electric shock. All 22 patients were subsequently treated with other modes of antiarrhythmic therapy. Using the technique described, the short-term efficacy of map-directed transcatheter intracardiac electric shock in eliminating VT is poor.

Adult↗

Sensitivity of an automatic external defibrillator for ventricular tachyarrhythmias in patients undergoing electrophysiologic studies.

An automatic advisory external defibrillator (AED) was activated during all arrhythmias occurring at the time of 77 electrophysiologic studies in 45 patients. Sustained ventricular tachycardia (VT) occurred during 55 studies in 31 patients and nonsustained VT was induced during 10 studies in 9 patients. Ventricular fibrillation was induced 5 times in 5 patients and atrial arrhythmias with a rapid ventricular response occurred during 7 studies in 4 patients. The AED detection algorithm advised "shock" during 36 of 55 (65%) episodes of sustained VT and all 5 episodes of ventricular fibrillation. The device correctly advised "shock" for all 6 episodes of nonsustained VT that spontaneously terminated after analysis was complete. Thus, the sensitivity of the device for all ventricular arrhythmias analyzed was 47 of 66 (71%). The device recommended "shock" for all 31 episodes of rapid VT and 1 of 2 episodes of atrial fibrillation associated with systemic hypotension (32 of 33, 97%). The 19 episodes of VT for which "no shock" was advised were comparatively slow and were hemodynamically well tolerated. The device recommended "no shock" during all 21 episodes of normal sinus rhythm and all 20 episodes of rapid atrial pacing (cycle length 400 ms) analyzed. "No shock" was advised during 4 episodes of sustained narrow QRS complex supraventricular tachycardia and 4 brief episodes of nonsustained VT that terminated before analysis was complete. Thus, in this study the specificity of the AED for wide complex tachycardias was 100%.

Algorithms↗

Out-of-hospital cardiac arrest. Use of electrophysiologic testing in the prediction of long-term outcome.

We examined the role of electrophysiologic testing in the prediction of long-term outcome in 166 survivors of out-of-hospital cardiac arrest not associated with acute myocardial infarction. Ventricular arrhythmias were inducible in 131 patients (79 percent) at base line and were suppressed by antiarrhythmic drugs or surgery (or both) in 91 of 127 (72 percent). During a median follow-up period of 21 months, cardiac arrest recurred in 29 patients: 11 (12 percent) of the 91 in whom inducible arrhythmias had been suppressed (including 5 patients in whom treatment had been discontinued), 12 (33 percent) of the 36 in whom inducible arrhythmias persisted, and 6 (17 percent) of the 35 in whom arrhythmias could not be induced at the initial electrophysiologic study. Cox survival analysis identified the following three variables as significant independent predictors of recurrent cardiac arrest: persistence of inducible ventricular arrhythmias (relative risk, 3.97 [95 percent confidence interval, 1.80 to 8.75], P = 0.0006), a left ventricular ejection fraction of 30 percent or less (relative risk, 2.60 [1.21 to 5.53], P = 0.0138), and the absence of cardiac surgery (relative risk, 4.20 [0.99 to 17.77], P = 0.0512). We conclude that electrophysiologic testing is useful in quantifying the subsequent risk of cardiac arrest among survivors of out-of-hospital cardiac arrest.

Anti-Arrhythmia Agents↗

Long-term efficacy of mexiletine alone and in combination with class Ia antiarrhythmic drugs for refractory ventricular arrhythmias.

The efficacy of mexiletine used alone, and in combination with a class Ia antiarrhythmic drug, was assessed in 159 previously drug-refractory patients with ventricular tachycardia (VT) during serial electrophysiologic studies and during long-term (5-year) clinical follow-up. Electrically-inducible ventricular tachycardia was suppressed by mexiletine alone in 23% of patients tested, and a combined antiarrhythmic drug regimen was effective in 29% of the trials performed. Mexiletine was much more likely to be effective in patients presenting with nonsustained VT or ventricular fibrillation than in patients with sustained VT (p less than 0.005). After 1 and 4 years of treatment, 18% and 42% of the patients treated with mexiletine alone had died suddenly or suffered recurrent symptomatic VT, compared to 11% and 25% of patients treated with the combined antiarrhythmic drug regimens (p = NS). Mexiletine therapy was associated with frequent, though readily reversible, adverse reactions. However, mexiletine treatment had to be discontinued permanently in 8 of 92 patients (9%) because of intolerable side effects. We conclude that the added efficacy and possible improved arrhythmia-free survival associated with combining mexiletine with a class Ia agent should be further investigated.

Anti-Arrhythmia Agents↗

Treatment of ventricular arrhythmias.

Within the past 20 years, our knowledge concerning the epidemiology, natural history, and treatment of VT has expanded greatly. A variety of effective pharmacologic, surgical and electrical therapies for VT are now available to the clinician. Patients who present with ventricular tachyarrhythmias should undergo a comprehensive medical evaluation directed at identifying and treating such factors as ischemia, congestive heart failure, valvular heart disease, sensitivity to cardioactive drugs, and metabolic derangements. Many patients who present with asymptomatic ventricular arrhythmias do not require specific antiarrhythmic drug therapy. However, certain patients who have already suffered a life-threatening arrhythmia or who are at high risk for such arrhythmia should be vigorously treated with specific antiarrhythmic therapy guided for that individual patient. The efficacy of any antiarrhythmic treatment should be assessed by ECG monitoring, exercise testing, and/or electrophysiologic study. In the near future, potentially revolutionary new electrical therapies for ventricular tachyarrhythmias will be evaluated. It is to be hoped that these devices used in combination with pharmacologic and surgical therapies may dramatically reduce the incidence of sudden cardiac death in high-risk patients.

Anti-Arrhythmia Agents↗

The automatic implantable cardioverter-defibrillator: efficacy, complications and survival in patients with malignant ventricular arrhythmias.

Ninety-four patients underwent surgery for automatic implantable cardioverter-defibrillator implantation. Ninety patients were discharged from the hospital with the device and were followed up for a mean period of 17 +/- 10 months. Forty-six patients experienced at least one discharge of the device under circumstances consistent with a malignant ventricular arrhythmia. One sudden death occurred. Complications included perioperative death (3 patients), post-operative ventricular tachycardia (12 patients) and atrial fibrillation (8 patients), perioperative myocardial infarction (1 patient) and device discharges for sinus tachycardia and supraventricular arrhythmias (17 patients). Six and 12 month survival rates by life table analysis were 98.7 and 95.4%, respectively. Thus, the automatic implantable cardioverter-defibrillator is a highly effective and relatively low risk treatment modality for patients with refractory life-threatening ventricular arrhythmias.

Adolescent↗

Prediction of successful suppression of sustained ventricular tachyarrhythmias by serial drug testing from data derived at the initial electrophysiologic study.

This study investigated whether data available after the initial electrophysiologic study in patients with sustained ventricular tachyarrhythmia could identify those patients in whom serial drug testing is likely to be efficacious. One hundred six patients with inducible sustained ventricular tachyarrhythmia, whose initial study included short-term drug testing with intravenous procainamide, were evaluated. The baseline arrhythmia induced (in the absence of all antiarrhythmic drugs) was monomorphic tachycardia with a cycle length greater than 200 ms in 81 patients and ventricular flutter or fibrillation in the remaining 25 patients. After intravenous infusion of procainamide (1,250 +/- 300 mg), a ventricular tachyarrhythmia could still be induced in 80 patients during testing with up to three extrastimuli. Serial drug testing with one to four trials of oral conventional and investigational agents was then undertaken. Evaluation of 15 clinical, hemodynamic and electrophysiologic variables by stepwise logistic regression identified two independent predictors of successful response to oral antiarrhythmic drugs: 1) noninducibility of ventricular tachycardia after intravenous procainamide (p less than 0.001), and 2) left ventricular ejection fraction greater than or equal to 40% (p less than 0.05). Subgroup analysis combining each of these variables identified patients with a high, intermediate or low probability of finding a successful oral drug regimen. Patients whose arrhythmia was suppressed by intravenous procainamide had a 100% likelihood (if left ventricular ejection fraction was greater than or equal to 40%) or an 87% likelihood (if ejection fraction was less than 40%) of responding to an oral regimen.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Spontaneous and electrically induced ventricular arrhythmias during acute ischemia superimposed on 2 week old canine myocardial infarction.

The arrhythmogenic effect of acute reversible myocardial ischemia before and 2 weeks after experimental myocardial infarction was investigated in 37 dogs that underwent reversible 10 min occlusion of the first major marginal branch of the left circumflex coronary artery. Subsequently, 24 of the dogs underwent experimental myocardial infarction with permanent left anterior descending coronary ligation, and 13 dogs served as sham-operated controls. Two weeks later, an open chest programmed electrical stimulation was performed in the 13 sham-operated and 24 postinfarction dogs to determine its accuracy in predicting the ventricular arrhythmias that develop during a subsequent episode of acute reversible ischemia. After programmed electrical stimulation, the left circumflex marginal branch was reversibly occluded for 10 min at the same site. The incidence of spontaneous ventricular fibrillation during reversible left circumflex marginal coronary occlusion did not differ from the first to the second study in sham-operated dogs, whereas in the postinfarction dogs, it increased from 13% before infarction to 54% after infarction (p = 0.005). The outcome of programmed electrical stimulation predicted spontaneous ventricular arrhythmias during coronary occlusion in only 21% of the postinfarction dogs. The accuracy of programmed electrical stimulation was 42% and its predictive value was 47% in detecting the dogs with spontaneous ventricular fibrillation. Regional myocardial blood flow measurements by microsphere technique identified the severity of reversible ischemia in the infarct border and periinfarction zones as a correlate of spontaneous ventricular fibrillation during coronary occlusion. In contrast, total infarct size correlated with electrically induced but not with spontaneous ventricular arrhythmias.

Acute Disease↗

Effect of intracarotid administration of ouabain in dogs.

Recent work has documented both centrally mediated vasoconstriction and, paradoxically, a withdrawal of sympathetic activity in response to cardiac glycosides. In the present study the possibility that these different neurogenic responses might be dose related was investigated by infusing ouabain (5, 10, and 20 micrograms) for 5 min into the right common carotid artery of 51 anesthetized mongrel dogs. Effects on vascular resistance in the isolated, separately perfused but innervated gracilis muscle were measured. A 5-microgram infusion of ouabain (n = 6) produced a prolonged decrease in gracilis vascular resistance (GVR) of 19.4 +/- 5.4% (SE) from 43.4 +/- 6.7 (SE) to 33.7 +/- 4.2 mmHg.ml-1.100 g muscle.min (resistance units, RU). This vasodilatory response was not present in nine additional dogs following denervation of the carotid bifurcation. A 10-microgram infusion had no significant effect on GVR (n = 5), but the 20-microgram infusion of ouabain (n = 8) caused a rapid increase in GVR from 42.1 +/- 5.0 to 47.6 +/- 5.7 RU, an increase of 14.4 +/- 5.6%, which was not influenced by denervation of the carotid bifurcation (n = 8). This vasoconstriction was transient returning toward the control levels by 20 min following the infusion. These data indicate important dose-related differences in vascular responses to ouabain that are directionally opposite and mediated by separate neurogenic mechanisms. At high doses a centrally mediated vasoconstriction dominates, whereas at low doses carotid bifurcation mediated vascular dilatation occurs.

Animals↗

The effect of potassium ion depletion on postinfarction canine cardiac arrhythmias.

The effect of potassium ion (K+) depletion on postmyocardial infarction ventricular arrhythmias was investigated in 32 dogs: 12 control animals, 10 animals that ate a diet extremely low in K+ for 15 days, and 10 others that, in addition to dietary K+ deprivation, received 50 mg of hydrochlorothiazide four times. The experimental myocardial infarction was created by proximal left anterior descending coronary artery ligation. In a subgroup of 24 animals selected for relatively uniform size of myocardial infarction (14% to 22% of left ventricular mass), eight animals with mean cumulative K+ balance of -4.01 +/- 2.19 meq/kg developed spontaneous ventricular fibrillation within 4 to 17 min of coronary ligation, whereas 16 animals with a mean cumulative K+ balance of -0.11 +/- 1.82 meq/kg didn't. By univariate analysis cumulative K+ deficit (p = .001) and plasma K+ concentration (p = .039) correlated significantly with spontaneous ventricular fibrillation. Multivariate analysis of the entire population of 32 animals identified cumulative K+ deficit and size of myocardial infarction as the only independent predictors of ventricular fibrillation. Cumulative K+ deficit was also an independent predictor of ventricular fibrillation induced by programmed cardiac stimulation in the conscious state 1 day after myocardial infarction.

Animals↗