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F J Venditti

Publications and source records attributed to F J Venditti.

35 records · Page 2Linked to original sources
PubMed1994

Appropriate sensing of ventricular fibrillation after failed shocks in a transvenous cardioverter-defibrillator system.

BACKGROUND: Reduction in R-wave amplitude immediately after defibrillation shocks in an integrated shock/sense transvenous cardioverter-defibrillator (TCD) lead system has prompted concerns regarding adequate sensing after failed shocks. We therefore studied redetection characteristics for ventricular fibrillation after unsuccessful defibrillation shocks in a TCD system to determine if these observations have clinical relevance. METHODS AND RESULTS: Fifty patients with this shock/sense TCD lead system underwent conversion testing of their TCD at several time intervals. There were a total of 142 failed shocks events recorded, including 10, 15, 70, and 47 events at implantation, predischarge, and 2- and 6-month testing, respectively. Initial detection time (IDT) and redetection time (RDT) for ventricular fibrillation were measured from event markers for all unsuccessful defibrillation shocks. To assess the effect of failed shocks on electrogram quality, 54 failed shock episodes were evaluated in 37 of the 50 patients by measuring electrograms during VF before and after shock. Mean RDT for the entire group was 5.3 +/- 3.5 seconds compared with an IDT of 4.5 +/- 3.3 seconds (P = NS). There were no significant differences between IDT and RDT at implantation or any follow-up testing period, despite a significant decline in R-wave amplitude from 8.1 +/- 3.5 to 6.8 +/- 2.8 mV (P < .0001) measured 3 to 6 seconds after shock delivery. Analysis of 8 individuals with any extended RDT (> or = 10 seconds) showed no significant differences in clinical or implantation characteristics when compared with 42 individuals without extended RDT. CONCLUSIONS: In this integrated shock/sense TCD lead system, unsuccessful shock delivery has no significant effect on redetection of ventricular fibrillation at device implantation or up to 6 months of follow-up, despite an observed reduction in postshock R-wave amplitude. Therefore, the reported reduction in electrogram quality after a shock is of no practical importance because sensing of ventricular fibrillation does not appear to be compromised in this particular TCD system. Whether this applies to other implantable cardioverter-defibrillator pulse generators and lead systems with different sensing characteristics requires further evaluation.

Aged↗
PubMed1993

Infection of implantable cardioverter defibrillator systems: a preventable complication?

In a consecutive series of 164 patients undergoing primary implantation of an implantable cardioverter defibrillator (ICD), two patients died in the hospital (1.2%) and early system infection developed in one patient requiring explantation of the device (0.61%). Late infection developed in one additional patient (0.61%) 7 months after transvenous ICD implantation, and was thought to be due to a recent intravascular catheterization. Symptomatic generator pocket hematomas developed in three patients, two of which were treated by simple evacuation and one with temporary generator explanation and subsequent reimplantation of the unit in a new pocket. No infection developed in these three patients during follow-up. Generator erosion without obvious system infection developed in a fourth patient. Guidelines for the prevention of infection in ICD systems are presented.

Defibrillators, Implantable↗
PubMed1993

Effect of extracorporeal shock wave lithotripsy on implantable cardioverter defibrillator.

Extracorporeal shock wave lithotripsy (ESWL) is frequently used for nephrolithiasis of the upper urinary tract. Because of the powerful shock wave and electromechanical forces created, this therapy has been contraindicated in the patient with an implantable cardioverter defibrillator (ICD). To determine whether or not ESWL affects ICD devices, we subjected ten devices to a full course of ESWL. The devices were then returned to the manufacturer to undergo bench analysis, which revealed no abnormalities in function. Additionally, one device was placed in the pathway of the shock wave, resulting in a discharge of the device despite a frequency of ESWL of 100 shocks/min (well below the rate cutoff of that device). Manufacturer analysis of this device, likewise, revealed no abnormalities even though the device had been exposed to the focal point of the shock wave. We conclude that contralateral ESWL is not contraindicated for the patient with an ICD. We do, however, recommend a post-procedure evaluation to ensure appropriate function of the ICD.

Contraindications↗
PubMed1992

Subfascial implantation of implantable cardioverter defibrillator generator.

The automatic cardioverter defibrillator generator is a relatively large unit, which has most often been implanted in a subcutaneous pocket. In a consecutive series of 120 primary implantations, we employed a subrectus fascia pocket that has resulted in a cosmetically superior result with a 0.8% incidence of system infection. The technique of subfascial implantation is described.

Electric Countershock↗
PubMed1992

Use of event markers during exercise testing to optimize morphology criterion programming of implantable defibrillator.

The present generation implantable defibrillator introduced on-line event markers that can be used to evaluate tachycardia detection in the electrophysiological testing mode. These markers were used to assess the appropriateness of programming the morphology criterion for detection of ventricular tachycardia. Twenty-one consecutive patients (19 men, 2 women) performed 29 bicycle exercise tests with real-time recording of the electrocardiogram and the event markers on a multichannel recorder. Mean ejection fraction was 29% (range 15%-69%). Seven patients were taking antiarrhythmic agents. Twelve patients satisfied the morphology criterion at rest (n = 1) or during exercise (group I), and nine patients did not (group II). One patient was excluded from analysis because of continuous ventricular pacing. Mean peak heart rate was 130 beats/min in group I and 125 beats/min in group II. No statistical differences existed between the groups in relation to cycle length of ventricular tachycardia and mode of induction of arrhythmia, QRS duration on the electrocardiogram, during native rhythm, amplitude and duration of defibrillation patch R wave, calculated duty cycle at peak heart rate, and number of discharges of the automatic implantable cardioverter defibrillator at 2 to 14 months of follow-up time. It is concluded that clinical, electrocardiographic, and implantation data are unreliable in predicting satisfaction of the morphology criterion during high heart rates in native rhythm. Formal exercise testing in the electrophysiological mode enables a rational decision to be made about the appropriateness of the use of probability density function in each patient.

Algorithms↗
PubMed1992

Hemothorax associated with anticoagulation after placement of implantable cardioverter defibrillator: possible similarity to postinfarction Dressler's syndrome.

Massive hemothorax developed after placement of an implantable cardioverter defibrillator (ICD) in two patients who received postoperative anticoagulants. The possible relationship of this complication to polyserositis after ICD implantation is discussed as are the possible adverse sequelae of early anticoagulation after ICD implantation.

Anticoagulants↗
PubMed1991

Renal extracorporeal shock wave lithotripsy performed in patient with implantable cardioverter defibrillator.

The effect of extracorporeal shock wave lithotripsy on the automatic implantable cardioverter defibrillator is unknown. To evaluate what effect might occur, a non-implanted automatic implantable cardioverter defibrillator was subjected to a full course of extracorporeal shock wave lithotripsy while inactive. Bench testing by the manufacturer after lithotripsy demonstrated normal function of the device. A patient with an automatic implanted cardioverter defibrillator who required contralateral extracorporeal shock wave lithotripsy then underwent this procedure. The right renal calculus was destroyed successfully with no apparent damage to the automatic implantable cardioverter defibrillator. A test of the automatic implantable cardioverter defibrillator after lithotripsy demonstrated normal sensing and conversion of induced ventricular tachycardia.

Aged↗
PubMed1991

Clinical experience in patients with implantable cardioverter defibrillators.

Forty patients (36 men and 4 women) with life-threatening arrhythmia received an implantable cardioverter defibrillator (ICD). Mean age was 63 years (range, 46 to 80 years). All patients had structural heart disease, with coronary artery disease in 32 patients, idiopathic cardiomyopathy in 7 patients, and hypertensive heart disease in 1 patient. Mean left ventricular ejection fraction was 29 +/- 13%. The clinical arrhythmia was out-of-hospital cardiac arrest in 14 patients (35%), symptomatic sustained ventricular tachycardia in 21 patients (53%), and episodes of syncope without documented spontaneous ventricular arrhythmia but ventricular tachycardia that was easily provoked at the time of electrophysiologic testing in 5 patients (13%). Sustained ventricular tachycardia was induced in 37 patients (93%) at basic electrophysiologic testing. The average number of drug failures was 2.9 +/- 1.4 per patient. One patient (2.5%) died perioperatively because of intractable ventricular tachycardia and ventricular fibrillation. During a median follow-up period of 5.5 months (range 2-21 months) 2 sudden deaths occurred. No patient had a serious complication during the follow-up period. Ten patients (25%) received antiarrhythmic drugs to suppress spontaneous ventricular tachycardia. Appropriate shock treatment was received by 18 patients (45%), and inappropriate shock treatment was received by 2 patients (5%). Several issues regarding use of the ICD must be considered, but the device seems to be useful, and it is associated with an acceptable rate of complications and good long-term success at the present time.

Aged↗
PubMed1990

Revised implantation procedure for programmable automatic implantable cardioverter defibrillator: don't discard the magnet.

The newest implantable defibrillator (Ventak 1550 AICD) introduces radiofrequency telemetric communication that obviates the need for activation and deactivation of the device by a magnet during implantation. We present three of our first ten cases of implantation in which difficulties in intraoperative sensing would have been undetected without use of the magnet for audible evaluation of sensing. Based on this experience, we recommend a revised implantation protocol in which audible confirmation of sensing for 30 to 60 seconds by means of a sterile magnet is performed twice (with a pacemaker, if present in DOO or VOO mode): at the time of system test before induction of arrhythmia with testing cables connected to permit recording of rate, morphology, and ECG interpretation channel signals; and after final connection of the leads to the AICD. This simple additional maneuver is a powerful troubleshooting tool during implantation that permits prompt identification of sensing problems.

Adult↗
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↗
PubMed1988

The role of exercise testing in evaluation of arrhythmias.

Exercise testing has been widely applied for the evaluation of patients with coronary artery disease. The principles underlying its use for this indication make it a useful adjunctive technique, when combined with ambulatory monitoring, to diagnose arrhythmias and monitor antiarrhythmic drug therapy. During exercise, there is a withdrawal of vagal tone and a marked increase in circulating catecholamines and sympathetic inputs to the heart. These changes may directly cause arrhythmias (e.g., catecholamines can enhance automaticity and delayed afterpotentials and can shorten myocardial conduction time and refractory periods). However, they also augment myocardial oxygen demands by increasing myocardial inotropy, heart rate and blood pressure. Such changes may cause ischemia in patients with heart disease, which is a powerful stimulus for arrhythmia, or lead to dysfunction in left ventricular contraction and increased myocardial wall stress, factors that also may precipitate arrhythmia. In approximately 10% of patients with a history of serious arrhythmia, exercise represents the only means for exposing arrhythmia. Importantly, this technique is useful for evaluating the effect of antiarrhythmic drugs. These agents work by reducing membrane automaticity, slowing impulse conduction through the myocardium and prolonging membrane refractoriness. In contrast, catecholamines, which are secreted in response to exercise, have the opposite effect. Thus, exercise may negate the important effects of the antiarrhythmic drugs. Additionally, exercise testing may expose potentially serious toxic drug reactions that may not be obvious at rest. These include conduction abnormalities, negative inotropic effects, congestive heart failure and aggravation of arrhythmia. Although the presence and frequency of arrhythmia with exercise is highly variable in patients with benign arrhythmia, results are more consistent in patients with a history of serious arrhythmia. If arrhythmia is reproducibly provoked with exercise, this technique can be used to judge drug effect. Thus, exercise testing is an important, reliable and helpful technique for exposing arrhythmia, evaluating drug efficacy and identifying potentially serious toxic drug effects.

Anti-Arrhythmia Agents↗
PubMed1988

Therapeutic and diagnostic benefits of intentional crosstalk mediated ventricular output inhibition.

Ventricular output inhibition due to crosstalk is generally considered unsafe and something that should be avoided. Special circuits have been incorporated in some dual chamber pacing systems to absolutely prevent this from happening. However, in patients with intact atrioventricular conduction, crosstalk mediated ventricular output inhibition can be beneficial to the evaluation and management of the patient. Utilizing this technique, one can achieve single chamber atrial paced rates which greatly exceed the rates allowed by lower rate limit programming to facilitate an assessment of the integrity of AV nodal conduction and to both convert and suppress some pathological tachyarrhythmias. The methods of achieving crosstalk and its utilization in four patients is discussed in this report.

Atrioventricular Node↗
PubMed1987

Electrophysiologic effects of beta blockers in ventricular arrhythmias.

Beta-adrenergic receptor blocking agents are effective antiarrhythmic drugs in patients with ventricular arrhythmias. However, these agents exert little or no measurable electrophysiologic effect on normal Purkinje and ventricular muscle fibers when administered acutely. They prevent catecholamine-induced increases in Purkinje fiber automaticity and may interfere with catecholamine-dependent slow responses. beta-adrenergic blocking drugs also prevent the decrease in ventricular fibrillation threshold induced by catecholamines. In the acutely ischemic ventricle, some beta blockers selectively depress conduction within the ischemic zone. The long-term administration of some beta blockers has, in contrast to their short-term effects, been shown to prolong action potential duration and effective refractory period in the ventricle. Which of these observed electrophysiologic effects, either alone or in combination, contributes to the ventricular antiarrhythmic effects of beta-blocking drugs in man is at present unknown.

Adrenergic beta-Antagonists↗
PubMed1987

Hypophosphatemia and cardiac arrhythmias.

In a prospective study of 34 hospitalized patients with moderate hypophosphatemia as an isolated electrolyte abnormality, the incidence of cardiac arrhythmias has been assessed in the absence of evident cardiac disease. Holter monitoring revealed that those without arrhythmias initially, group A, remained arrhythmia-free on follow-up. Group B (n = 8) had significant arrhythmias (Lown class II or above) and differed at p less than 0.02 from 28 controls. After phosphate replacement the arrhythmias in group B improved or disappeared (p less than 0.02). Thus, in the absence of known causes of cardiac arrhythmia, hypophosphatemia can be associated with significant ventricular ectopic activity.

Adult↗