Enrico P. Veltri

Predictors of first discharge and subsequent survival in patients with automatic implantable cardioverter-defibrillators.

BackgroundTwo hundred eighteen patients were evaluated in a two-phase approach (time to first appropriate discharge, survival after discharge) to identify factors that may be related to maximal benefit derived from use of an automatic implantable cardioverter-defibrillator (AICD). Methods and ResultsOne hundred ninety-seven patients survived implantation of AICD, with or without concomitant cardiac surgery. One hundred five patients had an AICD discharge associated with syncope, presyncope, documented sustained ventricular tachycardia or fibrillation, or sleep at 9.1 ± 11.1 months after implantation. Patients survived 23.8 ± 18.0 months after AICD discharge. Left ventricular dysfunction (p =0.008 for ejection fraction less than 25%) was associated with earlier AICD discharge and shortened survival after AICD discharge (p =0.008 for ejection fraction less than 25%;p=0.01 for New York Heart Association functional class III and IV). B-Blocker administration (p =0.006) and coronary bypass surgery (p =0.06) were associated with later AICD discharge. Coronary bypass surgery (p =0.035) but not P-blockers was associated with more prolonged survival after AICD discharge. ConclusionsThese data suggest that a relatively easy algorithm can be applied to predict which patient will benefit most from AICD implantation.

Clinical interactions between pacemakers and automatic implantable cardioverter-defibrillators

Concomitant use of a pacemaker and an automatic implantable cardioverter-defibrillator (AICD) is common. Seventeen percent of patients receiving an AICD at The Johns Hopkins Hospital also had a permanent pacemaker implanted before (16 patients), at the same time as (2 patients) or after (12 patients) AICD implantation. Four types of interactions were noted: 1) transient failure to sense or capture immediately after AICD discharge (seven patients); 2) oversensing of the pacemaker stimulus by the AICD, leading to double counting (one patient); 3) AICD failure to sense ventricular fibrillation resulting from pacemaker stimulus oversensing (three patients, one only at high asynchronous output); and 4) pacemaker reprogramming caused by AICD discharge (three patients). No clinical sequelae of these interactions were noted during follow-up study. Thus, potentially adverse clinical interactions are common and routine screening is recommended. With proper attention to lead placements and programming of the devices, clinical consequences of these interactions can be avoided.

Programmed electrical stimulation and long-term follow-up in asymptomatic, nonsustained ventricular tachycardia

Thirty-three patients with ventricular tachycardia (VT) (3 or more beats, less than 30 seconds in duration, rate more than 100 per minute) on 24-hour Holter monitoring and no history of clinical arrhythmia (presyncope, syncope or sudden death) were studied using programmed electrical stimulation (PES). PES induced VT in 14 patients (42%), sustained VT in 7 (21%) and nonsustained VT in 7 (21%). Inducible VT was associated with underlying heart disease in 9 of 19 patients with coronary artery disease, 3 of 6 patients with idiopathic dilated cardiomyopathy and 2 of 4 patients with mitral valve prolapse. Patients without structural heart disease did not have inducible VT. Ejection fraction (EF) was not significantly different in patients with or without inducible VT. Twenty-three patients were discharged with drug therapy and 10 patients without therapy. At 23 +/- 16 months (mean +/- standard deviation) follow-up, 28 patients (85%) were alive, 4 (12%) had died from a cardiac cause (EF 49 +/- 17% vs 28 +/- 20%, p less than 0.03). Another patient died from cerebrovascular accident. Twenty-six patients (79%) were free of clinical arrhythmia and 7 patients (21%) had arrhythmic events (EF 49 +/- 18% vs 31 +/- 17%, p less than 0.04). Two of 8 patients with noninducible VT who were discharged without drug treatment had clinical arrhythmic events and neither of 2 patients with inducible VT discharged off drugs had such events.(ABSTRACT TRUNCATED AT 250 WORDS)

Results of late programmed electrical stimulation and long-term electrophysiologic effects of amiodarone therapy in patients with refractory ventricular tachycardia

Thirteen patients with refractory, recurrent, life-threatening ventricular tachycardia (VT) underwent electrophysiologic testing before and after long-term amiodarone therapy. Nine patients (69%) had coronary artery disease, 3 (23%) had nonischemic cardiomyopathy and 1 patient (8%) had mitral valve prolapse. At control electrophysiologic study, programmed electrical stimulation (PES) induced VT in all patients: sustained VT in 11 and nonsustained VT in 2 (9 beats and 31 beats). After oral loading with amiodarone, 1200 mg/day for 14 days, followed by maintenance therapy with 408 +/- 20 mg/day (mean +/- standard error of the mean), repeat PES at 6 +/- 1.6 months revealed inducible VT in 12 of 13 patients: sustained VT in 11 and nonsustained VT (32 beats) in 1 patient. Inducible VT was suppressed in only 1 patient. Amiodarone significantly increased sinus cycle length, PR interval, QRS duration and right ventricular effective refractory period. Insignificant increases in AH, HV and QTc intervals were noted. At 24 +/- 2 months, 8 patients (62%) (all with inducible VT at late PES) were free of clinical arrhythmic events (syncope or sudden death), compared with 5 patients (38%) (4 with inducible VT at late PES) with events. There were no significant differences in the induced VT cycle length, VT cycle length change, ease of inducibility or hemodynamic response to induced VT at late PES in patients with and without arrhythmic events.(ABSTRACT TRUNCATED AT 250 WORDS)

Serial lung function testing in patients treated with Amiodarone: A prospective study

PURPOSE Amiodarone has proven to be effective in many cases of cardiac arrhythmias, refractory ventricular tachycardia, and ventricular fibrillation. Pulmonary toxicity is a possible side effect of the drug, with a reported incidence of 2 to 15 percent per year. To determine the effect of amiodarone on lung function, we prospectively studied serial lung function tests in a cohort of 91 patients with refractory cardiac arrhythmias treated with this agent. PATIENTS AND METHODS Spirometry and carbon monoxide diffusing capacity (DLCO) were measured at zero, three, six, 12, 18, and 24 months, with a mean follow-up of 351 days. RESULTS For the whole population taking a mean dose of amiodarone of 367 mg daily (range: 136 to 512 mg), there was no accelerated rate of decline in spirometric indices or DLCO. Analysis of lung function changes by multivariate analysis demonstrated that an accelerated decline in DLCO values occurred in elderly patients (p less than 0.05) but not in patients with pre-existing lung disease or cigarette smokers. In four patients (4.5 percent), clinical evidence of amiodarone pulmonary toxicity developed that was associated with a fall in DLCO of greater than 20 percent. All four patients recovered after the drug was stopped. Another 15 patients, without clinical evidence of pulmonary toxicity, had a sustained decline in DLCO of greater than 20 percent. These 15 patients remained asymptomatic over the next 11 months without interruption of therapy. A greater than 20 percent fall in DLCO was a sensitive test for clinically evident amiodarone pulmonary toxicity, but had a positive predictive value of only 21 percent. CONCLUSION An isolated fall in DLCO, in the absence of clinical evidence of toxicity, does not necessitate stopping amiodarone. An unchanged DLCO value appears to be a reliable negative predictor of pulmonary toxicity.

Amiodarone in the treatment of life-threatening ventricular tachycardia: Role of Holter monitoring in predicting long-term clinical efficacy

Forty-two patients with refractory, recurrent life-threatening ventricular tachycardia and spontaneous ventricular tachycardia (greater than or equal to 3 beats, heart rate greater than 100 beats/min) on baseline 24 hour Holter recording were treated with amiodarone. After 1 week of amiodarone therapy and during the follow-up period (22 +/- 11 months, mean +/- SD), patients had serial 24 hour Holter recordings (10.6 +/- 3.8 per patient). Twenty-four hour, 48 hour or 72 hour Holter monitoring was performed during the second week of therapy. Ventricular tachycardia was suppressed on all follow-up serial Holter recordings in 17 patients (40%). Ventricular tachycardia was suppressed in 34 (81%) of 42 patients with 24 hour Holter recordings, 21 (72%) of 29 patients with 48 hour recordings and 20 (69%) of 29 patients with 72 hour recordings during the second week of therapy. At follow-up 24 patients (57%) were free of clinical arrhythmic events (Sustained ventricular tachycardia or sudden death). The sensitivity, specificity, positive and negative predictive values and predictive accuracy of ventricular tachycardia on 24, 48 and 72 hour Holter recordings during the second week of therapy for predicting subsequent events were analyzed. The positive and negative predictive values were 100 and 71% for 24 hour Holter recordings, 88 and 71% for 48 hour recordings and 89 and 75% for 72 hour recordings. Overall predictive accuracy was 76, 76 and 79%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Twiddler's Syndrome: A New Twist

Twiddlers syndrome, characterized by dislodgment of pacemaker leads due to twisting of pulse generalors within the subcutaneous pocket with subsequent retraction of leads and loss of pacing function, has been well described in patients with permanent pacemakers implanted for bradyarrhythmias. The case presented here is the first report of a patient with an internal automatic cardioverter‐defibrillator with lead dislodgment due to pulse generator rotation. This case exemplifies a new subset of patients prone to the Twiddlers syndrome.

The Automatic Implantable Cardioverter Defibrillator: T Wave Sensing in the Newest Generation

The AICD uses an automatic gain control amplifier for detecting the small electrograms during ventricular fibrillation. The latest generation of the AICD appears to have a more sensitive lock on gain amplifier, as 6 of 76 patients implanted with the new AICD had double counting of the QHS‐T wave complex resulting in asymptomatic discharges. Solutions to the problem of limiting these asymptomatic discharges are difficult and include slowing of the heart rate with beta blockers, changing the lead system, or replacement of the device. One of the six patients was treated with beta blockers. Three patients had their device changed, two patients requested the inactivation of their device until a rate programmable unit was available. The potential for T wave sensing in a lock on gain amplifier represents the unique dilemma between detecting small electrograms of ventricular fibrillation, and detecting diastolic events which occur shortly after the QRS complex.

Impending sudden cardiac death: treatment with myocardial revascularization and the automatic implantable cardioverter defibrillator.

Myocardial revascularization and implantation of the automatic implantable cardioverter defibrillator (AICD) have individually been shown to improve survival in patients after sudden cardiac death. Their combined role has not been well defined. Twenty-three survivors of sudden death underwent revascularization and AICD implantation at an average age of 59 years. The initial arrest was caused by ventricular fibrillation in 15 and ventricular tachycardia in 8. Exercise stress tests, ambulatory ECGs, and electrophysiological monitoring with programmed electrical stimulation were done preoperatively and postoperatively. Follow-up averaged 24 months with a two-year survival of 91%. Eight patients (35%) required AICD resuscitation an average of 8 months postoperatively, and electrophysiological testing did not accurately predict arrhythmia recurrence. The addition of AICD implantation to revascularization substantially improves survival of patients with sudden cardiac death.

Amiodarone pulmonary toxicity: Early changes in pulmonary function tests during amiodarone rechallenge

Amiodarone is an investigational antiarrhythmic agent known to cause pulmonary toxicity. This report describes two patients with previous amiodarone pulmonary toxicity and complete resolution who at rechallenge 5 to 6 months later developed within 2 weeks of therapy a significant reduction in lung diffusion capacity before overt clinical toxicity occurred. This suggests that toxicity may present early with reduction in diffusion capacity and that such changes may warrant the need to alter treatment.