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Biomedical subjects

C Haffajee

Publications and source records attributed to C Haffajee.

7 recordsLinked to original sources
PubMed1998

Aborted implantable cardioverter defibrillator shock during facial electrosurgery.

A patient with a fourth-generation transvenous implantable cardioverter-defibrillator system nearly received an inappropriate defibrillation discharge while undergoing electrofulguration of keratotic facial skin lesions. The incident was confirmed by analyses of the implantable cardioverter-defibrillator's time/date stamped event log and stored electrogram record. Therapy was withheld by the noncommitted implantable cardioverter-defibrillator as the pulsed electrocautery was not continued beyond the charging period.

Aged↗
PubMed1997

A multicenter, randomized trial comparing an active can implantable defibrillator with a passive can system. Jewel Active Can Investigators.

Replacing one defibrillation electrode lead by the defibrillator can may simplify implantation of the ICD. In this multicenter study, 304 patients were randomized to receive either the biphasic active can (AC) (model 7219C system, Medtronic, Inc.) or the passive can (PC) (model 7219D system). The AC and PC systems were compared with respect to their ability to meet the implant defibrillation criterion and to defibrillate VF, and to DFTs, implant time, patient adverse events, and survival rates. A higher percentage fulfilled the implant defibrillation criterion on the first configuration with the AC (86.3% vs 75.9% for PC; P = 0.023), and the first shock success for terminating induced VF was 94% for AC compared to 89% for PC (P = 0.026). DFTs were significantly lower (10.9 vs 12.7 J; P = 0.031), and implant time was significantly shorter for the AC patients (99.2 vs 112.0 min; P = 0.002). The two groups showed no significant differences in 3-month adverse event rates, 3-month survival, and hospital stay.

Adolescent↗
PubMed1996

Combined third-generation implantable cardioverter defibrillator with permanent unipolar pacemakers: preliminary observations.

UNLABELLED: As implantable cardioverter defibrillators (ICDs) are strictly contraindicated in the presence of unipolar pacemakers, currently available options in patients having such chronic pacing systems include: abandoning the implanted pacemaker and selecting an ICD with ventricular demand (VVI) pacing; or replacing the chronic (dual chamber) unipolar pacing system with a dedicated bipolar version prior to ICD implantation. In three patients with previously implanted unipolar pacemakers, we challenged the premise that all ICD systems are incompatible by combining with a third-generation transvenous ICD system (Medtronic 7217B PCD) incorporating true bipolar sensing, a self-limiting auto-adjusting sensitivity, and a tolerant VF detection algorithm. The potential for pacemaker-ICD interaction was minimized by separating the tip of the ICDs transvenous right ventricular pace/sense-defibrillation coil lead from that of the chronic pacemaker lead by > or = 2-3 cm, and by performing "worst case" intraoperative testing. Although ICD double-counting of the dual chamber pacemaker's atrial and ventricular pacing spikes could be provoked at extreme high output settings, it did not occur at clinically appropriate settings. More importantly, continuous high output asynchronous pacing during ventricular fibrillation (VF) did not interfere with ICD detection. During a mean follow-up period of 18 months, one patient has had VF appropriately terminated by the ICD. In the remaining two patients, proper VF detection and ICD function was reassessed at 3 months and/or at 1 year during noninvasive testing. CONCLUSION: These preliminary findings demonstrate that this transvenous ICD system's VF sensing and detection features combined with careful implant technique, rigorous "worst case" testing for possible pacemaker-ICD interaction with regular follow-up, may permit implantation of this ICD system in patients with chronic unipolar pacing systems. Further studies are needed to validate the long-term clinical safety of this promising revised approach to a currently contraindicated device combination.

Aged↗
PubMed1987

Electrocardiographic and electrophysiologic effects of pirmenol in ventricular tachycardia.

Twenty patients with ventricular tachycardia refractory to drug treatment underwent electrophysiologic study with pirmenol. Patients ranged in age from 39 to 84 years (mean 61); the presenting arrhythmia was sustained ventricular tachycardia in 15, nonsustained ventricular tachycardia in 3 and ventricular fibrillation in 2. After discontinuation of all antiarrhythmic drugs (for at least 5 half-lives) and assessment of electrocardiographic and electrophysiologic parameters in the drug-free state, patients underwent comprehensive intracardiac electrophysiologic evaluation with intravenous pirmenol (mean dose 195 +/- 46 mg). Programmed ventricular stimulation began at least 30 minutes after pirmenol infusion was started in each patient. There was significant shortening of sinus cycle length in all patients, from 746 +/- 155 to 683 +/- 107 ms (mean +/- standard deviation). In 7 patients in whom ventricular tachycardia could not be induced after intravenous pirmenol, an oral pirmenol regimen was begun. The dosage was 200 or 250 mg (both 3 times/day) in 2 and 5 patients, respectively. Seven hours after the third dose of oral drug was given, these patients underwent repeat electrophysiologic testing. Intravenous and oral pirmenol significantly prolonged the PR, QT, QTc and JT intervals compared with baseline. Intravenous pirmenol also significantly prolonged the QRS interval compared with baseline. Oral pirmenol significantly prolonged the sinus node recovery time compared with intravenous pirmenol. Intravenous pirmenol significantly increased the HV interval compared with control; oral pirmenol did not demonstrate a significant prolongation of the HV interval, but this is due to the smaller number of patients studied while taking oral drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1984

Environmental iodine intake and thyroid dysfunction during chronic amiodarone therapy.

Amiodarone, an iodine-containing drug used frequently in the treatment of cardiac arrhythmias and angina pectoris, has many effects on thyroid hormone metabolism, including decreasing the production of triiodothyronine (T3) and decreasing the clearance of thyroxine and reverse T3. These effects result in elevated serum thyroxine and reverse T3 concentrations and decreased serum T3 concentrations. In addition, iodine-induced hyperthyroidism or hypothyroidism may occur in patients chronically treated with amiodarone. This study is a retrospective analysis of the incidence of thyroid dysfunction in Lucca and Pisa, West Tuscany, Italy, and in Worcester, Massachusetts. Hyperthyroidism was a more frequent (9.6%) complication of amiodarone therapy in West Tuscany, where iodine intake is moderately low; hypothyroidism was more frequent (22%) in Worcester, where iodine intake is sufficient. In patients receiving chronic amiodarone therapy, clinically suspected hyperthyroidism is best confirmed by showing elevations in serum T3 or free T3 concentrations; hypothyroidism is best diagnosed by showing an elevated serum thyrotrophin concentration. Thyroid function should be carefully monitored in patients receiving amiodarone chronically, especially if they have goiter or Hashimoto's thyroiditis.

Adult↗