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Biomedical subjects

Sami Viskin

Publications and source records attributed to Sami Viskin.

31 records · Page 2Linked to original sources

Reentry in a pulmonary vein as a possible mechanism of focal atrial fibrillation.

The case of an 18-year-old woman with recurrent idiopathic catecholamine-sensitive paroxysmal atrial fibrillation is reported. Recordings of multiple initiations of atrial fibrillation at the proximal part of the right superior pulmonary vein suggested local reentry in the vein as the mechanism of atrial fibrillation. A single radiofrequency pulse delivered at this site resulted in definite cure of the arrhythmia.

Adolescent↗

Incidence of dual AV node physiology following termination of AV nodal reentrant tachycardia by adenosine-5'-triphosphate: a comparison with drug administration in sinus rhythm.

Administration of adenosine triphosphate (ATP) in sinus rhythm identifies dual atrioventricular node physiology (DAVNP) in 75% of patients with inducible slow/fast AV nodal reentrant tachycardia (AVNRT). The incidence of DAVNP following termination of AVNRT with ATP is unknown. Incremental doses of ATP (10-60 mg) were administered, first in sinus rhythm and then during tachycardia induced at electrophysiologic study, to 84 patients with inducible AVNRT and to 18 control patients with inducible AV reentrant tachycardia (AVRT) and no electrophysiologic evidence of DAVNP. Study end-points were the occurrence of DAVNP or > or = 2nd degree AV block following administration of ATP in sinus rhythm and tachycardia termination following administration of ATP during tachycardia. Of the 82 patients with AVNRT who completed the study, 62 (75.6%) exhibited DAVNP following administration of 17.1 +/- 9.4 mg ATP in sinus rhythm, while 30 (36.5%) exhibited DAVNP at the termination of AVNRT following administration of 10.6 +/- 2.4 mg ATP. The occurrence of DAVNP following the administration of 10 mg ATP in sinus rhythm.was a good predictor (62%) of its occurrence after termination of AVNRT with ATP. The dose of ATP had a strong correlation between the presence of DAVNP following AVNRT termination and the ATP doses needed for tachycardia termination. Of the 18 control patients, none had DAVNP at ATP test during sinus rhythm but 1 (5.5%) showed slight (60 msec) PR jump after termination of AVRT with ATP. In conclusion, DAVNP is present in a relatively high proportion (36.5%) of patients following termination of AVNRT with ATP but is much less frequent (5.5%) in control patients. Thus, findings at termination of tachycardia by ATP may be useful in the noninvasive diagnosis of the mechanism of a paroxysmal supraventricular tachycardia.

Journal Article↗

Ventricular flutter induced during electrophysiologic studies in patients with old myocardial infarction: clinical and electrophysiologic predictors, and prognostic significance.

INTRODUCTION: Induction of ventricular flutter during electrophysiologic (EP) studies (similar to that of ventricular fibrillation [VF]) often is viewed as a nonspecific response with limited prognostic significance. However, data supporting this dogma originate from patients without previously documented ventricular tachyarrhythmias. We examined the significance of ventricular flutter in patients with and without spontaneous ventricular arrhythmias. METHODS AND RESULTS: We conducted a cohort study of all patients with myocardial infarction (MI) undergoing EP studies at our institution. Of 344 consecutive patients, 181 had previously documented spontaneous sustained ventricular arrhythmias, 61 had suspected ventricular arrhythmias, and 102 had neither. Ventricular flutter was induced in 65 (19%) of the patients. Left ventricular ejection fraction was highest among patients with inducible VF (35 +/- 13), lowest for patients with inducible sustained monomorphic ventricular tachycardia (SMVT; 27 +/- 9), and intermediate for patients with inducible ventricular flutter (30 +/- 10). Similarly, the coupling intervals needed to induce the arrhythmia were shortest for VF (200 +/- 28 msec), intermediate for ventricular flutter (209 +/- 27 msec), and longest for SMVT (230 +/- 35 msec). During 5 +/- 8 years of follow-up, the risk for ventricular tachycardia/VF was high for patients with SMVT and ventricular flutter and low for patients with inducible VF and noninducible patients (46%, 34%, 17%, and 14%, P < 0.005). CONCLUSION: Patients with inducible ventricular flutter appear to be "intermediate" between patients with inducible VF and patients with SMVT in terms of clinical and electrophysiologic correlates. However, the prognostic value of inducible ventricular flutter is comparable to that of SMVT.

Aged↗

Torsade de pointes due to noncardiac drugs: most patients have easily identifiable risk factors.

Numerous medications, including drugs prescribed for noncardiac indications, can lead to QT prolongation and trigger torsade de pointes. Although this complication occurs only rarely, it may have lethal consequences. It is therefore important to know if patients with torsade de pointes associated with noncardiac drugs have risk factors that are easy to identify. We reviewed reports of drug-induced torsade de pointes and analyzed each case of torsade de pointes associated with a noncardiac drug for the presence of risk factors for the long QT syndrome that can be easily identified from the medical history or clinical evaluation (female gender, heart disease, electrolyte disturbances, excessive dosing, drug interactions, and history of familial long QT syndrome). We identified 249 patients with torsade de pointes caused by noncardiac drugs. The most commonly identified risk factor was female gender (71%). Other risk factors were frequently present (18%-41%). Virtually all patients had at least 1 of these risk factors, and 71% of patients had 2 or more risk factors. Our study suggests that almost all patients with torsade de pointes secondary to noncardiac drugs have risk factors that can be easily identified from the medical history before the initiation of therapy with the culprit drug.

Anti-Bacterial Agents↗

Long QT syndrome caused by noncardiac drugs.

Numerous medications not intended for cardiac use (including antibiotics, histamine blockers, and antipsychotic medications) incidentally block potassium channels in myocardial cells, prolong the QT interval, and may trigger malignant arrhythmias. Although the odds for a given patient for developing arrhythmias are small, the number of patients receiving such drugs is enormous. Most patients developing proarrhythmia have additional risk factors that could be easily identified from their medical history. The list of risk factors includes female gender, organic heart disease, hypokalemia, and a history of long QT or drug-induced arrhythmias. Patients without risk factors are at very low risk. For these patients, it is neither practical nor necessary to record an electrocardiogram before therapy is initiated and the most important preventive measure is to avoid concurrent administration of 2 or more drugs that prolong the QT interval or administration of a medication that impairs the metabolism of a QT-prolonging drug. We performed a computerized literature search using the key words "long QT," "torsade," "drug-adverse effects," and "drug-ventricular arrhythmias," searching for published reports of drug-induced torsade de pointes. The references in each of these reports also were reviewed to identify additional publications. In addition, we reviewed the published reviews and the Internet sites dealing with drug-induced arrhythmias. All the original articles quoted in these reviews and Web sites were examined critically.

Anti-Bacterial Agents↗