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Sami Viskin

Publications and source records attributed to Sami Viskin.

At least 19 recordsLinked to original sources
PubMed2026

Risk stratification in short QT syndrome: Findings from a pooled analysis.

BACKGROUND: In long QT syndrome, longer QT intervals indicate increased arrhythmic risk, and a rate-corrected QT interval (QTc) of ≥500 ms denotes high risk. Establishing similar associations in short QT syndrome (SQTS) remains elusive. OBJECTIVE: This study aimed to demonstrate that shorter QT intervals denote a higher risk of malignant arrhythmias in SQTS and to define the "high-risk" QTc value in SQTS. METHODS: Pooled analysis of patients treated in our institutions or those reported in the literature revealed 162 patients with SQTS and known symptomatic status; 57 of them (35.2%) had arrhythmic symptoms (sudden death, cardiac arrest, or malignant syncope). RESULTS: There was a significant inverse association between the QTc and arrhythmic symptoms (with a median QTc of 315.0 ms [interquartile range 300.5-338.0] among symptomatic patients vs 330.0 ms [interquartile range 312.5-355.0] among asymptomatic patients; P = .0023). Receiver operator characteristics analysis showed that shorter QTc values were associated with a higher risk (area under the curve 0.64 ± 0.04; P = .0024). When patients were grouped by QTc range, most of those with a QTc of ≤320 ms had malignant arrhythmic symptoms, whereas the reverse was true for those with a QTc of ≥320 ms. Male patients were overrepresented in the SQTS cohort and more so in the subgroup with malignant symptoms. CONCLUSION: This pooled analysis of patients with SQTS demonstrates that, among patients with congenital SQTS, a shorter QTc is associated with a higher risk of malignant ventricular arrhythmias. A QTc shorter than 320 ms correlates with a higher arrhythmic risk. Men seem to be at higher risk.

Humans↗
PubMed2006

The role of induced sputum in amiodarone-associated interstitial lung diseases.

Amiodarone, a highly effective medication for suppressing cardiac rhythm disturbances, may cause pulmonary injury, such as chronic interstitial lung diseases, in 5-15% of the patients who take it. We applied induced sputum (IS), a non-invasive technique, for diagnosing amiodarone-induced pulmonary toxicity. Four patients with interstitial lung disease who were treated by amiodarone for ischemic heart diseases were evaluated by a conventional clinical workup. All four patients showed marked interstitial pattern on computerized tomography and decreased diffusion capacity (DLCO-SB 51-76%). IS showed lymphocytosis, a high CD4 or CD8 count, eosinophilia and amiodarone in 3 of 4 patients. IS may be a useful tool for assessing amiodarone toxicity in patients with ischemic heart diseases and concomitant pulmonary side effects.

Aged↗
PubMed2006

Frequency of spontaneous and inducible atrioventricular nodal reentry tachycardia in patients with idiopathic outflow tract ventricular arrhythmias.

OBJECTIVES: We sought to assess the frequency of spontaneous or inducible atrioventricular nodal reentry tachycardia (AVNRT) in patients referred for radiofrequency ablation (RFA) of idiopathic outflow tract ventricular arrhythmias. BACKGROUND: In patients with no obvious heart disease, AVNRT and outflow tract ventricular tachycardia (VT) are the most frequently encountered supraventricular and ventricular tachycardias, respectively. An increased coexistence of the two arrhythmias has been recently suggested. METHODS: In 68 consecutive patients referred for RFA of an idiopathic ventricular outflow tract arrhythmia, a stimulation protocol including repeated bursts of rapid atrial pacing, up to triple atrial extrastimuli during sinus rhythm and rapid ventricular pacing was performed before and after isoproterenol infusion following RFA of the ventricular arrhythmia. In patients with inducible AVNRT, RFA of the slow pathway was performed. RESULTS: Of the 68 study patients, 17 (25%) had either spontaneous AVNRT documented prior to RFA of the ventricular arrhythmia (n = 4) or inducible AVNRT at the time of RFA of the ventricular arrhythmia (n = 13). AVNRT was induced by atrial pacing in 15 (88%) of 17 patients: in 3 patients without isoproterenol and in 12 patients during isoproterenol infusion. Uncomplicated RFA of the slow pathway was successfully achieved in all patients with inducible AVNRT. CONCLUSION: Spontaneous or inducible AVNRT is relatively common in patients with idiopathic outflow tract ventricular arrhythmias. Atrial stimulation, especially when performed after isoproterenol infusion plays a major role in AVNRT inducibility. Although we performed RFA of the slow pathway in patients with inducible AVNRT and no prior tachycardia documentation, the question whether this is mandatory remains unsettled.

Adolescent↗
PubMed2006

Radiofrequency ablation of atrioventricular nodal reentry tachycardia: a 14 year experience with 901 patients at the Tel Aviv Sourasky Medical Center.

BACKGROUND: Atrioventricular nodal reentry tachycardia is the most frequent cause of regular, paroxysmal supraventricular tachycardia. Radiofrequency ablation of the slow pathway has been recommended as first-line therapy for curing AVNRT. OBJECTIVES: To report a 14 year experience of RFA of the slow pathway in patients with AVNRT treated in our laboratory. METHODS: A total of 901 consecutive patients (aged 9-92, mean 50.8 +/- 18.2 years) underwent RFA of the slow pathway. All patients had sustained AVNRT induced with or without intravenous administration of isoproterenol. A standard electrophysiologic method with three diagnostic and one ablation catheter was used in 317 patients (35.2%); in the remaining 584 patients (64.8%), only two electrode catheters (one diagnostic, one ablation) were used ("two-catheter approach"). RESULTS: Catheter ablation of the slow pathway abolished AVNRT induction in 877 patients (97.3%). In 14 patients (1.6%) the procedure was discontinued while in 10 (1.1%) the procedure failed. In 864 patients (95.9%) there were no complications. Transient or permanent AV block occurred during the procedure in 31 patients (3.4%), of whom 8 (0.9%) eventually required pacemaker insertion (n = 7) or upgrade of a previously implanted WI pacemaker (n = 1) during the month following the procedure. The number of catheters used did not significantly affect the rate of results or complications of the ablation procedure. The success and complication rates remained stable over the years, although a significant trend for increased age and associated heart disease was observed during the study period. CONCLUSIONS: The results of this single-center large study, which included patients with a wide age range, showed results similar to those of previous studies. The use of a "two-catheter approach" (one diagnostic and one ablation) was as effective and safe as a multi-catheter approach.

Adolescent↗
PubMed2005

Provocation of sudden heart rate oscillation with adenosine exposes abnormal QT responses in patients with long QT syndrome: a bedside test for diagnosing long QT syndrome.

AIMS: As arrhythmias in the long QT syndrome (LQTS) are triggered by heart rate deceleration or acceleration, we speculated that the sudden bradycardia and subsequent tachycardia that follow adenosine injection would unravel QT changes of diagnostic value in patients with LQTS. METHODS AND RESULTS: Patients (18 LQTS and 20 controls) received intravenous adenosine during sinus rhythm. Adenosine was injected at incremental doses until atrioventricular block or sinus pauses lasting 3 s occurred. The QT duration and morphology were studied at baseline and at the time of maximal bradycardia and subsequent tachycardia. Despite similar degree of adenosine-induced bradycardia (longest R-R 1.7+/-0.7 vs. 2.2+/-1.3 s for LQTS and controls, P=NS), the QT interval of LQT patients increased by 15.8+/-13.1%, whereas the QT of controls increased by only 1.5+/-6.7% (P<0.001). Similarly, despite similar reflex tachycardia (shortest R-R 0.58+/-0.07 vs. 0.55+/-0.07 s for LQT patients and controls, P=NS), LQTS patients developed greater QT prolongation (QTc=569+/-53 vs. 458+/-58 ms for LQT patients and controls, P<0.001). The best discriminator was the QTc during maximal bradycardia. Notched T-waves were observed in 72% of LQT patients but in only 5% of controls during adenosine-induced bradycardia (P<0.001). CONCLUSION: By provoking transient bradycardia followed by sinus tachycardia, this adenosine challenge test triggers QT changes that appear to be useful in distinguishing patients with LQTS from healthy controls.

Adenosine↗
PubMed2005

Inaccurate electrocardiographic interpretation of long QT: the majority of physicians cannot recognize a long QT when they see one.

BACKGROUND: Physicians in all fields of medicine may encounter patients with long QT syndrome (LQTS). It is important to define the percentage of physicians capable of distinguishing QT intervals that are long from those that are normal because LQTS can be lethal when left untreated. OBJECTIVES: The purpose of this study was to define the percentage of physicians in the different disciplines of medicine who can recognize a long QT when they see one. METHODS: We presented the ECGs of two patients with LQTS and two healthy females to 902 physicians (25 world-renowned QT experts, 106 arrhythmia specialists, 329 cardiologists, and 442 noncardiologists) from 12 countries. They were asked to measure the QT, calculate the QTc (the QT interval corrected for the heart rate), and determine whether the QT is normal or prolonged. RESULTS: For patients with LQTS, >80% of arrhythmia experts but <50% of cardiologists and <40% of noncardiologists calculated the QTc correctly. Underestimation of the QTc of patients with LQTS and overestimation of the QTc of healthy patients were common. Interobserver agreement was excellent among QT experts, moderate among arrhythmia experts, and low among cardiologists and noncardiologists (kappa coefficient = 0.82, 0.44, and < 0.3, respectively). Correct classification of all QT intervals as either "long" or "normal" was achieved by 96% of QT experts and 62% of arrhythmia experts, but by only <25% of cardiologists and noncardiologists. CONCLUSIONS: Most physicians, including many cardiologists, cannot accurately calculate a QTc and cannot correctly identify a long QT.

Cardiology↗
PubMed2005

The "short-coupled" variant of right ventricular outflow ventricular tachycardia: a not-so-benign form of benign ventricular tachycardia?

Idiopathic ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT-VT) and idiopathic RVOT-extrasystoles are generally considered benign arrhythmias. We described three cases who originally presented with typical "benign looking" RVOT-extrasystoles or RVOT-VT but developed malignant polymorphic VT during follow-up. The unusual aspect of their RVOT-extrasystoles was their coupling interval, which appears to be intermediate between the ultra-short coupling interval of idiopathic VF and the long coupling interval seen in the truly benign RVOT-VT.

Adult↗
PubMed2005

Intravenous chlorpromazine for the emergency treatment of uncontrolled symptomatic hypertension in the pre-hospital setting: data from 500 consecutive cases.

BACKGROUND: Chlorpromazine is a dopamine-receptor antagonist antipsychotic agent. Because of its strong alpha-blocking and sedative actions, it has also been used as emergency therapy for extreme arterial hypertension. Published reports to date have included very small numbers of patients (i.e., 5-30). OBJECTIVES: To analyze data on almost 500 patients who received intravenous chlorpromazine for the emergency treatment of uncontrolled symptomatic hypertension in the pre-hospital setting. METHODS: We reviewed data from 496 consecutive patients who received intravenous chlorpromazine as emergency therapy for uncontrolled symptomatic hypertension. Chlorpromazine was injected intravenously. The dose was 1 mg every 2-5 minutes until the systolic pressure was < or =140 mmHg and the diastolic pressure < or =100 mmHg with alleviation of symptoms. RESULTS: The mean dose of chlorpromazine administered was 4.5 +/- 5 mg (range 1-50 mg). Only 33 patients (7%) required >10 mg. Chlorpromazine reduced systolic BP from 222.82 +/- 26.31 to 164.93 +/- 22.66 mmHg (P< 0.001) and diastolic BP from 113.5 +/-16.63 to 85.83 +/- 11.61 mmHg (P< 0.001). The sinus rate decreased from 97.9 +/- 23.5 to 92.2 +/- 19.7 beats per minute (P< 0.001). These results were achieved within the first 37 +/- 11 minutes. CONCLUSIONS: Intravenous chlorpromazine is safe and effective when used as emergency treatment for uncontrolled symptomatic hypertension.

Aged↗
PubMed2004

Efficacy of quinidine in high-risk patients with Brugada syndrome.

BACKGROUND: Automatic implantable cardioverter-defibrillator therapy is considered the only effective treatment for high-risk patients with Brugada syndrome. Quinidine depresses I(to) current, which may play an important role in the arrhythmogenesis of this disease. METHODS AND RESULTS: The effects of quinidine bisulfate (mean dose, 1483+/-240 mg) on the prevention of inducible and spontaneous ventricular fibrillation (VF) were prospectively evaluated in 25 patients (24 men, 1 woman; age, 19 to 80 years) with Brugada syndrome. There were 15 symptomatic patients (including 7 cardiac arrest survivors and 7 patients with unexplained syncope) and 10 asymptomatic patients. All 25 patients had inducible VF at baseline electrophysiological study. Quinidine prevented VF induction in 22 of the 25 patients (88%). After a follow-up period of 6 months to 22.2 years, all patients are alive. Nineteen patients were treated with quinidine for 6 to 219 months (mean+/-SD, 56+/-67 months). None had an arrhythmic event, although 2 had non-arrhythmia-related syncope. Administration of quinidine was associated with a 36% incidence of side effects that resolved after drug discontinuation. CONCLUSIONS: Quinidine effectively prevents VF induction in patients with Brugada syndrome. Our data suggest that quinidine also suppresses spontaneous arrhythmias and could prove to be a safe alternative to automatic implantable cardioverter-defibrillator therapy for a substantial proportion of patients with Brugada syndrome. Randomized studies comparing these two therapies seem warranted.

Adult↗
PubMed2004

Drug-induced atrioventricular block: prognosis after discontinuation of the culprit drug.

OBJECTIVES: The goal of this study was to determine how often atrioventricular (AV) block is really caused by medications. BACKGROUND: Beta-blockers, verapamil, and diltiazem are considered a cause of AV block for which pacemaker implantation is not indicated. However, it is not known if such patients can expect a benign course after discontinuation of the culprit medication. METHODS: Consecutive patients with II or III degree AV block not related to acute myocardial infarction, digitalis toxicity, or vasovagal syncope were studied. The level of AV block (AV-nodal or infranodal) was defined by electrocardiographic criteria. The cause and effect relation between AV block and drugs was defined according to the response to drug discontinuation. RESULTS: Of 169 patients with AV block, 92 (54%) were receiving beta-blockers and/or verapamil or diltiazem. Patients receiving medications had similar clinical and electrocardiographic characteristics with patients who had AV block in the absence of drugs. Drug discontinuation was followed by resolution of AV block in 41% of cases, whereas spontaneous improvement of AV conduction occurred in 23% of patients who had AV block in the absence of drugs. However, 56% of the patients for whom drug discontinuation led to resolution of AV block had recurrence of AV block in the absence of therapy. Atrioventricular block that was "truly caused by drugs" was found in only 15% of patients who had II or III degree AV block during therapy with beta-blockers, verapamil, or diltiazem. CONCLUSIONS: Atrioventricular block is commonly "related to drugs" but is rarely "caused by drugs."

Adrenergic beta-Antagonists↗
PubMed2004

Long-term prognosis of inducible ventricular flutter: not an innocent finding.

BACKGROUND: The prognostic significance of ventricular flutter (VFL) induced during programmed electrical stimulation (PES) is currently unknown. METHODS: This study examined patients who had PES-induced VFL and assessed their long-term prognosis compared with patients who had inducible sustained monomorphic ventricular tachycardia (SMVT). RESULTS: Of 3414 patients undergoing PES, 74 (2%) had sustained VFL. They were compared with a group of 71 patients undergoing PES in the same time frame who had inducible SMVT. Patients with inducible VFL had a higher ejection fraction than patients with SMVT (0.39 vs 0.33; P =.05). More aggressive pacing was required for arrhythmia induction in patients with VFL, with more stimuli (2.7 +/- 0.5 vs 2.2 +/- 0.6; P <.01) and tighter S(2), S(3), and S(4) intervals. After a mean follow-up of 30 +/- 31 months, the mortality rate was 34% in patients with VFL and 30% in patients with SMVT (P =.41). No difference in the 2 groups in overall survival or a combined end point of sudden death or appropriate implantable cardioverter defibrillator shock was revealed with Kaplan-Meier analysis. CONCLUSION: The long-term prognosis of patients with inducible VFL is similar to that of patients with inducible SMVT, even when VFL is induced with a relatively aggressive protocol.

Arrhythmias, Cardiac↗
PubMed2004

Is idiopathic ventricular fibrillation a short QT syndrome? Comparison of QT intervals of patients with idiopathic ventricular fibrillation and healthy controls.

OBJECTIVE: The purpose of this study was to determine if patients with idiopathic ventricular fibrillation (VF) have shorter QT intervals than comparable healthy controls. BACKGROUND: The upper limit of the normal QT is well defined. Less is known about the lower limit of the normal QT. Patients with the recently described "short QT syndrome" have characteristics resembling those of patients with idiopathic VF. METHODS: The ECGs of 28 consecutive patients with idiopathic VF (17 men and 11 women, age 31 +/- 17 years) were compared to those of 270 age- and gender- matched healthy controls. Based on published literature, we defined "short QT" as QTc < or = 360 ms for males and < or = 370 ms for females. RESULTS: Despite significant overlapping, the QTc of males with idiopathic VF was shorter than the QTc of healthy males (371 +/- 22 ms vs 385 +/- 19 ms, P = .034). Short QT intervals were found more frequently among males with idiopathic VF (35% vs 10%, P = .003). No such differences were apparent among women. Short QTc intervals were more commonly seen during bradycardia. However, the correlation between short QT and a history of VF was independent of heart rate. CONCLUSIONS: "Short" QTc values are commonly seen in male patients with idiopathic VF. However, "short" QTc values are not rare among healthy adults, especially at slow heart rates. Further studies are needed to define when a given QT is really "too short."

Adult↗
PubMed2004

Long-term outcome of patients who received implantable cardioverter defibrillators for stable ventricular tachycardia.

INTRODUCTION: Evidence is inconclusive concerning the role of implantable cardioverter defibrillators (ICDs) to treat patients with hemodynamically stable ventricular tachycardia (VT). The goal of this study was to estimate future risk of unstable ventricular arrhythmias in patients who received ICDs for stable VT. METHODS AND RESULTS: We reviewed complete ICD follow-up data from 82 patients (age 66.1 +/- 11.3 years; left ventricular ejection fraction 32.3%+/- 11.2%; mean +/- SD) who received ICDs for stable VT. During the follow-up period of 23.6 +/- 21.5 months (mean +/- SD), 15 patients (18%) died, and 10 (12%) developed unstable ventricular arrhythmia, 8 of whom had the unstable arrhythmia as the first arrhythmia after ICD placement. Estimated 2- and 4-year survival in the whole group was 80% and 74%, respectively. Estimated 2- and 4-year probability of any VT and unstable VT was 67% and 77% and 11% and 25%, respectively. There were no differences in age, ejection fraction, sex, underlying heart disease, cycle length, symptoms, baseline electrophysiologic study results, or QRS characteristics of qualifying VT between patients who developed unstable ventricular arrhythmia and patients who did not. Twenty-nine patients (35%) had at least one inappropriate shock, and 11 (13%) underwent further surgery for ICD-related complications. CONCLUSION: Patients who present with hemodynamically stable VT are at risk for subsequent unstable VT. ICD treatment offers potential salvage of patients with stable VT who subsequently develop unstable VT/ventricular fibrillation, although complications and inappropriate shocks are considerable. No predictors could be found for high and low risk for unstable arrhythmias. These findings support ICD treatment for stable VT survivors.

Aged↗