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Biomedical subjects

Pamela Karasik

Publications and source records attributed to Pamela Karasik.

5 recordsLinked to original sources

Role of amiodarone or implantable cardioverter/defibrillator in patients with atrial fibrillation and heart failure.

BACKGROUND: Heart failure complicated by atrial fibrillation (AF) is associated with excessive mortality and morbidity. The aim of the study was to determine the role of amiodarone or implantable cardioverter/defibrillator (ICD) in patients with AF and heart failure. METHODS: Patients were determined to be in sinus rhythm (SR) or AF on the baseline electrocardiogram. Mortality, ICD discharge, or change in rhythm was assessed. RESULTS: Of the 2521 patients at baseline, 2328 were in SR and 173 were in AF. Overall, after adjusting for differences in baseline variables, there was no difference in mortality between patients with SR and patients with AF (P = .98), nor within assigned groups: placebo (P) (P = .82), amiodarone (A) (P = .68), and ICD (P = .40). For patients with SR, ICD decreased mortality (P vs ICD, P = .004; A vs ICD, P = .004; P vs A, P = .75). For patients with AF, there were no differences in mortality among groups (P vs ICD, P = .99; A vs ICD, P = .88; P vs A, P = .88). Of patients with SR at baseline, 11% (264) developed AF by any electrocardiogram during follow-up (P 12%, A 8%, ICD 15%; A vs P, P = .019; A vs ICD, P = .001; P vs ICD, P = .044). Of patients with AF, 70% (121) developed SR during follow-up (P 66%, A 67%, ICD 75%, all P = not significant against each other). Any ICD shock was seen in 52% (34) of patients with AF vs 30% (222) of patients with SR (P = .001). Inappropriate shocks were seen in 37% (24) of patients with AF vs 14% (107) of patients with SR (P = .001). Appropriate shocks were more often seen in AF vs SR (P = .03). CONCLUSION: After adjustments for baseline differences, patients with AF and patients with SR have similar overall mortality rates. Compared to P or A, ICD improves survival in patients with SR, but may not in patients with AF. Amiodarone is effective in reducing new AF, but not in converting AF to SR. Implantable cardioverter/defibrillator, inappropriate, and appropriate shocks were more often seen in AF than in SR.

Aged↗

Comparison of mental stress-induced myocardial ischemia in coronary artery disease patients with versus without left ventricular dysfunction.

To examine the susceptibility to myocardial ischemia with mental stress in patients who have coronary artery disease and normal left ventricular (LV) function versus those who have impaired LV function, we examined 58 patients who had coronary artery disease, including 22 who had normal LV function (ejection fraction >/=50%), 16 who had mild to moderate LV dysfunction (ejection fraction 30% to 50%), and 20 who had severe LV dysfunction (ejection fraction </=30%) and underwent bicycle and mental stress testing with myocardial perfusion scintigraphy on consecutive days in random order. Ischemia was assessed based on summed difference scores in regional rest versus stress myocardial perfusion and defined as a summed difference score >3. At comparable double products across the 3 groups, ischemia was induced with mental stress more frequently in patients who had severe LV dysfunction (50%) than in those who had normal LV function (9%; p <0.01). The frequency of exercise-induced ischemia was different only between those who had mild/moderate LV dysfunction and those who had normal LV function (56% vs 18%, respectively, p <0.05). The pattern of mental stress versus exercise ischemia differed between groups (p <0.02): there was a higher prevalence of mental stress ischemia versus exercise ischemia in patients who had severe LV dysfunction (p = 0.06), a marginally higher prevalence of exercise versus mental stress ischemia in those who had moderate LV dysfunction (p = 0.07), and no difference in mental stress versus exercise ischemia in those who had normal LV function. Thus, at comparable double products during mental stress and similar extent of coronary artery disease, ischemia with mental stress was induced more frequently in patients who had severe LV dysfunction than in those who had normal LV function. These data suggest that mental stress ischemia may be of particular clinical importance in patients who have coronary artery disease and LV dysfunction.

Analysis of Variance↗

Effects of acute mental stress and exercise on T-wave alternans in patients with implantable cardioverter defibrillators and controls.

BACKGROUND: Malignant cardiac arrhythmias can be triggered by exercise and by mental stress in vulnerable patients. Exercise-induced T-wave alternans (TWA) is an established marker of cardiac electrical instability. However, the effects of acute mental stress on TWA have not been investigated as a vulnerability marker in humans. METHODS AND RESULTS: TWA responses to mental stress (anger recall and mental arithmetic) and bicycle ergometry were evaluated in patients with implantable cardioverter defibrillators (ICDs) and documented coronary artery disease (n=23, age 62.1+/-12.3 years) and controls (n=17, age 54.2+/-12.1 years). TWA was assessed from digitized ECGs by modified moving average analysis. Dual-isotope single photon emission computed tomography was used to assess myocardial ischemia. TWA increased during mental stress and exercise (P values <0.001), and TWA responses were higher in ICD patients than in controls (arithmetic Delta=8.9+/-1.4 versus 4.3+/-2.2 microV, P=0.043; exercise Delta=21.4+/-2.8 versus 13.8+/-3.2 microV, P=0.038). TWA increases with mental stress occurred at substantially lower heart rates (anger recall Delta=9.7+/-7.7 bpm, arithmetic Delta=14.3+/-13.3 bpm) versus exercise (Delta=53.7+/-22.7 bpm; P values <0.001). After adjustment for heart rate increases, mental stress and exercise provoked increased TWA in ICD patients (P values <0.05), but not in controls (P values >0.2). Ejection fraction and stress-induced myocardial ischemia were not associated with TWA. CONCLUSIONS: Mental stress can induce cardiac electrical instability, as assessed via TWA, among patients with arrhythmic vulnerability and occurs at lower heart rates than with exercise. Pathophysiological mechanisms of mental stress-induced arrhythmias may therefore involve central and autonomic nervous system pathways that differ from exercise-induced arrhythmias.

Acute Disease↗

Upstream stimulation versus downstream stimulation: arrhythmogenesis based on repolarization dispersion in the human heart.

OBJECTIVE: The purpose of this study was to test the hypothesis that a ventricular tachycardia (VT) induction site has a shorter action potential duration (APD) and effective refractory period (ERP) than a noninducing site, resulting in collision against longer ERP ("upstream") as opposed to shorter ERP ("downstream," no collision). BACKGROUND: Induction of sustained VT is often feasible at one stimulation site while application of an identical pacing protocol to another site fails to provoke VT. METHODS: Sixty-nine patients undergoing programmed stimulation for VT inducibility had monophasic action potential recording/pacing catheters placed in the right ventricular outflow tract (RVOT) and right ventricular apex (RVA) simultaneously. Up to three extra-stimuli were introduced in 5 to 10 ms decrements until ERP was reached. Upon completion of a drive cycle at one stimulation site, it was repeated at the other. RESULTS: Thirty-eight patients had inducible VT, nine exclusively by RVA pacing and nine exclusively by RVOT pacing. Action potential duration and ERP at the induction site were significantly shorter (12 +/- 15 ms, p <0.05 and 22 +/- 14 ms, p < 0.01, respectively, at 600 ms basic cycle length) than at the noninduction site. Dispersion of repolarization between corresponding APD at the two sites was 58 +/- 41 ms during baseline stimulation (S1) at the inducing site but only 37 +/- 23 ms at the noninducing site (p < 0.05). Dispersion increased during extra-stimulus application (p < 0.05), reaching a maximum of 75 +/- 45 ms during VT induction, but only 53 +/- 33 ms during extra-stimulation at the noninduction site. CONCLUSIONS: Site specificity of VT induction underscores the role of dispersion of repolarization and refractoriness in facilitating re-entry arrhythmias. Upstream stimulation at a site with short repolarization produces larger dispersion and facilitates VT induction.

Action Potentials↗