Search PubMed⌕ Search

Biomedical subjects

J Somberg

Publications and source records attributed to J Somberg.

At least 19 recordsLinked to original sources
PubMed2000

Hypercalcemia, arrhythmia, and mood stabilizers.

Recent findings in a bipolar patient receiving maintenance lithium therapy who developed hypercalcemia and severe bradyarrhythmia prompted the authors to conduct a retrospective study of bipolar patients with lithium-associated hypercalcemia. A printout of all cases of hypercalcemia that presented during a 1-year period was generated. After eliminating spurious hypercalcemias or those associated with intravenous fluids, the authors identified 18 non-lithium-treated patients with hypercalcemias related to malignancies and other medical conditions (group A) and 12 patients with lithium-associated hypercalcemia (group B). Patients in group B were not comparable to those in group A, as the latter were medically compromised and were receiving multiple pharmacotherapies. Thus, two control groups were generated: group C1, which included age- and sex-comparable lithium-treated bipolar normocalcemic patients, and group C2, which included bipolar normocalcemic patients treated with anticonvulsant mood stabilizers. The electrocardiographic (ECG) findings for patients in group B were compared with those of patients in groups C1 and C2. It was found that these groups did not differ in their overall frequency of ECG abnormalities; however, there were significant differences in the frequency of conduction defects. Patients with hypercalcemia resulting from medical diseases and bipolar patients with lithium-associated hypercalcemia had significantly higher frequencies of conduction defects. Patients in group A had significant mortality at 2-year follow-up (28%), in contrast to zero mortality in the other three groups. The clinical implications of these findings are discussed.

Adult↗
PubMed1993

Risk factors not addressed in antihypertensive therapy based solely on blood pressure control.

There has been a considerable revolution in the field of hypertension therapy. We have gone through an era in which patients with severe hypertension and those with accelerated hypertension had a very short life expectancy. Currently blood pressure can be readily controlled with a marked improvement in longevity. We have gone from an era in which stroke was common due to hypertensive cardiovascular disease to an era in which patients are effectively treated and there has been a marked reduction in the incidence of stroke. The challenge is whether we can reduce the very high mortality due to coronary artery disease in patients with hypertension as we have done with stroke. New groups of drugs that may have a more favorable effect on metabolic and hemodynamic risk considerations have been developed over the last decade. These agents may reduce the risk for coronary heart disease to a greater extent than previously employed therapy. While there are no randomized placebo-controlled studies demonstration this, a theoretical basis does exist to give the physician reason to think about prioritizing therapies and tailoring them to the needs of the individual patient.

Animals↗
PubMed1993

The clinical implications of first-pass metabolism: treatment strategies for the 1990s.

The first-pass effect is real. It may pose obstacles to the treatment of disease, and strategies need to be developed to address the problem that first pass can cause. First we have to look at identifying the problem, and this symposium has helped to further emphasize that the problem exists and awareness is increasing. The first-pass effect has been a basic tenant of pharmacology but an area not receiving active research interest and one that is often overlooked in the clinical arena. Avoiding drug interactions is a consideration, and that is a major challenge to the field of clinical pharmacology. Clinicians need to be aware of the problem, aware of the danger areas with drugs, and first pass. Another alternative is to turn to chemical modification of a drug that avoids needing to take first pass into consideration.

Drug Therapy↗
PubMed1993

Mild heart failure: why the switch to ACE inhibitors?

Management of congestive heart failure in the past has focused on sodium and fluid restriction, rest, and digitalis glycosides. Now, significant new evidence justifies early and aggressive ACE inhibitor therapy in patients with asymptomatic or mildly symptomatic LV dysfunction. ACE inhibitors reduce the likelihood of symptomatic heart failure in asymptomatic patients with reduced ejection fraction. Patients with reduced LV function following acute MI who receive ACE inhibitors have a decreased risk of death, a lower probability of developing systematic heart failure, and fewer MI recurrences. Hypotension and azotemia can be avoided by reducing the concomitant dose of diuretics and carefully titrating the ACE inhibitor dosage to target levels.

Aged↗
PubMed1993

A randomized comparative study of the electrophysiological and electrocardiographic effects of isradipine vs verapamil.

Isradipine is a new dihydropyridine calcium antagonist reported to have minimal effects on cardiac electrophysiology. Of 19 patients with normal cardiac electrophysiological profiles, 11 received isradipine intravenously at doses of 0.0010, 0.0020, 0.0040 and 0.0080 mg.kg-1 (0.0150 mg.kg-1 total dose), and eight received verapamil intravenously at 0.0125, 0.0250, 0.0500 and 0.1000 mg.kg-1 (0.1875 mg.kg-1 total dose). One patient experienced hypotension several minutes after receiving the third isradipine dose. With isradipine, systolic blood pressure (BP) decreased from 154 +/- 24 to 151 +/- 22, 143 +/- 25, 133 +/- 19 and 124 +/- 17 mmHg, respectively. Diastolic BP decreased from 83 +/- 10 (baseline) to 80 +/- 12, 76 +/- 10, 74 +/- 7 and 68 +/- 9 mmHg, respectively. With verapamil, systolic BP changed from 132 +/- 20 (baseline) to 135 +/- 29, 132 +/- 24, 130 +/- 25 and 115 +/- 17 mmHg, respectively, and diastolic BP changed from 80 +/- 14 to 84 +/- 14, 81 +/- 9, 78 +/- 6 and 73 +/- 5 mmHg, respectively. Isradipine had no significant effect on the PR, QRS, QT and QTc intervals, nor were there changes in the atrial-His (AH) and His-ventricle (HV) intervals, atrioventricular nodal effective refractory period. Wenckebach cycle length or sinus node recovery time. Similarly, verapamil at the doses studied did not significantly affect PR, QRS, QT, QTc, AH or HV intervals. However, with verapamil, the Wenckebach cycle length changed significantly from 394 +/- 82 (baseline) to 448 +/- 93 ms. Despite the significant fall in BP with isradipine, heart rate did not change significantly. These results support the electrophysiological neutrality of isradipine on the cardiac conduction system.

Adult↗
PubMed1987

Electrophysiology of Ethmozine (moricizine HCl) for ventricular tachycardia.

Moricizine HCl, an antiarrhythmic phenothiazine drug, was investigated for its efficacy against ventricular tachycardia (VT) in a group of 60 patients from 8 institutions using electrophysiologic testing before and after oral administration. Moricizine HCl significantly prolonged PR, QRS, AH and HV intervals and cycle length for atrioventricular nodal block, but had minimal or no effect on repolarization or cardiac refractory periods. Induction of sustained VT (in 33 patients) and nonsustained VT (in 14 patients) occurred at baseline. During moricizine HCl therapy, sustained VT was induced in 31 patients and nonsustained VT in 7 patients. In individual patients, suppression of VT induction was obtained in 18% of patients with sustained VT and in 27% of patients with nonsustained VT. Cycle length of induced VT was significantly prolonged by moricizine HCl therapy. During prospective follow-up of 37 patients, electrophysiologic study predicted recurrence of nonrecurrence of VT with a sensitivity value of 82% and specificity of 65%.

Adult↗
PubMed1986

Antiarrhythmic drug efficacy at electrophysiology testing: predictive effectiveness of procainamide and flecainide.

In an effort to assess the ability of procainamide to predict effectiveness of antiarrhythmic agents at programmed electrical stimulation (PES) testing, we compared the result of procainamide at PES testing with that of all of the other agents studied. One hundred fifty-three patients underwent PES studies because of either sustained or nonsustained ventricular tachycardia (VT). Procainamide prevented VT induction in 79 of 153 patients. Seventy-four of the remaining 153 were inducible for VT on procainamide, with 55 of these being protected by another antiarrhythmic agent (p less than 0.001). If procainamide failed to prevent VT induction, other conventional and experimental agents were equally as likely to be effective in preventing VT induction. Analysis of flecainide acetate as a predictor of efficacy was also evaluated. Fifty-five patients received flecainide and 29 of these were protected at PES testing; 26 of these patients were also protected with another agent. When VT was inducible in patients who received flecainide, 15 of these 26 patients were protected by another agent, either conventional or experimental (p less than 0.01). Thus, if procainamide or flecainide prevented VT induction they accurately predicted effectiveness of other drugs; however, when they did not prevent VT induction, they served as a poor predictor of the possible effectiveness of other drugs. Serial drug testing at PES studies with multiple conventional and experimental drugs increases the likelihood of finding an effective antiarrhythmic agent.

Anti-Arrhythmia Agents↗
PubMed1986

N-acetylprocainamide's antiarrhythmic action in patients with ventricular tachycardia.

Antiarrhythmic properties of N-acetylprocainamide, an active metabolite of procainamide, were studied in 15 patients who presented with a cardiac arrest or documented sustained ventricular tachycardia. Programmed electrical stimulation studies were performed. All patients tested had inducible ventricular tachycardia by programmed electrical stimulation techniques while off all antiarrhythmic therapy. Patients were then tested on procainamide 1000 mg administered intravenously, and ventricular tachycardia could be provoked in 8 of 10 patients. Twenty-four to 36 hours later, N-acetylprocainamide was administered, intravenously, and programmed stimulation was performed after 20 minutes. N-acetylprocainamide did not significantly change heart rate, mean arterial blood pressure, electrocardiographic intervals, A-H or H-V conduction times. N-acetylprocainamide prevented ventricular tachycardia induction in 6 of 15 patients. The mean serum N-acetylprocainamide levels in the group protected was 15.7 +/- 4 micrograms/ml and 16.2 +/- 4 micrograms/ml in the group not protected. These 6 patients were discharged on N-acetylprocainamide 1.5 grams orally every 8 hours. Three patients have been maintained on chronic N-acetylprocainamide every 8 hours. Three patients have been maintained on chronic N-acetylprocainamide therapy (6 +/- 2 months), two patients had breakthrough ventricular tachycardia on follow-up Holter monitoring and alternative therapy was given. N-acetylprocainamide has antiarrhythmic efficacy in preventing induction of ventricular tachycardia by programmed electrical stimulation in a high risk group of patients. On chronic oral therapy, N-acetylprocainamide appears to be well tolerated with antiarrhythmic efficacy that may be enhanced with further upward dose titration.

Acecainide↗
PubMed1985

Prolongation of QT interval and antiarrhythmic action of bepridil.

Studies were undertaken with bepridil, a new calcium blocker that prolongs the QT interval, to determine the antiarrhythmic and possible arrhythmogenic properties of this agent. The technique of programmed electrical stimulation was employed to evaluate bepridil in 15 patients with symptomatic ventricular tachycardia (VT). Bepridil prevented VT induction in 7 of 15 patients. Bepridil prolonged the QT and refractoriness and a linear correlation could be demonstrated between the percent change in QTc and refractory period prolongation for the bepridil-protected group. Bepridil in one patient reduced by one the number of stimuli required to induce VT, but no spontaneous arrhythmias were noted. Bepridil thus possesses antiarrhythmic properties with a minimal proarrhythmic effect.

Aged↗
PubMed1985

Long-term lorcainide therapy in patients with ventricular tachycardia.

One hundred patients inducible at electrophysiologic studies underwent serial drug testing with procainamide, lidocaine, and lorcainide to determine comparative efficacy. Acute intravenous administration was followed by repeat programmed electrical stimulation (PES) studies on separate days for each antiarrhythmic drug. Lorcainide prevented ventricular tachycardia (VT) induction in 69% of the 100 patients studied, procainamide was effective in 50% of the 75 patients studied, and lidocaine prevented VT induction in 30% of 53 patients. Following PES and serial drug testing, 46 patients were started on lorcainide, nine patients on procainamide, and 45 patients were started on other antiarrhythmic drug regimens. Seventy percent of the patients have remained on lorcainide therapy, while 47% have continued on other drug therapies started over a 20.5 +/- 3.2-month mean follow-up period. Despite sleep-wake disturbances and a need for sedation at night, lorcainide therapy was tolerated well in this population and remained an effective antiarrhythmic with prolonged administration.

Benzeneacetamides↗