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Biomedical subjects

J C Somberg

Publications and source records attributed to J C Somberg.

At least 37 records · Page 2Linked to original sources
PubMed1997

QT interval dispersion in healthy subjects and survivors of sudden cardiac death: circadian variation in a twenty-four-hour assessment.

Twenty-four-hour acquisition of QT dispersion (QTd) from the Holter and the circadian variation of QTd were evaluated in 20 survivors of sudden cardiac death (SCD), in 20 healthy subjects, and in 14 control patients without a history of cardiac arrest who were age, sex, diagnosis and therapy matched to 14 SCD patients. Computer-assisted QT measurements were performed on 24-hour Holter recordings; each recording was divided into 288 5-minute segments and templates representing the average QRST were generated. QTd was calculated as the difference between QT intervals in leads V1 and V5 for each template on Holter. The 24-hour mean QTd was significantly greater in SCD patients (40 +/- 28 ms) than in healthy subjects (20 +/- 10 ms) and control patients (15 +/- 5 ms) (p <0.05). There was a circadian variation in QTd with greater values at night (0 to 6 A.M.) than at daytime (10 A.M. to 4 P.M.) in healthy subjects (25 +/- 13 vs 15 +/- 8 ms, p <0.001) and control patients (18 +/- 10 vs 12 +/- 4 ms p <0.05), whereas in SCD patients there was no significant difference between night and day values (45 +/- 31 vs 37 +/- 28 ms, p = NS). It is concluded that QTd measured by Holter was greater in SCD patients than in healthy subjects and matched control patients during the entire day. QTd has a clear circadian variation in normal subjects, whereas this variation is blunted in SCD patients. QTd measured on Holter differentiates survivors of cardiac arrest and may be a useful tool for risk stratification.

Adult↗
PubMed1996

Gender differences in drug therapy.

Patient response to drug therapy is affected by multiple factors, including age, renal function, diet, smoking, congestive heart failure and gender. However, the data on gender differences in pharmacotherapy are limited, predominantly because women are excluded from clinical research due to the potential risks involved during pregnancy and co-existing illnesses in elderly women. Currently some information is available on gender differences in drug therapy. Differences in drug distribution and response due to different body composition as well as the effects of hormonal differences are the few that have been documented. Differences in drug metabolism due to differences in blood concentration of enzymes such as alcohol dehydrogenase has been recently described. Pharmacotherapy may also have to be altered due to differences in disease expression, like increased vasomotor tone in women. Drug efficacy has been found to be affected by gender---an example is antiplatelet therapy for stroke prevention. Finally, the side effects of drugs may differ depending on gender. Those involved in pharmacotherapy should be aware of these differences when prescribing drugs to female patients, since the majority of clinical data regarding pharmaceuticals has been derived primarily from a population of young males.

Journal Article↗
PubMed1995

Can nitroglycerin convert effort-induced angina in men into silent myocardial ischemia?

The relief of anginal pain with nitroglycerin may not correspond to the disappearance of ischemia. To evaluate the possible lack of the elimination of ischemia with sublingual nitroglycerin, we studied 25 male patients with stable angina pectoris who underwent exercise stress testing with recording of blood pressure, pulse, and ST-segment displacement. The stress test was repeated 30 minutes after administration of 0.4 mg of sublingual nitroglycerin. All 25 patients had angina and ischemic ST-segment changes in the first stress test. On repeat stress testing, 15 patients had angina and ST-segment changes, 2 patients had angina but no ST-segment changes, and 4 patients had no ST-segment changes and no angina. Four patients, however, had no angina but persistent ischemic ST-segment changes suggesting that angina was converted into silent ischemia. The mean exercise duration was 311 +/- 66 seconds before and 421 +/- 81 seconds after the nitroglycerin test. Peak heart rate and systolic blood pressure before the nitroglycerin stress test were 109 +/- 18 and 155 +/- 23 mm Hg; in the repeat stress test, they increased to 123 +/- 21 and 162 +/- 20 mm Hg, respectively.

Administration, Sublingual↗
PubMed1993

Branded generics.

Explore the source record for details and available documents.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

New FDA initiatives.

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Adverse Drug Reaction Reporting Systems↗
PubMed1993

Proarrhythmia of nonantiarrhythmic drugs.

Proarrhythmic effects of nonantiarrhythmic drugs have not been as extensively studied or reported compared with the effects of antiarrhythmic drugs. The proarrhythmic incidence of many of these agents is not accurately known. In some instances, the facilitation of arrhythmias may be the result of compounding clinical factors. Many agents, however, share structural similarities to antiarrhythmics and manifest the same arrhythmic tendencies. Many reports of proarrhythmia may represent toxic rather than proarrhythmic effects, and in vitro studies to elicit the underlying mechanisms may be warranted for the more common drugs. This report summarizes reported arrhythmic effects of a variety of commonly utilized nonantiarrhythmic drugs. The incidence and mechanism of the proarrhythmia is not always clear. The clinician, however, should be aware of reported events to appropriately diagnose and treat the arrhythmia.

Anti-Bacterial Agents↗
PubMed1992

Hypothyroidism complicated by angina pectoris: therapeutic approaches.

The association of hypothyroidism and coronary artery disease is not uncommon. The precipitation of angina pectoris, cardiac arrhythmia, and even myocardial infarction may occur in patients when initiating rapid replacement therapy for hypothyroidism. This is particularly true when replacement therapy is instituted in elderly persons or in patients with preexisting coronary artery disease. A starting daily dose of 12.5 to 25 micrograms and increments of 25 micrograms every 2 to 3 weeks is recommended. Close monitoring of cardiac symptoms is essential to avoid side effects. Medical management of angina pectoris includes administration of beta-blockers, nitrates, or at times combination antianginal therapy may be most effective. Persistence of angina in these patients may require coronary angiography with subsequent angioplasty or coronary artery bypass surgery.

Adrenergic beta-Antagonists↗