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Biomedical subjects

S C Seagren

Publications and source records attributed to S C Seagren.

10 recordsLinked to original sources
PubMed1991

Metabolic consequences of treating hypertension.

Reduction of morbidity and mortality has been the aim of drug treatment for hypertension since its beginning in the 1950s. Its efficacy has been tested in many trials. An outstanding result of these trials has been their clear success in preventing stroke and stroke-related deaths and in decreasing the incidence of congestive heart failure (CHF) and renal disease. A similar success has not been achieved in reducing coronary heart disease endpoints. Diuretics and beta-blockers played a central role in these studies; however, their adverse effects on lipid metabolism have been cited as a possible explanation for the failure of antihypertensive therapy to affect coronary heart disease (CHD). Recently, the extent and significance of these lipid changes has been put into perspective, and new insights into the role of carbohydrate metabolism and insulin resistance in hypertension have emerged. The same drugs which adversely affect lipid metabolism also adversely affect carbohydrate metabolism, and more is becoming known about these mechanisms and their role in hypertension and its sequelae. Other classes of antihypertensive drugs such as the calcium antagonists, angiotensin converting enzyme (ACE) inhibitors, and alpha 1-antagonists do not share these adverse effects. It has become increasingly clear that effective antihypertensive therapy includes both the lowering of blood pressure and containment of the abnormalities that accompany the hypertensive state.

Adrenergic beta-Antagonists↗
PubMed1989

Effects of encainide on the function of implanted pacemakers.

The effect of encainide on chronic pacing thresholds was evaluated in 10 patients, age 64-89, who were exposed to weekly increased encainide dosing (25 mg TID, 50 mg TID, 75 mg TID). Median pacing threshold (mujoules) increased modestly at each period compared to placebo and returned rapidly to baseline after discontinuation. (table; see text) No patient experienced a pacing-related clinical event. One patient had a large threshold increase (566%), but no failure to capture on 24-hour ECG, and one patient whose threshold increased minimally had clinically insignificant capture failure, the longest event being 3 beats. No other failure to capture was noted. Thus, encainide, like a number of other antiarrhythmic drugs, appears to affect pacing thresholds. At the highest dose of 225 mg/day (75 mg TID, which exceeds the generally recommended dose of 50 mg TID), but not at lower doses, some patients may experience loss of capture that does not appear related to the change in threshold energy required. Increases in the duration of the paced QRS induced by encainide did not predict increases in threshold. Therefore, when higher doses of encainide are required in patients with pacemakers, clinical observation and ambulatory electrocardiographic monitoring should be carried out.

Aged↗
PubMed1986

Diltiazem as monotherapy for systemic hypertension: a multicenter, randomized, placebo-controlled trial.

A multicenter, randomized, placebo-controlled, parallel group study of diltiazem in essential hypertension was carried out in 77 patients (40 diltiazem, 37 placebo) with stable supine diastolic blood pressure (BP) between 95 and 110 mm Hg. Patients were withdrawn from previous antihypertensive therapy for at least 4 weeks, titrated to the optimal dose, and followed for a total of 12 weeks during therapy. A diltiazem dose of 360 mg/day was required in 85% of the patients. Average BP in all positions was significantly (p less than 0.0001) reduced by diltiazem compared with placebo. With diltiazem, average supine BP fell from 156/100 mm Hg at baseline to 141/87 at end titration and 145/90 mm Hg at week 12, whereas average standing BP fell from 152/101 mm Hg to 136/90 and 143/91 mm Hg, respectively, at those times. There was no significant change in heart rate at week 12. Diltiazem tended to be more effective in older patients, but caused no increase in orthostatic BP drop. There were no statistically significant changes in BP in the placebo group. Two patients receiving placebo and 1 patient receiving diltiazem discontinued therapy as a result of adverse effects, and overall, side effects were only slightly more common with diltiazem treatment. Thus, diltiazem was effective and well tolerated single therapy for mild to moderate systemic hypertension and appears to compare favorably to most agents being used.

Age Factors↗
PubMed1985

Effects of diltiazem on serum lipids, exercise performance and blood pressure: randomized, double-blind, placebo-controlled evaluation for systemic hypertension.

Treatment of hypertension with diuretics, beta blockers and alpha blockers may be associated with adverse effects on exercise performance, serum lipids and blood chemistries, as well as with orthostatic effects and fluid retention. A randomized, double-blind, placebo-controlled trial of a sustained-release preparation of diltiazem as sole therapy for moderate essential hypertension was conducted. Diltiazem was administered 2 times a day (360 mg/day) to 16 patients and placebo to 14 patients in a 12-week study. Average supine blood pressure with diltiazem therapy fell from 161/100 to 144/87 mm Hg without fluid retention or orthostatic effects. In an open-label study, patients from the placebo and diltiazem groups continued with diltiazem therapy. At an average of over 8 months, supine blood pressure on diltiazem was 147/88 mm Hg, and after withdrawal to single-blind placebo, average supine blood pressure increased to 173/104 mm Hg. All changes were significant compared with baseline and placebo (p less than 0.01). On diltiazem therapy, maximal treadmill exercise was increased by an average of 55 seconds (p less than 0.01), whereas heart rate, blood pressure and double product (heart rate X blood pressure) were reduced at submaximal exercise, and heart rate and double product were reduced at maximal exercise. No changes in serum glucose, potassium or uric acid were found. No adverse effects on serum lipids occurred. Diltiazem treatment was associated with an increase in high-density lipoprotein cholesterol (52 to 60 mg/dl, p less than 0.006) and a decrease in total cholesterol:high-density lipoprotein cholesterol ratio (4.7 to 4.2, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Benzazepines↗
PubMed1985

Long-term monotherapy of angina pectoris with diltiazem.

Eighteen patients with exertional angina were treated with diltiazem (360 mg/day). Serial exercise testing was performed and the results were compared to evaluations when patients were receiving placebo at the initiation and termination of the study. Serial exercise tests indicated significant improvement in duration of exercise (+18%, p less than 0.001), time to 1 mm ST depression (+32%, p less than 0.005), and time to angina (+46%, p less than 0.001) when patients were receiving diltiazem. During diltiazem treatment, there was a significant reduction in myocardial oxygen demand as indicated by the change in submaximal pressure rate product. This may contribute to the beneficial effect of diltiazem in patients with exertional angina. The reduction in pressure rate product was due primarily to a change in heart rate. This study provides evidence that diltiazem is an effective long-term monotherapy for angina; no evidence of drug tachyphylaxis was apparent after a total of 16 months treatment with diltiazem.

Aged↗
PubMed1976

Augmented right ventricular function in systemic hypertension-induced hypertrophy.

The contractile properties of right ventricular papillary muscles from the hearts of 15 rats which had developed hypertension 6 weeks following renal artery ligation were compared with those from 14 normal litter-mates. In the experimental group, the heart weight-body weight ratio was increased by 39%, while the right ventricular weight-body weight ratio increased 20%. Right ventricular papillary muscles from the hypertensive rats demonstrated increased tension development at the apex of the length-active tension curve (P less than 0 X 0001), elevated maximal rate of tension development (P less than 0 X 001), and increased maximal velocity of contraction at muscle lengths corresponding to both a light preload and at Lmax (P less than 0 X 05). Resting tension and time-to-peak tension in the muscles from the hypertensive group were not significantly different from the normal group. Thus, improved right ventricular performance, in the presence of increased left ventricular afterload, may indicate the existence of a stimulus to increased function in hypertrophied muscle not yet negated by the adverse effects of direct exposure to stress.

Animals↗
PubMed1971

Mechanochemistry of cardiac muscle. V. Influence of thyroid state on energy utilization.

The possibility that alterations in the rate or efficiency of energy utilization could be involved in the control of cellular oxygen consumption by thyroid hormone was examined in right ventricular papillary muscles isolated from normal euthyroid cats and cats with experimentally induced hyperthyroidism and hypothyroidism. Energy production in the muscles was inhibited and isolated from the process of energy utilization by exposure to iodoacetic acid and nitrogen. After resting or performing variable amounts of contractile element work under isometric conditions, muscles were frozen, and the total amount of chemical energy ( approximately P = creatine phosphate + ATP) used was determined. The resting rate of energy utilization in muscles from euthyroid animals was 0.78+/-0.07 mumoles/g per min of approximately P. This rate was elevated in muscles from hyperthyroid cats to 1.00+/-0.09 mumoles/g per min and decreased in muscles from hypothyroid cats to 0.23+/-0.14 mumoles/g per min. Isometrically contracting muscles from cats with hypothyroidism utilized only 64% as much energy as muscles from euthyroid cats while performing 81% as much contractile element work at a moderately decreased level of contractile state. Muscles from hyperthyroid cats utilized an average of 41% more energy than did muscles from euthyroid cats while contracting an identical number of times and performing an equal amount of contractile element work at a slightly increased level of contractile state. These results suggest that thyroid hormone directly influences the rate of cellular energy utilization. Furthermore, the increase in energy utilization in muscles from hyperthyroid cats could not be attributed entirely to observed alterations in contractile behavior, which indicates that excess thyroid hormone may decrease the efficiency of the conversion of cellular energy to work. However, the opposite effect, an increased efficiency of energy utilization, was not observed in muscles from hypothyroid cats. Thus, it is concluded that the calorigenic effects of thyroid hormone may be explained, at least in part, by alterations in the process of energy utilization.

Adenosine Triphosphate↗