PubMed HealthSearch

PubMed · 25112

Beta-blockers and plasma triglycerides.

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Shaw, J D England, A S Hua. 1978-04-15. Beta-blockers and plasma triglycerides.. https://doi.org/10.1136/bmj.1.6118.986-a

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Selective beta 1 and beta 2 adrenoceptor blockade on epinephrine-induced arrhythmias in halothane anaesthetized dogs.

Beta 2 as well as beta 1 adrenoceptors have been recognized in the heart of vertebrates. They mediate a positive chronotropic action of catecholamines. We compared the effect of selective beta 1 and beta 2 adrenoceptor antagonists on the genesis of halothane-epinephrine arrhythmias in dogs. The arrhythmogenic dose (AD) of epinephrine was increased in the presence of l-metoprolol, a selective beta 1 antagonist (8.40 +/- 1.13 micrograms.kg-1 x min-1; mean +/- SEM), compared with control value (2.62 +/- 0.56) (P < 0.05). In contrast, ICI-118,551, a selective beta 2 antagonist, did not change the AD (2.36 +/- 0.43). Adding ICI-118,551 to l-metoprolol did not affect the AD of epinephrine in the presence of l-metoprolol alone (6.34 +/- 0.74 vs 8.40 +/- 1.13). These results suggest that selective beta 1 blockade is effective in preventing halothane-epinephrine arrhythmias, but selective beta 2 blockade is not.

Adrenergic beta-Antagonists

Beta-blockers: primary and secondary prevention.

Coronary heart disease is the most frequent cause of death in Western, industrialized countries. Coronary risk factors are prevalent in such countries and sometimes combine to constitute the so-called syndrome X--hypertension, central obesity, serum lipid and clotting disturbances, and insulin resistance. beta-Blockers, unlike calcium antagonists, have proved highly effective in secondary prevention of myocardial infarction. If present at the time of the myocardial infarction, beta-blockers (unlike calcium antagonists and diuretics) probably decrease mortality 1 month later. Early intervention (within 12 h) of chest pain with intravenous beta-blockers results in a 15% reduction in cardiovascular mortality at 1 week. Later intervention (3-28 days) with oral non-ISA beta-blockers results in a 30% reduction in mortality after 1 year; ISA-containing beta-blockers are probably less effective (less decrease in heart rate). Hydrophilicity/lipophilicity of beta-blockers is unimportant in terms of decreased mortality. Primary prevention of myocardial infarction, unlike stroke, in hypertensive patients has been disappointing, possibly due to treatment-induced biochemical/lipid changes or inappropriate lowering of diastolic blood pressure in high-risk subjects (J-curve effect). beta-Blockers should be first-line therapy for hypertensive patients up to the age of 65 years, particularly men (and nonsmokers) as Q-wave myocardial infarction is significantly decreased by beta-blockers and significantly increased by diuretics. However, in elderly hypertensive subjects, beta-blockers have not significantly decreased myocardial infarction (unlike stroke), whereas diuretics have. The effects of beta-blockers and diuretics on heart size (and thus coronary flow reserve) in the elderly may be important. Thus, beta-blockers should be second-line therapy for the elderly hypertensive individual but first-line if overt ischemia (e.g., angina or recent myocardial infarction) also is present. In patients with angina but normal blood pressure, beta-blockers tend to decrease and calcium antagonists increase cardiovascular events. Thus, beta-blockers are highly effective agents in the secondary prevention of myocardial infarction and are moderately effective in primary prevention of myocardial infarction in hypertensive patients (particularly men) under the age of 65 years.

Adrenergic beta-Antagonists

Effects of nifedipine and diltiazem on myocardial ischemia in patients with severe stable angina pectoris treated with nitrates and beta-blockers.

In a randomized, cross-over, double-blind study, the effects of nifedipine were compared with those of diltiazem in 20 patients with severe stable angina pectoris and multivessel coronary artery disease treated with nitrates and beta-blockers. The comparison was performed by bicycle ergometry, clinical evaluation, and ambulatory 24-h ECG monitoring for 7-8 weeks. As compared with placebo, both nifedipine and diltiazem significantly reduced the daily number of anginal attacks and nitroglycerin consumption; prolonged exercise duration, time to 1-mm ST segment depression, and to onset of angina; and reduced the sum of ST segment depressions at maximal identical load in ergometry. In ambulatory ECG monitoring, only nifedipine significantly diminished the duration of asymptomatic ST segment depression as compared with placebo. Antianginal and antiischemic effects of nifedipine and diltiazem were similar. Both nifedipine and diltiazem significantly increased the effects of treatment with nitrates and beta-blockers. Administration of nifedipine was safer because at night diltiazem caused significant bradycardia despite careful titration of optimum doses of the drug. Although the maximum well-tolerated doses of conventional medication suppressed anginal symptoms in some patients, they did not abolish ischemia either at ergometry or in daily life.

Adrenergic beta-Antagonists