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Metabolic considerations in the choice of therapy for the patient with hypertension
1Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510.
Insights
Antihypertensive therapies like thiazide diuretics and beta-blockers may increase coronary artery disease risk. Newer agents like ACE inhibitors and calcium channel blockers offer better metabolic profiles for hypertension management.
Area of Science:
- Cardiology
- Pharmacology
- Internal Medicine
Background:
- Hypertension treatment aims to prevent morbidity and mortality, not just lower blood pressure.
- Clinical trials show antihypertensive therapy reduces stroke risk but not coronary artery disease (CAD) risk effectively.
- Traditional therapies (thiazide diuretics, beta-blockers) may paradoxically increase CAD risk through metabolic effects or arrhythmias.
Purpose of the Study:
- To evaluate the metabolic effects of commonly prescribed antihypertensive agents.
- To compare the risks and benefits of different classes of antihypertensive drugs concerning CAD prevention.
- To identify antihypertensive therapies with favorable metabolic profiles.
Main Methods:
- Review of clinical trial data and pharmacological assessments of antihypertensive agents.
- Analysis of metabolic side effects associated with thiazide diuretics, beta-adrenoreceptor blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium entry blockers.
- Comparison of adverse effects on lipids, glucose metabolism, and electrolytes.
Main Results:
- Thiazide diuretics cause electrolyte disturbances, dyslipidemia, and glucose metabolism abnormalities.
- Non-selective beta-blockers share similar metabolic adverse effects; selective beta-blockers with intrinsic sympathomimetic activity (ISA) or third-generation agents show improved metabolic profiles.
- Angiotensin-converting enzyme (ACE) inhibitors may improve lipid profiles and insulin sensitivity, while calcium entry blockers are metabolically neutral.
Conclusions:
- The choice of antihypertensive therapy significantly impacts patient outcomes beyond blood pressure reduction.
- Certain traditional antihypertensive drugs may contribute to CAD progression, necessitating careful selection.
- Angiotensin-converting enzyme (ACE) inhibitors and calcium entry blockers represent safer alternatives regarding metabolic complications and potential CAD risk.
Abstract:
The objective of treating patients with hypertension is not simply to reduce blood pressure but rather to prevent the associated morbidity and mortality. Recent assessments of clinical trials have shown that while the risk of stroke is consistently lower with antihypertensive therapy, the same degree of success has not been demonstrated for coronary artery disease (CAD). Although there are many explanations of why we have not done as well in preventing CAD, one possibility is that the therapy used in clinical trials, primarily thiazide diuretics and beta-adrenoreceptor blockers, has increased the patient's risk of developing coronary atherosclerosis or lethal arrhythmias. Four classes of antihypertensive agents are recommended for initial therapy--thiazide diuretics, beta-adrenoreceptor blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium entry blockers. The metabolic effects of thiazide diuretics include electrolyte disturbances (hypokalemia, hypomagnesemia, and hyponatremia), dyslipidemia (increased triglycerides), abnormalities of glucose metabolism (hyperglycemia, hyperinsulinemia, and peripheral insulin resistance), and hyperuricemia. beta-Adrenoreceptor blockers have many of the same metabolic adverse reactions. beta-Adrenoreceptor blockers without intrinsic sympathomimetic activity (ISA) also cause dyslipidemias (lowered high-density lipoprotein cholesterol and increased triglycerides) and abnormalities of glucose metabolism (hyperglycemia, hyperinsulinemia, and peripheral insulin resistance). beta-Adrenoreceptor blockers with ISA and third-generation beta-blockers with selective partial agonist activity (celiprolol and dilevalol) do not cause dyslipidemia and to date do not appear to induce abnormalities in glucose metabolism. ACE inhibitors may decrease triglycerides and increase high-density lipoprotein cholesterol, and captopril may improve insulin sensitivity. Calcium entry blockers are metabolically neutral.(ABSTRACT TRUNCATED AT 250 WORDS)