Background: Antihypertensive drug combinations have two major advantages: First, dosage of the single components can be reduced, and second, putative side effects can be minimized. Therefore, we analysed in a cohort of patients with multiple cardiovascular risk factors the metabolic effects of two fixed antihypertensive drug combinations.
Patients and methods: 225 patients with essential hypertension (dBP > or = 95 < or = 115 mm Hg) and adipositas (BMI 30.6 +/- 2.5) were randomly treated during 6 months with either quinapril and hydrochlorothiazide (HCTZ) or with metoprolol and hydrochlorothiazide. Compared with healthy controls, patients exhibited significant elevated concentrations of triglycerides (226 +/- 86 vs. 146 +/- 73 mg/dl) and fasting insulin (22.2 +/- 1.8 vs. 9.8 +/- 4.6 microU/ml).
Results: The antihypertensive effects and the tolerance of both substances were good and comparable after 3 and 6 months. Serum triglycerides increased during metoprolol/hydrochlorothiazide treatment (230 +/- 81 vs. 244 +/- 185 mg/dl; median 174 vs. 204; + 17%), as well as during treatment with quinapril/hydrochlorothiazide (222 +/- 155 vs. 235 +/- 162 mg/dl; median 166 vs. 174; + 5%). Fasting blood glucose levels, insulin, fructosamine, HbA1c and free fatty acids remained unchanged. In a subgroup of 88 postmenopausal women with upper body obesity (WHR > 0.85) treatment with quinapril/hydrochlorothiazide normalized the VLDL-triglyceride/VLDL-cholesterol ratio (3.8 vs. 5.9, p < 0.05), whereas the ratio only increased from 3.6 to 4.2 in the metoprolol/hydrochlorothiazide group. These changes in the ACE-inhibitor group were due to a decrease in VLDL-cholesterol (41.4 +/- 4.2 vs. 33.9 +/- 9.6).
Conclusion: These data demonstrate that quinapril or metoprolol in combination with hydrochlorothiazide do not differ significantly with regard to their effects on blood-pressure lowering, lipoprotein profile, and glucose metabolism. Only in the subgroup of adipose postmenopausal women, the modulated VLDL-composition might suggest the elimination of atherogenic VLDL-remnants/IDL during quinapril/hydrochlorothiazide treatment.