Carlo Pasotti

Influence of losartan and atenolol on memory function in very elderly hypertensive patients

The aim of this study was to compare the effect of the beta-adrenergic blocker atenolol and the Angiotensin II type 1 (AT1) receptor antagonist losartan on cognitive function in very elderly hypertensive patients. A total of 120 mild to moderate essential hypertensive (DBP >90 and <105 mmHg) patients, aged 75–89 years, were studied. After a 4-week wash-out period on placebo, they were randomized to receive atenolol 50 mg or losartan 50 mg for 24 weeks according to a parallel arm design. At the end of the placebo period and of each active treatment period, BP was measured (by mercury sphygmomanometer, Korotkoff I and V) and cognitive function was evaluated through three different tests (word list memory, word list recall and word list fluency). Both atenolol and losartan were equally effective in reducing SBP (−22.1 and −23.1 mmHg, respectively, P< 0.01 vs baseline) and DBP (−10.3 and −11.2 mmHg, respectively, P< 0.01 vs baseline). Atenolol treatment did not induce significant changes in any test score, whereas losartan significantly increased the score of both the word list memory (+2.2, P<0.05 vs baseline) and the word list recall test (+2.1, P<0.05 vs baseline). The comparison between losartan and atenolol was significant (P<0.05) for both memory tests. These data suggest that in very elderly hypertensive patients, chronic AT1 receptor blockade by losartan could improve cognitive function, in particular immediate and delayed memory.

Plasma lipids during chronic antihypertensive therapy with different β-blockers

The aim of this study was to compare the effects of long-term monotherapy with five different beta-blockers on plasma lipids in patients with essential hypertension. We studied 99 male patients, aged 35-55 years, with mild to moderate hypertension, who worked in the same community. After a 1-month placebo period, patients were assigned to receive propranolol (160 mg/day), atenolol (100 mg/day), bisoprolol (10 mg/day), mepindolol (10 mg/day), or celiprolol (400 mg/day). Therapy was continued for 2 years. Blood pressure (BP), heart rate, and blood samples for evaluation of total cholesterol (TC), LDL-cholesterol (LDL-C), triglycerides (TG) and HDL-cholesterol (HDL-C) were taken before and after the initial placebo period, and subsequently every 6 months from the beginning of active treatment. All beta-blockers caused similar reductions in BP that were maintained throughout the study. None of the beta-blockers significantly affected TC or LDL-C. Propranolol, a nonselective beta-blocker, caused the most pronounced changes in TG (+33 to 43%) and in HDL-C (-30 to -32%). Atenolol, a beta 1-selective agent, had the same quantitative effects, but to a lesser extent (TG + 23 to 30%; HDL-C -15 to -19%). Bisoprolol, more beta 1-selective than atenolol, and mepindolol, nonselective with ISA, increased TG (+20 to 28% and +14 to 25%, respectively) but did not significantly affect HDL-C. In contrast, celiprolol, a highly cardioselective beta-blocker with beta 2-partial agonism, improved lipid risk factors by significantly reducing TG (-14 to -21%) and increasing HDL-C (+8 to 14%).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of celiprolol on the blood lipid profile in hypertensive patients with high cholesterol levels

SummaryThe aim of this study was to compare the effects of chronic antihypertensive therapy with either celiprolol or atenolol on plasma lipids in patients with hypercholesterolemia. Forty-six patients with essential hypertension and a total cholesterol (TC) concentration > 220 mg/dl were studied. After 1 month on placebo, patients were stratified into five classes on the basis of their plasma TC levels and then randomized to receive atenolol 100 mg/day or celiprolol 400 mg/day for 1 year. Blood pressure (BP), heart rate (HR), and blood samples for evaluation of TC, HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), and triglycerides (TG) were taken before and after the placebo period, and every 6 months from the beginning of the active treatment. Celiprolol and atenolol caused similar reduction in BP. Both atenolol and celiprolol decreased TC. Atenolol significantly reduced HDL-C, while celiprolol increased it (p<0.01 at 12 months), and the difference between the two drugs was statistically significant in this regard. LDL-C levels were not significantly affected by atenolol, but were progressively reduced by celiprolol (p<0.05 at 6 months, p<0.01 at 12 months). TG rose under atenolol but was reduced by celiprolol (p<0.05). The results of this study show that the celiprolol-induced changes in plasma lipids may be favorable and suggest that, in hypertensive patients with high cholesterol levels, beta-blocker therapy with celiprolol may be effective in lowering BP without worsening the lipid profile.

β-blocker effects on plasma lipids in antihypertensive therapy : importance of the duration of treatment and the lipid status before treatment

The aim of this study was to evaluate the effects of long-term monotherapy with four β-blockers provided with different pharmacological properties on plasma lipids in both normocholesterolemic and hypercholesterolemic hypertensive patients. After a 1-month run-in period on placebo. 70 hypertensive patients with basal total cholesterol (TC) 220 mg/dl were treated for 3 years with propranolol 160 mg/day or atenolol 100 mg/day or bisoprolol 10 mg/day or mepindolol 10 mg/day, while 59 hypertensive patients with basal TC > 220 mg/dl were given the same β-blockers at the same dosage for 6 months. In both normocholesterolemic and hypercholesterolemic hypertensive patients. HDL-C and triglyceride (TG) levels showed significant changes that appeared to be related to the type of β-blocker used and to the duration of therapy. Nonselective, non-ISA (intrinsic sympathomimetic activity) propranolol caused the most pronounced changes, decreasing HDL-C and increasing TG concentrations; β1-selective atenolol and bisoprolol had similar, but less remarkable effects; even more discrete changes were observed on mepindolol (with ISA). The variations in HDL-C and TG values reached their peak in 6–12 months of β-blocker therapy; then, after a plateau phase, they showed a progressive trend toward pretreatment levels. In hypercholesterolemic patients, the percent change in both HDL-C and TG values was lower compared to normocholesterolemic patients.

EFFECT OF BENAZEPRIL AMLODIPINE COMBINATION ON LEFT VENTRICULAR HYPERTROPHY IN HYPERTENSIVE TYPE 2 DIABETIC PATIENTS: P3.266

(AA), and ( ) -blockers. We reviewed our primary care database of 70,264 HT patients and identified 5703 with a clinical diagnosis of HF (8%). Findings are summarized in the Table for all HT and all HF patients and for HF patients treated at VA and non-(n)VA primary care clinics. HT patients with HF are older and more likely to have hyperlipidemia and diabetes than all HT, and they are more likely to receive ACEI, AA, and ( ) -blockers (all p 0.001). The greater use of these meds as well as loop diuretics, spirinolactone, and CCBs (all p 0.001) may contribute to higher rates of BP control in HF than non-HF patients, despite their advanced age. HF patients at the VA were more likely to receive ACEI and less likely to receive ARBs than nVA HF patients (p 0.001), which likely reflects formulary restrictions. HF patients at the VA were also more likely to receive ( ) -blockers and statins than nVA HF patients (p 0.001), which may reflect differences in prescribing patterns and/or better access to these medications at the VA. Primary care providers are more aggressive in treating HT and comorbid risk factors in patients with than without HF. There are several similarities but also striking differences between treatment of HT patients with HF at VA and nVA settings that could favor better outcomes (more [ ] -blockers, statins, better LDL, HbA1c) for HF patients at the VA.

Effect of manidipine and atenolol on platelet aggregability in isolated systolic hypertension with and without type 2 diabetes mellitus

Abstract P-90 Key Words: Isolated Systolic Hypertension, Diabetes, Platelet Aggregability