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Biomedical subjects

R Fogari

Publications and source records attributed to R Fogari.

At least 91 records · Page 5Linked to original sources
PubMed1991

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

The 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 greater than 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 less than 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 less than 0.05 at 6 months, p less than 0.01 at 12 months). TG rose under atenolol but was reduced by celiprolol (p less than 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.

Adult↗
PubMed1991

Comparison of the effects on blood pressure and left ventricular hypertrophy of lacidipine and hydrochlorothiazide in hypertensive patients.

We evaluated the effects of lacidipine and hydrochlorothiazide on blood pressure and left ventricular mass in hypertensive patients of mild-to-moderate degree. Both antihypertensive agents significantly decreased systolic and diastolic blood pressure without relevant symptoms and signs of reflex activation of the sympathetic nervous system. Posterior wall and interventricular septal thickness and the left ventricular mass were significantly decreased by lacidipine and hydrochlorothiazide after 3 and 6 months of treatment without clinical symptoms of reduced cardiac function.

Blood Pressure↗
PubMed1990

Comparative effects of celiprolol, propranolol, oxprenolol, and atenolol on respiratory function in hypertensive patients with chronic obstructive lung disease.

The aim of the study was to compare the pulmonary effects of four beta-blockers with different ancillary properties: propranolol (non-beta 1 selective without ISA), oxprenolol (non-beta 1 selective with ISA), atenolol (beta 1 selective), and celipropol (beta 1 selective with mild beta 2-agonist and alpha 2-antagonist activity) in hypertensive patients with chronic obstructive lung disease. Ten asthmatic patients, all males, aged 50-66 years were studied. Entry criteria were a) DBP greater than or equal to 95 mmHg and less than or equal to 115 mmHg; b) FEV1 less than 70% of the theoretical values; c) FEV1 increase of at least 20% after salbutamol inhalation (200 micrograms). After a 2-week washout period on placebo, each patient received propranolol (80 mg/day), oxprenolol (80 mg/day), atenolol (100 mg/day), and celiprolol (200 mg/day) for 1 week, according to a randomized, cross-over design. At the end of the washout and of each treatment period, airway function, assessed by FEV1, FVC, and FEV1%, was evaluated by spirometry both in the basal condition and after salbutamol inhalation. Unlike propranolol and oxprenolol, which significantly reduced FEV1 and inhibited the bronchodilator response to inhaled salbutamol, atenolol and celiprolol did not significantly affect respiratory function and did not antagonize salbutamol effects. Celiprolol more closely approached placebo in its respiratory effects than did atenolol, although the differences were not statistically significant.

Adrenergic beta-Antagonists↗
PubMed1990

Beta-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 beta-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) < or = 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 beta-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 beta-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; beta1-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 beta-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.

Adrenergic beta-Antagonists↗
PubMed1990

Beta-blockers and primary cardioprotection in hypertension.

Theoretical and experimental data coupled with findings from several studies, showing the beneficial effect of beta-blocking therapy in reducing the risk of death and re-infarction among infarct patients (secondary cardioprotection), suggested that beta-blockers could reduce the incidence of coronary events also in hypertensive patients with no clinical evidence of coronary heart disease (CHD) (primary cardioprotection). In order to evaluate the primary cardioprotective potential of beta-blockers as compared to diuretics in the treatment of hypertension, some large-scale, randomized, prospective studies were set up in the middle and late 1970s. The results of three of these trials, the MRC, the IPPPSH and the HAPPHY studies, were negative or non-conclusive and somehow conflicting. None of them showed any difference between beta-blockers and diuretics in reducing the incidence of CHD, but the MRC and the IPPPSH studies suggested that beta-blockers were better than diuretics in male non-smokers. However, the HAPPHY study did not confirm such a hypothesis. More recently, two studies, the Clatterbridge study (retrospective, non-controlled) and the MAPHY study (prospective, controlled) gave positive results about the primary cardioprotective effect of beta-blockers. In particular, the MAPHY study demonstrated that starting antihypertensive treatment with the beta1-selective beta-blocker metoprolol instead of a thiazide diuretic led to lower total and cardiovascular mortality, mainly by reducing fatal CHD and fatal stroke. Although more evidence is needed, the primary cardioprotective effect demonstrated with metoprolol in the MAPHY study might have important implications for clinical practice and public health.

Adrenergic beta-Antagonists↗
PubMed1990

Antihypertensive activity and duration of action of dilevalol in hypertensive patients at rest and during exercise. A comparison with captopril.

The aim of this study was to compare the effect of dilevalol and captopril on blood pressure and heart rate in hypertensive subjects, both at rest and during bicycle exercise. Thirty mild hypertensive patients (24 men, 6 women), aged 34-55, were studied in a randomized, double-blind, parallel group trial. After a 3-week placebo run-in, patients were randomized to receive either dilevalol (200 mg once daily) or captopril (50 mg twice daily) for 4 weeks. Dilevalol-treated patients whose diastolic blood pressure had not decreased by more than 8 mmHg from baseline (or to less than 95 mmHg) were given 400 mg once daily for a further 2 weeks. Treatment was stopped for all other patients. Blood pressure and heart rate were measured at rest and during bicycle exercise tests 4 ("peak") and 24 hours ("trough") after dosing in the dilevalol group and 4 ("peak") and 12 hours ("trough") after dosing in the captopril group. At the end of the placebo run-in, mean resting blood pressure was 156/102 mmHg in the dilevalol group and 157/103 in the captopril group. Six patients had blood pressure normalization with captopril and 9 with dilevalol 200 mg; a further 2 patients achieved normalized blood pressure levels with dilevalol 400 mg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Ketanserin in chronic treatment of hypertension in type 2 diabetes mellitus.

This study was performed in order to evaluate the effects of ketanserin monotherapy on blood pressure and glucose metabolism in essential hypertensives with type 2 diabetes. Twenty-nine patients, 17 males and 12 females, aged 45 to 78 years, with mild hypertension (DBP greater than or equal to 95 and less than or equal to 105 mmHg) and type 2 diabetes were studied. After a 4 week run-in period on placebo, each patient received ketanserin 20 mg b.i.d. for 6 months, with no modification in previous antidiabetic therapy. SBP, DBP, HR, fasting and post-prandial glycemia were monitored monthly. An oral glucose tolerance test (OGTT), glycosilated hemoglobin (HbA1c), urinary C-peptide, serum electrolytes, creatinine, uric acid, total cholesterol and 24 h protein and glucose urinary excretion were evaluated before and after 3 and 6 months of treatment. Ketanserin significantly reduced both SBP and DBP (p less than 0.005) with no changes in HR. No significant modifications of fasting and post-prandial glycemia, HbA1c and C-peptide were observed. Besides, ketanserin did not affect glucose tolerance, the levels of glucose during the OGTT were not significantly different before and after treatment. None of the patients required any change in antidiabetic therapy. In conclusion, ketanserin was effective in the treatment of mild hypertension in patients with type 2 diabetes. The absence of effects on glucose metabolism makes it an especially interesting drug in such patients.

Aged↗
PubMed1990

Benazepril at incremental doses in essential hypertension.

The antihypertensive effect of the new non-sulphydryl ACE-inhibitor benzepril was studied in 30 patients (16 men, 14 women; mean age 50 +/- 7 years) with essential hypertension at WHO stage I or II. After a 2-week placebo treatment, patients with lying diastolic blood pressure (DBP) greater than or equal to 95 mmHg were given benzepril 10 mg once daily for 2 weeks. At the end of this period, patients with lying DBP less than 95 mmHg continued with the same dosage, while those with lying DBP greater than or equal to 95 mmHg were blindly up-titrated to benazepril 20 mg once daily. In both cases treatment was continued for further 4 weeks. BP was measured every two weeks 24-26 h after last drug administration. After the run-in period, mean group lying BP was 160/104 +/- 8/5 mmHg. Benazepril significantly reduced systolic blood pressure (SBP) and DBP, both supine and standing (p less than 0.01), while heart rate (HR) did not change. After the first 2 weeks, 13 patients (43%) had lying DBP less than 95 mmHg ("fast responders"), while 17 patients (57%) had DBP greater than or equal to 95 mmHg. By increasing the dosage to 20 mg, a further 5 patients became responder and mean group blood pressure in patients up-titrated with benazepril dropped significantly (-16/-10 mmHg from baseline; p less than 0.01, "slow responders"). Fast responders were younger (47 +/- 5 vs 54 +/- 8 years), had lower baseline BP (160/99 +/- 4/3 vs 173/107 +/- 7/3) and had shorter duration of hypertension (20 +/- 14 vs 61 +/- 27 months) than "slow responders".(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Community control of hypertension at the worksite in a metallurgical factory: results of 1-year follow-up.

This study was designed to assess advantages and cost-effectiveness of community control of hypertension at the worksite in a metallurgical factory in Pavia. Under consent of managers and trade-unionists, a screening program was undertaken. 2701 subjects (95% of the total number of employees) were screened: 277 (10.2%) were hypertensive, 101 (38%) did not know to be hypertensive, 56 (22%) knew to be hypertensive but they were untreated and only 20 (8%) of those under treatment were adequately treated. Of the 277 essential hypertensives, 262 (94%) adhered to the program. They were assigned to beta-blocking or diuretic treatment following WHO rules. Then an aggressive follow-up was started (the hypertensives were periodically called to control at the worksite). 257 (98%) were participants 1 year later. Our worksite hypertension control program allowed us to identify many cases of undiagnosed or untreated hypertension and to start an early treatment. One year after entry, the percentage of hypertensives achieving a normal blood pressure (85%) was almost twice as that obtained by conventional clinical approach employing the same type of treatment. Besides, more than 95% of hypertensives remained under control at 1 year. Regarding the costs, it is difficult to generalize, but our study suggests that, if there is the will, it is possible to realize programs of hypertension community control at a very low cost (in our experience: 43 dollars per hypertensive per year).

Blood Pressure↗
PubMed1989

Heart and hypertension.

The manifestations of cardiac involvement in hypertension include: (1) the development of hypertensive heart disease characterized by left ventricular hypertrophy (LVH), and (2) the consequences of coronary atherosclerosis, as angina pectoris, myocardial infarction, and sudden cardiac death. Whereas the former is directly related to increased blood pressure, the latter are sequelae of atherosclerosis per se, and hypertension acts only as a risk factor in this regard. This can partially explain why antihypertensive treatment is effective in diminishing the incidence of congestive heart failure, which is the final consequence of LVH, but is not very effective in preventing coronary complications. It is generally accepted about LVH that increased arterial pressure is the major stimulus to cardiac hypertrophy in hypertension; however, there are a lot of both quantitative and qualitative events suggesting that other factors beside blood pressure levels can modulate the development of LVH, in particular neurohumoral influences. From a morphological point of view, hypertrophy of the cardiac muscle is defined as an increase in the size of existing myocardial fibers. In most experimental models, myocardial hypertrophy is associated with myosin isoenzymatic changes, consisting in a shift from the faster migrating isoenzyme V1 to V3, a form that migrates more slowly. However these changes do not occur in all animal species and particularly in humans. In the hypertrophied human ventricle, a decreased ATPase activity of myofibrils was observed, probably related to changes in myosin light chains. Presently the changes in ATPase activity and in ventricular contractility do not still have a clear molecular basis in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1989

Plasma lipids during chronic antihypertensive therapy with different beta-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)

Adrenergic beta-Antagonists↗
PubMed1989

Beta-blockers in chronic treatment after acute myocardial infarction.

Postinfarction treatment trials have demonstrated that beta-blockers are beneficial after myocardial infarction (MI), significantly reducing postinfarction cardiac mortality and nonfatal reinfarction, aside from bringing about an improved quality of life. Such cardioprotective action is probably mediated by both antiarrhythmic and anti-ischemic effects of these drugs. Beta-Blockers without ISA seem to be more effective in reducing cardiac mortality than those with ISA, which is probably due to their different effects on heart rate. Patients deriving major benefit from beta-blocker therapy after MI should be "high risk," elderly, and, perhaps, hypertensive patients. The suitable duration of postinfarction beta-blocker therapy is unknown: results from recent long-term trials speak in favor of continuous postinfarction beta-blocker therapy.

Adrenergic beta-Antagonists↗
PubMed1989

[Antihypertensive effect and tolerability of slow-release nicardipine].

In order to evaluate the antihypertensive efficacy and tolerability of a new nicardipine formulation, 26 mild-to-moderate essential hypertensive patients were given slow-release nicardipine, 40 mg, twice daily for 6 weeks. Systolic (SBP) and diastolic (DBP) blood pressure were measured after a 1 week single-blind placebo run-in period and after 1, 2, 4 and 6 weeks of active treatment, just before the morning administration. After 1 week, nicardipine induced a significant blood pressure reduction (p less than 0.01), with a decrease in mean SBP/DBP values of -15/-11 mmHg (from baseline values of 165/104 to 150/93 mmHg) in supine and of -16/-12 mmHg (from 158/110 to 142/98 mmHg) in standing position. After 6 weeks the decrease was of -15/-12 mmHg in supine and of -15/-14 mmHg in standing position. The responder rate (DBP decrease of at least 10 mmHg) was 62% (16/26). Normalization rate (DBP less than 95 mmHg with a concomitant decrease of at least 10 mmHg) was 54% (14/26). Eleven patients reported adverse events (headache, peripheral oedema, palpitations, nausea, constipation, flush, dizziness and asthenia). Due to an improved pharmacokinetic profile, the slow-release formulation prolongs to 12 hours the antihypertensive effect of nicardipine, thus facilitating patient's compliance.

Adult↗
PubMed1988

Effects of captopril on cold pressor test responses in normotensive and hypertensive subjects.

The aim of this study was to evaluate the effects of short-term captopril administration on the response to cold pressor testing in normotensive and hypertensive subjects. Cold pressor testing was performed in 15 normotensive subjects and 15 hypertensive patients before and 90 minutes after captopril administration. Blood pressure and heart rate were measured before testing and at one-minute intervals from the beginning of cold pressor testing. Systolic time intervals were also assessed before and after testing. Captopril did not affect pressor responses to cold pressor testing in normotensive subjects or hypertensive patients. Basal heart rate (before testing) did not change, despite the decrease in blood pressure and showed a smaller increase in response to cold pressor testing in normotensive subjects, suggesting that captopril might interfere with arterial baroreflexes. The systolic time intervals were not modified by captopril except isometric contraction time; its basal value was reduced by captopril in both normotensive subjects and hypertensive patients. Cold exposure caused a similar increase in isometric contraction time before and after captopril in normotensive subjects, and the increase in isometric contraction time in hypertensive patients was greater. These findings suggest that captopril did not affect cardiac performance, indeed improving it, at least in basal conditions.

Adult↗
PubMed1988

Effects of different beta-blockers on lipid metabolism in chronic therapy of hypertension.

The aim of this study was to evaluate the possible time-related effects of long-term monotherapy with different beta-blockers on plasma lipids in patients with essential hypertension. We studied 69 mild-moderate hypertensives, all males, aged 35-56 years belonging to the same working community. After 1-month placebo period, patients were assigned to receive propranolol 160 mg/day or atenolol 100 mg/day or bisoprolol 10 mg/day or mepindolol 10 mg/day. They were followed-up 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 placebo period and every 6 months from the beginning of the active treatment. All beta-blockers caused similar reduction in BP values which persisted throughout the study. None of the beta-blockers significantly affected TC and LDL-C. Propranolol caused the most pronounced changes in TG (+35-43%) and in HDL-C (-36-44%). Atenolol had the same qualitative effects but to a lesser extent (TG: +26-30%; HDL: -15-25%). Bisoprolol has more beta 1-selective than atenolol, and mepindolol, non-selective with ISA, increased TG (+15-28% and +13-23%) but did not significantly affect HDL-C. Consequently, HDL-C and TG changes appeared to be related to the ancillary properties of the different beta-blockers and, in a lesser degree, to the duration of therapy.

Adrenergic beta-Antagonists↗