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Biomedical subjects

A Zoppi

Publications and source records attributed to A Zoppi.

At least 73 records · Page 4Linked to original sources
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↗
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↗
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↗
PubMed1987

[The electrocardiogram in hypothermia].

Hypothermia is reflected in the electrocardiogram in the form of alterations that permit early recognition of the condition. In fact the electrocardiogram is a more sensitive indicator of temperature than the standard measurements of body temperature used in clinical practice. The various aetiological aspects of hypothermia are described as are its electrocardiographic features.

Atrial Fibrillation↗
PubMed1987

Chronic beta 1-blockade and control of left ventricular hypertrophy in hypertension.

The aim of this study is to evaluate the effects of chronic beta-blocking therapy (atenolol 100 mg/d) on ECG and ECG indexes of left ventricular hypertrophy (LVH) in hypertensive patients. Seventy one subjects with essential hypertension (mean age 47 y) were studied for 5 years. Sokolow-Lyon voltage criteria for ECGLVH (S wave in V1 plus R wave in V5 greater than or equal to 35 mm) were employed in: 38 treated patients with ECGLVH, 12 treated patients without ECGLVH and 21 untreated patients with ECGLVH. Beta-blocking therapy significantly reduced blood pressure (BP) in the treated patients. In the patients with ECGLVH, treatment significantly improved Sokolow-Lyon Index (SLI) reducing it from 55.04 +/- 16.2 mm to 47.6 +/- 15.04 mm (p less than 0.05) but only 11.4% of the treated patients returned within the normality range (SLI less than 35 mm). No significant change was present in the treated patients without ECGLVH. On the contrary, the group of untreated patients showed an increase in SLI from 45.19 +/- 7.08 mm to 50.52 +/- 11.09 mm (p less than 0.05) and no change in hypertension levels. We conclude, therefore, that: ineffective BP control allows progression of LVH; BP reduction by beta-blocking drugs reduces LVH but does not produce complete regression of the hypertrophy, if not in the early stages; if no LVH is present, BP control by these drugs prevents LVH. We emphasize the importance of early detection and treatment of hypertension.

Adult↗
PubMed1986

Effect of beta-blockers on plasma lipids.

Forty-five hypertensive patients (I-II WHO), after two weeks wash out, were randomly allocated to receive 100 mg/day atenolol, 200 mg/day metoprolol and 10 mg/day mepindolol for three months, in order to evaluate their possible effect on lipid metabolism. Plasma triglyceride levels were increased by the three drug treatments; the increase was, however, greater after mepindolol. Total cholesterol was unchanged by atenolol, increased by metoprolol and decreased by mepindolol. HDL-cholesterol was unchanged by atenolol, decreased by metoprolol and increased by mepindolol, whereas LDL-cholesterol was increased by atenolol, unchanged by metoprolol and decreased by mepindolol. Therefore, the LDL/HDL ratio was decreased by mepindolol (from 3.15 +/- 1.71 to 2.92 +/- 1.17) and increased by atenolol and metoprolol. The results show that the treatment with atenolol, metoprolol and mepindolol does not significantly affect the lipid levels suggesting that cardioselective beta-blockers as well as those with ISA have no untoward effect on lipid metabolism.

Adult↗
PubMed1985

Time-related effects of chronic atenolol treatment on cardiovascular responses to handgrip.

To assess the influence of chronic atenolol therapy on the cardiovascular responses to isometric exercise, we evaluated the behavior of blood pressure, heart rate and double product in 75 hypertensive patients treated with atenolol 100 mg once daily for 6 months. During the 1st month of treatment, both systolic blood pressure (SBP) and diastolic blood pressure (DBP) increases rose more than before treatment. SBP increase to handgrip became lower than before treatment on the 2nd months of therapy (p less than 0.05) and fell even more afterwards (p less than 0.01 on the 6th month). On the contrary, DBP increase subsequently steadied on levels not significantly different from those before treatment. Double product increase was inferior to that recorded before atenolol administration; the difference became significant after 2 months and reached its apex after 6 months of treatment. The conclusion was that chronic atenolol therapy affected some cardiovascular responses to handgrip although to a different extent depending on treatment length; it would seem sensible to pay attention to how long a patient has been on beta-blocker when evaluating the response to isometric exercise.

Adult↗
PubMed1984

[Central alpha 2-adrenergic receptors in the rat: effect of sodium in vitro].

Characteristics of the (3H) Rauwolscine binding were studied in homogenates of rat cerebral cortex, particularly in presence of NaCl. We had shown that (3H) Rauwolscine specifically bind the alpha 2-adrenoceptors. The Scatchard plot analysis had demonstrated 2 sites: a high affinity site (B 41,06 +/- 5,21 KD = 1,31 +/- 0,16) and a low affinity site (B = 203,41 +/- 13,37 KD = 11,62 +/- 0,55 nM). Incubation of cerebral cortex homogenates with NaCl 150 mM induced an increase (53,97 p less than 0.001) of the high affinity site density. These results indicate that (3H) Rauwolscine is a useful alpha 2-adrenoceptor ligand to study in animal models various central nervous system abnormalities or diseases induced by ion disorders.

Animals↗
PubMed1984

Half-strength atenolol-chlorthalidone combination (tenoretic mite) in the treatment of elderly hypertensive patients.

The antihypertensive efficacy and tolerance of a new fixed combination of 50 mg atenolol and 12.5 mg chlorthalidone (Tenoretic Mite, TM) was studied in 37 patients with arterial hypertension, aged 61-80 years (mean, 70.2 years), who had been randomized to either 50 mg atenolol or 12.5 mg chlorthalidone for a 4-week period. At the end of this period, the fixed combination of atenolol and chlorthalidone was given to all patients for 6 months at a dose of one tablet daily in the morning. In both atenolol- and chlorthalidone-pretreated patients, treatment with the fixed combination resulted in a further significant drop in blood pressure, whereas the heart rate decreased only in the latter group. The mean blood pressure reduction achieved by the fixed combination was 30/15 mmHg in the standing position. Serum potassium levels significantly increased with the fixed combination compared with values on chlorthalidone alone. Unwanted effects were rare, and their frequency tended to decrease over time. In conclusion, the fixed combination of 50 mg atenolol plus 12.5 mg chlorthalidone tested in this study proved highly effective in lowering elevated blood pressure values in a population of elderly hypertensive patients treated over a 6-month period without noticeable unwanted effects.

Age Factors↗
PubMed1983

[A case of Morquio's syndrome with long survival time].

A long-surviving clinical case of suspected Morquio's syndrome is described. The locomotorium (vertebral dwarfism, hyphoscoliosis, but no hypoplasia of the odontoid process of the epistropheus, platyspondylia), cardiopulmonary (aortic insufficiency, arterial calcification, varices) visual (opaque lens on right eye, sclerosis of the lenticular lamellae but no corneal opacity on left eye) acoustic (deafness) and gastroenteric systems (hepatomegaly) are analysed. No pathological granulations were noted in the leukocytes. The plasmatic lysosome enzymes were normal and alpha-fucosidase subnormal. Abnormal keratan sulphate secretion was noted in the daily urine. All this would explain the patient's long survival.

Adult↗
PubMedDate not supplied

Hydrochlorothiazide added to valsartan is more effective than when added to olmesartan in reducing blood pressure in moderately hypertensive patients inadequately controlled by monotherapy.

This study was undertaken to evaluate the effects on blood pressure of hydrochlorothiazide (HCTZ) 12.5 mg added to valsartan 160 mg or to olmesartan 20 mg in hypertensive patients. After a 2-wk placebo period, 130 patients, aged 35 to 75 y, with diastolic blood pressure (DBP) >or=99 and 110 mm Hg were randomly assigned to olmesartan 20 mg once daily or to valsartan 160 mg once daily according to a prospective, parallel-arm study design. After 4 wk of monotherapy, patients whose BP was not controlled (DBP >or=90 mm Hg) were given combination treatment with HCTZ 12.5 mg for an additional 4 wk. At the end of the placebo period and at the end of each treatment period, clinical and ambulatory BP measurements were recorded. At the end of the combination therapy period, venous blood samples were drawn 2, 4, and 24 h after drug intake for evaluation of HCTZ plasma concentrations. Both combinations induced a greater ambulatory BP reduction than monotherapy. However, mean reduction from baseline in the valsartan/HCTZ-treated patients (-21.5)-14.6 mm Hg for 24 h, -21.8/-14.9 mm Hg for daytime, and -20.4/-13.7 mm Hg for nighttime systolic blood pressure [SBP]/DBP) was greater than in the olmesartan/HCTZ-treated patients )-18.8/-12.3 mm Hg for 24 h, -19.3/-12.8 mm Hg for daytime, and 17.4/-10.6 mm Hg for nighttime SBP/DBP). The difference between the effects of the 2 treatments was significant (P<.01). In particular, compared with monotherapy, the add-on effect of HCTZ 12.5 mg was significantly greater in the valsartan group than in those treated with olmesartan; the difference was more evident for nighttime BP values. Plasma concentrations of HCTZ were significantly greater with valsartan than with olmesartan at each determination time (P<.05). These findings suggest that the addition of HCTZ 12.5 mg to valsartan 160 mg monotherapy produces a greater BP reduction than the addition of the same dose of HCTZ to olmesartan 20 mg monotherapy.

Adult↗