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Biomedical subjects

P Verdecchia

Publications and source records attributed to P Verdecchia.

At least 145 records · Page 8Linked to original sources
PubMed1983

Echocardiography in clinical pharmacology: developing new concepts on the pathophysiology of left ventricular hypertrophy in arterial hypertension.

By using echocardiography it is possible to quantify accurately and repeatedly the degree of left ventricular hypertrophy (LVH) in patients with arterial hypertension. It therefore appears to be a valuable tool for investigating the mechanisms that may be involved in the pathogenesis of this condition in hypertensive patients. The role of increased afterload in LVH induction is well established, and results of several independent laboratories concord in indicating blood pressure as a major independent factor in the pathogenesis of LVH in hypertensive patients. The role of factors other than blood pressure has not yet been fully established, however, in this setting. Animal and human studies from different laboratories are providing conflicting results on the possible role of factors such as the catecholamines or the renin-angiotensin system as additional stimuli facilitating LVH development. Clinical pharmacology could be a useful tool in seeking to clarify this important question. Drugs that lower blood pressure without consistently affecting the humoral factors possibly responsible for LVH might be expected to induce a lesser degree of LVH reversal than drugs that lower blood pressure while at the same time reducing or inhibiting the factors responsible for LVH. This experimental approach raises several methodological and technical points which are crucial in the trial planning stages. The question whether borderline hypertensive patients should be considered separately from stable hypertensive patients in the search for relationships between LVH and possible pathogenic factors is also discussed.

Animals↗
PubMed1983

[Hemodynamic and humoral changes in long-distance athletes].

Cardiac anatomy and function, and some biohumoral parameters, have been examined in 11 long-distance olympic runners, and in 11 healthy untrained control subjects. Echocardiographic methods and computed reading of tracings were adopted. Long-distance runners were also studied within 2 minutes after the end of a 30 Km race. At rest, the athletes had thicker interventricular septa and, posterior walls, higher left ventricular mass index, larger end-diastolic dimensions, cardiac index and stroke index compared to the untrained subjects (all P less than 0.01). Resting heart rate was lower in runners (P less than 0.01). In runners, competitive exercise test induced significant haemodynamic changes (increases in cardiac index, heart rate, stroke index, ejection fraction [all P less than 0.01], decreases in end-systolic dimensions and peripheral vascular resistance [both P less than 0.01]). After exercise, runners showed massive increases both of norepinephrine and epinephrine serum levels (measured in 4 subjects), an increase, in haematocrit and plasma glucose concentration, and a decrease in plasma potassium concentration (all P less than 0.01). In conclusion, olympic long-distance runners have increased cardiac dimensions and wall thickness at rest as compared with healthy untrained subjects matched for age and resting blood pressure. In the former group, a competitive long-distance test results in marked haemodynamic changes, with massive increase in plasma catecholamine concentration and concomitant reduction in plasma potassium concentration. This combination is potentially hazardous, and warrants further investigation.

Cardiac Output↗
PubMed1983

Effects of hydrochlorothiazide combined with amiloride in atenolol-resistant hypertensive patients.

Twenty hypertensive outpatients WHO stage I or II, with supine diastolic blood pressure greater than or equal to 95 mmHg at the end of a 4-week treatment period with atenolol (Tenormin) 100 mg daily, continued atenolol in free association with half a tablet of Moduretic (i.e., hydrochlorothiazide 25 mg + amiloride 2.5 mg) for a further 4 weeks. Atenolol monotherapy induced a drop of systolic blood pressure from 175.0 +/- 11 (mean +/- s.d.) mmHg to 158.7 +/- 6 mmHg (p less than 0.01), and of diastolic blood pressure from 113.5 +/- 8 mmHg to 102.7 +/- 5 mmHg (p less than 0.01). After 4 weeks with atenolol in association with half a tablet of Moduretic, systolic blood pressure further decreased to 145.7 +/- 8 mmHg (p less than 0.01), and diastolic blood pressure to 90.2 +/- 10 mmHg (p less than 0.01). Seven out of 20 patients remained with diastolic blood pressure greater than or equal to 95 mmHg despite the above combination therapy. In these patients, the doubling of diuretic dose (hydrochlorothiazide 50 mg + amiloride 5 mg) in combination with atenolol resulted in a further drop in systolic pressure (to 142.1 +/- 9 mmHg) and diastolic (to 92.1 +/- 6 mmHg) (both p less than 0.01). Plasma potassium concentration showed a slight and non-significant increase during atenolol monotherapy (from 4.4 +/- 0.5 mEq/l to 4.6 +/- 0.7 mEq/l; n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

A fixed combination of metoprolol slow-release and chlorthalidone, given once daily, in the long-term treatment of arterial hypertension.

A fixed combination of metoprolol slow-release 200 mg and chlorthalidone 25 mg was given once daily over a 3 months period in forty out-patients with mild-to-moderate arterial hypertension stage I or II WHO. The combination elicited a clear-cut antihypertensive effect lasting at least 24 hours after drug. As compared with pre-treatment values, systolic and diastolic blood pressures were gradually reduced within the first month of treatment, remaining nearly constant in the following 2 months. Treatment was well tolerated by all patients. Neither serum potassium nor any other laboratory test (creative, glucose, uric acid, etc) showed significant changes. In conclusion, slow-release metoprolol fixed association with chlorthalidone provides a safe and effective treatment of arterial hypertension even on a long-term basis. The once daily dosing schedule may considerably improve patient's compliance.

Adult↗
PubMed1981

[Exercise tolerance in angina patients 3 and 24 hours after administration of a new delayed-action preparation of metoprolol].

To assess the duration of improved exercise tolerance by metoprolol given in a new sustained-release formulation, 40 in-patients affected by stable exercise-induced angina pectoris received single-blind placebo in day 1 and thereafter, in double-blind cross-over once daily administration, metoprolol RETARD 100 mg and 200 mg in days 3 and 5. Symptom-limited cycloergometric exercise tests were performed at 3 and 24 hours after placebo and after each of the two doses of metoprolol RETARD. Duration of exercise, maximal workload and total work performed did significantly increase at 3 and 24 hours after metoprolol RETARD 100 mg (P less than 0.01) and 200 mg (P less than 0.01), without any significant difference between the two doses. Peak systolic arterial pressure and heart rate were lowered by metoprolol RETARD 200 mg at 3 (P less than 0.01) and 24 (P less than 0.01) hours, whereas only the peak heart rate at 3 hours was lowered (P less than 0.05) by the 100 mg dose. It is concluded that in patients with stable exercise-induced angina pectoris, metoprolol RETARD 200 mg appears to be able to increase exercise tolerance and to reduce exercise-induced myocardial oxygen consumption throughout 24 hours period. This may justify a once daily dosing schedule of the 200 mg dose, aimed at improving patient compliance.

Adult↗
PubMedDate not supplied

Prognostic significance of serial changes in left ventricular mass in essential hypertension.

BACKGROUND: Increased left ventricular (LV) mass predicts an adverse outcome in patients with essential hypertension. The purpose of this study was to determine the relation between changes in LV mass during antihypertensive treatment and subsequent prognosis. METHODS AND RESULTS: Procedures including echocardiography and 24-hour ambulatory blood pressure (BP) monitoring were performed in 430 patients with essential hypertension before therapy and after 1217 patient-years. Months or years after the follow-up visit, 31 patients suffered a first cardiovascular morbid event. The patients with a decrease in LV mass from the baseline to follow-up visit were compared with those with an increase in LV mass. There were 15 events (1.78 per 100 person-years) in the group with a decrease in LV mass and 16 events (3.03 per 100 person-years) in the group with an increase in LV mass (P=.029). In a Cox model, the lesser cardiovascular risk in the group with a decrease in LV mass (hazard ratio [HR], 0.46; 95% CI, 0.22 to 0.99) remained significant (P=.04) after adjustment for age (HR, 1.06; 95% CI, 1.03 to 1.10; P=.0008) and baseline LVH at ECG (HR, 3.85; 95% CI, 1.52 to 9.78; P=.012). In that model, baseline LV mass bordered on statistical significance (HR, 1.01; 95% CI, 1.00 to 1.03; P=.06). In the subset with LV mass > 125 g/m2 at the baseline visit (26% of subjects), the event rate was lower among the subjects who achieved regression of LVH than in those who did not (1.58 versus 6.27 events per 100 person-years; P=.002). This difference held in the multivariate analysis (HR, 0.18; 95% CI, 0.05 to 0.68). CONCLUSIONS: In essential hypertension, a reduction in LV mass during treatment is a favorable prognostic marker that predicts a lesser risk for subsequent cardiovascular morbid events. Such an association is independent of baseline LV mass, baseline clinic and ambulatory BP, and degree of BP reduction.

Blood Pressure Monitoring, Ambulatory↗
PubMedDate not supplied

Systolic time intervals as possible predictors of pressure response to sustained beta-adrenergic blockade in arterial hypertension. A within-patient, placebo-controlled study.

Systolic time intervals (STI) were recorded at rest and during isometric exercise (IHG) in 20 hypertensive outpatients, WHO Stage 1 or 2. In a double-blind crossover study, slow-release metoprolol 200 mg once daily and matched placebo were given for 4 weeks each, at the end of a 2-week placebo washout. Blood pressure and STI were taken in the last day of washout and of either crossover period. Treatment decreased blood pressure and heart rate values at rest and on peak IHG; it didn't modify preejection period index (PEPI), left ventricular ejection time index (LVETI), and their ratio at rest, but decreased the ratio between diastolic blood pressure and PEPI (DBP/PEPI ratio) at rest and on peak IHG and lengthened the PEPI at peak IHG. Resting PEPI values on placebo treatment showed a negative correlation with systolic (r = -0.72) as well as diastolic (r = -0.80) pressure reduction on slow-release metoprolol as compared with placebo treatment. The PEP/LVET ratio at rest on placebo treatment showed a negative correlation with systolic (r = -0.78) as well as diastolic (r = -0.82) pressure reduction at rest on metoprolol compared with placebo treatment. Patients with a resting PEP/LVET ratio less than 0.43 showed a reduction in both systolic and diastolic pressure approximating or exceeding 20 mm Hg, whereas patients with a PEP/LVET ratio greater than 0.47 showed a decrease in systolic and diastolic blood pressure of less than 10 mm Hg. In patients with a PEP/LVET ratio of 0.43 to 0.47 (50% of the trial population), STI didn't show any correlation with the pressure response to beta-blockade. A positive correlation was found between the DBP/PEPI ratio at rest on placebo treatment and systolic (r = 0.56) as well as diastolic (r = 0.76) pressure reduction at rest on slow-release metoprolol compared with placebo treatment. Thus, STI appeared as promising predictors of the magnitude of blood pressure response to sustained beta-blocking therapy in mild-to-moderate essential hypertension, mostly in patients with a resting PEP/LVET ratio less then 0.43 or greater then 0.47.

Adult↗
PubMedDate not supplied

Low-dose captopril therapy in mild and moderate hypertension. Randomized comparison of twice daily vs three times daily doses.

We have investigated the antihypertensive activity of relatively low daily doses of captopril in patients with mild and moderate arterial hypertension. In a first trial, at the end of a 2-week placebo washout period, 18 patients with essential hypertension WHO Stage I or II were treated with captopril, 25 mg three times daily (t.i.d.), 25 mg twice daily (b.i.d.), 50 mg t.i.d., and 50 mg b.i.d., according to a randomized within-patient open design, with each regimen lasting for a 2-week period. In a second trial, 12 hypertensive patients not adequately controlled by chlorthalidone 25 mg daily as monotherapy (supine diastolic blood pressure at rest greater than 95 mm Hg), continued the diuretic treatment in combination with captopril, 25 mg t.i.d. and 25 mg b.i.d. according to a randomized within-patient open design. Analysis of variance did not reveal differences between the four captopril dosing schedules (1st trial), or between the two captopril dosing schedules (2nd trial). Both the patients on captopril monotherapy (1st trial) and those cotreated with chlorthalidone (2nd trial) showed lower systolic and diastolic blood pressure values on each captopril regimen compared to prerandomization values (all p less than 0.01). No relevant unwanted effects were noted. We conclude that in patients with mild or moderate essential hypertension, either untreated or resistant to chlorthalidone, captopril is effective in reducing blood pressure even at daily doses not exceeding 150 mg, without differences between a t.i.d. and a b.i.d. dosing schedule.

Adult↗