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Biomedical subjects

D Rizzoni

Publications and source records attributed to D Rizzoni.

At least 73 records · Page 4Linked to original sources
PubMed1993

[Antihypertensive treatment and left ventricular hypertrophy].

Left ventricular hypertrophy in arterial hypertension can be considered as an adaptive response of the heart to the increased afterload, in order to reduce wall stress; however, cardiac hypertrophy can also represent the first step toward a pathological process that leads to the development of congestive heart failure. Epidemiological studies have documented that left ventricular hypertrophy in essential hypertension represents an independent risk factor for cardiovascular morbidity and mortality. The possibility of reversing, or even preventing, left ventricular hypertrophy through a reduction in elevated blood pressure values and modification of some other pathogenetic factors should represent a major therapeutic need in the treatment of hypertensive patients. It has been demonstrated that different classes of antihypertensive drugs do not have the same effect in reducing left ventricular mass, probably because beyond control of blood pressure, the pharmacological interference with adrenergic system, the renin-angiotensin-aldosterone system or other growth factors can influence the development and the reduction of cardiac hypertrophy. Two recent meta-analyses of the principal regression studies have shown that ACE-inhibitors, followed by calcium antagonists and drugs capable of reducing sympathetic nervous system activity, are more effective in decreasing left ventricular mass. The results of experimental and clinical studies have demonstrated that the reversal of cardiac hypertrophy is associated with an improvement of the functional consequences of an increased left ventricular mass. Further studies are needed in order to verify whether the reversal of left ventricular hypertrophy per se increases survival in essential hypertensive patients.

Adaptation, Physiological↗
PubMed1993

Effect of antihypertensive treatment on daytime and nighttime power spectral analysis of heart rate.

Power spectral analysis of heart rate may provide useful information about cardiac neural activity. The aim of this study was to evaluate cardiac sympathetic and parasympathetic activity, as assessed by power spectral analysis of heart rate, in hypertensive patients before and after antihypertensive treatment. In 14 hypertensive patients and in 7 normotensive subjects 24 h Holter electrocardiogram monitoring was performed under basal conditions and after 6 months of treatment with nifedipine (n = 7) or enalapril (n = 7). Sequences of 512 RR intervals were taken for the evaluation of power spectral analysis (autoregressive method); absolute and normalized power spectral density of the peak at 0.10 Hz (low frequency peak: LF) and at 0.25 Hz (high frequency peak: HF), as well as their ratio (index of sympatovagal interaction: SVI) were calculated. Under basal conditions SVI was significantly decreased from daytime to nighttime in normotensives, while no change was observed in hypertensive patients. In all hypertensive patients a reduction of SVI during nighttime in respect to basal values was observed after treatment. SVI during nighttime was significantly reduced with both nifedipine and enalapril, while SVI during daytime was slightly increased during nifedipine treatment, and significantly reduced during enalapril treatment. Systolic and diastolic arterial pressure as well as left ventricular mass index were significantly reduced with both treatments. In conclusion, long term treatment with nifedipine or enalapril seems to be able to restore an impaired daytime to nighttime SVI modulation in hypertensive patients, even considering the potential limitations of power spectral analysis of heart rate.

Adult↗
PubMed1992

Relationship between initial cardiovascular structural changes and daytime and nighttime blood pressure monitoring.

It has been shown that in hypertensive patients the degree of target organ damage correlates more closely with average blood pressure as recorded by ambulatory monitoring (ABPM) throughout 24 h than with clinic blood pressure. We examined a group of 91 clinically healthy subjects, 23 normotensives and 68 hypertensives according to clinic blood pressure. Cardiac anatomy was investigated by echocardiography. As an index of arterial structural changes forearm minimal vascular resistance was calculated from mean arterial pressure and maximal postischemic blood flow, as assessed by venous occlusion plethysmography. The results were correlated to clinic blood pressure or ABPM values (measured by noninvasive ABPM ICR 5200, Spacelabs, Bellevue, CA). Left ventricular mass was correlated more closely with the average blood pressure recorded during 24 h, or during daytime or nighttime periods, than with clinic blood pressure. Minimal vascular resistance was also significantly correlated to ABPM values, but the correlation was similar to that observed with clinic blood pressure. Minimal vascular resistance was significantly correlated to blood pressure variability, as evaluated by the standard deviation of the mean. Minimal vascular resistance and left ventricular mass were higher in a subgroup of patients in whom blood pressure was not significantly reduced during the night. The results of this study confirm that elevated average ABPM values are associated to higher left ventricular mass; in addition, they suggest that increased blood pressure variability may be associated with vascular structural changes, as evaluated by minimal vascular resistance. It remains to be clarified whether cardiac hypertrophy and/or vascular structural changes are a cause or consequence of increased blood pressure values and variability.

Adult↗
PubMed1992

Antidiuretic hormone and atrial natriuretic peptide during lower body negative or positive pressure in hypertensive patients with and without left ventricular hypertrophy.

Aim of the study was to evaluate the effect of cardiopulmonary receptors activation and deactivation on antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) incretion in hypertensive and normotensive subjects. Twenty-one male subjects, 7 normotensives and 14 mild hypertensives, 7 without and 7 with left ventricular hypertrophy (LVH) were admitted to the study. Each subject underwent selective loading and unloading of cardiopulmonary receptors, by application of a positive (LBPP) or negative (LBNP) pressure to the lower body. Blood samples were taken for measurement of ANP, ADH, PRA, immunoreactive renin, aldosterone, noradrenaline and adrenaline. ADH plasma concentration increased during cardiopulmonary receptors inhibition, but this increase became statistically significant (p less than 0.05) at a step of LBNP (-40 mm Hg), in which an involvement of the sinoaortic receptors cannot be excluded. ANP plasma levels increased progressively during LBPP (p less than 0.05 at least). These changes were significantly reduced in hypertensive patients with LVH.

Adolescent↗
PubMed1992

Reduction of left ventricular hypertrophy after longterm antihypertensive treatment with doxazosin.

The aim of this study was to evaluate the effect of antihypertensive treatment with doxazosin on left ventricular anatomy and function. Therefore, after 4 weeks of washout with placebo (phase 1), doxazosin (dosage range from 1 to 16 mg, plus hydrochlorothiazide when necessary) was given to 11 essential hypertensive patients (6 M, 5 F, age range 34-63 years) for 8 weeks (phase 2) in order to achieve diastolic blood pressure values less than 90 mmHg; this dosage was then maintained for a further 20 weeks up to the end of the study (phase 3). Blood pressure was significantly reduced (Anova P less than 0.05), while heart rate did not change. A significant reduction of left ventricular mass index (from 128.5 +/- 26 to 114 +/- 23 g/m2, at the end of phase 1 and 3 respectively, P less than .001)) was observed. Before and during treatment left ventricular systolic function, both at rest and during stress (handgrip and cold pressor tests), evaluated by fractional shortening as related to end-systolic stress, in every case within 95% confidence limits, was calculated in normal subjects. Diastolic function, as evaluated by the ratio between peak early and atrial velocities of transmitral flow examined by pulsed doppler was significantly improved. Plasma catecholamine concentrations, plasma renin activity and plasma aldosterone did not change. A significant reduction of plasma cholesterol concentration was observed. These results confirm that doxazosin is a well tolerated and effective antihypertensive drug, with a favourable effect on blood lipids and they indicate that its longterm administration can induce a significant reduction of left ventricular mass.

Adrenergic alpha-Antagonists↗
PubMed1991

Renal and hemodynamic effects of atrial natriuretic peptide infusion are not mediated by peripheral dopaminergic mechanisms.

The possible involvement of peripheral dopaminergic mechanisms in the action of atrial natriuretic peptides was investigated in 10 subjects by administering 200 micrograms h-ANP 99-126 intravenously for 30 min during treatment with 50 mg carbidopa, a peripheral inhibitor of dopamine synthesis, every 8 h, or during placebo. Atrial natriuretic peptide (ANP) infusion during placebo was associated with a significant increase of diuresis, natriuresis, kaliuresis, urinary noradrenaline, and dopamine excretion. Plasma aldosterone significantly decreased. Blood pressure was slightly reduced. The administration of carbidopa significantly reduced urinary dopamine excretion but did not modify natriuresis, diuresis, indexes of adrenergic and renin-aldosterone system activity, blood pressure, or heart rate, both in basal conditions and in response to ANP infusion. We conclude that the effects of exogenous ANP administration are independent from dopaminergic mechanisms that involve the synthesis of dopamine outside the central nervous system, particularly in the kidney.

Adult↗
PubMed1991

Improved left ventricular systolic and diastolic function after regression of cardiac hypertrophy, treatment withdrawal, and redevelopment of hypertension.

The aim of this study was to differentiate the effects of changes of arterial pressure from those of regression of left ventricular hypertrophy (LVH) on systolic and diastolic function at rest and during a rapid increase in afterload, induced by handgrip and cold pressor tests. An additional purpose was to assess the hemodynamic mechanisms responsible for the increase in arterial pressure after treatment withdrawal. Therefore, we evaluated the cardiac anatomy and function (TM echo) at rest and during handgrip and cold pressor tests in 23 hypertensive patients, before therapy and 20-30 days after withdrawal of treatment, which had lasted 6-12 months, when left ventricular mass index (LVMI) was significantly reduced (from 140 +/- 44 to 113 +/- 13 g/m2, p less than 0.001) but the arterial pressure had increased again to pretreatment values (166 +/- 19/105 +/- 7 mm Hg before treatment vs. 162 +/- 15/100 +/- 12 mm Hg). The LVMI reduction was due to a decrease in LV wall thickness, whereas the LV internal dimensions did not change. Systolic function was evaluated by the relationship between LV end-systolic stress (ESS) and fractional shortening (FS): at rest as well as at the peak of handgrip and cold pressor tests, highly significant negative correlations between ESS and FS (range of -0.71 to -0.96) were found. Considering each point of relation between ESS and FS in hypertensive patients, in comparison with 95% prediction limits of the correlation obtained in normal subjects, a "supernormal" systolic function at rest was observed in 10 of 23 patients and a reduced systolic function was not present after treatment withdrawal and redevelopment of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Regression of cardiovascular structural changes after long-term antihypertensive treatment with the calcium antagonist nitrendipine.

Regression of cardiovascular structural changes is a main goal of antihypertensive treatment. Nitrendipine is a calcium antagonist of the dihydropiridine group that may be given once daily. In different animal models of experimental hypertension, nitrendipine was shown to reduce blood pressure (BP) and left ventricular (LV) mass, to prevent early mortality, and to limit the development of vascular lesions. It has also been proposed that nitrendipine is able to preserve tissue integrity and increase life span in malignant hypertension, because it prevents a deleterious calcium overload in the heart and arterial vessels. In humans, the effect of nitrendipine on LV mass has been evaluated in a limited number of studies with conflicting results. It has been shown that nitrendipine is able to increase the compliance of large arteries; its effect on vascular structural changes has never been reported. In this study, nitrendipine (20 mg o.d.) was given to 10 hypertensive patients. BP, (ambulatory BP monitoring) heart rate (HR), LV mass and function (TM echo, 2D guided), forearm minimal vascular resistance (min VR = BP/max blood flow--venous occlusion plethysmography--taken as an index of vascular STC), plasma renin activity (PRA), plasma catecholamines (NE and E), and aldosterone (ALD) were measured during placebo, after 2 and 6 months of treatment. BP was significantly reduced and HR was slightly increased. After 6 months of treatment a significant reduction of LV mass index (p less than 0.001) and of min VR (p less than 0.002) was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Increase by ANP and ADH of the duration of activation and deactivation of the cardiopulmonary baroreceptor reflex: modification in the presence of left ventricular hypertrophy].

The involvement of cardiopulmonary and arterial sinoaortic receptors in the control of antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) release is still controversial in humans. Moreover, it is not clear if this control may be impaired in hypertensive patients with left ventricular hypertrophy (LVH). We studied 17 male subjects, age 18-58 (6 normotensives and 9 mild hypertensives, 5 without and 4 with LVH). Each subject underwent selective loading and unloading of cardiopulmonary receptors, in a randomized sequence, by application of a positive (LBPP) or negative (LENP) pressure to the lower body (steps: +10, +20, +40, -10, -40 mmHg, each for about 30 min), through a plexyglass-constructed tubular apparatus with a rubber adhesion round the patients' waist. Blood samples were taken at the end of every step for measurement of ADH, ANP, PRA, immunoreactive renin, aldosterone, noradrenaline and adrenaline. Cuff arterial pressure was measured every 5 min, while heart rate was evaluated by continuous ECG recording. Hypertensive subjects underwent right atrial pressure measurement by an iv catheter and forearm blood flow evaluation at rest and during the different steps (venous occlusion plethysmography). During LBNP, ADH plasma levels increased progressively, but the increase became statistically significant only at the step of -40 mmHg. ANP increased significantly during LBPP. Taking into account only hypertensive patients, a consistent reduction in the changes of ADH and ANP plasma levels, respectively during LBNP and LBPP in patients with LVH in respect to those without LVH was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗