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Biomedical subjects

C Giannattasio

Publications and source records attributed to C Giannattasio.

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

New aspects of antihypertensive treatment. Metabolism, the kidney and the heart.

This paper briefly reviews recent evidence concerning the relationship between hypertension and alterations in glucose and lipid metabolism and renal and cardiac damage. It is now clear that high blood pressure is frequently associated with insulin resistance and dyslipidaemia. This suggests a possible pathogenetic link between hypertension and deranged metabolism. It also suggests, however, that the hypertensive patient is likely to have other cardiovascular risk factors in addition to hypertension. It is also clear that lowering blood pressure may not only reduce the overall cardiovascular risk but may be specifically nephro- and cardioprotective. However, it is difficult to assess the effect of antihypertensive treatment in these areas, because there are no simple and sensitive measures of the progression of renal disease, and antihypertensive therapy does not provide consistent protection against coronary heart disease. Furthermore, the degree of protection obtained is less than would be expected on the basis of epidemiological evidence. Further trials are needed to fully resolve these issues.

Animals↗
PubMed1993

Vasovagal syncope with bradycardia during lower body negative pressure in a heart transplant recipient.

Vasovagal syncope has been ascribed to the vagal excitation and the sympathetic inhibition induced reflexly by mechanical stimulation of receptors in the ventricles. In this case report we describe a vasovagal syncope with bradycardia triggered by a reduction in venous return obtained via mild lower body negative pressure, in a patient with cardiac denervation due to heart transplantation. This suggests that the mechanisms involved in this phenomenon may not exclusively depend on a reflex originating from ventricular receptors. It also suggests that non-neural factors may be involved in the genesis of the bradycardia.

Blood Pressure↗
PubMed1993

[Hypertension, left ventricular hypertrophy and heart failure].

Epidemiological and clinical studies carried out over the past 30 years have unequivocally shown that cardiac hypertrophy is frequently associated with high blood pressure values adversely affecting, from a pathophysiological and prognostic view point, the clinical evolution of the hypertensive disease. From a pathophysiological view point, it has been reported that a pathologic increase in cardiac wall thickness not only impairs diastolic function, coronary circulation and reflex control of circulation exerted by cardiopulmonary volume receptors, but also enhances cardiac work and myocardial oxygen consumption. From a clinical view point, cardiac hypertrophy has been shown to increase the risk of occurrence of cardiac arrhythmias, myocardial infarction, heart failure and sudden cardiac death. Antihypertensive drugs, such as ACE-inhibitors, calcium antagonists and alpha and beta-blocking agents, by reducing high blood pressure values and concomitantly by favouring the regression of the echo- and electrocardiographic signs of cardiac hypertrophy, have been shown to physiologically restore normal cardiac function and reflex homeostatic cardiovascular control.

Heart Failure↗
PubMed1993

RAA system and cardiovascular control in normal subjects, hypertensives and patients with congestive heart failure.

The involvement of the renin-angiotensin-aldosterone (RAA) system, particularly angiotensin II, in the pathogenesis of hypertension is widely acknowledged and is supported by several observations: the RAA system has been shown to be critically involved in the development of some experimental hypertensions; activation of the RAA system appears to be the crucial factor involved in the maintenance of the BP elevation in some antihypertensive patients; while drugs which interfere with the production of angiotensin II reduce BP in a large number of hypertensive patients. It is now clear that the chronic BP elevations caused by circulating (and perhaps locally produced) angiotension II may have adverse effects on organ function and protection: for example, induction of cardiac hypertrophy and vascular hypertrophy and/or hyperplasia, reduction of arterial compliance and reduction in vagal tone and facilitation of sympathetic activity on cardiac and vascular targets. At the cardiac level, the renin-angiotensin sympathetic interaction may enhance electrical instability, thereby favouring arrhythmias and increasing mortality after a myocardial infarction. It finally enhances coronary vasoconstriction in man, producing or favouring myocardial ischaemia.

Angiotensin II↗
PubMed1992

Reflex cardiovascular control in congestive heart failure.

This article reviews evidence that the reflex control of the cardiovascular system provided by negative feedback mechanisms is impaired in congestive heart failure (CHF). The impairment involves vagal and sympathetic modulation of the heart exerted by arterial baroreceptors. It also affects baroreceptor control of blood pressure and peripheral vascular resistance, as well as the cardiopulmonary receptor's ability to modulate sympathetic activity. The degree of such impairment is most marked in severe CHF but is also apparent, to a minor degree, in mild heart failure. Reflex impairment is due to a reduction in the receptor signal, but other factor under investigation are probably also involved. Digoxin and other pharmacologic treatments of CHF improve reflex function, thereby facilitating a reduction in the elevated sympathetic activity and a stepping up of the reduced vagal activity typical of CHF. This may be relevant to a patient's prognosis.

Animals↗
PubMed1992

Cardiopulmonary receptor and arterial baroreceptor reflexes after acute myocardial infarction.

The baroreceptor-heart rate reflex in human is impaired 2 days after a myocardial infarction but it improves 10 days after the acute coronary event. This study investigated whether (1) the baroreceptor-heart rate reflex improvement takes the reflex back to normal, and (2) the cardiopulmonary reflex is affected by myocardial infarction. In subjects studied 8 to 11 days after a transmural anterior or inferior myocardial infarction the baroreceptor-heart rate reflex sensitivity (slope of the linear regression between negative neck chamber pressures and lengthenings in RR interval) was similar to that seen in control subjects (-6.2 +/- 0.8 vs -6.0 +/- 0.6 ms/mm Hg, mean +/- SEM) and did not change when reassessed 10 days later. In contrast, the cardiopulmonary reflex sensitivity (changes in forearm vascular resistance induced by changing central venous pressure through nonhypotensive lower body suction and leg raising) was markedly less in subjects studied 8 to 11 days after myocardial infarction than in control subjects; the reduction amounted to 58.1 +/- 8% (p less than 0.01). The cardiopulmonary reflex sensitivity greatly improved when reassessed 28 to 45 days later. Thus, the baroreflex is normal about 10 days after myocardial infarction. This condition markedly impairs the cardiopulmonary reflex, but the impairment is also transient.

Blood Pressure↗
PubMed1992

Effect of detraining on the cardiopulmonary reflex in professional runners and hammer throwers.

In professional athletes with marked cardiac hypertrophy, reflex influences originating from cardiopulmonary receptors are impaired. To determine whether the reflex is restored after termination of physical training and regression of cardiac hypertrophy 8 former athletes (age 31 +/- 6 years, mean +/- SD) who stopped agonistic activity for 5 +/- 1 years were compared with 15 sedentary subjects (27 +/- 7 years) and 19 active professional athletes (22 +/- 7 years). Cardiopulmonary receptor stimulation and deactivation were obtained by increasing and reducing left ventricular end-diastolic diameter (echocardiography) through leg raising and nonhypotensive lower body negative pressure, respectively. Left ventricular mass index (echocardiography) was markedly and significantly (p less than 0.01) greater in athletes (135 +/- 6 g/m2) than in former athletes (105 +/- 4 g/m2) whose value was similar to that of sedentary subjects (98 +/- 4 g/m2). The reduction in forearm vascular resistance and plasma norepinephrine induced by increasing left ventricular end-diastolic diameter was 24 and 23% less in athletes than in former athletes whose responses were similar to those of sedentary subjects. This was the case also for the responses induced by reducing left ventricular end-diastolic diameter. In contrast, the hemodynamic responses to cold pressor test were similar in the 3 groups. It is concluded that the impairment of the cardiopulmonary reflex observed in athletes is largely reversible when physical training is terminated. This may be due to regression of left ventricular hypertrophy.

Adaptation, Physiological↗
PubMed1992

Ambulatory blood pressure monitoring and antihypertensive treatment.

This paper outlines the advantages of ambulatory blood pressure monitoring (ABPM) in the evaluation of the efficacy of antihypertensive drugs. The main advantage is that ABPM allows the antihypertensive effect of a drug or drug regimen to be determined in daily life conditions and to uncover whether the treatment employed is associated with untoward hypotensive episodes. Furthermore, ABPM facilitates the design of studies on antihypertensive drug efficacy because the 24 h mean blood pressure is devoid of a placebo effect and its reproducibility is much greater than office blood pressure. This has permitted demonstration of the efficacy of several antihypertensive drug regimens, including diuretic studies, based on relatively small numbers of subjects. A further advantage of ABPM is that it allows drug treatment efficacy to be evaluated in relation to blood pressure variability, another possible determinant of the organ damage related to hypertension.

Antihypertensive Agents↗
PubMed1992

Sympathomoderating influence of benazepril in essential hypertension.

OBJECTIVE: In essential hypertension, captopril attenuates forearm vasoconstriction reflexly induced by deactivation of cardiopulmonary and arterial baroreceptors, thus exerting a sympathomoderating effect. We investigated whether this is a common effect of angiotensin converting enzyme (ACE) inhibitors. METHODS AND DESIGN: Cardiopulmonary and arterial baroreceptors were deactivated by progressively reducing central venous pressure (CVP) through progressively greater lower body negative pressures in eight untreated mild essential hypertensives on a moderately low-sodium diet (50 mmol/l per day). This deactivation was performed after oral administration of the non-sulphidrylic ACE inhibitor benazepril (10 mg) and placebo according to a double-blind randomized crossover experimental design. RESULTS: After placebo, the reduction in CVP increased forearm vascular resistance (FVR; mean arterial pressure: plethysmographic forearm blood flow ratio). After benazepril, baseline blood pressure (beat-to-beat finger pressure) and FVR were significantly reduced whilst plasma angiotensin II was suppressed and PRA increased (both measured by radioimmunoassay). The FVR increases induced by progressive CVP reduction were less than after placebo administration, and the overall difference was statistically significant. Benazepril did not affect the reflex FVR reduction observed by increasing CVP through leg raising, nor the reflex changes in plasma norepinephrine measured by high-performance liquid chromatography accompanying the changes in FVR. CONCLUSIONS: Benazepril attenuates sympathetic vasoconstriction as does captopril. This effect (which is mainly operative during an increased sympathetic drive and exerted through a reduction of adrenoceptor responsiveness) is thus likely to be a class- rather than a compound-related feature.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Effect of oral dilevalol on forearm circulation in essential hypertension.

In 7 patients with untreated mild essential hypertension, a single 200-mg dilevalol dose was administered orally. Blood pressure (BP, left brachial artery catheter), heart rate (HR), and left and right forearm blood flows were measured and left and right forearm vascular resistances were calculated before and for approximately 3 h after drug administration. Dilevalol administration was followed by a sustained reduction in BP, little change in HR, and a similar pronounced and sustained increase in left and right forearm blood flows and reduction in left and right forearm vascular resistances. At the end of the observation period, the changes in left forearm circulation were unaffected by left brachial artery infusion of saline but markedly reduced by left brachial artery infusion of propranolol at doses that had no effect on BP, HR, and contralateral forearm vasodilatation. Thus, at an oral dose exerting an antihypertensive effect, dilevalol induces a marked and persistent vasodilation due largely to the beta-adrenoceptor agonism of the drug.

Administration, Oral↗
PubMed1992

Alpha 1-blocking properties of carvedilol during acute and chronic administration.

Carvedilol is a beta-adrenergic-blocking drug with vasodilating properties. This vasodilation has been ascribed to alpha 1-adrenergic blockade, but it has never been shown in the clinical setting. We addressed this issue by studying eight patients with mild essential hypertension who were given prazosin, 2 mg or carvedilol, 25 mg p.o. following a 2-week washout from previous treatment, according to a randomized double-blind, crossover experimental design. Before and 2 h after the administration of either prazosin or carvedilol, the patients were infused i.v. with increasing doses of phenylephrine (0.2-1.2 microgram/kg/min) and isoproterenol (0.01-0.05 microgram/kg/min). The patients were thereafter maintained on carvedilol 25 mg daily for 3 weeks, and the i.v. phenylephrine and isoproterenol infusions were repeated 2 h after the last tablet administration. The results showed that the single dose of carvedilol and prazosin lowered blood pressure (beat-to-beat finger pressure measurement) to a similar extent, but that heart rate was unaffected by prazosin and reduced by carvedilol. The tachycardic response to isoproterenol was abolished by carvedilol and unaffected by prazosin, whereas the pressor response to phenylephrine was reduced by carvedilol and virtually abolished by prazosin. The antihypertensive, beta-blocking and alpha 1-adrenergic-blocking effects of carvedilol were unchanged following prolonged administration of the drug. Thus, at a clinically effective dose, carvedilol not only has beta- but also sizeable alpha 1-blocking effects. These effects are preserved during prolonged administration of the drug. For a comparable antihypertensive action, however, the alpha 1-blocking effect is less pronounced than that of an alpha 1-blocker such as prazosin.

Adrenergic alpha-Antagonists↗
PubMed1992

Changes in 24 hour blood pressure and in cardiac and vascular structure in normotensive subjects with parental hypertension.

Subjects with family history of hypertension represent a suitable model to investigate the mechanisms responsible for early cardiovascular structural and functional changes occurring in essential hypertension. In our study we have addressed the factors involved in determining the mild elevation in office blood pressure frequently observed in normotensive subjects with hypertensive parents. In 15 normotensive subjects with both parents hypertensive (FH++) and in 15 normotensive subjects with one parent hypertensive (FH(+)-) we found no evidence of a hyperreactivity to stress as compared to the responses of 15 normotensive subjects with no parental hypertension (FH--). On the contrary FH++ subjects were characterized by a significant although mild increase in their blood pressure values recorded either at rest and in ambulatory conditions over the 24 hours, including night sleep. FH++ and FH(+)- subjects also showed a greater left ventricular mass thickness and a greater minimal forearm vascular resistance than FH-- subjects. Thus, the elevation in blood pressure found in the pre-hypertensive stage in subjects with positive family history for hypertension does not reflect a hyperreactivity to the stress associated with physician's visit but indicates an early and persistent blood pressure elevation. This blood pressure elevation is accompanied by early cardiovascular structural changes which may indicate that these subjects are exposed to a higher risk even before developing overt hypertension.

Adult↗
PubMed1992

Changes in arterial compliance induced by physical training in hammer-throwers.

OBJECTIVE: Physical training induces multiple changes in the cardiovascular system which allow an increased performance along with increased oxygen consumption. The present study was designed to investigate whether the changes include an increase in arterial compliance. METHODS AND DESIGN: In six normotensive right-handed hammer-throwers (aged 21.3 +/- 1.8 years, mean +/- SE) we measured radial artery diameter continuously via a new non-invasive echo-tracking device, and beat-to-beat blood pressure. Arterial compliance was calculated by an arctangent model. In each subject measurements were made from both the left and the right arm. The data were compared with those obtained in six age-matched normotensive controls. RESULTS: Compared to the controls, the hammer-throwers had similar blood pressure, a lower heart rate and plasma norepinephrine and a higher left ventricular mass index and radial artery diameter. In the athletes, right radial artery compliance was significantly greater than either right or left radial artery compliance in the sedentary subjects (+61 and 63%, P < 0.05). It was also significantly greater than contralateral radial artery compliance (+53 +/- 8%, P < 0.05). CONCLUSIONS: Physical training is accompanied by an increase in arterial compliance. In our hammer-throwers this increase was mainly evident in the more highly trained arm, suggesting that local mechanisms are involved in this phenomenon.

Adult↗
PubMed1991

Reflex control of circulation in the elderly.

Baroreceptor control of heart rate is markedly reduced in elderly subjects. However, the effects of aging on baroreceptor control of blood pressure and on the vascular and neurohumoral influences of volume cardiopulmonary receptors are unknown. In this paper we report evidence that in both conscious rats and humans aging is associated with a fall in the baroreceptor ability to rapidly cause blood pressure changes, but that the more long-term carotid baroreceptor control of blood pressure remains similar to that observed in younger individuals. Early and late cardiopulmonary receptor modulation of vascular resistance is impaired by aging, which also reduces the influence of this reflex on renin secretion. These dynamic and steady-state alterations in reflex cardiovascular control account for several hemodynamic abnormalities of the advanced age.

Aged↗