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Biomedical subjects

G Grassi

Publications and source records attributed to G Grassi.

At least 145 records · Page 8Linked to original sources
PubMed1995

[The intervention trial in the evaluation of antihypertensive therapy].

Several epidemiological studies carried out over the past 30 years have unequivocally shown that hypertension is a major risk factor for cardiovascular diseases, the incidence of cerebral, coronary, and peripheral artery disease being progressively higher as blood pressure values become more and more elevated. Interventional clinical trials have also shown that antihypertensive treatment is able, by decreasing high blood pressure values, to reduce the cardiovascular risk profile of the hypertensive patient, although not to normalize it. Furthermore, antihypertensive treatment has been demonstrated to be more effective in protecting against stroke and congestive heart failure than against coronary artery disease. This paper will review the results of the various interventional trials carried out in hypertensive states of different clinical severity and in isolated systolic hypertension of the elderly. It will also briefly discuss the peculiar features of the ongoing interventional clinical trials, whose results will allow clarification of important and still unsolved issues concerning antihypertensive therapy.

Aged↗
PubMed1995

[The role of the sympathetic nervous system in essential arterial hypertension and organ damage].

Experimental evidence collected in animals and man supports the concept that adrenergic neural factors may be involved in the development of the hypertensive state and hypertension-related cardiovascular and metabolic complications. The various methodological approaches employed in evaluating sympathetic tone in man have shown that a hyperadrenergic state is evident in the early hypertensive phases. Sympathetic activation becomes more evident in stable hypertension and contributes to the maintenance of high blood pressure values. Adrenergic factors are also involved in the pathogenesis of cardiac and vascular hypertrophy, i.e. cardiovascular hypertensive complications that in the past have been regarded as mainly dependent on hemodynamic mechanisms. Sympathetic overactivity may also play an important role in the atherogenic process and may contribute to the insulin resistance state that often characterizes the hypertensive patient. The role of neural sympathetic factors in the pathophysiology of hypertension and its complications suggests that modulation of sympathetic activity should be an important target of modern antihypertensive treatment, aimed not only at lowering blood pressure, but also at reducing the patient's cardiovascular risk profile.

Animals↗
PubMed1994

Surgical pathology of valve disease in the elderly.

Since age is no longer considered an additional risk factor for cardiac surgery, the epidemiology of valve disease in the elderly at present may be estimated from the surgical pathology evaluation of valve specimens which are resected at the time of valve replacement. In the time interval 1991-1993, 500 patients underwent native cardiac valve replacement or repair at our University, with a total of 549 valves available for gross and histological examination. Single valve surgery was performed in 451 patients (300 aortic, 148 mitral, 3 tricuspid), and double valve replacement in 49 (47 mitral-aortic, 1 aorto-tricuspid and 1 mitral-tricuspid). Two hundred and eighteen patients (44%) were older than 65 years; the mean age was 70.4 +/- 4.3 years, and the male to female ratio was 0.9 to 1. Two-thirds of the interventions in the elderly group were aortic operations. However, regardless of the age group, 50 and 60% of the cases with respectively aortic and mitral valve disease were due to rheumatic disease. Age-related degenerative valve diseases were prominent; senile dystrophic calcification with aortic stenosis mostly in the elderly, anuloaortic ectasia with aortic incompetence mostly in adults, and floppy valve with mitral incompetence in both age groups. Bicuspid aortic valve, a congenital anomaly which is silent until adulthood, accounted for both aortic stenosis and stenoincompetence by dystrophic calcification, and pure aortic incompetence by endocarditis or anuloaortic ectasia. Our findings suggest that although age-related degenerative valve diseases are increasing, rheumatic disease still remains the leading cause of valve dysfunction in our country even in the elderly. These data may have an impact on prevention strategies and health-care costs. However, it has to be pointed out that the high prevalence of rheumatic disease is a feature of this particular study but is different from the findings of other studies around the world.

Adolescent↗
PubMed1994

Hypertension--when is the clinical problem solved? When patients are rendered normotensive.

Hypertension is usually symptomless and associated with little or no alterations in well-being. However, conclusive evidence demonstrates that hypertension is a major risk factor for cardiovascular disease. A reduction of the elevated blood pressure with antihypertensive medication can reduce this risk, but not to that of a normotensive patient. Furthermore, antihypertensive treatment is more effective against stroke and congestive heart failure than against coronary heart disease. Antihypertensive treatment is costly due to its extensive use and life-long indication. Future progress in this area will aim to identify those hypertensive patients at greatest risk of cardiovascular disease, in order to limit treatment to those patients who may benefit most. This paper will consider the effects of blood pressure reduction on cardiovascular morbidity and mortality, the differing effects of antihypertensive treatment on the complications of hypertension, and how antihypertensive therapy can be optimized.

Antihypertensive Agents↗
PubMed1994

Mechanisms responsible for sympathetic activation by cigarette smoking in humans.

BACKGROUND: The pressor and tachycardic effects of cigarette smoking are associated with an increase in plasma catecholamines, suggesting the dependence of these effects on adrenergic stimulation. Whether the stimulation occurs at a central or a peripheral level and whether reflex mechanisms are involved is unknown. METHODS AND RESULTS: In nine normotensive healthy subjects (age, 33.0 +/- 3.5 years, mean +/- SEM), we measured blood pressure (Finapres device), heart rate (ECG), calf blood flow and vascular resistance (venous occlusion plethysmography), plasma norepinephrine and epinephrine (high-performance liquid chromatography assay), and postganglionic muscle sympathetic nerve activity (microneurography from the peroneal nerve) while subjects were smoking a filter cigarette (nicotine content, 1.1 mg) or were in control condition. Cigarette smoking (which raised plasma nicotine measured by high-performance liquid chromatography from 1.0 +/- 0.9 to 44.2 +/- 7.1 ng/mL) markedly and significantly increased mean arterial pressure (+13.2 +/- 2.3%), heart rate (+30.3 +/- 4.7%), calf vascular resistance (+12.1 +/- 4.9%), plasma norepinephrine (+34.8 +/- 7.0%), and plasma epinephrine (+90.5 +/- 39.0%). In contrast, muscle sympathetic nerve activity showed a marked reduction (integrated activity -31.8 +/- 5.1%, P < .01). The reduction was inversely related to the increase in mean arterial pressure (r = -.67, P < .05), but the slope of the relation was markedly less (-54.1 +/- 7.5%, P < .05) than that obtained by intravenous infusion of phenylephrine in absence of smoking. The hemodynamic and neurohumoral changes were still visible 30 minutes after smoking and occurred again on smoking a second cigarette. Sham smoking was devoid of any hemodynamic and neurohumoral effect. CONCLUSIONS: These data support the hypothesis that in humans the sympathetic activation induced by smoking depends on an increased release and/or a reduced clearance of catecholamines at the neuroeffector junctions. Central sympathetic activity is inhibited by smoking, presumably via a baroreceptor stimulation triggered by the smoking-related pressor response. The baroreflex is impaired by smoking, however, indicating that partial inability to reflexly counteract the effect of sympathetic activation is also responsible for the pressor response.

Adult↗
PubMed1994

Physical training and baroreceptor control of sympathetic nerve activity in humans.

In nine sedentary subjects (16.5 +/- 0.4 years, mean +/- SEM) we measured blood pressure (Finapres device), heart rate (electrocardiogram), and postganglionic muscle sympathetic nerve activity (microneurography from the peroneal nerve) at rest and during intravenous infusion of phenylephrine and nitroprusside. These measurements were performed before and after 10 weeks of endurance training (2 h/d, 5 d/wk) that increased maximum oxygen consumption from 34.8 +/- 2.1 to 40.4 +/- 1.8 mL/kg per minute (P < .02). Basal mean blood pressure and muscle sympathetic nerve activity were lower after than before endurance training (86.5 +/- 2.6 versus 97.5 +/- 1.8 mm Hg, P < .05, and 14.0 +/- 1.8 versus 21.2 +/- 2.3 bursts per minute, P < .02), and the changes in these variables were closely related (r = .95, P < .01). Similar mean blood pressure increases induced by phenylephrine caused greater reductions in heart rate and muscle sympathetic nerve activity after than before endurance training (-8.6 +/- 0.8 versus -6.1 +/- 1.1 beats per minute, P = NS, and -78.0 +/- 4.6% versus -53.6 +/- 4.8%, P < .05). Likewise, similar mean blood pressure reductions induced by nitroprusside caused greater increases in heart rate and muscle sympathetic nerve activity after than before endurance training (18.6 +/- 3.0 versus 12.4 +/- 2.4 beats per minute, P < .05, and 128.1 +/- 26% versus 63.2 +/- 11%, P < .02). No alteration in hemodynamics, oxygen consumption, muscle sympathetic nerve activity, and baroreceptor reflex sensitivity occurred in four other age-matched sedentary subjects studied before and after a 10-week observation period without endurance training.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

[Physiopathologic and clinical features of hypertensive cardiopathy].

Several studies, performed during the past 20 years in different experimental animal models of hypertension and in men, have allowed to clarify important pathophysiological and clinical aspects of the hypertensive cardiovascular disease, i.e. the pathological condition characterized by marked structural and functional alterations of the heart induced by arterial hypertension. Epidemiological studies have indeed clearly shown that the prevalence of left ventricular hypertrophy in large hypertensive population samples is markedly high (40-50%) and that the electrocardiographic evidence of cardiac hypertrophy adversely affects patient's prognosis, by significantly increasing cardiovascular morbidity (myocardial infarction, congestive heart failure and cardiac arrhythmias) and mortality (sudden death). It has also been shown that cardiac hypertrophy is characterized by profound functional alterations in myocardial contractility and impairs neural reflex responses to beta-adrenergic stimulation and to deactivation of cardiopulmonary volume receptors, which are involved in physiological conditions in blood volume homeostasis control. Finally, several interventional studies have unequivocally shown that antihypertensive drugs may allow to obtain, even following 3-6 months of treatment, along with a blood pressure reduction, a clearcut regression of cardiac hypertrophy. By improving cardiovascular hemodynamics and neural control of circulation, regression of cardiac structural alterations is associated with a significant reduction in the patient's cardiovascular risk profile.

Humans↗
PubMed1994

Mid-term results of heart transplantation in diabetic patients.

BACKGROUND: Diabetes mellitus (DM) has been considered a relative contraindication to heart transplantation (HTx) because of possible increased infection rates and worsening DM with prednisone immunosuppression. The introduction of cyclosporine has allowed us to reduce the dosage of oral steroids and to accept DM patients (pts) for HTx. We reviewed the mid-term outcome of our DM pts who had undergone HTx. MATERIALS AND METHODS: Out of 257 HTx recipients, 19 males and 3 females, aged 53 +/- 8 years, were diabetic. Prior to HTx, DM was controlled with insulin in 5, with oral hypoglycemic agents in 7 and with diet in the remaining patients. Immunosuppression consisted of cyclosporine and azathioprine; low-dose prednisone was added in 10 patients because of repeated rejections. RESULTS: All patients survived HTx and were followed 2 to 75 (mean 38 +/- 21) months. There were 4 late deaths, with actuarial survival of 84% at 5 years. DM was more difficult to control after HTx (12 patients requiring insulin vs 5 pre-HTx), but comparison of diabetic vs non diabetic patients following HTx showed no significant difference in frequency of rejection or infection during the 1st year (2.6 +/- 1.6 vs 2.1 +/- 1.5; 0.5 +/- 0.4 vs 0.4 +/- 0.3 episode/patient respectively) and in 5-year actuarial survival (84% vs 77%). Renal function is preserved in all DM patients, hypertension has developed in 11/18 (61%); annual post-HTx cardiac catheterisation has shown normal graft function and coronary arteries in all but 2 patients. CONCLUSIONS: Mid-term results indicate that HTx can be safely performed in diabetic patients; a longer follow-up is required to determine whether DM is no longer a contraindication to HTx.

Actuarial Analysis↗
PubMed1994

Hemodynamic and neural effects of urapidil and prazosin in essential hypertensives.

Assessment of the effects of antihypertensive drugs on sympathetic cardiovascular modulation is aimed not only at exploring the neural mechanisms of the hypotensive action of different pharmacological compounds but also at evaluating the effects of these drugs on neural cardiovascular homeostatic control. This paper, after reviewing the effects of different antihypertensive drugs on efferent postganglionic muscle sympathetic nerve activity directly assessed in man via the microneurographic technique, will report the preliminary results of a study we have recently performed in 12 untreated mild essential hypertensives. This study was aimed at examining the effects of a single oral administration of either the hybrid drug urapidil (30 mg) or the pure alpha-blocker prazosin (2 mg) on arterial blood pressure (Finapres technique), heart rate (electrocardiogram) and muscle sympathetic nerve activity (microneurography at the peroneal nerve). For similar blood pressure reductions, urapidil caused a lesser degree of tachycardia in comparison with prazosin (+5.1 +/- 1.2 vs +8.4 +/- 0.8 beats/min, p < 0.05) but superimposable increases in muscle sympathetic nerve traffic (+15.4 +/- 2.8 vs 17.5 +/- 3.5 bursts/min). These results suggest that the two drugs induce similar degrees of blood pressure reduction as well as of muscle sympathetic activation. Urapidil, however, is accompanied by less tachycardia than prazosin, presumably because of a selective drug's action on either parasympathetic or sympathetic modulation of heart rate, triggered by the stimulation of central 5HT1A-receptors.

Administration, Oral↗
PubMed1994

[Neurohumoral mechanisms in cardiocirculatory decompensation].

Congestive heart failure is characterized by profound alterations in systemic haemodynamics as well as in neurohumoral profile with activation of the sympathetic nervous system, reninangiotensin axis, plasma vasopressin and atrial natriuretic peptides, i.e. factors involved in homeostatic control of the cardiovascular system. The sympathetic stimulation, which has been documented by a variety of methodological approaches (plasma norepinephrine measurement, norepinephrine spillover technique, microneurographic recording of efferent post-ganglionic muscle sympathetic nerve traffic) is already evident in the initial stages of the disease (NYHA classes I-II) and more manifest in severe heart failure (NYHA classes III-IV). Although representing in mild heart failure a compensatory mechanism aimed at preserving cardiac output, the sympathetic and neurohumoral activation, which can be likely ascribed to arterial baroreceptor dysfunction, may represent, in the clinical course of the disease, a maladaptative phenomenon. Thus pharmacological treatment of heart failure should be aimed not only at improving systemic haemodynamics but also at reversing neurohumoral activation and baroreflex impairment. Recent experimental clinical evidence suggests that these therapeutical goals can be satisfactorily achieved by digitalis glycosides and ACE-inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Acute effects of smoking on radial artery compliance in humans.

OBJECTIVE: To clarify whether the acute and marked increase in blood pressure associated with smoking is accompanied by an alteration in arterial compliance. DESIGN: Arterial compliance was measured in 13 subjects before and after smoking a cigarette with a nicotine content of 1.2 mg, or before and after sham smoking. Measurements were obtained with the subjects at rest and after prolonged brachial artery occlusion (12 min). METHODS: Compliance was measured using an echo-tracking system capable of continuously providing (300 readings/s) radial diameter data and, with the addition of a photoplesythmographic device, blood pressure measurement. RESULTS: Acute cigarette smoking caused a pressor and tachycardic response, and decreased markedly both resting radial artery diameter and compliance, at blood pressure values identical to those before smoking. The marked increase in radial artery diameter and compliance brought about by local ischaemia was unaffected by smoking, and no changes were observed both at rest and after ischaemia as a result of sham smoking. CONCLUSIONS: Smoking causes a marked reduction in radial artery compliance, and the effect is independent of the increase in blood pressure. However, the marked increase in compliance due to ischaemia is not modified by smoking.

Adult↗
PubMed1994

[Contusion of the liver. Importance of associated lesions in polytraumatized patients].

Between January 1984 and June 1993, we treated 120 contusions of the liver in a situation of polytrauma. There were 24 patients in Stage I, 47 in Stage II, 22 in Stage III, 13 in Stage IV and 14 in Stage V according to the Organ Injury Scaling Committee of the American Association for the Surgery of Trauma. A total of 107 patients were operated. Polytrauma related mortality was high. Besides the gravity of the liver lesion, prognosis was a function of other associated intra or extra abdominal lesions. In our series, other associated lesions were the cause fo death in 26 patients (64%) and 15 deaths (36%) were directly related to the hepatic lesion. The gravity of the Stage V lesions was related both to the state of shock of operation and the difficulties in reestablishing haemostasis. Packing decreased the effect of hypovolaemia and coagulopathy. The prognosis of supra hepatic venous lesions and hepatic resections remain disastrous. Our surgical schema has changed towards more conservative surgery and, when haemodynamic stability has been achieved, to abstention and careful monitoring. Different extra-hepatic trauma causing damage to other organs directly compromises simple hepatic lesions. The result of our series confirms the correlation between mortality and the gravity of the polytrauma as evaluated according to the Injury Severity Score proposed by Baker.

Abdominal Injuries↗