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Biomedical subjects

G Grassi

Publications and source records attributed to G Grassi.

At least 163 records · Page 9Linked to original sources
PubMed1993

Endomyocardial biopsy in heterotopic heart transplant recipients via the femoral vein.

The results of endomyocardial biopsy (EMB) via the femoral vein in heterotopic heart transplant recipients were retrospectively analyzed and compared with those obtained using the right internal jugular vein approach. A total of 139 EMB were performed in 8 patients using the femoral (35) or the jugular (104) approach. Twenty three (64.7%) of the procedures performed via the femoral vein were part of the yearly hemodynamic and coronary artery study, and 12 (35.3%) constituted a routine postoperative evaluation of the myocardium rejection state in patients with imperviousness of the right internal jugular vein. Comparing the results obtained with the femoral approach, we observed a higher overall success rate (94.3 vs 88.5%, NS) and obtained more samples that were useful for histologic evaluation (95.5 vs 85.9%, NS); with the jugular procedure, the fragments were significatively larger in diameter (1.28 +/- 0.55 vs 1.61 +/- 0.85 mm, mean +/- SD) and in area (1.49 +/- 1.16 vs 2.28 +/- 2.24 mm2, mean +/- SD). No cardiac or local complications were noted when the femoral approach was used, while two attempts to perform biopsy via the jugular vein resulted in obstruction of this vessel. Our data suggest that the femoral venous approach for endomyocardial biopsy in heterotopic heart transplant recipients is a valid alternative to the more commonly used routes.

Biopsy↗
PubMed1993

Reflex vasopressin and renin modulation by cardiac receptors in humans.

Animal studies have shown that vasopressin secretion is modulated by arterial baroreceptors and cardiopulmonary volume receptors. Whether this is the case also in humans is controversial, however. To determine whether vasopressin is reflexly modulated by cardiac volume receptors, we studied the effect on plasma vasopressin (venous blood, radioimmunoassay) of reducing venous return and left ventricular end-diastolic diameter (echocardiography) by producing a 20-minute lower body negative pressure in 14 healthy subjects (aged 49.3 +/- 3.8 years, mean +/- SEM). The data were compared with those of 14 age-matched heart-transplant recipients, i.e., subjects with cardiac denervation. In healthy subjects, lower body negative pressure at -15 mm Hg caused a modest reduction in left ventricular end-diastolic diameter (-5 +/- 3.4%) and no change in vasopressin, whereas lower body negative pressure at -37.5 mm Hg caused a more marked reduction in left ventricular end-diastolic diameter (-12 +/- 2.5%) and a small, variable, but overall statistically significant (p < 0.05) increase in vasopressin (+145 +/- 46%, p < 0.01). The left ventricular end-diastolic diameter changes induced by the two lower body negative pressure stimuli were similar in heart-transplant recipients, but the vasopressin increase seen with the lower body negative pressure at -37.5 mm Hg was abolished. The marked increase in plasma renin activity and forearm vascular resistance induced by lower body negative pressure in healthy subjects was also abolished or drastically attenuated in heart-transplant recipients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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

[Arterial hypertension and myocardial infarction].

Several epidemiological and clinical studies, carried over the past 30 years, have unequivocally shown that high blood pressure is an important risk factor for development of myocardial infarction. The risk level, which has been documented for an increase both in systolic and diastolic blood pressure values, further increases when hypertension is accompanied with other conditions (e.g. hyperlipidemia, diabetes, cigarette smoking) well-known to adversely affect the cardiovascular system. Antihypertensive treatment significantly decreases, although without normalizing, the incidence of coronary events in the hypertensive patient, the reasons for this only partial cardioprotection being so far largely unknown. More complex and less documented are the relationships between hypertension and myocardial reinfarction. Although there is no doubt that high blood pressure levels increase the incidence of reinfarction, it should be emphasized that no study so far has been undertaken to clarify the effectiveness of antihypertensive treatment in reducing the risk of myocardial infarction and in improving the prognosis of the disease.

Humans↗
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

Evaluating sympathetic activity in human hypertension.

AIM: To review the use of plasma norepinephrine to evaluate sympathetic activity in humans, and to discuss the improvement in assessment of human sympathetic activity brought about by the norepinephrine spillover method and by microneurography. METHOD: Literature survey. RESULTS: These methods have limitations, and an accurate assessment of sympathetic cardiovascular control should not be limited to an investigation of sympathetic nerve firing or norepinephrine secretion but include cardiac and vascular responses. These responses can be assessed by traditional pharmacological means (for example, a reduction in vascular resistance induced by alpha-adrenergic blockade) or by a variety of approaches aimed at examining sympathetic cardiovascular modulation in a more integrated fashion, such as the recently developed power spectrum analysis of blood pressure and heart rate. CONCLUSION: The sensitivity and specificity of all these methods is still under investigation, but in almost every case an increase in sympathetic cardiovascular influence has been reported to occur in hypertension, indicating that sympathetic activation has a pathogenic effect on this condition.

Blood Pressure↗
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

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↗