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Biomedical subjects

A Zanchetti

Publications and source records attributed to A Zanchetti.

At least 199 records · Page 11Linked to original sources
PubMed1993

Evaluation of organ damage in hypertension.

INTRODUCTION: This document is the result of discussions held during a Scientific Workshop in Brescia, Italy, where the numerous methods, old and new, for evaluation of organ damage in hypertension were considered. Not all of the methods can be recommended as routine diagnostic procedures for every hypertensive subject. Current routine diagnosis of organ damage by clinic blood pressure, retinal appearances, the electrocardiogram, serum creatinine estimation and urinary analysis will probably suffice; of the more refined methods, only the echocardiogram is likely to be often included in the examination of hypertensive patients. All of the other techniques will be useful in the diagnostic approach to patients with particular problems, or for the purposes of special investigation. RECOMMENDATIONS: It is recommended that the validity of the methods, the clinical relevance of the abnormalities (including left ventricular hypertrophy, reduced coronary reserve, arterial changes in the eye grounds, reduced large artery compliance and microalbuminuria) and the potential benefits of therapeutically reverting these alterations should be assessed by including organ damage evaluation in future epidemiological and interventional trials in hypertension.

Ambulatory Care↗
PubMed1993

Ultrasonographic evaluation of cardiac and vascular changes in young borderline hypertensives.

We measured the intima-media thickness of the common carotid artery (CCA) and of its bifurcation (BIF) in 20 borderline hypertensives (age 24 +/- 4 years) and in 20 normotensive subjects (age 23 +/- 6 years), as a control group. Both carotid axes have been scanned from different views on a transversal and longitudinal section. Carotid diameter and thickness were measured in the longitudinal section. CCA parameters were assessed 20 mm caudally to the flow divider. In borderline patients blood pressure (147.8 +/- 10.5/90.7 +/- 6.6 mm Hg) and left ventricular mass index (102.5 +/- 15.3 g/m2) were significantly higher than in normotensive subjects (blood pressure 120.5 +/- 11.5/78.0 +/- 5.4 mm Hg; left ventricular mass 90.5 +/- 14.3 g/m2, p < 0.01 and p < 0.05 respectively). The intima-media thickness of both the CCA and BIF was significantly higher in borderline hypertensives than in normotensives (CCA 0.6 +/- 0.08 vs. 0.4 +/- 0.05 mm, p < 0.01; BIF 0.7 +/- 0.08 vs. 0.5 +/- 0.08, p < 0.01). In the whole population there was a statistically significant correlation between the carotid wall thickness and the left ventricular mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Renal afferents signaling diuretic activity in the cat.

Mechanoreceptors and chemoreceptors have been identified inside the kidney, but their functional role is still largely unclear. The aim of this study was to investigate whether changes in urine output could modify the discharge rate of renal afferent fibers. Experiments were performed in anesthetized cats in which afferent renal nerve activity (ARNA) was recorded by standard electrophysiological techniques from a centrally cut renal nerve. Arterial pressure, renal blood flow velocity, urine flow rate, and renal pelvic pressure were also measured. Three diuretic maneuvers were tested in the same cat: intravenous administration of physiological saline (8 to 13 mL/min for 2 minutes), furosemide (1 mg/kg), and atrial natriuretic peptide (ANP, 1 microgram/kg). The three maneuvers increased urine flow rate and pelvic pressure, respectively, 137.0 +/- 20.6% and 136.8 +/- 21.1% (saline), 148.6 +/- 31.7% and 139.6 +/- 43.5% (furosemide), and 75.9 +/- 7.9% and 62.1 +/- 21.2% (ANP) at the time of the maximum response. Arterial pressure slightly increased after saline, did not change after furosemide, and slightly decreased after ANP. Renal blood flow increased after saline and did not change after furosemide and ANP. The three maneuvers increased ARNA by 98.4 +/- 15.2% (saline), 270.7 +/- 100.8% (furosemide), and 59.6 +/- 23.4% (ANP). Changes in ARNA significantly correlate with changes in both pelvic pressure and urine flow rate. Our data demonstrate that increments in urine flow rate increase the firing rate of renal afferent fibers and suggest that (1) pelvic pressure is the major determinant of the neural response, and (2) this increased afferent discharge is due to activation of renal mechanoreceptors.

Animals↗
PubMed1993

Ambulatory blood pressure monitoring in hypertension.

Ambulatory blood pressure monitoring generates a greater interest among investigators and clinicians because of its potential to 1) study the mechanisms involved in cardiovascular control in daily life (particularly if monitoring is performed on a beat-to-beat basis) and 2) improve the diagnosis of hypertension, the estimate of the patient's risk and the assessment of the efficacy of antihypertensive treatment. This paper will discuss the evidence pros and cons the latter indications of this approach. It will be shown that 24 hour blood pressure values correlate more closely than clinic blood pressure with various measures of the end organ damage of hypertension, suggesting that it may reflect better than traditional blood pressure measurements the cardiovascular consequences of this condition. Wider use of ambulatory blood pressure monitoring in the medical practice, however, must await a more clear demonstration of its prognostic importance, by longitudinal studies based on cardiovascular morbidity and mortality or on surrogate end points with undisputable clinical significance (e.g. left ventricular hypertrophy). It must also await clear definition of ambulatory blood pressure normality based on population studies. Until then ambulatory blood pressure monitoring should be employed to resolve special problems, e.g. identification of white coat hypertension and false non response to treatment.

Ambulatory Care↗
PubMed1993

The issue of quality of life in antihypertensive therapy.

The treatment of hypertension is based on an assessment of the balance between the effects of therapy on survival on the one hand and effects of the patient's symptoms and well-being on the other. The concept of quality of life is used to summarise the latter effects. Preservation of quality of life involves both the prevention of hypertensive complications and detrimental effects on well-being induced by drugs. However, scientific accumulation of data in this area has been severely hampered by the lack of consensus as to how quality of life should be defined and measured. The scientific power of the quality of life concept has also yet to be proven. Although recent studies indicate that specific aspects of quality of life could be adequately assessed the relative importance of minor shifts in questionnaire or test scores remains an unresolved scientific and clinical issue. Despite these shortcomings a series of studies now available suggests that there are only minor differences between the first-line antihypertensive drugs (e.g. beta-blockers and ACE inhibitors) regarding their effect on quality of life.

Antihypertensive Agents↗
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

What blood pressure levels should be treated?

Information concerning the level of blood pressure at which treatment should be commenced is incomplete, and current guidelines have to be considered of provisional suggestions on which many experts have a consensus. There is general agreement on the need to administer anti-hypertensive therapy when diastolic pressure is 100 mmHg or above. At diastolic values of 90-99 mmHg the risk, albeit increased, is relatively low. The wisest practical solution, which coincides with guidelines from the World Health Organization and the International Society of Hypertension, is to commence treatment if diastolic pressure is between 95 and 100 mmHg, but only after several months of observation with repeated measurements. At values between 90 and 95 mmHg, a decision in favor of treatment will be influenced by concomitant elevation of systolic values and by the occurrence of other risk factors or a strong family history of cardiovascular disease.

Antihypertensive Agents↗
PubMed1992

Coronary response to diving in subjects with mild and severe left coronary artery disease.

The cold pressor test (CPT) is commonly used to determine the vasospastic origin of angina and to investigate the factors modulating coronary vasomotor tone. However, coronary vasoconstriction associated with this manoeuvre is often limited, particularly in patients with mild coronary atherosclerosis. To identify stimuli that can more powerfully constrict the coronary arteries we compared the effects on coronary blood flow (thermodilution) and vascular resistance (mean aortic pressure divided by coronary blood flow) of CPT (2 min) and diving (D, 45 s) in subjects with angiographically documented mild (n = 11) or severe (n = 11) left anterior descending coronary artery stenosis. In subjects with severe coronary artery stenosis the rate-pressure product increased to a similar extent with CPT and D. The latter stimulus, however, caused a more marked fall in coronary blood flow and a much more pronounced increase in coronary resistance as compared to CPT (+44 +/- 3.1% vs +19 +/- 1.6%, P less than 0.01). In the face of a similar increase in rate-pressure product, D caused a significant increase in coronary vascular resistance also in patients with mild coronary artery stenosis (less than or equal to 50%) in which CPT failed to induce any coronary vasoconstriction (+16 +/- 1.8% vs +0.3 +/- 1.3%, P less than 0.01). Thus, diving is a much more powerful coronary vasoconstrictor stimulus than CPT. It can thus replace CPT when an increase in coronary resistance is needed for diagnostic purposes or for investigating abnormalities in coronary vascular regulation.

Cold Temperature↗
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↗