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G Mancia

Publications and source records attributed to G Mancia.

At least 163 records · Page 9Linked to original sources
PubMed1998

Clinical relevance blood pressure variability.

Blood pressure fluctuates continuously over time, either spontaneously or in response to a variety of external stimulations. The occurrence of these continuous and often marked blood pressure variations is not only of pathophysiologic interest, but it may also have a clinical relevance. Indeed, it has been shown that the occurrence of pronounced blood pressure changes at the time of the physician's visit may introduce errors in the diagnosis of hypertension and in the assessment of the efficacy of antihypertensive treatment. Moreover, several studies have reported that the end-organ damage of hypertension is significantly and independently related to the degree of blood pressure variability during the day and night. This was shown by reports that assessed blood pressure variability by a variety of different methods, i.e. by computing the 24 h or daytime blood pressure standard deviation, the degree of morning blood pressure rise or that of night-time blood pressure fall, the frequency of blood pressure peaks over the 24 h, and the blood pressure increases under stressful conditions or during physical exercise. Results from a recent follow-up study have provided evidence that the degree of blood pressure variability may also have prognostic relevance in hypertensive patients. Thus, optimal antihypertensive treatment might also need to reduce the degree of blood pressure fluctuations together with the 24 h average blood pressure levels. Until recently, however, available antihypertensive drugs have been ineffective in buffering blood pressure variability or have even been responsible for an increase in the degree of blood pressure fluctuations. Further studies are needed to assess whether recently developed antihypertensive agents, and in particular those able to induce a smooth reduction in blood pressure over the 24 h or to modulate the sympathetic influences exerted on the cardiovascular system, may represent better tools to reduce the magnitude of an enhanced blood pressure variability in hypertensive patients over the 24 h. Recent progress in technology has offered us more powerful tools to address this issue. They include devices for continuous noninvasive ambulatory blood pressure monitoring (Portapres, TNO), and techniques for a more comprehensive analysis of all components which contribute to overall blood pressure variability (broad-band spectral analysis).

Blood Pressure↗
PubMed1998

Clinical advantages of lipophilic dihydropyridines.

Lipophilic dihydropyridines have many theoretical and practical clinical advantages owing to their long permanence at the cell membrane. They have a greater chance of smoothly and permanently reducing blood pressure over 24 h than other dihydropyridines, a feature that may have positive prognostic implications since 24-h blood pressure is more closely related to the end-organ damage of hypertension. They may avoid the sympathetic activation consequent to an excessive early-dose hypotension, which is responsible for an increase in 24-h blood-pressure variability and reflex tachycardia, two phenomena that may worsen the prognosis of hypertensive patients. A further advantage which has been shown in experimental and clinical settings is the possibility of reducing the extension and progression of atherogenic lesions in blood vessels, which are responsible for cardiovascular complications in hypertension. Some of these features have been shown by the novel lipophilic dihydropyridine lercanidipine. In particular, clinical studies have shown that (i) this drug is effective in homogeneously reducing blood pressure over 24 h, (ii) its antihypertensive effect is similar to that of some common antihypertensive drugs, and (iii) the rate of adverse events experienced with lercanidipine is no greater than that observed with other antihypertensive drugs, with special reference to non-lipophilic calcium antagonists. In particular, studies performed so far have shown that lercanidipine does not exert a dangerous reflex tachycardia.

Adolescent↗
PubMed1998

Calcium antagonists and sympathetic activity in congestive heart failure.

OBJECTIVE: To review the sympathetic abnormalities occurring in heart failure, their pathophysiological importance and clinical relevance, and the effects of drug treatment, with particular reference to calcium antagonists. SYMPATHETIC ACTIVATION IN HEART FAILURE: Indirect and direct approaches to study sympathetic function in humans have documented conclusively that sympathetic activation represents a hallmark of cardiac failure syndrome. Evidence indicates that sympathetic overactivity is associated with, and probably caused by, a baroreflex impairment and that it has adverse effects on patients' prognosis and survival. GOALS OF DRUG TREATMENT IN CONGESTIVE HEART FAILURE: In the past, drug treatment in heart failure was aimed at improving patients' survival by ameliorating cardiac hemodynamics. It is now established that a major goal of therapeutic intervention is also to reduce sympathetic activation characterizing heart failure. CALCIUM ANTAGONISTS IN HEART FAILURE: Studies with short-acting calcium antagonists show that they enhance sympathetic activation and that this has an adverse effect on patients' survival. In contrast, third generation calcium antagonists such as amlodipine, which have a slow onset and long duration of action, do not adversely affect sympathetic function and reflex cardiovascular control. Indeed, evidence suggests calcium antagonists with this profile may exert favorable clinical effects.

Baroreflex↗
PubMed1998

Clinical benefits of a consistent reduction in blood pressure.

This paper briefly reviews the epidemiological evidence that hypertension is a major cardiovascular risk factor. It also summarizes the data from controlled intervention trials that show antihypertensive treatment to be accompanied by a reduction in cardiovascular morbidity and mortality. The inability of antihypertensive treatment to offer full protection to the hypertensive individual is then discussed, together with the therapeutic strategies to increase the benefits, particularly with respect to limiting end-organ damage and reduction of cardiovascular events. In this context, emphasis is given to the potential additional benefit conferred by control of 24-h blood pressure and to the compliance advantage of using drugs with a long duration of action. The longevity of the blood pressure lowering effect can compensate for delayed or missed drug consumption, a frequent phenomenon in the chronically treated hypertensive patient.

Aged↗
PubMed1998

Can good surrogate end-points predict the prognosis of hypertensive patients?

SURROGATE END-POINTS FOR PROGNOSIS OF HYPERTENSION: The identification of surrogate measures of cardiovascular risk in patients with hypertension may allow clinicians to better estimate a patient's long-term prognosis and monitor the effects of antihypertensive therapy in reducing risk and thereby reducing the cardiovascular complications of hypertension. PROGNOSTIC LIMITATIONS OF OFFICE BLOOD PRESSURE: Previous studies have shown that office blood pressure may predict the incidence of fatal and nonfatal cardiovascular complications of hypertension. However, evidence also suggests that the predictive value of office blood pressure is limited and that it does not provide accurate estimates of the changes in the cardiovascular risk profile that can occur with antihypertensive treatment. PROGNOSTIC VALUE OF 24-H AMBULATORY BLOOD PRESSURE: Cross-sectional studies have shown that 24-h average blood pressure values are more closely correlated with hypertensive target-organ damage [e.g. left ventricular hypertrophy (LVH), retinopathy, increased serum creatinine, albuminuria, and microalbuminuria] than are office blood pressure values. Although longitudinal evidence of the clinical relevance of 24-h ambulatory blood pressure monitoring is limited, preliminary data from a recently completed trial, the Study on Ambulatory Pressure and Lisinopril Evaluation (SAMPLE), have clearly shown the superiority of 24-h blood pressure monitoring over office readings in predicting the regression of LVH in hypertensive patients following treatment to reduce blood pressure.

Blood Pressure↗
PubMed1998

Study population and treatment titration in the International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT).

OBJECTIVES: To ascertain the baseline characteristics of the high-risk hypertensive patients entering the International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT). To determine the success of single and combination therapy in achieving target blood pressures in such a population. DESIGN: INSIGHT is a double-blind, prospective outcome trial comparing the efficacy of the calcium channel blocker, nifedipine GITS, and the thiazide, co-amilozide, in preventing myocardial infarction and stroke. We recruited 2996 men and 3454 women, aged 55-80 years, with blood pressure during placebo run-in >150/95 mmHg or isolated systolic blood pressure >160 mmHg from nine countries. Treatment allocation to nifedipine GITS 30 mg daily or co-amilozide (hydrochlorothiazide 25 mg/amiloride 5 mg) once daily was performed by minimization rather than randomization to balance additional risk factors. This was followed by four optional increases in treatment: dose-doubling of the primary drug, addition of atenolol 25/50 mg or enalapril 5/10 mg, and then any other hypotensive drug excluding calcium blockers or diuretics. Target blood pressure was 140/90 mmHg or a fall > or = 20/10 mmHg. RESULTS: Blood pressure at randomization was 172+/-15 / 99+/-9 mmHg. Thirteen per cent of the patients were previously untreated. The proportions of each additional risk factors were: smoking > 10/day, 29%; cholesterol > 6.43 mmol/l, 52%; family history of premature myocardial infarction or stroke, 21%; diabetes mellitus 20%; left ventricular hypertrophy, 10%; previous myocardial infarction, other presentations of coronary heart disease, and peripheral vascular disease, each 6%; proteinuria, 3%. Fifty-five per cent of patients had one additional risk factor, whereas 33%, 9% and 3% had two, three or more additional risk factors, respectively. The blood pressure (and falls in blood pressure) at the end of titration and at 1 year after minimization was 139+/-12 / 82+/-7 mmHg (33+/-15 / 17+/-9) in the 5226 patients still on randomized treatment The numbers requiring the four treatment increments were, respectively, 1591, 780, 597 and 294, meaning that almost 70% of patients on randomized treatment in INSIGHT are receiving only the primary drug. At one year, 69% of patients had a blood pressure < or = 140/90 mmHg. CONCLUSION: INSIGHT is one of the first double-blind comparisons of active antihypertensive treatments, requiring high-risk patients to achieve sufficient power. Despite this requirement, it is possible to achieve good blood pressure control in most patients without the addition of multiple additional treatments that may dilute any differences between the primary agents.

Aged↗
PubMed1997

Effects of chronic ACE inhibition on sympathetic nerve traffic and baroreflex control of circulation in heart failure.

BACKGROUND: In congestive heart failure ACE inhibitors chronically reduce plasma norepinephrine. No information exists, however, on whether and to what extent this reduction reflects a true chronic inhibition of sympathetic outflow and which mechanisms may be responsible. METHODS AND RESULTS: In 24 patients aged 60.3+/-2.0 years (mean+/-SEM) affected by congestive heart failure (New York Heart Association class II) and treated with diuretics and digitalis, we measured mean arterial pressure (Finapres), plasma renin activity and angiotensin II levels (radioimmunoassay), plasma norepinephrine (high-performance liquid chromatography), and muscle sympathetic nerve activity (microneurography at a peroneal nerve) at rest and during baroreceptor stimulation and deactivation caused by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. In 12 patients measurements were repeated after a 2-month addition of the ACE inhibitor benazepril (10 mg/d P.O.), while in the remaining 12 patients they were performed again after 2 months without any treatment modifications. Benazepril did not alter mean arterial pressure, markedly increased plasma renin activity, reduced plasma angiotensin II, and caused a nonsignificant reduction in plasma norepinephrine. In contrast, muscle sympathetic nerve traffic was significantly reduced (-30.5+/-5.3%, P<.01). This reduction was accompanied by no change in the sympathoexcitatory responses to baroreceptor deactivation but by a marked enhancement of the sympathoinhibitory responses to baroreceptor stimulation (103.5+/-3.4%). CONCLUSIONS: These results provide the first direct evidence that in congestive heart failure chronic ACE inhibitor treatment is accompanied by a marked reduction in central sympathetic outflow. This reduction may depend on a persistent restoration of baroreflex restraint on the sympathetic neural drive.

Angiotensin II↗
PubMed1997

Intracoronary angiotensin II potentiates coronary sympathetic vasoconstriction in humans.

BACKGROUND: In humans with coronary artery disease, ACE inhibition attenuates coronary sympathetic vasoconstriction. Whether this is due to removal of angiotensin (Ang) II production or to a reduced bradykinin breakdown, however, is unknown. METHODS AND RESULTS: In eight normotensive patients with angiographic evidence of mild left coronary artery lesions (< or = 50%), mean arterial pressure (MAP, intra-arterial catheter), heart rate (HR, ECG lead), coronary sinus blood flow (CBF, thermodilution method), and coronary vascular resistance (CVR, ratio between MAP and CBF) were measured before and during a 15-minute left intracoronary infusion of Ang II at a dose that had no direct coronary or systemic vasomotor effects. The same measurements were made before and during a 15-minute infusion of saline. A 2-minute cold pressor test (CPT) and a 45-second diving were performed at the end of either infusion period. These maneuvers were used because their coronary vasomotor effects are abolished by phentolamine and thus depend on sympathetic activation. During saline infusion, both CPT and diving caused a marked increase in MAP. HR increased with CPT and fell with diving. CBF increased in parallel to the MAP increase, with little change in CVR. The MAP and HR responses were similar during Ang II infusion, which, however, caused either no change or a reduction in CBF with a consequent marked increase in CVR with both CPT and diving. In four additional patients, the diameter of the stenotic vessels remained unchanged during the CPT performed under saline and Ang II infusion. CONCLUSIONS: Ang II markedly enhances sympathetic influences on coronary circulation in humans, presumably by acting at the arteriolar level. This may explain the blunting effect of ACE inhibition on sympathetic coronary vasoconstriction in patients with coronary artery disease.

Aged↗
PubMed1997

Randomised study of effect of ibopamine on survival in patients with advanced severe heart failure. Second Prospective Randomised Study of Ibopamine on Mortality and Efficacy (PRIME II) Investigators.

BACKGROUND: Drugs that improve symptoms in patients with heart failure must also be assessed for their effects on survival. Ibopamine stimulates DA-1 and DA-2 receptors and causes peripheral and renal vasodilatation; the drug improves symptoms of heart failure. We assessed the effect of ibopamine on survival in patients with advanced heart failure in a multicentre, randomised placebo-controlled study. METHODS: Patients with advanced severe heart failure (New York Heart Association classes III and IV) and evidence of severe left-ventricular disease, who were already receiving optimum treatment for heart failure, were randomly allocated oral ibopamine 100 mg three times daily or placebo. The primary endpoint was all-cause mortality. The study was designed to recruit 2200 patients, and the minimum duration of treatment would be 6 months. We did intention-to-treat and on-treatment analyses; a post-hoc subgroup analysis was also done. FINDINGS: After we had recruited 1906 patients the trial was stopped early, because of an excess of deaths among patients in the ibopamine group. 232 (25%) of 953 patients in the ibopamine group died, compared with 193 (20%) of 953 patients in the placebo group (relative risk 1.26 [95% CI 1.04-1.53], p = 0.017). The average length of follow-up was 347 days in the ibopamine group and 363 days in the placebo group. In multivariate analysis, only the use of antiarrhythmic drugs at baseline was a significant independent predictor of increased fatality in ibopamine-treated patients. INTERPRETATION: Ibopamine seems to increase the risk of death among patients with advanced heart failure who are already receiving optimum therapy, but the reasons for this increase are not clear. Our finding that antiarrhythmic treatment was a significant predictor of increased mortality in ibopamine-treated patients may be important, but exploratory analyses must be interpreted with caution.

Adult↗
PubMed1997

Ambulatory blood pressure is superior to clinic blood pressure in predicting treatment-induced regression of left ventricular hypertrophy. SAMPLE Study Group. Study on Ambulatory Monitoring of Blood Pressure and Lisinopril Evaluation.

BACKGROUND: In cross-sectional studies, ambulatory blood pressure (ABP) correlates more closely than clinic BP with the organ damage of hypertension. Whether ABP predicts development or regression of organ damage over time better than clinic BP, however, is unknown. METHODS AND RESULTS: In 206 essential hypertensive subjects with left ventricular hypertrophy (LVH), we measured clinic supine BP, 24-hour ABP, and left ventricular mass index (LVMI, echocardiography) before and after 12 months of treatment with lisinopril (20 mg UID) without or with hydrochlorothiazide (12.5 or 25 mg UID). Measurements included random-zero, clinic orthostatic, and home BP. In all, 184 subjects completed the 12-month treatment period. Before treatment, clinic supine BP was 165 +/- 15/105 +/- 5 mm Hg (systolic/diastolic), 24-hour average BP was 149 +/- 16/95 +/- 11 mm Hg, and LVMI was 158 +/- 32 g/m2. At the end of treatment, they were 139 +/- 12/87 +/- 7 mm Hg, 131 +/- 12/83 +/- 10 mm Hg, and 133 +/- 26 g/m2, respectively (P < .01 for all). Before treatment, LVMI did not correlate with clinic BP, but it showed a correlation with systolic and diastolic 24-hour average BP (r = .34/.27, P < .01). The LVMI reduction was not related to the reduction in clinic BP, but it was related to the reduction in 24-hour average BP (r = .42/.38, P < .01). Treatment-induced changes in average daytime and nighttime BPs correlated with LVMI changes as strongly as 24-hour BP changes. No substantial advantage over clinic supine BP was shown by clinic orthostatic, random-zero, and home BP. CONCLUSIONS: In hypertensive subjects with LVH, regression of LVH was predicted much more closely by treatment-induced changes in ABP than in the clinic BP. This provides the first longitudinally controlled evidence that ABP may be clinically superior to traditional BP measurements.

Adult↗
PubMed1997

Blood-pressure control in the hypertensive population.

BACKGROUND: In large-scale surveys of individuals with hypertension those whose clinic blood pressure is reduced to 140/90 mm Hg or less have been found to represent only a small fraction of the hypertensive population. We assessed whether these results arise because of a white-coat effect elevating clinic blood pressure. METHODS: We randomly selected 2400 individuals from the town of Monza, Italy, and invited them to take part in our study. We measured clinic blood pressure as well as home (morning and evening measurements), and 24 h ambulatory blood pressure-ie, blood pressures largely devoid of a white-coat effect. Based on clinic blood pressure participants were then classified as normotensive, untreated hypertensive (clinic blood pressure > 140 mm Hg systolic and/or > 90 mm Hg diastolic), or treated hypertensive (having antihypertensive treatment). The mean blood pressures for each group were calculated. FINDINGS: 1651 people took part in the study. The clinic blood pressure of treated hypertensives (n = 207; 146.9 [SD 18] mm Hg/90.2 [8.6] mm Hg) was only slightly less than in untreated hypertensives (n = 402; 148 [15.2] mm Hg/93.3 [8] mm Hg) and in both groups the blood pressure values were much greater than those of normotensive individuals (n = 1042; 119.5 [10.3] mm Hg/78.1 [6.6] mm Hg) p < 0.001. Averaged home and 24 h blood pressures were lower than clinic blood pressures but similarly higher in untreated and treated hypertensive individuals when compared with normotensive individuals. This was also the case for day and night average blood pressures. The number of treated hypertensive patients found to have blood pressures within the normal limits was small not only when based on clinic blood pressure values but also when based on ambulatory blood-pressure values. INTERPRETATION: In the hypertensive population the number of patients with inadequate blood-pressure control is high not only when assessed in the clinic but also when assessed by ambulatory-blood-pressure monitoring or at home. The high blood-pressure values commonly found in treated hypertensive individuals cannot be accounted for by a white-coat effect but by a true lack of daily-life blood-pressure control.

Adult↗
PubMed1997

Scipione Riva-Rocci.

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Blood Pressure Determination↗
PubMed1997

Evidence of functional and structural cardiac abnormalities in cirrhotic patients with and without ascites.

Cirrhosis is associated with cardiovascular abnormalities. Scanty information is available as to whether these include left ventricle diastolic dysfunction and wall thickness increase. To this aim in 27 cirrhotic patients with tense ascites, 17 cirrhotic patients with previous episodes of ascites (not actual), and 11 controls we investigated by echocardiography and echocolor Doppler left ventricle diastolic function (E wave, A wave, E/A ratio, deceleration time of E wave), systolic function (ejection fraction), and wall thickness (left ventricle posterior wall thickness + interventricular septum thickness) along with neurohumoral variables. All measurements (supine position) were repeated after total paracentesis (10.7 +/- 0.6 L of ascites) in ascitic patients. Both in patients with and without ascites E/A ratio was reduced as compared with controls (0.93 +/- 0.07 and 0.97 +/- 0.06 vs. 1.18 +/- 0.08, P < .05) while left ventricle wall thickness was increased (18.6 +/- 0.6 and 20.1 +/- 0.8 vs. 17.2 +/- 0.7, P < .05 and P < .01, respectively), irrespective of the postviral or alcoholic cause of liver disease. In all cirrhotics both right and left atrial and right ventricle diameters were significantly greater. Ejection fraction was slightly but significantly (P < .01) reduced in ascitic patients. Paracentesis induced a reduction of the highly increased basal plasma renin activity, aldosterone, norepinephrine (P < .01), and epinephrine (P < .05) and improved diastolic function (E/A, P < .05). Systolic function was unaffected. Thus, irrespective of ascites and cause, advanced cirrhosis is associated with left ventricle diastolic dysfunction and wall thickness increase. We can speculate that neurohumoral overactivity, known to stimulate cardiac tissue growth, may challenge the heart, promoting fibrosis and exerting a further hindrance to ventricular relaxation in patients with cirrhosis experiencing episodes of ascites.

Aged↗
PubMed1997

Time and frequency domain estimates of spontaneous baroreflex sensitivity provide early detection of autonomic dysfunction in diabetes mellitus.

Diabetic autonomic dysfunction is associated with a high risk of mortality which makes its early identification clinically important. The aim of our study was to compare the detection of autonomic dysfunction provided by classical laboratory autonomic function tests with that obtained through computer assessment of the spontaneous sensitivity of the baroreceptor-heart rate reflex (BRS) by time domain and frequency domain techniques. In 20 normotensive diabetic patients (mean age +/- SD 41.9 +/- 8.1 years) with no evidence of autonomic dysfunction on laboratory autonomic testing (D0) blood pressure (BP) and ECG were continuously monitored over 15 min in the supine position. BRS was assessed as the slope of the regression line between spontaneous increases or reductions in systolic BP and linearly related lengthening or shortening in RR interval over sequences of at least 4 consecutive beats (sequence method), or as the squared ratio between RR interval and systolic BP spectral powers around 0.1 Hz. We compared the results with those of 32 age-matched normotensive diabetic patients with abnormal autonomic function tests (D1) and with those of 24 healthy age-matched control subjects with normal autonomic function tests (C). Compared to C, BRS was markedly less in D1 when assessed by both the slope of the two types of sequences (data pooled) and by the spectral method (-71.3% and -60.2% respectively, both p < 0.01). However, BRS was consistently although somewhat less markedly reduced in D0, the reduction being clearly evident for all the estimates (-57.0% and -43.5%, both p < 0.01). The effects were more evident than those obtained by the simple quantification of the RR interval variability. These data suggest that time and frequency domain estimates of spontaneous BRS allow earlier detection of diabetic autonomic dysfunction than classical laboratory autonomic tests. The estimates can be obtained by short non-invasive recording of the BP and RR interval signals in the supine patient, i.e. under conditions suitable for routine outpatient evaluation.

Adult↗
PubMed1997

Combination treatment in hypertension: the VeraTran Study.

In the past few years, the combination of two antihypertensive drugs has become a popular approach to hypertension treatment, because this procedure allows one to obtain satisfactory blood pressure control when monotherapy is partially ineffective and also to improve a patient's adherence to the therapeutic regimen, thereby enhancing the tolerance/effectiveness ratio of the treatment. This paper will briefly review the theoretical background and the requirements for an effective combination treatment. It will also discuss the results of the VeraTran Study, a multicenter study performed according to a double-blind parallel group design and aimed at assessing the antihypertensive efficacy of the fixed combination verapamil slow release (SR) and trandolapril, administered for 8 weeks, on clinic and 24-h ambulatory blood pressure. The results of the study demonstrate that the fixed combination of a calcium antagonist and an angiotensin converting enzyme (ACE) inhibitor allows one to obtain an effective and balanced blood pressure control throughout the 24 h.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Treatment of heart failure with fosinopril: an angiotensin converting enzyme inhibitor with a dual and compensatory route of excretion.

Congestive heart failure (CHF) is one of the most common and clinically important cardiovascular diseases. This pathologic state is characterized not only by well-defined hemodynamic alterations, but also by complex abnormalities involving the sympathetic nervous system, the renin-angiotensin system, and other hormones involved in cardiovascular homeostasis. In addition, there is an abnormality in the homeostatic cardiovascular control exerted by arterial baroreceptors and the viscoelastic properties of medium-size arteries are altered, causing a reduction in arterial compliance. All of these abnormalities can be favorably affected by angiotensin converting enzyme (ACE) inhibitors, which have been shown to improve not only the hemodynamic and neurohumoral profiles of CHF, but also patient survival. CHF is accompanied with a decline or some sort of effect on renal function. An ACE inhibitor with a dual route of excretion, such as fosinopril, may be especially useful in treating patients with CHF.

Aged↗