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Biomedical subjects

Gino Seravalle

Publications and source records attributed to Gino Seravalle.

14 recordsLinked to original sources
PubMed2007

Excessive sympathetic activation in heart failure with obesity and metabolic syndrome: characteristics and mechanisms.

Congestive heart failure is characterized by sympathetic activation, which has also been described in the metabolic syndrome. No information exists, however, as to whether the sympathostimulating effects of these 2 conditions summate when heart failure is complicated by the metabolic syndrome, leading to an exceedingly high adrenergic drive. This is clinically relevant, because in heart failure sympathetic activation is closely related to mortality. We studied 48 control subjects (age: 58.4+/-1.6 years, mean+/-SEM) and 89 age-matched heart failure patients (New York Heart Association class II), of whom 47 were without and 42 were with metabolic syndrome. Measurements included blood pressure (Finapres), heart rate (ECG), and sympathetic nerve traffic (microneurography) at rest and during baroreceptor manipulation. Waist circumference, blood pressure, and metabolic variables were greater in heart failure with metabolic syndrome than in heart failure without metabolic syndrome and in control subjects. Left ventricular ejection fraction and end-diastolic diameter were similarly altered in the 2 heart failure groups. Compared with control subjects, sympathetic nerve activity was greater in heart failure patients without metabolic syndrome (64.7+/-3.2 versus 45.8+/-2.9 bursts/100 heartbeats; P<0.01), a further pronounced increase being detected in those with metabolic syndrome (80.9+/-3.2 bursts/100 heartbeats; P<0.01). In the multivariate analysis, waist circumference and body mass index were the variables most closely related to sympathetic activation. Compared with control subjects, baroreflex responses were significantly attenuated in the 2 heart failure groups, the impairment being more marked in the group with than without metabolic syndrome. Thus, obesity and metabolic syndrome potentiate the sympathetic activation characterizing heart failure. This potentiation is likely to mainly depend on metabolic and baroreflex mechanisms.

Aged↗
PubMed2004

Sympathetic and baroreflex function in hypertensive or heart failure patients with ventricular arrhythmias.

OBJECTIVE: To determine whether in hypertension and in heart failure the occurrence of ventricular arrhythmias is associated with alterations in sympathetic drive and baroreflex function. DESIGN AND METHODS: We studied 28 untreated essential hypertensives (age, 53.0 +/- 1.1 years, mean +/- standard error of the mean), 15 without and 13 with monofocal premature ventricular contractions (PVCs) in Lown class I, and 30 heart failure patients (age, 53.8 +/- 1.3 years) in New York Health Association class II-III, 17 without and 13 with PVCs also in Lown class I. In each patient we measured, along with echocardiographic variables, the beat-to-beat mean blood pressure (Finapress), heart rate (HR) (EKG), muscle sympathetic nerve traffic (MSNA) (microneurography), venous plasma norepinephrine and renin activity (high-pressure liquid chromatography and radioimmunoassay, respectively). Measurements were performed at rest and during arterial baroreceptor stimulation and deactivation via stepwise intravenous infusion of phenylephrine and nitroprusside, respectively. RESULTS: The mean blood pressure, HR and MSNA were similar in hypertensive patients without and with PVCs. However, compared with non-arrhythmic patients, hypertensives with PVCs displayed a baroreflex-HR and baroreflex-MSNA modulation reduced by 27.7 +/- 4.2 and 17.9 +/- 2.8%, respectively (P < 0.05). Heart failure patients with PVCs showed haemodynamic and echocardiographic variables superimposable to those without PVCs. Compared with these patients, however, they exhibited a significant increase in MSNA values (75.8 +/- 3.0 versus 63.6 +/- 2.8 bs/100 hb, P < 0.05), coupled with a significant impairment in baroreflex-HR and baroreflex-MSNA control (-52.5 +/- 5.4 and -37.5 +/- 3.6%, P < 0.01). CONCLUSIONS: These data provide evidence that in both hypertension and heart failure, sympathetic and baroreflex mechanisms exert a pro-arrhythmogenic role. This role, however, appears to be more pronounced in heart failure than in hypertension, in which the impaired vagal function may exert a concomitant favouring effect.

Adult↗
PubMed2003

Effects of hypertension and obesity on the sympathetic activation of heart failure patients.

Previous studies have shown that congestive heart failure is characterized by sympathetic and reflex dysfunctions. Whether these alterations are potentiated in the presence of obesity and hypertension, two conditions that also display neuroadrenergic abnormalities and markedly increase the risk of heart failure, is unknown. In 14 healthy control subjects (C; age, 55.1+/-3.0 years; mean+/-SEM), 13 lean hypertensive subjects (H), 15 obese normotensive subjects (O), 14 lean normotensive subjects with congestive heart failure (CHF, New York Heart Association class II), 14 lean hypertensive subjects with CHF (CHFH), 14 obese normotensive subjects with CHF (CHFO), and 13 obese hypertensive subjects with CHF (CHFOH), all age-matched with C, we measured mean blood pressure (Finapres), heart rate (ECG), and muscle sympathetic nerve traffic (MSNA, microneurography) at rest and during baroreflex testing. Compared with C, body mass index was similarly increased in O, CHFO, and CHFOH, whereas mean blood pressure was similarly increased in HF, CHFH, and CHFOH, and left ventricular ejection fraction (echocardiography) was similarly reduced in CHF, CHFH, CHFO and CHFOH. Compared with C, MSNA was significantly increased in O, H, and CHF (43.0+/-2.2 versus 54.1+/-2.8, 53.1+/-2.5, and 57.4+/-2.8 bursts/100 heart beats, P<0.01). When O or H was combined with CHF, the MSNA increase was significantly more pronounced and maximal when O and H were concomitantly associated with CHF. Baroreflex sensitivity was reduced in O and H, with a further reduction in CHF and a minimal value in CHFOH. These data show that the sympathetic activation characterizing CHF is markedly potentiated when O and H alone or combined together are associated with a low cardiac output state and that this may depend on an arterial baroreflex impairment.

Blood Pressure↗
PubMed2003

Impairment of thermoregulatory control of skin sympathetic nerve traffic in the elderly.

BACKGROUND: Human aging is characterized by a marked increase in muscle sympathetic nerve traffic (MSNA). No information exists, however, on the effects of aging on skin sympathetic nerve traffic (SSNA) and on its reflex modulation by thermoregulatory mechanisms. METHODS AND RESULTS: In 13 young, 11 middle-aged, and 12 elderly healthy subjects, we measured arterial blood pressure (Finapres), skin temperature (thermocouples), and resting MSNA and SSNA (microneurography). Measurements also included the SSNA responses to (1) an acute increase and reduction (+/-8 degrees C) in room temperature, each lasting 45 minutes and (2) an acoustic stimulus capable to trigger an emotional arousal. Although resting MSNA was progressively and significantly (P<0.05) increased from young to middle-aged and elderly groups, SSNA was significantly (P<0.05) reduced in the latter compared with the former 2 groups. Cold exposure induced a SSNA increase that was significantly (P<0.01) smaller in the elderly than in young and middle-aged subjects. Conversely, heat exposure induced a SSNA reduction that was significantly (P<0.05) smaller in elderly than in young and middle-aged subjects. Compared with SSNA in young individuals, the SSNA change from cold to warm temperature was reduced by 61% in the elderly group. This was not the case, however, for the SSNA responses to the arousal stimulus, which were superimposable in the 3 groups. CONCLUSIONS: These data provide the first demonstration of a dichotomy in the MSNA and SSNA responses to aging. They also show that aging markedly impairs thermoregulatory control of SSNA and that this impairment might participate at the age-related SSNA decrease.

Adolescent↗
PubMed2003

Short-versus long-term effects of different dihydropyridines on sympathetic and baroreflex function in hypertension.

Antihypertensive treatment with dihydropyridines may be accompanied by sympathetic activation. Data on whether this is common to all compounds and similar in the various phases of treatment are not univocal, however. In 28 untreated essential hypertensives (age, 56.4+/-1.8 years; mean+/-SEM) finger blood pressure (BP, Finapres), heart rate (HR, ECG), plasma norepinephrine (NE, high-performance liquid chromatography), and muscle sympathetic nerve traffic (MSNA, microneurography) were measured at rest and during baroreceptor manipulation (vasoactive drugs) in the placebo run-in period and after randomization to double-blind acute and chronic (8 weeks) felodipine (10 mg/d, n=14) or lercanidipine (10 mg/d, n=14). Acute administration of both drugs induced pronounced BP reductions and marked increases in HR, NE, and MSNA. After 8 weeks of treatment, BP reductions were similar to those observed after acute administration, whereas HR, NE, and MSNA responses were markedly attenuated (-7%, -32%, and -14%, respectively; P<0.05). There was a small residual increase in sympathetic activity in the felodipine group, whereas in the lercanidipine group, all adrenergic markers returned to baseline values. Baroreflex control of HR and MSNA was markedly impaired (-42% and -48%, respectively) after acute drug administration, with a recovery and complete resetting during chronic treatment. Thus, the sympathoexcitation induced by 2 different dihydropyridines is largely limited to the acute administration. The 2 drugs have, nevertheless, a different chronic sympathetic effect, indicating that dihydropyridines do not homogeneously affect this function. The acute sympathoexcitation, but not the small between-drugs differential chronic adrenergic effect, is accounted for by baroreflex impairment.

Antihypertensive Agents↗
PubMed2003

Tolerability and treatment compliance with angiotensin II receptor antagonists.

Several studies and intervention trials performed during the past 30 years have provided evidence that hypertension-related cardiovascular risk is not irreversible. This is because the reduction in blood pressure (BP) induced by antihypertensive drugs has been shown to be accompanied by a clear-cut decrease in the rate of cardiovascular events and complications. There is also evidence that BP control in the population is far from being optimal, and that no more than one quarter of treated hypertensive patients display BP values <140/90 mm Hg. The reasons for inadequate BP control are multiple, involving a combination of factors such as inadequate compliance with treatment, intolerance to side effects of currently prescribed drugs, and insufficient clinical use of combination drug treatment. This article focuses on three major areas. It first provides an overview of the current status of BP control in treated hypertensive persons. It then examines the factors potentially responsible for this phenomenon, with particular emphasis on the relevance of the so-called "compliance factor." Finally it provides an overview of the tolerability and compliance profile of the angiotensin II receptor antagonists, a new class of antihypertensive drugs characterized by an efficacy and safety profile.

Angiotensin Receptor Antagonists↗
PubMed2003

Behaviour of the adrenergic cardiovascular drive in atrial fibrillation and cardiac arrhythmias.

AIM: Animal studies have conclusively shown that the sympathetic nervous system plays a major role not only in regulating sinus node activity but also in promoting cardiac rhythm alterations. Less univocal and often circumstantial have been the evidences collected on this issue in humans. However, the introduction of the microneurographic technique in clinical research has allowed to gain new important insights on the role of neuroadrenergic factors in the pathophysiology of cardiac arrhythmias. METHODS: The present paper will review the results of microneurographic studies performed by our group and others in the field of cardiac rhythm disturbances by addressing three specific issues. First it will examine the relationships between heart rate and muscle sympathetic neural outflow in a variety of cardiovascular diseases characterized by sympathetic activation. This will be followed by an analysis of the behaviour of the sympathetic nerve traffic responses to paroxysmal atrial fibrillation. Finally, the sympathetic adjustments to spontaneously occurring or artificially induced pre-mature ventricular contractions will be highlighted.

Atrial Fibrillation↗
PubMed2003

Comparative effects of candesartan and hydrochlorothiazide on blood pressure, insulin sensitivity, and sympathetic drive in obese hypertensive individuals: results of the CROSS study.

OBJECTIVE: The increase in blood pressure that accompanies the obese state is almost invariably associated with alterations in metabolism (insulin resistance and dyslipidaemia) and the neurohumoral profile (activation of the renin-angiotensin system, sympathetic overactivity), which potentiate the cardiovascular risk associated with hypertension. However, debate remains as to the antihypertensive drug on which treatment of obesity-related hypertension should be based. The CROSS (Candesartan Role on Obesity and on Sympathetic System) study was undertaken to examine the antihypertensive, neuroadrenergic, and metabolic effects of an angiotensin II receptor blocker in comparison with a diuretic in obese hypertensive individuals. METHODS: In 127 obese hypertensive individuals aged 50.7 +/- 5.1 years (mean +/- SD), we measured clinic blood pressure, heart rate, plasma glucose, and insulin at rest and during an oral glucose load before and 12 weeks after treatment with either candesartan cilexetil (8-16 mg once daily) or hydrochlorothiazide (HCTZ, 25-50 mg once daily), administered orally in accordance with a double-blind, randomized, placebo-controlled, two-parallel-groups study design. Insulin sensitivity was expressed as insulin resistance index (IRI), calculated as the ratio of the area under the curve (AUC) for glucose to that for insulin. In a subgroup of patients, measurements also included direct microneurographic recording of muscle sympathetic nerve activity (MSNA) in the peroneal nerve. RESULTS: Candesartan cilexetil caused a significant (P < 0.01) reduction in both mean blood pressure (from 114.2 +/- 5.1 to 99.6 +/- 6.0 mmHg) and MSNA (from 51.0 +/- 12.3 to 40.4 +/- 12.5 bursts per 100 heart beats), and a significant (P < 0.02) increase in insulin sensitivity (AUC IRI: from -23.2 +/- 22.1 to -17.6 +/- 12.2). In contrast, HCTZ did not significantly affect MSNA and worsened insulin sensitivity, while achieving blood pressure reductions similar to those produced by candesartan cilexetil. CONCLUSIONS: These data provide evidence that, in obese hypertensive individuals, treatment with candesartan cilexetil has an antihypertensive effect similar to that of HCTZ. Unlike diuretic treatment, however, treatment with candesartan cilexetil improves insulin sensitivity and exerts sympathoinhibitory effects.

Adolescent↗
PubMed2002

Short- and long-term neuroadrenergic effects of moderate dietary sodium restriction in essential hypertension.

BACKGROUND: In essential hypertension, marked restrictions in dietary sodium intake cause in the short-term period an increase in muscle sympathetic nerve traffic (MSNA) and a baroreflex impairment. The present study was set out to assess on a long-term basis the neuroadrenergic and reflex effects of moderate sodium restriction. METHODS AND RESULTS: In 11 untreated mild to moderate essential hypertensive patients (age 42.0+/-2.6 years, mean+/-SEM), we measured beat-to-beat blood pressure (Finapres), heart rate (ECG), and MSNA (microneurography) at rest and during stepwise intravenous infusions of phenylephrine and nitroprusside. Measurements were performed at regular sodium intake, after 1 and 8 weeks of low-sodium diet (80 mmol NaCl/d), and repeated again at regular sodium intake. After 1 week, urinary sodium excretion was markedly reduced. This was accompanied by a slight blood pressure reduction, no heart rate change, and a significant increase in plasma renin activity, aldosterone, and MSNA (+23.0+/-4.6% P<0.05). Whereas baroreflex heart-rate control was unchanged, baroreflex modulation of MSNA was reduced by 46.8+/-5.1% (P<0.01). At the end of the 8-week low-sodium diet, the neurohumoral and baroreflex responses were similar to the ones observed after 1 week of the dietary intervention. All changes disappeared when regular sodium diet was restored. CONCLUSIONS: Thus, a moderate dietary sodium restriction triggers a sympathetic activation and a baroreflex impairment. Maintenance of low-sodium diet for several weeks does not attenuate these adverse adrenergic and reflex effects.

Adult↗
PubMed2002

Sympathetic response to ventricular extrasystolic beats in hypertension and heart failure.

Provoked premature ventricular contractions (PVCs) evoke, in concomitance with an early and late blood pressure fall and overshoot, an early sympathoexcitation and a later period of sympathoinhibition, respectively. The present study was designed to examine whether in healthy subjects this is the case for spontaneous PVCs. Because of their pathophysiological relevance for arrhythmogenesis, it was also designed to determine whether the sympathetic responses are different from those seen in essential hypertension and congestive heart failure. In 14 untreated mild essential hypertensives (EH; age, 53.8+/-2.6 years; mean+/-SEM), 20 untreated congestive heart failure patients (CHF; age, 56.7+/-2.5 years; New York Heart Association class, II or III), and 16 age-matched healthy subjects (control) in Lown class <II, we evaluated the blood pressure (Finapres), heart rate (ECG), and muscle sympathetic nerve traffic (MSNA; by microneurography) responses to isolated monofocal PVCs. MSNA, quantified as bursts/100 heart beats, was significantly increased in EH (57.8+/-3.8, P<0.05) and CHF patients (77.7+/-4.0, P<0.01) compared with controls (44.6+/-4.4). In controls, the PVC-induced blood pressure fall and overshoot were accompanied by a sympathoexcitation (144.2+/-14%), followed by a period of sympathoinhibition (average duration, 12043+/-985 ms). The responses were similar in EH but not in CHF, in whom the magnitude of the sympathoexcitation and particularly the duration of the subsequent sympathoinhibition were strikingly reduced (average reduction, -46.1 and -72.8%, respectively). The most important factor accounting for this reduction appeared to be an altered baroreflex response to the PVC-induced BP changes. These data demonstrate that the MSNA responses to spontaneous PVCs are similar in controls and EH but markedly impaired in CHF, presumably because of the baroreflex alteration. This may represent an important factor for the genesis of the life-threatening ventricular arrhythmias that characterize CHF.

Aged↗
PubMed2002

Pathophysiological aspects of hypertensive disease in women.

Although during the past two decades there has been considerable progress in the understanding of the pathophysiology of human essential hypertension, the basic mechanisms responsible for the development and progression of the disease still remain largely undefined. This also applies to the pathophysiology of hypertension in women, although a number of haemodynamic, vascular, metabolic and neurohumoral factors have been identified throughout the years as being characterized by a gender-specific relation. This paper will examine the main differences in the haemodynamic, vascular, metabolic and neurohumoral profile characterizing normotensive as well as hypertensive females as compared with age-matched males. Although in some instances clearcut differences between genders can be found, overall the pathophysiological picture of the hypertensive state does not seem to have significant differences in men and women, at least up to the years when the menopausal-related hormonal changes take place.

Evidence-Based Medicine↗
PubMed2002

Systolic blood pressure: an underestimated cardiovascular risk factor.

Classification of the severity of hypertension and recommendations on the blood pressure values to be achieved during antihypertensive drug treatment have for decades been based on diastolic values. It is now clear, however, that systolic blood pressure is by no means less important. This paper will focus on the following sets of evidence: (1) that epidemiologically a selective elevation of systolic blood pressure has a major prevalence in the elderly population; (2) that isolated systolic hypertension carries a marked increase in the risk of cardiovascular disease and that even in systo-diastolic hypertension this risk may be more closely related to systolic than to diastolic blood pressure; (3) that treatment of systolic hypertension greatly reduces cardiovascular complications and that in all conditions this reduction is related to the treatment-induced reduction in systolic blood pressure to a degree similar to or superior to the relationship with the reduction in diastolic blood pressure; and (4) that in the hypertensive fraction of the population, control of systolic blood pressure is achieved much less often than control of diastolic blood pressure. That this last point is also the case in major intervention trials suggests that normalization of systolic blood pressure may be intrinsically more difficult than normalization of diastolic blood pressure, possibly because of the difficulty of reversing the pathophysiological abnormalities responsible for the elevation of systolic blood pressure. This emphasizes the importance of research into new drugs or treatment types with greater efficacy in systolic hypertension.

Aged↗
PubMedDate not supplied

Baroreflex function in hypertension: consequences for antihypertensive therapy.

Studies performed in experimental animal models of hypertension as well as in human hypertension have unequivocally shown that reflex cardiovascular control undergoes profound changes with high blood pressure and participates throughout direct and indirect mechanisms at the development and progression of hypertension-related target organ damage. This explains why investigation of the effects of antihypertensive drugs on neural cardiovascular control has a significant impact on hypertension treatment. This review will examine the main features of cardiovascular reflex control in hypertension and the effects of the different classes of antihypertensive drugs in uncomplicated and complicated hypertension.

Antihypertensive Agents↗