Rosario Scaglione

The Usefulness of Bioelectrical Impedance Analysis in Differentiating Dyspnea Due to Decompensated Heart Failure

BACKGROUND Acute dyspnea poses a diagnostic challenge for physicians, and the current methods in differentiating cardiac from non-cardiac causes have been limited to date. Recently, the brain natriuretic peptide (BNP) rapid test has been validated in the emergency room. Nevertheless, the early accumulation of fluid in the interstitial space in the body and in the lungs, which characterizes patients with ADHF, is well estimated by BIA. We investigate whether bioelectrical impedance analysis (BIA) can serve as a noninvasive diagnostic tool in the differential diagnosis of acute decompensated heart failure (ADHF) in the emergency department (ED). METHODS AND RESULTS A total of 292 patients presenting with acute dyspnea to the ED were evaluated by using a conventional diagnostic strategy and rapid BNP measures. Segmental (Seg) and whole-body (WB) BIA resistance (Rz) and reactance (Xc) on entry were immediately detected. After hospital discharge, an expert team classified enrolled patients into ADHF and non-ADHF. A total of 58.9% of patients had ADHF, whereas 41.1% were non-ADHF. ADHF patients showed significantly (P < .001) higher BNP values (591.8 +/- 501 versus 69.5 +/- 42 pg/mL), a significant (P < .001) reduction of Seg (35.5 + 8.2 versus 66.4 + 10.5) and WB (402.3 + 55.5 versus 513.2 + 41.8) Rz (Ohm), and a significant correlation (P < .0001) between BNP and Seg (r = -0,62) and WB (r = -0.63) bioelectrical Rz was also identified. Multiple regression analysis revealed that whole body and segmental BIA were strong predictors of ADHF alone or in combination with BNP. CONCLUSIONS Our data suggest that Seg and WB BIA are a useful, simple, rapid, and noninvasive diagnostic adjunct in the early diagnosis of dyspnea from ADHF.

Central obesity and hypertension: The role of plasma endothelin

Hypertension and central obesity are two conditions closely linked, but the mechanisms responsible for obesity-associated hypertension are still unclear. In the last few years, several studies addressed the role of endothelin-1 (ET-1) in the development and maintenance of hypertension. This study was designed to evaluate plasma ET-1 in normotensive and hypertensive central obese subjects compared with a lean healthy group. Our final goal was to analyze the relationship between plasma ET-1, blood pressure, and left ventricular structure and function in central obese subjects (both normotensives and hypertensives). ET-levels have been assessed by the radioimmunoassay method in 20 lean normotensives and in 57 central obese subjects; 30 of them were hypertensives and 27 of them were normotensives. Twenty-four-hour mean blood pressure (MBP/24 h) by noninvasive ambulatory blood pressure monitoring, left ventricular mass/ height (LVM/H), and left ventricular ejection fraction (LVEF) by echocardiography and peak filling rate (PFR) by radionuclide study were also measured. ET levels were significantly (P < .05) higher in obese hypertensives and obese normotensives than in lean normotensives. In addition, ET levels were significantly (P < .05) higher in obese hypertensives than in obese normotensives. ET were directly related to LVM/ H (r = 0.86; P < .001) and MBP/24 h (r = 0.48; P < .009) but only in obese hypertensives. Multiple regression analysis indicated that ET-1 plasma levels remain an independent predictor of MBP/ 24 h and LVM/H also when age was included in the analysis. These data suggest that obesity-associated hypertension is characterized by an endothelial dysfunction that may contribute to the higher cardiovascular risk detectable in these patients.

Hemostatic function in young subjects with central obesity: relationship with left ventricular function.

This study was designed to evaluate coagulation and fibrinolysis activity and their relationship with left ventricular function in young obese subjects with central fat distribution. We assessed coagulation and fibrinolysis activity by evaluation of factor VII activity, fibrinogen and plasminogen, plasminogen activator inhibitor (PAI), and tissue plasminogen activator antigen basally (tPA1) and after venous occlusion (tPA2). These measures were evaluated in young (< 40 years) obese subjects with central fat distribution (n = 19) and in comparable lean subjects (n = 20). Blood glucose, triglycerides, total and high-density lipoprotein (HDL) cholesterol, apolipoprotein (apo) A1 and apo B, fasting immunoreactive insulin, and lipoprotein(a) levels were also measured by current methods. Left ventricular ejection fraction (LVEF) and peak filling rate (PFR) determined by radionuclide angiocardiography and left ventricular mass (LVM) and LVM indexed for body height (LVM/H) determined by echocardiographic study were calculated. Central obesity was evaluated by the waist to hip ratio (WHR) according to the criteria of the Italian Consensus Conference of Obesity. Factor VII (P < .001), fibrinogen (P < .001), plasminogen (P < .001), PAI activity (P < .001), tPA1 (P < .02), fasting blood glucose (P < .01), apo B (P < .02), and immunoreactive insulin (P < .01) were significantly higher in obese than in lean subjects. In contrast, HDL cholesterol (P < .01), tPA2 (P < .01), LVEF (P < .001), and PFR (P < .02) were significantly lower in obese than in lean subjects. In all subjects, WHR correlated directly with fibrinogen and inversely with tPA2; LVEF correlated inversely with tPA1, PAI, and fibrinogen; and PFR correlated inversely with factor VII activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Echo-Doppler left ventricular filling abnormalities in patients with rheumatoid arthritis without clinically evident cardiovascular disease.

Our investigation aimed at verifying diastolic abnormalities in rheumatoid patients, without clinically evident cardiovascular disease and other confounding complaints, by using pulsed Doppler examination of transmitral blood flow. We selected 40 patients fulfilling revised American Rheumatism Association (ARA) criteria for the diagnosis of rheumatoid arthritis having no symptoms of cardiac disease or clinical findings of other extracardiac diseases. We also studied 40 rheumatoid‐matched healthy volunteers as a control group. An echocardiographic examination was carried out on each subject. Left ventricular structural and functional measurements were obtained. Interventricular septal thickness and left ventricular mass index were significantly higher in rheumatoid patients than in the control group. We also found in rheumatoid patients higher mean values of peak A velocity and A/E ratio. When multiple linear regression analysis was performed on the data of rheumatoid patients we found an independent relationship only between A/E ratio and left ventricular mass. In conclusion, our results confirm diastolic abnormalities in rheumatoid patients and point out that these abnormalities also affect echo‐Doppler parameters of left ventricular filling. Moreover, further analysis of our data may suggest the possibility that structural left ventricle changes could be responsible for left ventricular filling impairment.

Visceral obesity and metabolic syndrome: two faces of the same medal?

In this review, we have analyzed the role of visceral obesity in the occurrence of metabolic syndrome (MetS). MetS is a common metabolic disorder that has been related recently to the increasing prevalence of obesity. The disorder is defined in various ways, but in the near future a new definition(s) should be applicable worldwide. The pathophysiology has been largely attributed, in the past years, to insulin resistance, although several epidemiological and pathophysiological data now indicate visceral obesity as a main factor in the occurrence of all the components of MetS. In view of this, relationships among visceral obesity, free fatty acids, dyslipidemia and insulin resistance have been reported. In addition, the effects of some adipocytokines and other proinflammatory factors produced by fat accumulation on the occurrence of MetS have been also emphasized. Accordingly, the “hypoadiponectinemia hypothesis” has been proposed as the most interesting to explain the pathophysiology of MetS. The epidemiologic, pathophysiologic and clinical data reported seem to indicate that MetS might be considered a fatal consequence of visceral obesity.

Heart involvement in Rheumatoid Arthritis: Systematic review and meta-analysis

OBJECTIVE The aim of our study was to conduct a systematic review with meta-analysis of the current case-control studies about the valvular and pericardial involvement in patients with Rheumatoid Arthritis (RA), asymptomatic for cardiovascular diseases. METHODS Case-control studies were identified by searching PubMed (1975-2010) and the Cochrane Central Register of Controlled Trials (CENTRAL) (1975-2010). Participants were adult patients with RA asymptomatic for cardiovascular diseases, and the outcome measure was the presence of cardiac involvement. RESULTS Quantitative synthesis included 10 relevant studies out of 2326 bibliographic citations that had been found. RA resulted significantly associated to pericardial effusion (OR 10.7; 95% CI 5.0-23.0), valvular nodules (OR 12.5; 95% CI 2.8-55.4), tricuspidal valve insufficiency (OR 5.3; 95% CI 2.4-11.6), aortic valve stenosis (OR 5.2; 95% CI 1.1-24.1), mitral valve insufficiency (OR 3.4; 95% CI 1.7-6.7), aortic valve insufficiency (OR 1.7; 95% CI 1.0-2.7), combined valvular alterations (OR 4.3; 95% CI 2.3-8.0), mitral valve thickening and/or calcification (OR 5.0; 95% CI 2.0-12.7), aortic valve thickening and/or calcification (OR 4.4; 95% CI 1.1-17.4), valvular thickening and/or calcification (OR 4.8; 95% CI 2.2-10.5), and mitral valve prolapse (OR 2.2; 95% CI 1.2-4.0). CONCLUSIONS Our systematic review pointed out the strength and the grade of both pericardial and cardiac valvular involvement in RA patients. Our findings underscore the importance of an echocardiographic assessment at least in clinical research when RA patients are involved. Moreover, further research is needed to understand the possible relationship of our findings and the increased cardiovascular mortality.

Heredity and obesity-associated hypertension: impact of hormonal characteristics and left ventricular mass

Objectives: To investigate the influence of heredity on obesity-associated hypertension, we evaluated casual and 24-h blood pressure, left ventricular mass and some metabolic and hormonal measurements in normotensive obese subjects. Design: Healthy, normotensive obese subjects (n=81) with positive or negative family history of hypertension were studied. Both groups were also subdivided according to a positive or a negative family history of obesity. Accordingly, 45 obese subjects had a positive family history of hypertension, 25 of these having a positive (subgroup A) and 20 having a negative family history of obesity (subgroup B). The other 36 obese subjects had a negative family history of hypertension, 19 of these having a positive (subgroup C) and 17 having a negative family history of obesity (subgroup D). Methods: Casual and 24-h systolic (SBP), diastolic (DBP) and mean blood pressure (MBP) were evaluated. Serum fasting blood sugar, total cholesterol and triglycerides levels, urinary excretion of sodium, immunoreactive fasting insulin, plasma ANF levels, plasma renin activity (PRA), plasma aldosterone level, plasma adrenaline and noradrenaline levels and echocardiographic total left ventricular mass (LVM) and LVM: height ratio were also calculated. Results: Twenty-four-hour DBP, 24-h MBP, LVM, LVM:height ratio, total cholesterol and PRA values were significantly higher in normotensive obese offspring of hypertensive parents than in obese offspring of normotensive parents. Twenty-four-hour DBP and MBP, LVM, LVM:height ratio, insulin level, insulin:glucose ratio and PRA were significantly higher in subgroup A than in subgroup B. Fasting blood sugar level, 24-h DBP and MBP, insulin level, insulin:glucose ratio, PRA, noradrenaline, adrenaline and plasma aldosterone levels were significantly higher in subgroup C than in subgroup D. Multivariate analysis also indicated that 24-h MBP and PRA levels were significantly influenced by the association between a positive family history of hypertension and obesity. Conclusions: The present results suggest that a family history of obesity might increase the risk of developing hypertension in obese subjects. An elevated PRA may precede the development of hypertension in obese subjects who are at risk for developing hypertension.

Hypoadiponectinemia: A Link between Visceral Obesity and Metabolic Syndrome

Metabolic syndrome (MetS) represents a combination of cardiometabolic risk factors, including visceral obesity, glucose intolerance or type 2 diabetes, elevated triglycerides, reduced HDL cholesterol, and hypertension. MetS is rapidly increasing in prevalence worldwide as a consequence of the “epidemic” obesity, with a considerable impact on the global incidence of cardiovascular disease and type 2 diabetes. At present, there is a growing interest on the role of visceral fat accumulation in the occurrence of MetS. In this review, the effects of adipocytokines and other proinflammatory factors produced by fat accumulation on the occurrence of the MetS have been also emphasized. Accordingly, the “hypoadiponectinemia” has been proposed as the most interesting new hypothesis to explain the pathophysiology of MetS.

Central obesity and hypertensive renal disease: association between higher levels of BMI, circulating transforming growth factor beta1 and urinary albumin excretion.

Objective: In this study, the relationship between circulating transforming growth factor β1 (TGFβ1) and urinary albumin excretion (UAE) has been investigated in non‐obese and central obese hypertensive patients. Design and Patients: Fifty‐eight consecutive hypertensive outpatients both lean and with central obesity were enrolled and divided in three groups, according to their body mass index (BMI) values. Group A: 16 lean hypertensives (men with BMI <25 kg/m 2 and women with BMI <24.7 kg/m 2 ); Group B: 16 overweight hypertensives (men with BMI ≥25 kg/m 2 and <30 kg/m 2 and women with BMI ≥24.7 kg/m 2 and <27.3 kg/m 2 ); Group C: 26 obese hypertensives (men with BMI ≥30 kg/m 2 and women with BMI ≥27.3 kg/m 2 ). Measures: In all patients, UAE, by immunonephelometric assay, circulating TGFβ1 by a solid‐phase specific sandwich enzyme‐linked immunosorbent assay (ELISA) technique, blood urea nitrogen (BUN) and creatinine, by routine laboratory methods, were determined. In addition, left ventricular telediastolic internal diameter (LVIDd), interventricular septum diastolic (IVSTd), posterior wall thickness (PWT), total and normalized to height 2.7 left ventricular mass (LVM, LVM/h 2.7 ), relative wall thickness (RWT) and left ventricular ejection fraction (EF) by M‐B Mode echocardiography were calculated. Results: Overweight and obese hypertensives had significantly (p < 0.05) higher BMI, waist–hip ratio (WHR), UAE and TGFβ1 than lean hypertensives. Obese hypertensives had significantly (p < 0.05) higher total and indexed LVM values than lean hypertensives. Obese hypertensives had significantly (p < 0.05) higher BMI, UAE and TGFβ1 than overweight hypertensives. In all subjects, TGFβ1 correlated directly with BMI (r = 0.52; p < 0.0001), WHR (r = 0.48; p < 0.003), MBP (r = 0.31; p < 0.02) and UAE (r = 0.57; p < 0.0001). Multiple regression analysis indicated that BMI, MBP and UAE were able to explain the 47.9% TGFβ1 variability (r = 0.69; p < 0.0001), and that TGFβ1 was the best predictor of UAE changes (r = 0.60; p < 0.0001). Conclusion: Our data suggest that TGFβ1 levels are positively associated with BMI, MBP and UAE in hypertensive subjects. This also indicates that TGFβ1 overproduction might be considered a pathophysiology mechanism of progressive renal function impairment in obese hypertensives.

Left ventricular function response to exercise in normotensive obese subjects: influence of degree and duration of obesity

This study has been designed to evaluate whether duration and severity of obesity can influence left ventricular function response to exercise in obese subjects without other known cardiovascular risk factors such as hypertension, diabetes or hyperlipoproteinemia. A total of 29 obese subjects were included and they were divided, according to their body mass index and to Garrows criteria as follows: Overweight or mildly obese subjects: body mass index from 25 to 30 kg/m2; moderately obese subjects: body mass index > 30 and < 40 kg/m2. Both obese groups were further subdivided according to their duration of obesity evaluated by accurate anamnesis in subgroup A (duration of obesity less than 120 months) and subgroup B (duration of obesity more than 120 months). Left ventricular ejection fraction was detected by blood pool gated radionuclide angiocardiography both at rest and after symptom-limited bicycle ergometer procedure. At peak exercise left ventricular ejection fraction increased significantly (p < 0.05) only in overweight subjects. Exercise produced an increase of left ventricular ejection fraction in 14 overweight and in 5 moderately obese subjects and a decrease in 2 moderately obese subjects. At peak exercise mean heart rate and mean blood pressure increased significantly (p < 0.001) in both groups. When obese subjects were subgrouped according to duration of obesity, left ventricular ejection fraction increased significantly (p < 0.05) only in overweight subjects with duration of obesity less than 120 months. Duration of obesity correlated inversely with percent change in left ventricular ejection fraction (EF) at peak exercise (delta EF) (r = -0.59; p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)