N-terminal prohormone brain natriuretic peptide (NT-proBNP) as a noninvasive marker for restrictive syndromes

Constrictive pericarditis (CP) and restrictive cardiomyopathy share many similarities in both their clinical and hemodynamic characteristics and N-terminal prohormone brain natriuretic peptide (NT-proBNP) is a sensitive marker of cardiac diastolic dysfunction. The objectives of the present study were to determine whether serum NT-proBNP was high in patients with endomyocardial fibrosis (EMF) and CP, and to investigate how this relates to diastolic dysfunction. Thirty-three patients were divided into two groups: CP (16 patients) and EMF (17 patients). The control group consisted of 30 healthy individuals. Patients were evaluated by bidimensional echocardiography, with restriction syndrome evaluated by pulsed Doppler of the mitral flow and serum NT-proBNP measured by immunoassay and detected by electrochemiluminescence. Spearman correlation coefficient was used to analyze the association between log NT-proBNP and echocardiographic parameters. Log NT-proBNP was significantly higher (P < 0.05) in CP patients (log mean: 2.67 pg/mL; 95%CI: 2.43-2.92 log pg/mL) and in EMF patients (log mean: 2.91 pg/mL; 95%CI: 2.70-3.12 log pg/mL) compared with the control group (log mean: 1.45; 95%CI: 1.32-1.60 log pg/mL). There were no statistical differences between EMF and CP patients (P = 0.689) in terms of NT-proBNP. The NT-proBNP log tended to correlate with peak velocity of the E wave (r = 0.439; P = 0.060, but not with A wave (r = -0.399; P = 0.112). Serum NT-proBNP concentration can be used as a marker to detect the presence of diastolic dysfunction in patients with restrictive syndrome; however, serum NT-proBNP levels cannot be used to differentiate restrictive cardiomyopathy from CP

Myocardial T1 mapping and extracellular volume quantification in patients with left ventricular non-compaction cardiomyopathy

Aims: From pathophysiological mechanisms to risk stratification and management, much debate and discussion persist regarding left ventricular non-compaction cardiomyopathy (LVNC). This study aimed to characterize myocardial T1 mapping and extracellular volume (ECV) fraction by cardiovascular magnetic resonance (CMR), and investigate how these biomarkers relate to left ventricular ejection fraction (LVEF) and ventricular arrhythmias (VA) in LVNC. Methods and results: Patients with LVNC (n = 36) and healthy controls (n = 18) were enrolled to perform a CMR with T1 mapping. ECV was quantified in LV segments without late gadolinium enhancement (LGE) areas to investigate diffuse myocardial fibrosis. Patients with LVNC had slightly higher native T1 (1024 ± 43 ms vs. 995 ± 22 ms, P = 0.01) and substantially expanded ECV (28.0 ± 4.5% vs. 23.5 ± 2.2%, P &lt; 0.001) compared to controls. The ECV was independently associated with LVEF (β = -1.3, P = 0.001). Among patients without LGE, VAs were associated with higher ECV (27.7% with VA vs. 25.8% without VA, P = 0.002). Conclusion: In LVNC, tissue characterization by T1 mapping suggests an extracellular expansion by diffuse fibrosis in myocardium without LGE, which was associated with myocardial dysfunction and VA, but not with the amount of non-compacted myocardium

Subclinical Regional Left Ventricular Dysfunction In Obese Patients With And Without Hypertension Or Hypertrophy

We investigated the impact of obesity on the abnormalities of systolic and diastolic regional left ventricular (LV) function in patients with or without hypertension or hypertrophy, and without heart failure. We studied 120 individuals divided into 6 groups of 20 patients (42 6 years, 60 females) using standard and pulsed-wave tissue Doppler imaging (TDI) echocardiography, and heterogeneity index (HI): nonobese (I: no hypertension, no hypertrophy, control group; II: hypertension, no hypertrophy; III: hypertension and hypertrophy) and obese (IV: no hypertension, no hypertrophy; V: hypertension, no hypertrophy; VI: hypertension and hypertrophy). The criterion for obesity was BMI 30kg/m -2, for hypertension was blood pressure 140/90mmHg, for hypertrophy in nonobese was LV mass/body surface area (BSA) 134g/m -2 (men) and 110mg/m -2 (women), and in obese was LV mass/height (2.7) 50 (men) and 40 (women). Obese groups had normal LV ejection fraction compared with nonobese groups, but decreased longitudinal and radial systolic myocardial peak velocities (S′), and early diastolic myocardial peak velocity (E′). Also, a great variability of E′ and late diastolic myocardial peak velocity (A′) from the longitudinal basal region was observed in obese groups (E′basal nonobese: 11 7 vs. obese 19 11, P 0.001, A′basal nonobese: 7 4 vs. obese 11 7, P 0.001). Our findings were more evident when comparing groups IV with V and VI, with the latter having concentric hypertrophy and obvious segmental systolic and diastolic dysfunctions. Subclinical myocardial alterations and increased variability of the velocities were observed in obese groups, especially with hypertension and hypertrophy, reflecting impaired regional LV relaxation, segmental atrial, and systolic dysfunctions. © 2011 The Obesity Society.19612961303Casale, P.N., Devereux, R.B., Milner, M., Value of echocardiographic measurement of left ventricular mass in predicting cardiovascular morbid events in hypertensive men (1986) Annals of Internal Medicine, 105 (2), pp. 173-178Manson, J.E., Willett, W.C., Stampfer, M.J., Body weight and mortality among women (1995) N Engl J Med, 333, pp. 677-685Must, A., Spadano, J., Coakley, E.H., Field, A.E., Colditz, G., Dietz, W.H., The disease burden associated with overweight and obesity (1999) Journal of the American Medical Association, 282 (16), pp. 1523-1529. , DOI 10.1001/jama.282.16.1523Hubert, H.B., Feinleib, M., McNamara, P.M., Castelli, W.P., Obesity as an independent risk factor for cardiovascular disease: A 26-year follow-up of participants in the Framingham Heart Study (1983) Circulation, 67 (5), pp. 968-977Kenchaiah, S., Evans, J.C., Levy, D., Wilson, P.W.F., Benjamin, E.J., Larson, M.G., Kannel, W.B., Vasan, R.S., Obesity and the risk of heart failure (2002) New England Journal of Medicine, 347 (5), pp. 305-313. , DOI 10.1056/NEJMoa020245Murphy, N.F., MacIntyre, K., Stewart, S., Hart, C.L., Hole, D., McMurray, J.J.V., Long-term cardiovascular consequences of obesity: 20-Year follow-up of more than 15 000 middle-aged men and women (the Renfrew-Paisley study) (2006) European Heart Journal, 27 (1), pp. 96-106. , DOI 10.1093/eurheartj/ehi506Calle, E.E., Thun, M.J., Petrelli, J.M., Rodriguez, C., Heath Jr., C.W., Body-mass index and mortality in a prospective cohort of U.S. adults (1999) New England Journal of Medicine, 341 (15), pp. 1097-1105. , DOI 10.1056/NEJM199910073411501Levy, D., Garrison, R.J., Savage, D.D., Kannel, W.B., Castelli, W.P., Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study (1990) New England Journal of Medicine, 322 (22), pp. 1561-1566Devereux, R.B., Alonso, D.R., Lutas, E.M., Echocardiographic assessment of left ventricular hypertrophy: Comparison to necropsy findings (1986) American Journal of Cardiology, 57 (6), pp. 450-458. , DOI 10.1016/0002-9149(86)90771-XMacMahon, S.W., Wilcken, D.E.L., Macdonald, G.J., The effect of weight reduction on left ventricular mass. A randomized controlled trial in young, overweight hypertensive patients (1986) New England Journal of Medicine, 314 (6), pp. 334-339Messerli, F.H., Christie, B., DeCarvalho, J.G.R., Obesity and essential hypertension. Hemodynamics, intravascular volume, sodium excretion, and plasma renin activity (1981) Archives of Internal Medicine, 141 (1), pp. 81-85. , DOI 10.1001/archinte.141.1.81Barouch, L.A., Berkowitz, D.E., Harrison, R.W., O'Donnell, C.P., Hare, J.M., Disruption of leptin signaling contributes to cardiac hypertrophy independently of body weight in mice (2003) Circulation, 108 (6), pp. 754-759. , DOI 10.1161/01.CIR.0000083716.82622.FDAlpert, M.A., Obesity cardiomyopathy: Pathophysiology and evolution of the clinical syndrome (2001) American Journal of the Medical Sciences, 321 (4), pp. 225-236Redfield, M.M., Jacobsen, S.J., Burnett Jr., J.C., Mahoney, D.W., Bailey, K.R., Rodeheffer, R.J., Burden of systolic and diastolic ventricular dysfunction in the community: Appreciating the scope of the heart failure epidemic (2003) Journal of the American Medical Association, 289 (2), pp. 194-202. , DOI 10.1001/jama.289.2.194Levy, D., Larson, M.G., Vasan, R.S., Kannel, W.B., Ho, K.K.L., The progression from hypertension to congestive heart failure (1996) Journal of the American Medical Association, 275 (20), pp. 1557-1562. , DOI 10.1001/jama.275.20.1557Peterson, L.R., Waggoner, A.D., Schechtman, K.B., Meyer, T., Gropler, R.J., Barzilai, B., Davila-Roman, V.G., Alterations in left ventricular structure and function in young healthy obese women: Assessment by echocardiography and tissue Doppler imaging (2004) Journal of the American College of Cardiology, 43 (8), pp. 1399-1404. , DOI 10.1016/j.jacc.2003.10.062, PII S0735109704001974The 7th report of the joint national committee on prevention, detection, evaluation and treatment of high blood pressure -JNC VII (2003) JAMA, 289, pp. 1560-1572De Simone, G., Daniels, S.R., Devereux, R.B., Left ventricular mass and body size in normotensive children and adults: Assessment of allometric relations and impact of overweight (1992) J Am Coll Cardiol, 20, pp. 1251-1260Lang, R.M., Bierig, M., Devereux, R.B., Flachskampf, F.A., Foster, E., Pellikka, P.A., Picard, M.H., Stewart, W.J., Recommendations for chamber quantification: A report from the American Society of Echocardiography's guidelines and standards committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology (2005) Journal of the American Society of Echocardiography, 18 (12), pp. 1440-1463. , DOI 10.1016/j.echo.2005.10.005, PII S0894731705009831Quiñones, M.A., Otto, C.M., Stoddard, M., Waggoner, A., Zoghbi, W.A., Recommendations for quantification of Doppler echocardiography: A report from the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography (2002) J Am Soc Echocardiogr, 15, pp. 167-184. , Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of EchocardiographyNagueh, S.F., Appleton, C.P., Gillebert, T.C., Recommendations for the evaluation of left ventricular diastolic function by echocardiography (2009) J Am Soc Echocardiogr, 22, pp. 107-133Cardim, N., Oliveira, A.G., Longo, S., Ferreira, T., Pereira, A., Reis, R.P., Correia, J.M., Doppler tissue imaging: Regional myocardial function in hypertrophic cardiomyopathy and in athlete's heart (2003) Journal of the American Society of Echocardiography, 16 (3), pp. 223-232. , DOI 10.1067/mje.2003.13Krishnan, R., Becker, R.J., Beighley, L.M., Lopez-Candales, A., Impact of body mass index on markers of left ventricular thickness and mass calculation: Results of a pilot analysis (2005) Echocardiography, 22 (3), pp. 203-210. , DOI 10.1111/j.0742-2822.2005.03138.xLauer, M.S., Anderson, K.M., Levy, D., Separate and joint influences of obesity and mild hypertension on left ventricular mass and geometry: The Framingham Heart Study (1992) J Am Coll Cardiol, 19, pp. 130-134Willens, H.J., Chakko, S.C., Lowery, M.H., Byers, P., Labrador, E., Gallagher, A., Castrillon, J.C., Myerburg, R.J., Tissue Doppler imaging of the right and left ventricle in severe obesity (body mass index &gt;35 kg/m 2) (2004) American Journal of Cardiology, 94 (8), pp. 1087-1090. , DOI 10.1016/j.amjcard.2004.06.076, PII S0002914904010847Wong, C.Y., O'Moore-Sullivan, T., Leano, R., Byrne, N., Beller, E., Marwick, T.H., Alterations of left ventricular myocardial characteristics associated with obesity (2004) Circulation, 110 (19), pp. 3081-3087. , DOI 10.1161/01.CIR.0000147184.13872.0FRen, J., Sowers, J.R., Walsh, M.F., Brown, R.A., Reduced contractile response to insulin and IGF-I in ventricular myocytes from genetically obese Zucker rats (2000) Am J Physiol Heart Circ Physiol, 279, pp. H1708-H1714Amad, K.H., Brennan, J.C., Alexander, J.K., The cardiac pathology of chronic exogenous obesity (1965) Circulation, 32, pp. 740-745Alpert, M.A., Terry, B.E., Mulekar, M., Cohen, M.V., Massey, C.V., Fan, T.M., Panayiotou, H., Mukerji, V., Cardiac morphology and left ventricular function in normotensive morbidly obese patients with and without congestive heart failure, and effect of weight loss (1997) American Journal of Cardiology, 80 (6), pp. 736-740. , DOI 10.1016/S0002-9149(97)00505-5, PII S0002914997005055Rodriguez, L., Garcia, M., Ares, M., Griffin, B.P., Nakatani, S., Thomas, J.D., Assessment of mitral annular dynamics during diastole by Doppler tissue imaging: Comparison with mitral Doppler inflow in subjects without heart disease and in patients with left ventricular hypertrophy (1996) American Heart Journal, 131 (5), pp. 982-987. , DOI 10.1016/S0002-8703(96)90183-0Di Salvo, G., Pacileo, G., Del Giudice, E.M., Natale, F., Limongelli, G., Verrengia, M., Rea, A., Calabro, R., Abnormal myocardial deformation properties in obese, non-hypertensive children: An ambulatory blood pressure monitoring, standard echocardiographic, and strain rate imaging study (2006) European Heart Journal, 27 (22), pp. 2689-2695. , DOI 10.1093/eurheartj/ehl163Ballo, P., Motto, A., Mondillo, S., Faraguti, S.A., Impact of obesity on left ventricular mass and function in subjects with chronic volume overload (2007) Obesity, 15 (8), pp. 2019-2026Dasgupta, P., Ramhanmdany, E., Brigden, G., Improvement in left ventricular function after rapid weight loss in obesity (1992) Eur Heart J, 13, pp. 1060-1066Willens, H.J., Chakko, S.C., Byers, P., Chirinos, J.A., Labrador, E., Castrillon, J.C., Lowery, M.H., Effects of weight loss after gastric bypass on right and left ventricular function assessed by tissue doppler imaging (2005) American Journal of Cardiology, 95 (12), pp. 1521-1524. , DOI 10.1016/j.amjcard.2005.02.029, PII S000291490500490

Leptin levels in different forms of Chagas' disease

Leptin is produced primarily by adipocytes. Although originally associated with the central regulation of satiety and energy metabolism, increasing evidence indicates that leptin may be an important mediator in cardiovascular pathophysiology. The aim of the present study was to investigate plasma leptin levels in patient with Chagas' heart disease and their relation to different forms of the disease. We studied 52 chagasic patients and 30 controls matched for age and body mass index. All subjects underwent anthropometric, leptin and N-terminal pro-brain natriuretic peptide (NT-proBNP) measurements and were evaluated by echocardiography, 12-lead electrocardiogram (ECG), and chest X-ray. All patients had fasting blood samples taken between 8:00 and 9:00 am. Chagasic patients were divided into 3 groups: group I (indeterminate form, IF group) consisted of 24 subjects with 2 positive serologic reactions for Chagas' disease and no cardiac involvement as evaluated by chest X-rays, ECG and two-dimensional echocardiography; group II (showing ECG abnormalities and normal left ventricular systolic function, ECG group) consisted of 14 patients; group III consisted of 14 patients with congestive heart failure (CHF group) and left ventricular dysfunction. Serum leptin levels were significantly lower (P < 0.001) in the CHF group (1.4 ± 0.8 ng/mL) when compared to the IF group (5.3 ± 5.3 ng/mL), ECG group (9.7 ± 10.7 ng/mL), and control group (8.1 ± 7.8 ng/mL). NT-proBNP levels were significantly higher (P < 0.001) in the CHF group (831.8 ± 800.1 pg/mL) when compared to the IF group (53.2 ± 33.3 pg/mL), ECG group (83.3 ± 57.4 pg/mL), and control group (32 ± 22.7 pg/mL). Patients with Chagas' disease and an advanced stage of CHF have high levels of NT-ProBNP andlow plasma levels of leptin. One or more leptin-suppressing mechanisms may operate in chagasic patients

N-terminal-pro-brain natriuretic peptide, but not brain natriuretic peptide, is increased in patients with severe obesity

Elevated body mass index (BMI) has been reported as a risk factor for heart failure. Prevention of heart failure through identification and management of risk factors and preclinical phases of the disease is a priority. Levels of natriuretic peptides as well as activity of their receptors have been found altered in obese persons with some conflicting results. We investigated cardiac involvement in severely obese patients by determining N-terminal-pro-brain natriuretic peptide (NT-proBNP) and brain natriuretic peptide (BNP) and attempting to correlate the levels of these peptides in serum and plasma, respectively, with BMI, duration of obesity, waist circumference, and echocardiographic parameters. Thirty-three patients with severe obesity (mean BMI: 46.39 kg/m², mean age: 39 years) were studied. The control group contained 30 healthy age-matched individuals (BMI: <25 kg/m², mean age: 43 years). The t-test and Spearman correlation were used for statistical analysis. Log-NT-proBNP was significantly higher (P = 0.003) in obese patients (mean 1.67, 95% CI: 1.50-1.83 log pg/mL) compared to controls (mean: 1.32, 95% CI: 1.17-1.47 log pg/mL). The Log-NT-proBNP concentration correlated with duration of obesity (r = 0.339, P < 0.004). No difference was detected in the Log-BNP concentration (P = 0.63) of obese patients (mean: 0.73, 95% CI: 0.46-1.00 log pg/mL) compared to controls (mean: 0.66, 95% CI: 0.51-0.81 log pg/mL). NT-proBNP, but not BNP, is increased in severely obese patients and its concentration in serum is correlated with duration of obesity. NT-proBNP may be useful as an early diagnostic tool for the detection of cardiac burden due to severe obesity

Prolonged heart rate recovery time after 6-minute walk test is an independent risk factor for cardiac events in heart failure: A prospective cohort study

To determine whether the time for peak exercise heart rate to return to resting heart rate after the 6-minute walk test (6MWT) can predict cardiac events in patients with heart failure (HF) within 2 years. Prospective cohort study. HF outpatient facility at a tertiary teaching hospital. Seventy-six patients with HF, New York Heart Association functional classification II and III, and left ventricular ejection fraction <50%. Patients used a heart rate monitor to measure the time for peak exercise heart rate to return to resting heart rate after the 6MWT. Data were analysed using Polar Pro-Trainer 5 software (Kempele, Finland). Patients were followed for >2 years for cardiac events (hospitalisations and death). Thirty-four patients had cardiac events during the 2-year follow-up period. There was a significant difference in time to return to resting heart rate between the groups with and without cardiac events {with 3.6 [standard deviation (SD) A] vs without 2.8 (SD B) minutes; mean difference C; 95% confidence interval (CI) of the difference D to E; P=0.003}. No significant differences between patients with and without cardiac events were found for mean walking distance, mean heart rate recovery at 1minute and mean heart rate recovery at 2minutes. The receiver operating curve discriminated between patients with and without cardiac events (área under the curve 0.71, 95% CI 0.61 to 0.81; P<0.001). Using logistic regression analysis, prolonged time to return to resting heart rate (≥3minutes) independently increased the risk for cardiac events 6.9-fold (95% CI 2.34 to 20.12; P<0.001). The Kaplan–Meier curve showed more cardiac events in patients with prolonged time to return to resting heart rate (P=0.028). Prolonged time to return to resting heart rate (≥3minutes) after the 6MWT was an independent predictor of cardiac events in patients with HF

Collagen content, but not the ratios of collagen type III/I mRNAs, differs among hypertensive, alcoholic, and idiopathic dilated cardiomyopathy

Cardiac interstitial fibrosis may contribute to ventricular dysfunction and the prognosis of patients with dilated cardiomyopathy. The objective of the present study was to determine if total myocardial collagen content and collagen type III/I (III/I ratio) mRNAs differ in hypertensive, alcoholic, and idiopathic dilated cardiomyopathy subjects. Echocardiography and exercise cardiopulmonary testing were performed in patients with idiopathic (N = 22), hypertensive (N = 12), and alcoholic (N = 11) dilated cardiomyopathy. Morphometric analysis of collagen was performed in fragments obtained by endomyocardial biopsy with picrosirius red staining. The collagen III/I ratio was determined by reverse transcription polymerase chain reaction. Samples of controls (N = 10) were obtained from autopsy. Echocardiographic variables and maximal oxygen uptake were not different among dilated cardiomyopathy groups. Collagen was higher in all dilated cardiomyopathy groups (idiopathic, hypertensive and alcoholic, 7.36 ± 1.09%) versus controls (1.12 ± 0.18%), P < 0.05. Collagen was lower in idiopathic dilated cardiomyopathy (4.97 ± 0.83%) than hypertensive (8.50 ± 1.11%) and alcoholic (10.77 ± 2.09%) samples (P < 0.005 for both). The collagen III/I ratio in all samples from dilated cardiomyopathy patients was higher compared to that in controls (0.29 ± 0.04, P < 0.05) but was the same in the samples from idiopathic (0.77 ± 0.07), hypertensive (0.75 ± 0.07), and alcoholic (0.81 ± 0.16) dilated cardiomyopathy groups. Because of the different physical properties of the types of collagen, the higher III/I ratio may contribute to progressive ventricular dilation and dysfunction in dilated cardiomyopathy patients