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      Evaluation of Exercise Capacity with Cardiopulmonary Exercise Testing and Type B Natriuretic Peptide Concentrations in Adult Patients with Patent Atrial Septal Defect


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          Adults with patent atrial septal defect (ASD) usually find their exercise capacity satisfactory, and therefore hesitate to accept proposed surgical treatment of the heart disease. The aim of our study was to evaluate both the exercise capacity, using the cardio-pulmonary stress test, and brain natriuretic peptide (BNP) levels in asymptomatic adults with ASD. Thirty-six patients with patent secundum type ASD (aged mean 44.7 ± 8.2 years) were studied. The control group consisted of 25 healthy subjects at the mean age of 45.6 ± 6.1 years. Echocardiography and CPST were performed and BNP levels measured in all subjects. Oxygen uptake (VO<sub>2 max</sub>) was lower in ASD patients than in controls (22.1 ± 5.6 vs. 30.0 ± 6.8 ml/kg/min, p = 0.00001); the VE/VO<sub>2</sub> slope was elevated in ASD patients compared with healthy subjects (31.3 ± 6.6 vs. 26.9 ± 3.3, p = 0.001), and exceeded 34 in 5 patients. VO<sub>2 max</sub> showed a negative correlation with the pulmonary to systemic flow ratio Qp:Qs (r = –0.46, p = 0.004), and a positive correlation was found between the VE/VO<sub>2</sub> slope and Qp:Qs (r = 0.32, p = 0.05). BNP levels were higher in the ASD group than in the controls (60.6 ± 49.9 vs. 32.6 ± 24.5 pg/ml, p = 0.02). BNP correlated positively with RV diameter and Qp:Qs (r = 0.38 and 0.39 respectively, p = 0.03) and negatively with maximum VO<sub>2</sub> (r = –0.5, p = 0.004) and VO<sub>2</sub>% (r = –0.32, p = 0.07). Conclusions: Although most adult patients with ASD perceive their exercise capacity as satisfactory, objective assessment reveals that in fact it is significantly decreased. BNP levels are increased comparing to healthy individuals. Decreased exercise capacity and increased BNP levels seem to result from right ventricular volume overload.

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          Most cited references 29

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          Cardiopulmonary exercise testing for prognosis in chronic heart failure: continuous and independent prognostic value from VE/VCO(2)slope and peak VO(2).

          Chronic heart failure carries a poor prognosis. Cardiopulmonary exercise testing is useful in predicting survival. We set out to establish the prognostic value of peak VO(2)and VE/VCO(2)slope across a range of threshold values. Three hundred and three consecutive patients with stable chronic heart failure underwent cardiopulmonary exercise testing between 1992 and 1996. Their age was 59+/-11 years (mean+/-SD), peak VO(2)17. 8+/- 6.6 ml. kg(-1)min(-1), VE/VCO(2)slope 37+/-12. At the end of follow-up in January 1999, 91 patients had died (after a median of 7 months, interquartile range 3-16 months). The median follow-up for the survivors was 47 months (interquartile range 37-57 months). The areas under the receiver-operating characteristic curves for predicting mortality at 2 years were 0.77 for both peak VO(2)and VE/VCO(2)slope. With peak VO(2)and VE/VCO(2)slope viewed as continuous variables in the Cox proportional-hazards model, they were both highly significant prognostic indicators, both in univariate analysis and bivariate analysis (P<0.001 for VE/VCO(2)slope, P<0.003 for peak VO(2)). Lower peak VO(2)implies poorer prognosis across a range of values from 10 to 20 ml. kg(-1)min(-1), without a unique threshold. Gradations of elevation of the VE/VCO(2)slope also carry prognostic information over a wide range (30-55). The two parameters are comparable in terms of prognostic power, and contribute complementary prognostic information. Copyright 2000 The European Society of Cardiology.
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            Neurohormonal activation and the chronic heart failure syndrome in adults with congenital heart disease.

            Neurohormonal activation characterizes chronic heart failure, relates to outcome, and is a therapeutic target. It is not known whether a similar pattern of neurohormonal activation exists in adults with congenital heart disease and, if so, whether it relates to common measures of disease severity or whether cardiac anatomy is a better discriminant. Concentrations of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), endothelin-1 (ET-1), renin, aldosterone, norepinephrine, and epinephrine were determined in 53 adults with congenital heart disease, comprising 4 distinct anatomic subgroups (29 female; 33.5+/-1.5 years of age; New York Heart Association class 2.0+/-0.1, mean+/-SEM) and 15 healthy control subjects (8 female; 32.3+/-1.3 years of age). Systemic ventricular function was graded by a blinded echocardiographer as normal or mildly, moderately, or severely impaired. Adults with congenital heart disease had elevated levels of ANP (56.6 versus 3.1 pmol/L), BNP (35.8 versus 5.7 pmol/L), ET-1 (2.5 versus 0.7 pmol/L, all P<0.0001), renin (147 versus 16.3 pmol/L), norepinephrine (2.2 versus 1.6 pmol/L, both P<0.01) and aldosterone (546 versus 337 pmol/L, P<0.05). There was a highly significant stepwise increase in ANP, BNP, ET-1, and norepinephrine according to New York Heart Association class and systemic ventricular function, with even asymptomatic patients having evidence of significant neurohormonal activation. In contrast, there was no direct relationship between the 4 anatomic subgroups and any of the neurohormones studied. Neurohormonal activation in adult congenital heart disease bears the hallmarks of chronic heart failure, relating to symptom severity and ventricular dysfunction and not necessarily to anatomic substrate. Neurohormonal antagonism across this large and anatomically diverse population should be considered.
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              The impact of cardiac natriuretic peptide determination on the diagnosis and management of heart failure.

              The long-predicted endocrine function of the heart has been proven by the discovery of atrial natriuretic peptide (atrial natriuretic factor, A-type natriuretic peptide; ANP) 20 years ago. This subsequently led to the description of a whole family of structurally similar but genetically distinct peptides, the natriuretic peptide family, which contributes to cardiovascular homeostasis. These looped peptides promote natriuresis and diuresis, act as vasodilators, and exert antimitogenic effects on cardiovascular tissues. Two members, ANP and brain natriuretic peptide (B-type natriuretic peptide; BNP) are secreted by the heart mainly in response to myocardial stretch induced by volume load. The natriuretic peptides are synthesized as preprohormones. The C-terminal endocrinological active peptides (ANP, BNP) and their N-terminal prohormone fragments are found in plasma. The natriuretic peptide system is activated to its highest degree in ventricular dysfunction. However, natriuretic peptides are increased in all patients with edematous disorders which lead to an increase in atrial tension or central blood volume, such as renal failure or ascitic liver cirrhosis. It could be demonstrated that in chronic heart failure patients and during the subacute phase of myocardial infarction, of all tested neurohormones, the cardiac natriuretic peptides were best markers to identify heart failure and the most powerful predictors of morbidity and mortality. Natriuretic peptides are independent markers for risk assessment. In comparative studies BNP was superior to ANP and its N-terminal prohormone fragments in myocardial infarction as well as in chronic heart failure patients. Less data on N-terminal proBNP (NT-proBNP) is available, but BNP and NT-proBNP appear to be equivalent markers. For primary care physicians natriuretic peptide measurement is useful to decide which patient with suspected heart failure warrants further investigation, particularly when assessment of left ventricular function is not readily available. Natriuretic peptides have an excellent negative predictive value, particularly in high risk patients. An increase in BNP is serious enough to warrant follow-up examinations. For the cardiologists the natriuretic peptides are helpful for guidance of therapy and monitoring disease course in heart failure patients and for risk stratification in heart failure and myocardial infarction.

                Author and article information

                S. Karger AG
                September 2006
                29 September 2006
                : 106
                : 3
                : 154-160
                a1st Department of Cardiology, bDepartment of Clinical Pharmacology, and cCardiac Surgery Department, University of Medical Sciences, Poznan, Poland
                92770 Cardiology 2006;106:154–160
                © 2006 S. Karger AG, Basel

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                Figures: 3, Tables: 3, References: 40, Pages: 7
                Original Research


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