Acute Heart Failure Group Research Articles

Etiology of acute dyspnea and the role of N-terminal pro-B-type natriuretic peptide in etiologic diagnosis

Objective To investigate the causes of acute dyspnea and the clinical value of Nterminal pro-B-type natriuretic peptide ( NT-proBNP ) in identification of the early etiologies of acute dyspnea.Methods 290 patients presenting with acute wheezing or dyspnea during the period of Juanary 2010 to December 2010 were recruited.The etiologic diagnosis was made based on disease history,physical examination,lab tests,and responses to therapies.The causes of acute dyspnea were statistically analyzed and the patients were assigned to acute heart failure ( AHF ) group and non-heart failure ( NHF )group.Plasma NT-proBNP levels were compared between the two groups.Besults The four common causes of acute dyspnea were acute exacerbation of chronic obstructive pulmonary disease ( AECOPD )(n=110,37.9％),AHF (n=85,29.3％),acute asthma (n=36,12.4％),andpneumothorax (n =26,9.0％ ).NT-proBNP levels were markedly higher in AHF group than in NHF group ( P ＜ 0.01 ).As the cutoff value of plasma NT-proBNP was =1500 pg/ml,the sensitivity,specificity,and positive predictive value for diagnosing AHF were 91.8％,95.1％,and 88.6％.Conclusions The most frequent causes of acute dyspnea were AECOPD,AHF,acute asthma,and pneumothorax.Plasma NT-proBNP level is of importance in the primary screening of the causes of acute heart failure and the differentiation of cardiogenic from non-cardiogenic dyspnea. Key words: Dyspnea; NT-proBNP; Heart failure

Cardiac ultrasound helps for differentiating the causes of acute dyspnea with available B-type natriuretic peptide tests

Introduction The aim of this study was to evaluate the role of cardiac ultrasound in diagnosing acute heart failure (AHF) in patients with acute dyspnea with available plasma B-type natriuretic peptide (BNP) level. Methods Patients with acute dyspnea presenting to the emergency department (ED) of a tertiary medical center were prospectively enrolled. The enrolled 84 patients received both BNP tests and cardiac ultrasound studies and were classified into AHF and non–heart failure groups. Results Plasma BNP levels were higher in the AHF group (1236 ± 1123 vs 354 ± 410 pg/mL; P < .001). The AHF group had larger left ventricular end-diastolic dimension (LVEDD; 32 ± 7 vs 27 ± 4 mm/m 2; P < .001) and worse left ventricular ejection fraction (52% ± 18% vs 64% ± 15%; P = .003). Multiple logistic regression analysis showed that both BNP levels more than 100 pg/mL and LVEDD were independent predictors for AHF. In patients with plasma BNP levels within gray zone of 100 to 500 pg/mL, LVEDD was larger in the AHF group than that in the non–heart failure group (29 ± 4 vs 26 ± 4 mm/m 2; P = .044). Conclusion Both LVEDD by cardiac ultrasound and BNP levels can help emergency physicians independently diagnose AHF in the ED. In patients with plasma BNP levels within 100 to 500 pg/mL, cardiac ultrasound can help differentiate heart failure or not.

Endothelin-Converting Enzyme Inhibition in the Rat Model of Acute Heart Failure: Heart Function and Neurohormonal Activation

Endothelin-1 (ET-1) has been implicated in many cardiovascular diseases, including acute heart failure (AHF) due to myocardial ischemia. Previously we described the oral endothelin-converting enzyme (ECE) inhibitor, PP36, and in this study, we investigated its cardioprotective effect in more detail, and examined the role of PP36 in the neurohormonal activation in rats that had been subjected to acute myocardial ischemia due to the microsphere embolization of coronary microcirculation. PP36 treatment (3.5 x 10(-5) M/kg/day) led to a significant fourfold decrease in hypertensive response when big-ET-1 was administered to healthy, conscious rats. ECE inhibition did not affect mortality during the first 48 hours after ischemia initiation. Systemic hemodynamic, heart function, and neurohormonal activation were analyzed in the healthy control group, the AHF group, and the AHF+PP36 group two days after AHF induction. In conscious rats in the AHF+PP36 group, mean arterial pressure (MAP) was restored and became similar to that of the MAP of the control group. In anesthetized rats, in the AHF+PP36 group, MAP was not restored and was 22% lower than the MAP of the control group. Myocardial contractility was partially restored and cardiac relaxation significantly improved after PP36 application. Further analysis of cardiac output and peripheral resistance in anesthetized rats revealed no differences between the AHF group and the AHF+PP36 group. There were no differences in plasma ET-1 concentration, serum angiotensin converting enzyme activity, and in the adrenal glands' catecholamine content between the AHF group and the AHF+PP36 group. However, rats in the AHF+PP36 group demonstrated a 60% decrease in cardiac endothelial nitric oxide synthase (eNOS) protein expression, and a 56% reduction of myocardial norepinephrine release, when compared with the AHF group's animals. These results suggest that PP36 can preserve heart function during the recovery from acute ischemic injury, and may modulate the cardiac norepinephrine release and eNOS protein level.