Echocardiographic subtypes of heart failure in consecutive hospitalised patients with dyspnoea.

Heart failure with preserved ejection fraction (HFpEF) involves half of hospitalised patients with heart failure (HF), but estimates vary due to unclear diagnostic criteria. We performed a prospective observational study of hospitalised patients admitted with dyspnoea. The aim was to apply contemporary guidelines to diagnose HF due to valvular disease (HFvhd), HF due to reduced ejection fraction (HFrEF), HF due to midrange EF (HFmrEF) and HFpEF in relation to presumed cardiac or non-cardiac dyspnoea. Methods: We included consecutive hospitalised patients with presumed HF or dyspnoea and excluded patients with acute coronary syndrome, estimated glomerular filtration rate <30 mL/min/1.73 m² or low NT-proBNP (<296 ng/L). Higher age-adjusted NT-proBNP values excluded patients with presumptive non-cardiac dyspnoea. Contemporary criteria for HFpEF and diastolic dysfunction were assessed, and we adjudicated whether acute decompensated HF (ADHF) had been the primary diagnosis. Results: Of 707 eligible patients, we included 370 patients of whom 75 had non-cardiac dyspnoea. Of these, 10% (38/370) had no cardiac dysfunction. Cardiac dysfunction consisted of 18.4%, HFvhd, 30.1% HFrEF, 10.2% HFmrEF and 41.3% HFpEF. HFpEF was twice as common in presumptive non-cardiac dyspnoea versus cardiac dyspnoea (71% vs 34%, p<0.0001). However, adjudicated ADHF was the primary diagnosis in 80% of HFrEF, 62% of HFmrEF and just 28% of HFpEF. Conclusion: HF according to contemporary criteria applied to 90% of patients admitted with dyspnoea and elevated NT-proBNP irrespective of the presumptive cause of dyspnoea, of whom 10% had HFmrEF and 41% HFpEF. However, significant non-cardiac diagnoses related to 9 out of 10 with HFpEF with pulmonary disease as the predominant adjudicated problem.

High-sensitivity C-reactive protein and exercise-induced changes in subjects suspected of coronary artery disease.

BACKGROUND: Inflammation plays a major role in the development of atherosclerosis. We wanted to investigate the effects of exercise on high-sensitivity (hs) C-reactive protein (CRP) in subjects who were suspected of having coronary artery disease (CAD). METHODS: Blood samples were obtained before, 5 minutes after, and 20 hours after an exercise test in 155 subjects who were suspected of CAD. Coronary anatomy was evaluated by computed tomography coronary angiography and/or coronary angiography. RESULTS: Median baseline hs-CRP was higher in subjects with ≥50% coronary artery lumen diameter stenosis (n=41), compared with non-CAD-subjects (n=114), 2.93 mg/L (interquartile range 1.03-5.06 mg/L) and 1.30 mg/L (interquartile range 0.76-2.74 mg/L), respectively, P=0.007. In multivariate analyses testing conventional risk factors, hs-CRP proved borderline significant, odds ratio =2.32, P=0.065. Adding baseline hs-CRP to the results of the exercise test did not improve the diagnostic evaluation. Baseline natural logarithm (Ln) hs-CRP was positively associated with body mass index and baseline Ln-transformed hs troponin T levels, and negatively associated with the daily life activity level. An increase in hs-CRP of 0.13 mg/L (interquartile range 0.05-0.24 mg/L) from baseline to 5 minutes after peak exercise was found (P<0.0001), but the increase was not associated with presence of CAD. From baseline to 20 hours after exercise, no increase in hs-CRP was found. CONCLUSION: In conclusion, hs-CRP was not independently associated with CAD. Hs-CRP increased immediately as a response to the exercise, and the increase was modest and not associated with CAD. The results indicate that exercise has potential to cause unwanted variations in hs-CRP and that exercise prior to hs-CRP measurements in subjects included in epidemiological studies, therefore, should be avoided.

Diagnostic value of exercise-induced changes in circulating high sensitive troponin T in stable chest pain patients.

OBJECTIVE: We investigated the diagnostic value of exercise-induced increase in cardiac Troponin T (cTnT) in stable chest pain subjects. METHODS: CTnT was measured before and 20 h after an exercise test in 157 subjects suspected of coronary artery disease (CAD). RESULTS: CAD subjects (n = 41) had higher baseline cTnT levels compared to non-CAD subjects (n = 116), 6.39 ng/l and 3.00 ng/l, respectively, p < 0.0001, and were more likely to increase in cTnT (70.7% versus 27.6%, p < 0.0001). Net Reclassification Index for the combined variable was 19%, p = 0.02. CONCLUSIONS: Exercise-induced increase in cTnT was found to be associated with CAD and cTnT measurements improved the diagnostic evaluation.

Prevalence and prognosis of heart failure with preserved ejection fraction and elevated N-terminal pro brain natriuretic peptide: a 10-year analysis from the Copenhagen Hospital Heart Failure Study.

AIMS: The aim of this study was to assess the epidemiological features and prognosis of heart failure with preserved ejection fraction (HFPEF) and to compare these findings with those from patients with reduced ejection fraction. Furthermore the effects of N-terminal pro brain natriuretic peptide (NT-proBNP) requirement in the heart failure diagnosis were assessed by repeating the analyses in the subgroup of patients with elevated NT-proBNP. METHODS AND RESULTS: In 1844 patients admitted, a clinical diagnosis of heart failure was made in 433; amongst these 61% had HFPEF. An elevated NT-proBNP applied to the heart failure diagnosis reduced the number of heart failure patients to 191, and amongst these 29% had preserved ejection fraction. Use of NT-proBNP reduced clinical differences between heart failure patients with preserved and reduced ejection fraction. When not using NT-proBNP, patients with reduced ejection fraction had higher mortality [hazard ratio (HR) 1.24, 95% confidence interval (CI) 1.01-1.52; P = 0.04], even after adjustment for other significant predictors of mortality, except NT-proBNP (HR 1.29, 95% CI 1.04-1.59; P = 0.02). However, no difference in mortality was observed when NT-proBNP was adjusted for (HR 0.90, 95% CI 0.71-1.15; P = 0.4), or used for the heart failure diagnosis (HR 0.96; 95% CI 0.71-1.29; P = 0.8). CONCLUSION: Using a heart failure diagnosis requiring elevated NT-proBNP reduces the prevalence of HFPEF and results in a survival similar to that of heart failure with reduced ejection fraction. In contrast, when NT-proBNP is not used for the heart failure diagnosis or adjusted for, HFPEF is associated with a lower mortality in both univariate and multivariate analysis.