Nikolas Deubner

Airway obstruction in systolic heart failure – COPD or congestion?

BACKGROUND The diagnosis of chronic obstructive pulmonary disease (COPD) in patients with systolic heart failure (SHF) is challenging because symptoms of both conditions overlap. We aimed to estimate the prevalence, correlates and prognostic impact of true COPD in patients with SHF. METHODS To diagnose COPD under stable conditions according to the guidelines, pulmonary function testing (PFT) was performed in 619 patients six months after hospitalization for congestive SHF. In 272 patients, PFT had been also performed prior to discharge. RESULTS In the total cohort, COPD was reported in 23% (144/619). PFT under stable conditions revealed that COPD was absent in 73% (449/619), unconfirmed in 18% (112/619), and proven in 9% (58/619). In 272 patients with serial PFT, initial airway obstruction was found in 19% (51/272) but had resolved in 47% of those (24/51) after six months. Initial hyperinflation detected by bodyplethysmography strongly predicted proven COPD six months later: odds ratio for elevated intrathoracic gas volume 12.8, 95% confidence interval (CI) 2.5-65.9; p=0.002. After a median follow-up of 34 months, 27% of the total cohort (165/619) had died. Only proven COPD was associated with an increased mortality risk after adjustment for age, sex, NYHA functional class, ejection fraction, atrial fibrillation, smoking, renal dysfunction and diabetes: hazard ratio 1.64, 95%CI 1.03-2.63; p=0.039. CONCLUSIONS Airway obstruction is a dynamic phenomenon in SHF. Therefore, a valid diagnosis of COPD in SHF demands serial PFT under stable conditions with special attention to hyperinflation. COPD proven by PFT is associated with an increased all-cause mortality risk.

Cardiac β1‐adrenoceptor autoantibodies in human heart disease: rationale and design of the Etiology, Titre‐Course, and Survival (ETiCS) Study

Evidence for a pathophysiologic relevance of autoimmunity in human heart disease has substantially increased over the past years. Conformational autoantibodies stimulating the cardiac β1‐adrenoceptor (β1‐aabs) are considered of importance in heart failure development and clinical pilot studies have shown their prognostic significance in human ‘idiopathic’ cardiomyopathy.

Nurse‐coordinated collaborative disease management improves the quality of guideline‐recommended heart failure therapy, patient‐reported outcomes, and left ventricular remodelling

Heart failure (HF) pharmacotherapy is often not prescribed according to guidelines. This longitudinal study investigated prescription rates and dosages of angiotensin‐converting enzyme inhibitors/angiotensin receptor blockers (ACEi/ARB), beta‐blockers, and mineralocorticoid receptor antagonists (MRA), and concomitant changes of symptoms, echocardiographic parameters of left ventricular (LV) function and morphology and results of the Short Form‐36 (SF‐36) Health Survey in participants of the Interdisciplinary Network Heart Failure (INH) programme.

Dysnatraemia in heart failure

To investigate in detail the correlates of dysnatremia, and to estimate its differential prognostic relevance in patients with heart failure with reduced or preserved LVEF.

How safe are NOACs compared with phenprocoumon after pulmonary vein isolation with the cryoballoon technique using purse-string suture closure?

INTRODUCTION The aim of this observational study was to compare the postprocedural incidence of bleeding and thromboembolic complications associated with novel oral anticoagulants (NOACs) with that of interrupted and continuous phenprocoumon after pulmonary vein isolation (PVI) using a purse-string suture (PSS) closure of the puncture site. METHODS AND RESULTS Consecutive patients who had undergone PVI via cryoballoon ablation were divided into the following groups: (1) interrupted phenprocoumon with heparin bridging (n=101), (2) continuous phenprocoumon targeting an internationally normalized ratio>2 (n=70), and (3) NOACs without bridging that were restarted 2-4h after the procedure (n=185). Protamine was not administered after venous closure with PSS at the end of the procedure. The total complication rate was significantly lower in group 3 than in groups 1 and 2 (1.62% vs. 6.93% vs. 7.14%, p=0.04). The hospital costs were lower and the hospital stay length was significantly shorter (4484±3742 vs. 6082±4044 Euro vs. 4908±2925, p=0.03; 1.94±1.67 vs. 2.70±1.80 vs. 2.19±1.30days, p<0.01). No thromboembolic event occurred. Vascular complications were the most common complications noted (80%). The occurrence of any complication led to a significantly longer hospital stay (5 vs. 2days, p<0.01) and higher costs (10,052±6241 Euro vs. 4747±3447, p<0.01). The vascular complication rate after PSS was independent of intraprocedural heparin dosage and activated clotting time. CONCLUSIONS NOACs have a lower complication rate and appear to be safer in this setting than phenprocoumon. The hospital costs and hospital stay length after PVI was significantly reduced in patients treated with NOACs compared with phenprocoumon.

Frequency and prognostic impact of mid-expiratory flow reduction in stable patients six months after hospitalisation for heart failure with reduced ejection fraction.

AIM This study investigates the prevalence and prognostic impact of central and small airways obstruction (CAO and SAO) in patients with stable heart failure (HF). METHODS & RESULTS Spirometry was performed in 585 outpatients (mean age 65±12years, 75% male) six months after hospitalisation for acute decompensation secondary to HF with ejection fraction <40%. We assessed forced expiratory volume in the first second (FEV1), forced vital capacity (FVC) and mid-expiratory flow (MEF) at 50% of FVC. CAO was defined by FEV1/FVC <0.7. SAO was defined by FEV1/FVC ≥0.7 plus MEF <60% of predicted value. CAO and SAO were excluded in 359 patients (61% of all). MEF <60% predicted was found in 226 patients (39% of all), among those 88 with CAO (15% of all) and 138 (24% of all) with SAO. During a twelve month follow-up, 42 patients (7.2%) died. Mortality rates of patients with CAO and SAO were comparable (12.5% and 10.9%, respectively, p=0.74), and both higher than in patients without airways obstruction (4.5%, both p<0.01). In univariable Cox regression analysis, both CAO and SAO were associated with 2-fold increased all-cause mortality risk (hazard ratios [95% confidence intervals]: 2.78 [1.33-6.19], p=0.007 and 2.51 [1.24-5.08], p=0.010, respectively). Adjustment for determinants of CAO and SAO, prognostic markers of heart failure and comorbidities attenuated the association of mortality with CAO but not with SAO. CONCLUSIONS SAO is more common than CAO and indicates an increased mortality risk in HF. Thus, reduced MEF may be a feature of patients at risk and merits special attention in HF management.

Safety and feasibility of percutaneous skin closure using purse-string suture compared with compression bandage after pulmonary vein isolation

This observational study was designed to analyze the safety and feasibility of percutaneous skin closure using a purse‐string suture and compare it with the use of a compression bandage after pulmonary vein isolation.

Acute Myocarditis – A Trigger of Cardiac Autoimmunity? Expected Insights from the Etiology, Titre-Course, and Effect on Survival of Cardiac Autoantibodies (ETiCS) Study

Progressive cardiac dilatation and pump failure of unknown aetiology termed “idiopathic” dilated cardiomyopathy (DCM) (Richardson et al., 1996; Maron et al., 2006) represents one of the main causes of severe heart failure in Western populations with an annual incidence of about 100 and a prevalence of 300-400 patients per year (American Heart Association, 2009). The large majority of cases are thought to arise from an initial (mostly viral) infection leading to acute myocardial inflammation. Acute myocarditis may either heal (about one third of the cases) or progress to a chronic inflammatory process with continued fibrotic repair, subsequent dilatation of the left and/or right ventricle and –finally– severe congestive heart failure (about another third of the patients). Progression to DCM appears to occur particularly, when associated (a) with chronic inflammation of the myocardium due to viral persistence (Kuhl et al., 2005) and/or (b) with the development of autoantibodies directed against distinct sarcoplasmatic or myocyte membrane proteins that are essential for cardiac function (Freedman & Lefkowitz, 2004; Jahns et al., 2006). The latter findings are further strengthened by the fact that patients with DCM often have alterations in both, their innate and their adaptive immune system (Limas, 1997; Luppi et al., 1998; Jahns et al., 2006; Mahrholdt et al., 2006). Thus, under certain conditions an initial acute inflammatory reaction may proceed into a kind of low-grade inflammation (MacLellan & Lusis, 2003) facilitating the development of abnormal or misled immune responses to the primary (infectious)