Susanne Brenner

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.

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.

Chronic obstructive pulmonary disease in heart failure: accurate diagnosis and treatment

Coincidence of COPD and heart failure (HF) is challenging as both diseases interact on multiple levels with each other, and thus impact significantly on diagnosis, disease severity classification, and choice of medical therapy. The current overview aims to educate caregivers involved in the daily management of patients with HF and (possibly) concurrent COPD in how to deal with clinically relevant issues such as interpreting spirometry, the potential role of extensive pulmonary function testing, and finally, the potential beneficial, but also detrimental effects of medication used for HF and COPD on either disease.

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.

Prognostic potential of midregional pro-adrenomedullin following decompensation for systolic heart failure: comparison with cardiac natriuretic peptides

Whereas guidelines recommend the routine use of natriuretic peptides (NPs) in heart failure (HF) care, the clinical relevance and prognostic potential of midregional pro‐adrenomedullin (MR‐proADM) is less well established. We aimed to compare the prognostic potential of MR‐proADM after acute decompensation for systolic HF with that of N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) and midregional pro‐atrial NP (MR‐proANP), to investigate the significance of high/rising MR‐proADM, and to evaluate the incremental prognostic yield of repeat measurements.

Sleep-Disordered Breathing and Heart Failure: A Dangerous Liaison

In industrialized countries, heart failure has developed into a leading cause of death and hospitalization. It represents one of the most relevant drivers of health-related costs and is among the prime medical and societal challenges of future decades. Sleep-disordered breathing impacts adversely on quality of life and may further aggravate the heart failure syndrome, thus augmenting the high mortality risk associated with this disorder. This article reviews important pathophysiological interactions between both obstructive and central sleep apnea and coexistent heart failure and describes the available treatment options. Based on current evidence, an algorithm for the diagnosis and treatment of sleep-disordered breathing in heart failure is proposed, and future research perspectives are outlined.

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.

Prognostic significance of serial high-sensitivity troponin I measurements following acute cardiac decompensation-correlation with longer-term clinical outcomes and reverse remodelling

BACKGROUND This study investigated the correlation of levels of and changes in serial high-sensitivity cardiac troponin I (hsTnI) with subsequent clinical event rates and changes in cardiac morphology and function in patients hospitalized for acutely decompensated heart failure (ADHF). METHODS AND RESULTS HsTnI levels were determined in 875 ADHF patients before discharge from hospital (baseline cohort) and clinical outcomes assessed after 180days. HsTnI was re-measured at 180days in 456/875 patients (follow-up cohort). Follow-up hsTnI values were grouped according to baseline hsTnI tertiles; echocardiographic changes from 0-180days and event rates from 180-540days were assessed in these subgroups. At baseline and 180-day follow-up, hsTnI levels were elevated (>0.06ng/mL) in 322/875 (37%) and 68/456 (15%) patients, respectively. At 180days, 85/875 patients (9.7%) had died (cardiovascular causes: 56/875 [6.4%]). Hazard ratios (HR) and 95% confidence intervals (CI) for all-cause and cardiovascular mortality (per two-fold hsTnI increase) were 1.2 (1.0-1.3; p=0.004) and 1.2 (1.1-1.4; p=0.001), respectively. In the follow-up cohort, 35/456 patients (7.7%) died between days 180 and 540 (cardiovascular death: 20/456, 4.4%). HsTnI was a significant predictor of cardiovascular re-hospitalization within 180-540days (HR 1.2, 95% CI 1.0-1.4; p=0.028). Patients with hsTnI in the lowest tertile at follow-up had more frequent and more pronounced reverse cardiac remodelling on echocardiography. CONCLUSIONS Elevated baseline hsTnI was common and associated with adverse clinical outcomes. Changes in hsTnI from baseline to 180-day follow-up predicted longer-term risk. Low or decreasing hsTnI was associated with better reverse cardiac remodelling and more favourable long-term outcomes. CLINICAL TRIAL REGISTRATION URL: http://www.controlled-trials.com. Unique identifier: ISRCTN23325295.

Kardiales Remodelling nach Myokardinfarkt

ZusammenfassungDie Herzinsuffizienz ist eine führende Todesursache und häufigster Anlass für Hospitalisierungen in Deutschland, obwohl die therapeutischen Möglichkeiten v. a. bei reduzierter Pumpfunktion in den letzten Jahren erheblich zugenommen haben. Meist wird, bevor sich eine Herzinsuffizienz auch klinisch manifestiert, eine Phase des kardialen Remodellings durchlaufen. Remodelling wurde ursprünglich morphologisch und mechanisch definiert, vollzieht sich allerdings auch auf zellulärer und molekularer Ebene. So sind Heilungsvorgänge nach einem akuten Myokardinfarkt geprägt von Inflammation, zellulärer Migration und Narbenbildung. Das kardiale Remodelling wird zudem von systemischen Anpassungsvorgängen begleitet. Ein primäres Ziel der Therapie sollte daher sein, das Remodelling zu verhindern. Wichtig sind hierfür die möglichst schnelle Diagnostik und Therapieeinleitung. Frühzeitige Reperfusionstherapie limitiert die Infarktgröße und trägt dazu bei, die linksventrikuläre Pumpfunktion zu erhalten. Als medikamentöse Standardtherapie sind nach Myokardinfarkt Angiotensinkonversionshemmer, Angiotensin-1-Rezeptor-Blocker und Betablocker etabliert. Auch Mineralokortikoidrezeptorantagonisten zeigen günstige Wirkungen. Spezifische Medikamente, die darauf abzielen, schon in die Heilung des Infarkts einzugreifen, sind in Entwicklung.

Airway obstruction in patients with cardiac diseases.

We thank Dr. Aydogan for commenting on our article “Airway obstruction in systolic heart failure (SHF) — Chronic obstructive pulmonary disease (COPD) or congestion?” [1,2]. We agree that airway obstruction is a non-specific clinical sign [2,3]. We recently demonstrated that airway obstruction was often present during hospitalization for SHF (19%) but frequently resolved over time (48%) [2]. Furthermore, we revealed that a previously assigned diagnosis of COPD was often not confirmed if challenged by pulmonary function testing under stable conditions. Hence, COPD is indeed substantially over-diagnosed in patients with SHF (78%) [2]. In SHF, pulmonary congestion causes a transient airway obstruction with dyspnea, wheezing and cough mimicking the typical signs and symptoms of COPD. Even if chest X-ray then suggests pulmonary congestion, initial application of beta-agonists may be beneficial for fast symptom relief during an episode of acute cardiac failure. However, if the use of bronchodilators has been motivated by such circumstances, COPD may perpetuate in a patients diagnosis and treatment plan. Permanent application of potentially harmful substances in SHF may then be the consequence [4]. As stated by Aydogan and colleagues, a similar scenario is possible in patients with heart failure and preserved ejection fraction (HFpEF). There, it might be sometimes difficult to differentiate pulmonary disease with fixed airway obstruction and secondary diastolic failure [5] from HFpEFtriggered congestion with secondary airway obstruction. We agree that further studies investigating diastolic function in patients with airway obstruction are needed. In our cohort of patients with stable SHF, we detected a fixed airway obstruction as the spirometric criterion of COPD diagnosis [3] in 9% [2]. Of those, 28%were never-smokers; this proportion is in accordance with the results of large population-based studies [6]. It has been shown that occupational risk factors, such as organic dust exposure, significantly contribute to the development of COPD in never-smokers [6,7]. Such detailed exposure capture, however, was outside the scope of our study. Finally, pulmonary function testing should be performed in any patient with dyspnea, wheezing and cough, but diagnosis and treatmentmust of course also rely on further integral findings such as patient history, symptoms, risk factors, chest X-ray and echocardiography [3].