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Co-morbidities in acute heart failure

Session number: 140
Session title: Co-morbidities in acute heart failure
Authors: Stamatis Adamopoulos (Athens, Greece)



Pulmonary disease (presented by Dr. Frans Hendrik Rutten, Utrecht, NL)

Chronic obstructive pulmonary disease (COPD) and heart failure (HF) share some pathophysiological and clinical similarities, thus explaining why more than 20% of COPD patients are, in fact, unrecognized HF cases. Dr Rutten underlined the risk of overdiagnosing COPD, since 35% of acute heart failure (AHF) patients have wheezing. Only 9% of the 23% AHF patients initially thought to suffer from COPD remain with this diagnosis 3 months after the AHF episode. Therefore, a label of COPD does not always actually represent COPD, and HF treatment should precede the prescription of inhalers.

AHF patients with COPD have worse long-term prognosis, compared to non-COPD, not only because they have different clinical characteristics (more comorbidities) but also because they less frequently receive evidence-based HF treatment. In this context, beta-blocker prescription, preferably cardioselective, in COPD patients needs to improve, since it seems to reduce overall mortality and exacerbation of COPD. More than 80% of COPD patients tolerate beta-blockers.

Diabetes (presented by Prof PetarSeferovic, Belgrade, Serbia)

Nearly 30% of patients with HF and diabetes mellitus (DM) die within the first year, due to underlying coronary artery disease (CAD) and multiple comorbidities. In the ADHERE registry, 44% of AHF patients were diabetics. Insulin-dependent DM is associated with worse prognosis, whereas ACE-inhibition, beta-blockers and previous PCI were associated with better prognosis. The degree of hyperglycemia on admission predicts 30-day mortality, and new onset DM is characterized by increased in-hospital mortality in patients with AHF.

DM abolishes the obesity paradox in HF patients. Prof. Seferovic said that we are now less reluctant to treat DM with metformin. Large observational studies show no increase in mortality, hospitalisation or lactic acidosis with metformin. Glitazones are contraindicated and some (not all) DPP-4 inhibitors seem to be associated with higher incidence of HF hospitalization.

Kidney disease (presented by Kevin Damman, Groningen, NL)

An estimated glomerular filtration rate (eGFR) <60ml/min/1.73m2 is strongly prevalent in patients with AHF (50%), doubling the risk of death compared to AHF patients without renal impairment. In addition, a decline in GFR is associated with 60–80% higher mortality. Poor response to diuretics is also associated with worse prognosis.

Dr Damman gave an excellent description of the renal spectrum in AHF, dissociating, in pathophysiological, clinical and prognostic terms, worsening renal function (WRF) from acute kidney injury (AKI). He pointed out that not all WRFs are equal. He also pointed out the significance of increased venous congestion in the detrimental cardio-renal interplay, leading to WRF.  

A combination of diuretics and ultrafiltration is recommended on an individualised basis for resistance in diuretics, whereas dopamine is useful only in selected patients based on the results of the ROSE study.

Anemia-Iron Deficiency (presented by EwaJankowska, Wroclaw, Poland)

Relatively high haemoglobin levels and haemoconcentration on admission with AHF is associated with better prognosis. On the contrary, iron deficiency (ID), present in more than 50% of AHF patients, is a significant prognostic factor for 12-month mortality.

Iron status should be assessed in symptomatic HF patients both with and without anemia, and treatment of ID should be seriously considered. Hepcidin might better reflect iron stores, while soluble transferrin receptor (sTfR) might better detect iron utilisation. According to unpublished data by Prof Jankowska, low hepcidin and high sTfR better describe functional and/or absolute ID compared to ferritin (influenced by inflammation) and transferrin saturation (TSAT) and should, therefore, be used in clinical practice to identify ID in HF.

In addition, ID, but not anemia is associated with abnormal skeletal muscle energy metabolism, and high sTfR reflects unmet cellular metabolic needs for iron, thus contributing to the pathophysiological mechanisms underlying the muscle hypothesis in HF.

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.