Acute heart failure: Multiple clinical profiles and mechanisms require tailored therapy

Abstract

Acute heart failure (HF) is the most common diagnosis at discharge in patients aged >65years. It carries a dismal prognosis with a high in-hospital mortality and very high post-discharge mortality and re-hospitalization rates. It is a complex clinical syndrome that cannot be described as a single entity as it varies widely with respect to underlying pathophysiologic mechanisms, clinical presentations and, likely, treatments. It is the aim of this paper to describe some of the main clinical presentations of acute HF. Amongst them, we will consider de novo HF versus acutely decompensated chronic HF, HF caused, and/or worsened, by myocardial ischemia, acute HF with low, normal, or high systolic blood pressure, acute HF caused by lung congestion or fluid retention or fluid redistribution to the lungs, and acute HF with comorbidities (diabetes, anemia, renal insufficiency, etc.). Different pathophysiologic mechanisms and clinical presentations may coexist in the same patient. Identification and, whenever possible, treatment of underlying pathophysiologic mechanisms may become important for acute HF management.

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

“…Zaproponowano wiele różnych, częściowo nakłada-jących się klasyfikacji AHF, opartych na różnych kryteriach [510][511][512][513]. Najbardziej przydatne w praktyce są klasyfikacje, które powstają na podstawie obrazu klinicznego przy przyjęciu.…”

Postdischarge Assessment After a Heart Failure Hospitalization

“…Simple but powerful predictors of postdischarge events include blood pressure, QRS duration, renal dysfunction, serum levels of sodium, natriuretic peptides and troponin, and other comorbidities. 1,5,19 The hospital length of stay and the number of previous rehospitalizations are also major prognostic variables. 8,9,18 What Should the Postdischarge Assessment Accomplish?…”

Troponin T levels in patients with acute heart failure: clinical and prognostic significance of their detection and release during hospitalisation

“…Acute myocardial damage is one of the most likely mechanisms [2][3][4][5]. Increased left ventricular filling pressure and myocardial stress, hypotension, tachycardia, endothelial dysfunction, platelet aggregation, activation of neurohormonal and inflammatory mechanisms, oxidative stress, and altered calcium handling may all favour myocytes injury, necrosis or apoptosis, and/or troponin release even in patients with angiographically normal coronary arteries [3,6].…”