Vascular phenotypes of acute decompensated vs. new‐onset heart failure: treatment implications

Abstract

AimsAcute heart failure (HF) is a frequent and life‐threatening syndrome with heterogeneous clinical, haemodynamic, and neurohormonal features. This article describes the vascular phenotypes associated with acute decompensated chronic HF (ADCHF), and new‐onset acute HF (NOAHF).Data SynthesisWorsening of chronic HF occurs with full activation of adaptive mechanisms that maintain blood pressure (BP) and systemic perfusion. Rapid onset of HF in the setting of previous normal functioning heart not only does not allow full activation of adaptive mechanisms but also generates inappropriate responses from systemic endothelium leading to low BP/hypotension. Consequently, the treatment of ADCHF is based on diuretics and vasodilators, while in NOAHF, vasoconstrictors may be required to maintain BP to allow the correction of the acute cardiac disease.ConclusionsPatients with ADCHF and NOAHF present different vascular phenotypes with treatment implications.

Diagnostic accuracy of inferior vena cava evaluation in the diagnosis of acute heart failure among dyspneic patients

“…The main cause of dyspnea in AHF is the increase in pulmonary wedge pressure due to increased afterload and volume-shift lung congestion which is not always associated with increased right atrial pressure. This is particularly true among patients with new onset AHF compared to patient with chronic HF [20]. This explains way echocardiographic assessment of IVC cannot be alone the diagnostic method of choice for the diagnosis of AHF in patients with acute dyspnea.…”

Letter by Ferreira Regarding Article, “Extracorporeal Membrane Oxygenation in the Therapy of Cardiogenic Shock: Results of the ECMO-CS Randomized Clinical Trial”

“…However, systemic hypoperfusion triggers endothelial dysfunction with inappropriate vasodilation, hemostasis dysregulation, and systemic inflammatory response syndrome that reduce catecholamine responsivity, decrease myocardial contractility, and further depress perfusion pressure. 3,4 As a corollary of this new pathophysiologic concept, emergent vasoactive therapy and mechanical circulatory support must be implemented in early phases of CS to prevent triggering of endothelial dysfunction and systemic inflammatory response syndrome.The design of the ECMO-CS trial is apparently in line with this new paradigm because it included a therapeutic strategy of immediate implementation of veno-arterial ECMO in patients with CS. 1 However, the study included patients with rapidly deteriorating or severe CS, characterized by ongoing inappropriate endothelial and inflammatory responses.…”

Mecanismos fisiopatológicos, neurohormonales y objetivos terapéuticos en la insuficiencia cardiaca aguda

“…Para pacientes con SCA complicado por shock cardiogénico, se recomienda realizar inmediatamente una coronariografía (durante las primeras 2 horas tras el ingreso) con intención de revascularizar al paciente. El objetivo del tratamiento farmacológico es mejorar la perfusión orgánica mediante el aumento del gasto cardiaco y la PA. Tras realizar una carga de fluidos, el tratamiento farmacológico consiste en la administración de un inotrópico y un fármaco vasopresor, según la necesidad del caso individual (34)(35)(36)(37)(38) .…”