Hemodynamics play a central role in the pathophysiology of heart failure (HF), yet their proper assessment and optimization remains challenging. Heart failure is defined as the inability of the heart to deliver adequate perfusion (cardiac output) to the body at rest or exercise, or to require an elevation in cardiac filling pressures in order to do this. This bedrock definition is important because it relies on measurable quantities (filling pressures and output) that are readily assessed in the cardiac catheterization laboratory. Here we present three cases to illustrate how better understanding of the determinants of cardiac output and stroke volume: preload, afterload, contractility, and lusitropy, as well as the determinants of congestion (high filling pressures) may be used to guide optimization of hemodynamic status. The goal is that the readers will be able to think more critically when evaluating the hemodynamics of their patient in HF and recognize the complex interplay that determines the complex balance between cardiac ejection and filling capabilities, and how this alters symptoms and outcomes for patients with HF. KEY POINTS: Careful assessment of hemodynamics in the catheterization laboratory allows for actionable insight to a patient's volume status, cardiac function and can help prognosticate outcomes. Exercise hemodynamics in heart failure is a powerful tool to better understand the cause of symptoms and predict outcomes. Clinicians should aim to decrease biventricular filling pressures to normal values to improve morbidity and reduce risk for readmission. In patients with heart failure and reduced ejection fraction, clinicians should aim to decrease afterload as much as can be tolerated by the renal function and patient's symptoms. Low cardiac output can often be improved by optimizing preload and afterload rather than initiating inotropes, which should be reserved until needed. In advanced heart failure, the right heart function becomes a key determinant of symptoms and outcomes.
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http://dx.doi.org/10.1002/ccd.28490 | DOI Listing |
Can J Physiol Pharmacol
January 2025
Dalhousie University, Department of Physiology and Biophysics, Halifax, Canada;
A growing body of evidence suggest that the stem cell antigen-1 expressing (Sca-1) cells in the heart may be the cardiac endothelial stem/progenitor cells. Their endothelial cell (EC) functions, and their role in RV physiology and pathophysiology of right heart failure (RHF) remains poorly defined. This study investigated EC characteristics of rat cardiac Sca-1 cells, assessed spatial distribution and studied changes in Sca1 cells during RV remodelling in monocrotaline (MCT) model of pulmonary hypertension and RV remodeling.
View Article and Find Full Text PDFJ Cardiovasc Med (Hagerstown)
February 2025
Division of Cardiology, Department of Systems Medicine, Tor Vergata University, Rome.
Atrial cardiomyopathy (AC) has been defined by the European Heart Rhythm Association as "Any complex of structural, architectural, contractile, or electrophysiologic changes in the atria with the potential to produce clinically relevant manifestations".1 The left atrium (LA) plays a key role in maintaining normal cardiac function; in fact atrial dysfunction has emerged as an essential determinant of outcomes in different clinical scenarios, such as valvular diseases, heart failure (HF), coronary artery disease (CAD) and atrial fibrillation (AF). A comprehensive evaluation, both anatomical and functional, is routinely performed in cardiac imaging laboratories.
View Article and Find Full Text PDFJ Cardiovasc Med (Hagerstown)
February 2025
Cardiology Unit, Azienda Ospedaliera Universitaria di Ferrara, Cona, Ferrara, Italy.
Introduction: Cardiac amyloidosis typically causes restrictive cardiomyopathy, in which the impairment of diastolic function is dominant. Echocardiography provides prognostic information through some important parameters: left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS). However, LVEF often remains preserved despite disease progression, and GLS is not routinely performed as it is limited by suboptimal image quality.
View Article and Find Full Text PDFSci Adv
January 2025
Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Protein homeostasis is crucial for maintaining cardiomyocyte (CM) function. Disruption of proteostasis results in accumulation of protein aggregates causing cardiac pathologies such as hypertrophy, dilated cardiomyopathy (DCM), and heart failure. Here, we identify ubiquitin-specific peptidase 5 (USP5) as a critical determinant of protein quality control (PQC) in CM.
View Article and Find Full Text PDFSci Transl Med
January 2025
Center for Transplantation Sciences, Department of Surgery, Massachusetts General Hospital, Boston, MA 02114, USA.
Long-term, immunosuppression-free allograft survival has been induced in human and nonhuman primate (NHP) kidney recipients after nonmyeloablative conditioning and donor bone marrow transplantation (DBMT), resulting in transient mixed hematopoietic chimerism. However, the same strategy has consistently failed in NHP heart transplant recipients. Here, we investigated whether long-term heart allograft survival could be achieved by cotransplanting kidneys from the same donor.
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