Role of Pulsatile Hemodynamics in Acute Heart Failure: Implications for Type 1 Cardiorenal Syndrome

Heart failure has become a major health problem worldwide with a substantial financial burden mainly from hospitalization due to acute heart failure syndrome (AHFS). A considerable number of patients hospitalized for the treatment of AHFS experience significant worsening of renal function, which is now recognized as type 1 cardiorenal syndrome (CRS) and is associated with worse outcomes. Currently known risk factors for acute CRS in AHFS include obesity, cachexia, hypertension, diabetes, proteinuria, uremic solute retention, anemia, and repeated subclinical acute kidney injury events. Venous renal congestion due to hemodynamic changes also contributes to type 1 CRS. Vascular aging and its aggravated pulsatile hemodynamics have been shown to be involved in the pathogenesis of AHFS. Suboptimal recovery of the perturbation of the pulsatile hemodynamics may predict 6-month post-discharge cardiovascular outcomes in patients hospitalized due to AHFS. Furthermore, on-admission pulsatile hemodynamics may also be helpful to identify and stratify patients with aggravated pulsatile hemodynamics who may benefit from customized therapy. There are close interplays and feedback loops between heart and kidney dysfunction. Increased arterial stiffness accelerates pulse wave velocity and causes an earlier return of the reflected wave, resulting in higher systolic, lower diastolic, and higher pulse pressure in the central aorta and renal arteries. Increased pulsatile hemodynamics have been associated with deterioration of renal function in subjects with a high coronary risk and patients with hypertension or chronic kidney disease. Thus, there is a potential role of vascular aging/pulsatile hemodynamics in the pathophysiological pathways of acute CRS in AHFS.