Chapter 36 - Arterial stiffness and pulsatile hemodynamics in heart failure

Abstract

Arterial load exerts a profound impact on left ventricular structure and function. Assessments of pulsatile arterial hemodynamics have provided important insights into the pathophysiology of left ventricular remodeling and fibrosis, diastolic dysfunction, and failure. Moreover, pulsatile arterial load may interact with the distal microvasculature, promoting microvascular dysfunction and impaired oxygen delivery to peripheral skeletal muscle, all of which contribute to exercise intolerance in heart failure (HF). Arterial pulsatile hemodynamic mechanisms also contribute to the pathogenesis of comorbidities present among patients with HF, such as renal failure and cognitive dysfunction. Specific abnormalities in pulsatile load may be susceptible to novel pharmacologic interventions. Given the heterogeneity of HF, our therapeutic approach to HF can be enhanced by detailed phenotyping of arterial hemodynamics, which can contribute to the segmentation of the HF population into relevant pathophysiologic categories, or to identifying individuals exhibiting prominent physiologic abnormalities that can be targeted by pharmacologic interventions. This is particularly relevant for heart failure with preserved ejection fraction (HFpEF), which is now the most common form of HF, and for which limited therapeutic options exist.