Structural and Hemodynamic Changes of the Right Ventricle in PH-HFpEF

Abstract

One of the most important diagnostic challenges in clinical practice is the distinction between pulmonary hypertension (PH) due to primitive pulmonary arterial hypertension (PAH) and PH due to left heart diseases. Both conditions share some common characteristics and pathophysiological pathways, making the two processes similar in several aspects. Their diagnostic differentiation is based on hemodynamic data on right heart catheterization, cardiac structural modifications, and therapeutic response. More specifically, PH secondary to heart failure with preserved ejection fraction (HFpEF) shares features with type 1 PH (PAH), especially when the combined pre- and post-capillary form (CpcPH) takes place in advanced stages of the disease. Right ventricular (RV) dysfunction is a common consequence related to worse prognosis and lower survival. This condition has recently been identified with a new classification based on clinical signs and progression markers. The role and prevalence of PH and RV dysfunction in HFpEF remain poorly identified, with wide variability in the literature reported from the largest clinical trials. Different parenchymal and vascular alterations affect the two diseases. Capillaries and arteriole vasoconstriction, vascular obliteration, and pulmonary blood fluid redistribution from the basal to the apical district are typical manifestations of type 1 PH. Conversely, PH related to HFpEF is primarily due to an increase of venules/capillaries parietal fibrosis, extracellular matrix deposition, and myocyte hypertrophy with a secondary “arteriolarization” of the vessels. Since the development of structural changes and the therapeutic target substantially differ, a better understanding of pathobiological processes underneath PH-HFpEF, and the identification of potential maladaptive RV mechanisms with an appropriate diagnostic tool, become mandatory in order to distinguish and manage these two similar forms of pulmonary hypertension.

Pulmonary Embolism: An Update Based on the Revised AWMF-S2k Guideline

“…However, thrombolysis increases the risk of major bleeding (9.4%; OR: 2.84; 95% CI: 1.92–4.20) and especially intracranial bleeding (2%; OR: 7.59; 95% CI: 1.38–41.7). 38…”

“…However, thrombolysis increases the risk of major bleeding (9.4%; OR: 2.84; 95% CI: 1.92-4.20) and especially intracranial bleeding (2%; OR: 7.59; 95% CI: 1.38-41.7). 38 Table 1 Risk stratification and early mortality in patients with acute pulmonary embolism (modified from 24 ).…”

Risk Factors and Cellular Differences in Heart Failure: The Key Role of Sex Hormones

“…Further, the pathophysiological feature of HFpEF is the association with pulmonary hypertension. Pulmonary hypertension is more frequent in women, due to a higher prevalence of mitral regurgitation and a greater susceptibility to idiopathic pulmonary hypertension [85,86].…”

Pulmonary Arterial Hypertension in the Elderly: Peculiar Features and Challenges for a Proper Phenotyping Approach

“…These compensatory mechanisms are particularly deranged in elderly subjects, who are prone to modulating RV remodelling through cardiomyocyte loss, fiber reorientation, and replacement with fibrous tissue, thus providing a weaker age-related response to pulmonary afterload, compared to younger PAH patients [ 28 ]. A first reactive response of the RV to increased afterload (altogether called ventricular–arterial coupling) includes several adaptive mechanisms, like RV concentric hypertrophy and enhanced contractility, in order to decrease RV wall stress, thus preserving systolic and diastolic function, and allowing the RV to maintain the stroke volume at minimal energetic dissipation (homeometric adaptation) [ 29 ]. Whether RV systolic function cannot be enhanced any further, a maladaptive RV remodelling develops, as a consequence of a chronic right-sided pressure overload and pulmonary vascular lumen narrowing due to media thickening, which are common pathophysiologic findings of the advanced stage of the disease [ 4 , 30 , 31 ].…”