TAVR
Hemodynamic Stratification of the Pulmonary Vasculature in Patients Undergoing Transcatheter Aortic Valve Replacement
2022 Volume 86 Issue 3 Pages 391-392
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2022 Volume 86 Issue 3 Pages 391-392
Despite the past few years seeing considerable progress in the field of transcatheter aortic valve replacement (TAVR), between one-quarter and one-half of TAVR recipients experience hospital readmission within 1 year of the procedure. Readmission after an index hospitalization may be related to noncardiac causes (including patient comorbidities) and cardiac causes. Half of all readmissions stem from the latter, with heart failure (HF) being the leading cardiovascular trigger.1 Although the procedural success and outcomes of TAVR have established it as the standard of care for most patients with severe symptomatic aortic valve stenosis (AS), readmission for HF after TAVR is frequent and strongly associated with the 1-year mortality rate. For this reason, patient subgroups at risk of HF following TAVR have been identified as those with diabetes mellitus, chronic lung disease, a history of acute HF, grade III or IV aortic regurgitation, or pulmonary hypertension (PH). All these conditions independently predict readmission for HF.2
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Traditionally, the right atrium (RA) and right ventricle (RV) were not considered important in the determination of clinical outcomes of patients with severe AS; however, reports suggest that not only the stenotic aortic valve and left ventricle (LV), but also the right-side unit influence the clinical outcomes of patients with severe AS.3–5 Changes in LV structure and function, hemodynamic consequences beyond the LV (such as significant mitral and tricuspid regurgitation) and RV dysfunction have been associated with poor outcomes in patients with severe AS undergoing aortic valve replacement.3–5 Additionally, PH typically results from left atrial (LA) pressure elevation, due to the combined effects of LV pressure overload, which affects LV and LA function, and the development of functional mitral regurgitation. If substantial LA pressure elevation is sustained, post-capillary PH may occur following secondary pulmonary vascular remodeling. It has been reported that both patients with pre-capillary PH and those with isolated post-capillary PH have a significantly higher risk of death after TAVR compared with those without PH.6 Therefore, both detection of PH and hemodynamic stratification of PH are helpful for risk and response prediction in patients with AS undergoing TAVR.
In this issue of the Journal, Imamura et al7 demonstrate the effect of the diastolic pressure gradient (DPG), defined as the difference between the diastolic pulmonary artery pressure (PAP) and the measured pulmonary artery wedge pressure (PAWP), on clinical events following TAVR. In this retrospective study of 77 symptomatic patients with severe AS, approximately 20% of the cohort had post-TAVR decoupling, defined as DPG ≥3 mmHg. The existence of post-TAVR decoupling was associated with an increased risk of all-cause death or HF readmission in the 2 years after treatment. Among patients with post-TAVR decoupling, 6 (37.5%) had persistent increased DPG before and after TAVR, and 10 (62.5%) had de novo decoupling (increased DPG after TAVR). De novo decoupling was primarily caused by a decrease in PAWP and a smaller decrease in diastolic PAP, following LV unloading with TAVR. Moreover, the pulmonary vascular resistance index, both pre- and post-TAVR, was higher in patients with post-TAVR decoupling. These results suggest that the most prevalent mechanism that leads to de novo decoupling (i.e., persistently elevated diastolic PAP) may be the consequence of longstanding AS affecting the pulmonary vasculature, and/or the result of pre-existing, pre-capillary pulmonary vascular damage.
Although TAVR has been shown to immediately reduce pulmonary pressure and improve RV PAP coupling in some patients, pulmonary vascular damage may sometimes be irreversible.8 When assessing pulmonary vascular damage under these conditions, mean PAP is not a suitable predictor of clinical outcome because, in the case of endstage PH, RV dysfunction decreases stroke volume, which in turn decreases PAP. On the other hand, if PAWP is directly transmitted to diastolic PAP, there is: (1) a nonproportional increase in systolic and mean PAP, which depend on stroke volume; (2) an increase in the mean PAP/PAWP gradient; and (3) a consistent DPG, which is independent of both PAWP and stroke volume and therefore remains unchanged.9 DPG thus seems to be the best marker of pulmonary vascular damage.
Recently, a new staging system for severe AS has been proposed based on the extent of anatomic and functional cardiac damage.10 This classification has 4 stages: stage 0 indicates the absence of any cardiac damage; stage 1 corresponds to damage at the level of the LV; stage 2 is damage at the level of the mitral valve and LA; stage 3 at the level of pulmonary artery circulation and tricuspid valve; and stage 4, damage to the RV (Figure). A gradual increase in deaths was observed for each stage increment in symptomatic patients with severe AS undergoing aortic valve replacement. Stages 3 and 4 were associated with a marked increase in the short-term risk of death both before and after aortic valve replacement.10,11 Of note, in the current study, mean PAP following TAVR was comparable between patients with and without post TAVR decoupling, and post-TAVR decoupling was distributed widely regardless of mean PAP. These results suggest that post-TAVR decoupling indicates that pulmonary vascular damage is a preliminary step of pre-capillary PH, regardless of PAP (Figure). These findings present a strong argument in favor of early intervention at the time of pulmonary vascular damage, prior to cardiac damage resulting in PH and RV dysfunction.
Staging classification of cardiac damage in patients with aortic stenosis according to the extent of extra-aortic valvular cardiac injury. LA, left atrium; LV, left ventricular; MV, mitral valve; PA, pulmonary artery; PAWP, pulmonary artery wedge pressure; RV, right ventricular; TV, tricuspid valve.
The study published in this issue7 strongly supports the cardiac damage staging system. Understanding the effects of TAVR on PAP/PAWP decoupling has implications for both patient management and outcomes. Ideally, intervention should be performed before the onset of pulmonary vascular damage, and preprocedural risk stratification is needed to identify those at risk of developing decoupling. However, the existence of pre-TAVR decoupling was not associated with clinical outcome, whereas post-TAVR decoupling was an independent predictor of clinical outcome. Thus, further studies of post TAVR decoupling interventions, such as pulmonary vasodilators, prostanoids, endothelin-receptor antagonists, and phosphodiesterase type 5 (PDE5) inhibitors, in larger populations are needed.
The authors report no conflicts of interest.
