Tricuspid Regurgitation in Left Ventricular Systolic Dysfunction: Marker or Target?

Abstract

Far from being historically considered a primary healthcare problem, tricuspid regurgitation (TR) has recently gained much attention from the scientific community. In fact, in the last years, robust evidence has emerged regarding the epidemiological impact of TR, whose prevalence seems to be similar to that of other valvulopathies, such as aortic stenosis, with an estimated up to 4% of people >75 years affected by at least moderate TR in the United States, and up to 23% among patients suffering from heart failure with reduced ejection fraction. This recurrent coexistence of left ventricular systolic dysfunction (LVSD) and TR is not surprising, considered the multiple etiologies of tricuspid valve disease. TR can complicate heart failure mostly as a functional disease, because of pulmonary hypertension (PH), subsequent to elevated left ventricular end-diastolic pressure, leading to right ventricular dilatation, and valve tethering. Moreover, the so-called “functional isolated” TR can occur, in the absence of PH, as a result of right atrial dilatation associated with atrial fibrillation, a common finding in patients with LVSD. Finally, TR can result as a iatrogenic consequence of transvalvular lead insertion, another frequent scenario in this cohort of patients. Nonetheless, despite the significant coincidence of these two conditions, their mutual relation, and the independent prognostic role of TR is still a matter of debate. Whether significant TR is just a marker for advanced left-heart disease, or a crucial potential therapeutical target, remains unclear. Aim of the authors in this review is to present an update concerning the epidemiological features and the clinical burden of TR in the context of LVSD, its prognostic value, and the potential benefit for early tricuspid intervention in patients affected by contemporary TR and LVSD.

The accuracy and influencing factors of Doppler echocardiography in estimating pulmonary artery systolic pressure: comparison with right heart catheterization: a retrospective cross-sectional study

“…We assumed that the coupling mechanism between RV contractility and its load may account for this phenomenon. When sPAP RHC mildly elevates during the initial phase of PH, RV coupling could be maintained by enhanced RV contractility [ 13 , 14 ], and the estimation of sPAP RHC by DE is relatively reliable. However, as PH progresses and RV uncoupling occurs, CO would decrease and RV preload would increase, along with elevated RAP, so the right atrioventricular pressure gradient would decrease, and DE would underestimate sPAP RHC .…”

HRAS germline mutations impair LKB1/AMPK signaling and mitochondrial homeostasis in Costello syndrome models

“…The E wave velocity through the tricuspid valve was also increased ( Figure 1, L–N ), suggesting occurrence of tricuspid regurgitation. Tricuspid regurgitation, in combination with left ventricular dysfunction was associated with excess mortality in previous studies ( 25 ). Last, the pulmonary vein peak velocity was also reduced in 23-week-old CS mice ( Figure 1G ).…”

Artificial intelligence-enabled phenotyping of patients with severe aortic stenosis: on the recovery of extra-aortic valve cardiac damage after transcatheter aortic valve replacement

“…The significantly elevated prevalence of atrial fibrillation and/or flutter, ageing and possibly also genetic predisposition might have contributed to irreversible right atrial dilatation in patients from cluster 4, ultimately sustaining a vicious circle of arrhythmia, right atrial dilatation and worsening of TR. 19 …”

“…The significantly elevated prevalence of atrial fibrillation and/or flutter, ageing and possibly also genetic predisposition might have contributed to irreversible right atrial dilatation in patients from cluster 4, ultimately sustaining a vicious circle of arrhythmia, right atrial dilatation and worsening of TR. 19 Where have all the patients gone who have previously been reported to show right heart recovery after TAVR? It intuitively makes sense to cardiovascular practitioners that patients with recovering right heart function and structure after TAVR live longer than patients with persistent right heart dysfunction, and the compelling evidence that some patients do indeed improve in right heart function after TAVR cannot be ignored.…”

“…This finding emphasises that structural alterations such as right ventricular and atrial dilatation with concomitant development of severe TR can occur in some patients without the driving force of severely elevated pulmonary artery pressures, hence challenging the validity of the hypothesised sequential progression of accumulated pathologies caused by severe AS in a real-world scenario. The significantly elevated prevalence of atrial fibrillation and/or flutter, ageing and possibly also genetic predisposition might have contributed to irreversible right atrial dilatation in patients from cluster 4, ultimately sustaining a vicious circle of arrhythmia, right atrial dilatation and worsening of TR 19…”