Clinical Impact of Changes in Left Ventricular Function After Aortic Valve Replacement

Abstract

Background-Our objectives were to identify correlates of mortality and congestive heart failure after aortic valve replacement (AVR) according to preoperative left ventricular (LV) function and to describe the incidence, time course, and correlates of LV recovery and mass regression postoperatively. Methods and Results-A total of 3112 patients with AVR were assessed in a follow-up clinic with echocardiography (median follow-up, 6.0 years). At operation, their mean age was 67.8±13.4 years, one third were female, and 29% had LV dysfunction (ejection fraction <50%). In severe patients with severe aortic stenosis and LV dysfunction, transaortic valve mean pressure gradient <40 mm Hg, longer cardiopulmonary bypass duration, and prosthesis-patient mismatch (indexed effective orifice area ≤0.85 cm 2 /m 2 ) were independent correlates of the composite outcome of death or congestive heart failure after AVR. In patients with severe aortic regurgitation and LV dysfunction, older age and higher preoperative LV mass were identified. LV recovery correlated with better survival and freedom from heart failure in patients with aortic stenosis. Maximum LV mass regression took 24 months in patients with aortic stenosis and nearly 5 years with aortic regurgitation; independent correlates included smaller LV end-systolic diameter in patients with aortic stenosis and low New York Heart Association class with aortic regurgitation. Conclusions-Incomplete LV recovery, prosthesis-patient mismatch, low transaortic valve pressure gradient, and higher LV mass are associated with increased mortality or heart failure after AVR in patients with LV dysfunction. Higher LV end-systolic diameter and symptoms correlate with less LV mass regression, which takes at least 2 years. These findings help surgeons and cardiologists refine the indications, timing, prognostication, and follow-up of patients before and after AVR. (Circulation. 2015;132:741-747.

Renin–angiotensin system blockade therapy after transcatheter aortic valve implantation

“…Progressive myocardial hypertrophy causes fibrosis and myocyte degeneration, which contribute significantly to LV dysfunction 16. Several studies have demonstrated that persistent LV hypertrophy after SAVR is associated with worse clinical outcome and mortality,1 2 17 and regression of LV hypertrophy has been related to improved survival rates,1 as well as lower risk of myocardial infarction and stroke 18 19. Moreover, in patients who underwent SAVR for AS, postoperative RAS blockade therapy with ACE inhibitors or ARBs was associated with augmented regression of LV hypertrophy,4 20 as well as increased survival rates 6.…”

Women had favourable reverse left ventricle remodelling after TAVR

“…LV remodelling alone can greatly impact morbidity in this patient population. 17,18 TAVR causes an acute decrease in the transvalvular gradient that could lead to unloading the LV and, thus reverses LV remodelling and improves clinical outcomes. 18 Previous studies have suggested that female sex is associated with better mid-and long-term survival post-TAVR despite the increased rate of periprocedural complications.…”

“…17,18 TAVR causes an acute decrease in the transvalvular gradient that could lead to unloading the LV and, thus reverses LV remodelling and improves clinical outcomes. 18 Previous studies have suggested that female sex is associated with better mid-and long-term survival post-TAVR despite the increased rate of periprocedural complications. [2][3][4][5][6] There is currently no clear-cut explanation for why women fare better than men after TAVR.…”

Prognostic Significance of Occult Transthyretin Cardiac Amyloidosis in Patients With Severe Aortic Stenosis Undergoing Surgical Aortic Valve Replacement

“…6 Severity of coexisting coronary artery disease was associated with impaired clinical outcomes at 1 year after TAVR in 445 patients with severe AS (mean age, 82.5 years; 56% female). 7 Severe AS and left ventricular ejection fraction of <50% with or without aortic valve replacement, 8,9 low-flow, low-gradient AS with reduced stroke volume index, [10][11][12][13] and reduced global longitudinal strain by speckle-tracking echocardiography 14 have increased risk of mortality after sAVR or TAVR in patients with severe AS. Midwall myocardial fibrosis that can be detected by late gadolinium enhancement, 15 and prosthesispatient mismatch 16,17 have also been reported as prognosticators in patients with severe AS after sAVR or TAVR.…”

“…[6][7][8][9][10][11][12][13][14][15][16][17] The coexistence of wtATTR and severe AS may cause severe hypertrophy and left ventricular functional impairment, which can be misdiagnosed as low-flow, low-gradient severe AS. [10][11][12][13] Recent studies have suggested that patients with wtATTR are characterized by lower left ventricular ejection fraction, stroke volume index, left ventricular basal, and midradial strains compared with age and wall thickness matched mutant ATTR patients.…”