Impact of left ventricular hypertrophy late after aortic valve replacement for aortic stenosis on cardiovascular morbidity and mortality
Introduction
In patients with long-standing aortic stenosis, left ventricular (LV) mass increases and ventricular geometry changes in order to preserve the relation between intraventricular pressure and systolic wall stress.[1], [2] LV hypertrophy is a result of cellular myocardial hypertrophy and structural alternations of the extracellular matrix (i.e. interstitial fibrosis). Myocardial hypertrophy and interstitial fibrosis impair the diastolic function of the LV by increasing its stiffness and delaying its relaxation [3]. After successful aortic valve replacement, LV pressure and thereby LV systolic wall stress are substantially reduced [4]. As a consequence, regression of LV hypertrophy can be expected during the ensuing months.
In the general population, LV hypertrophy is a risk factor for cardiovascular morbidity and mortality independent of its aetiology [5]. In patients with aortic stenosis and LV hypertrophy, there are few data on the fate of patients with increased LV mass late after aortic valve replacement. A recent report of a small patient group suggested an increased mortality (23% mortality over a mean follow-up of 40 months) in patients with persistent LV hypertrophy after aortic valve replacement for aortic stenosis [6].
The current study was designed to assess the prevalence of LV hypertrophy late after aortic valve replacement in a large patient cohort and to test the hypothesis of increased cardiovascular morbidity and mortality related to LV hypertrophy despite successful aortic valve replacement.
Section snippets
Patient selection
All transthoracic echocardiographic studies performed at our institution between 1992 and 1998 were reviewed for the following four criteria: (i) aortic valve replacement for predominant aortic stenosis; (ii) no previous or concomitant replacement of another heart valve; (iii) sufficient echocardiographic image quality to allow determination of LV mass; (iv) the echocardiographic study was performed at least 6 months postoperatively. Each patient and/or the family doctor was located. In 5 cases
Patient characteristics
Patient characteristics are summarized in Table 1. Ninety-nine of 213 patients (46%) operated for aortic stenosis had LV hypertrophy > 6 months after aortic valve replacement. Patients with LV hypertrophy were 4 years older at the time of aortic valve replacement than patients with normal LV mass at follow-up (p = 0.03). They were treated more frequently with beta blocking agents than patients with normalized LV mass (27% vs. 11%, p = 0.02). Otherwise cardiac medication and clinical characteristics
Discussion
In nearly half of our patients with isolated aortic valve stenosis undergoing aortic valve replacement, LV mass is increased late after surgery independent of a history of arterial hypertension. In these patients, LV hypertrophy is associated with increased exertional dyspnoea and reduced exercise capacity. Overall mortality in patients > 6 months after replacement of a stenotic aortic valve was mainly related to age at surgery, coexisting coronary artery disease and smoking.
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Cited by (20)
Impact of Obesity on Persistent Left Ventricular Hypertrophy After Aortic Valve Replacement for Aortic Stenosis
2019, American Journal of CardiologyCitation Excerpt :These findings add to previous knowledge focusing on the impact of obesity on LV remodeling in preoperative studies in AS patients.3,5,6,19 Previous studies have documented the importance of LV hypertrophy regression for long-term postoperative prognosis.9,20 The present study expands previous findings from smaller studies by documenting that BMI ≥30 kg/m2 may independently impair normalization of LV mass during the first 6 months after surgical AVR for AS.13,14
A meta-analysis of effects of transcatheter versus surgical aortic valve replacement on left ventricular ejection fraction and mass
2017, International Journal of CardiologyCitation Excerpt :Gaudino et al. [4] demonstrated that the extent of LVM regression after SAVR did not correlate with 28 ± 9-month survival. Whereas, Zybach-Benz et al. [5] indicated that LVH at 5.8 ± 5.4 years after SAVR was an independent predictor of cardiac-related morbidity. The introduction of transcatheter aortic valve implantation (TAVI) in clinical practice has widened options for symptomatic patients at high surgical risk [1].
Left ventricular hypertrophy in valvular aortic stenosis: Mechanisms and clinical implications
2015, American Journal of MedicineLoad independent impairment of reverse remodeling after valve replacement in hypertensive aortic stenosis patients
2014, International Journal of CardiologyCitation Excerpt :LV hypertrophy (LVH) allows for normalization of systolic wall stress and has been considered as compensatory [5], but it is also associated with impaired coronary blood-flow reserve [6] and changes in cardiomyocytes and extracellular matrix (ECM) connective tissue, some of them irreversible [7]. Moreover, the presence of residual hypertrophy after aortic valve replacement (AVR) has been associated with incomplete recovery of left ventricular function and worse prognosis [8–10]. The coexistence of hypertension and valvular aortic stenosis (AS) is common, but few studies have assessed the impact of concomitant hypertension on LV structure and function in patients with AS.
Early regression of left ventricular mass associated with diastolic improvement after transcatheter aortic valve implantation
2012, Journal of the American Society of EchocardiographyCitation Excerpt :Furthermore, diastolic dysfunction is caused and worsened by cardiopulmonary bypass, ischemia-reperfusion injury, and myocardial edema, and it may be a major determinant of perioperative outcomes in elderly patients undergoing AVR.43,44 Improvement in diastolic function after AVR has been attributed mainly to the subsequent regression of LVH, but early improvement may precede regression of hypertrophy after surgery.45 Ikonomidis et al.23 previously showed that abnormal LV relaxation was associated with residual LVH in patients with isolated AVS who underwent to AVR.