Regression of left ventricular hypertrophy during 10 years after valve replacement for aortic stenosis is related to the preoperative risk profile

Lund, Ole; Emmertsen, K; Dørup, I; Jensen, F. T.; Flø, Christian

doi:10.1016/s0195-668x(03)00316-6

Cited by 101 publications

(76 citation statements)

References 25 publications

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“…It is known that, LVMI decreases with the reduction of LV afterload after s-AVR and as a result, improvement in myocardial ischemia, functional capacity and long-term prognosis is observed [12,13]. The regression in LVMI after s-AVR is believed to be more important than valvular gradient as a prognostic factor [14][15][16]. The rate and magnitude of regression in LVMI can also be used as a distinctive parameter for reverse cardiac remodeling [17].…”

Section: Discussionmentioning

confidence: 99%

Impact of transcatheter aortic valve implantation on the left ventricular mass

et al. 2015

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001). There were no significant changes between the baseline and discharge mean LVM and LVM index values (LVMI; p = 0.1). However, LVMI decreased significantly in the 1st month of follow-up compared to baseline (123.3 ± ± 20.3 to 127.9 ± 21.3 g/m 2 , respectively, p < 0.001). Also, significant regression of LVM was observed at the 1 st month of follow-up compared to baseline (228.3 ± 33.5 g vs. 236.5 ± 34.2 g, respectively, p < 0.001 (Cardiol J 2015; 22, 6: 645-650)

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Section: Discussionmentioning

confidence: 99%

Impact of transcatheter aortic valve implantation on the left ventricular mass

et al. 2015

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“…By the time of the late postoperative study, there were no longer any significant differences in LV muscle mass index. 7 Lund and associates 20 analyzed LV hypertrophy regression during 10 years after AVR with disc valves, caged ball valves, and stented porcine valves implantations for AS. The mean LVMI was 202 ± 46 g/m 2 preoperatively, 157 ± 48 g/m 2 at 1.5 years (P <0.0001), and 159 ± 70 g/m 2 at 10 years (P <0.0001).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, our patients, because of their advanced age, had been exposed to the harmful effects of severe AS for many years: long-standing LV hypertrophy eventually becomes irreversible, due to myocardial fibrosis. 20,22 In addition, 94.7% of patients had a history of hypertension. Postoperative medications were β-blockers in 15 patients (79%), angiotensin-converting enzyme inhibitors/angiotensin-1 receptor blockers in 11 (58%), calcium antagonists in 5 (26%), and diuretics in 10 (53%).…”

Section: Discussionmentioning

confidence: 99%

Regression of Left Ventricular Mass after Implantation of the Sutureless 3f Enable Aortic Bioprosthesis

Concistrè¹,

Miceli²,

Marchi³

et al. 2015

Texas Heart Institute Journal

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“…Patient-prosthesis mismatch and hypertension following AVR are each associated with attenuated LV reverse remodeling due to the persistence of elevated afterload [84,85]. Within the PARTNER trial, mean aortic valve gradient predicted early LV functional improvement after valve replacement, supporting the premise that low-gradient severe AS with LV dysfunction represents an advanced stage of LV remodeling characterized at least in part by irreversible LV pathology [73•].…”

Section: Invasive Therapiesmentioning

confidence: 99%

Patterns of Left Ventricular Remodeling in Aortic Stenosis: Therapeutic Implications

Elmariah

2015

Curr Treat Options Cardio Med

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Aortic valve stenosis is characterized by indolent progression followed by the late development of symptoms once left ventricular compensatory mechanisms fail. In this review, we describe the left ventricular response to aortic stenosis. Specifically, we highlight the process of adaptive remodeling, which begins as a beneficial compensatory mechanism but ultimately transitions to a maladaptive process characterized by inappropriate left ventricular hypertrophy, interstitial fibrosis, and diminished contractility. Myocardial fibrosis ensues as the remodeling process progresses with potentially irreversible consequences on diastolic and systolic function and on clinical symptoms and outcomes. Recent data suggest that fibrosis is largely responsible for the development of symptoms in patients with severe aortic stenosis, which unfortunately implies that fibrosis may be advanced by the time clinical symptomatology triggers evaluation for aortic valve replacement. Interstitial fibrosis persists for years after valve replacement and, when severe, can lessen the clinical benefits of valve replacement. Further evaluation of noninvasive measures capable of assessing the extent of maladaptive left ventricular remodeling and of predicting its reversal are desperately needed in order to enhance the personalized delivery of aortic valve replacement for severe aortic stenosis. We support aggressive assessment of symptomatic status with more frequent clinical follow-up and exercise testing in asymptomatic individuals with severe left ventricular hypertrophy or impaired longitudinal contractility. However, whether early valve replacement is advantageous in patients with evidence of maladaptive left ventricular remodeling in the absence of symptoms remains unknown, but is certainly worthy of further investigation.

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Regression of left ventricular hypertrophy during 10 years after valve replacement for aortic stenosis is related to the preoperative risk profile

Abstract: Left ventricular hypertrophy regression for patients who survived up to 10 years after AVR for AS is dependent on the preoperative risk profile indicating that irreversible myocardial disease is the underlying factor. Systemic hypertension is an important factor in its own right.

Cited by 101 publications

References 25 publications

Impact of transcatheter aortic valve implantation on the left ventricular mass

Impact of transcatheter aortic valve implantation on the left ventricular mass

Regression of Left Ventricular Mass after Implantation of the Sutureless 3f Enable Aortic Bioprosthesis

Patterns of Left Ventricular Remodeling in Aortic Stenosis: Therapeutic Implications

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