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Myocardial Fibrosis and Cardiac Decompensation in Aortic Stenosis.

ABSTRACT: OBJECTIVES:Cardiac magnetic resonance (CMR) was used to investigate the extracellular compartment and myocardial fibrosis in patients with aortic stenosis, as well as their association with other measures of left ventricular decompensation and mortality. BACKGROUND:Progressive myocardial fibrosis drives the transition from hypertrophy to heart failure in aortic stenosis. Diffuse fibrosis is associated with extracellular volume expansion that is detectable by T1 mapping, whereas late gadolinium enhancement (LGE) detects replacement fibrosis. METHODS:In a prospective observational cohort study, 203 subjects (166 with aortic stenosis [69 years; 69% male]; 37 healthy volunteers [68 years; 65% male]) underwent comprehensive phenotypic characterization with clinical imaging and biomarker evaluation. On CMR, we quantified the total extracellular volume of the myocardium indexed to body surface area (iECV). The iECV upper limit of normal from the control group (22.5 ml/m2) was used to define extracellular compartment expansion. Areas of replacement mid-wall LGE were also identified. All-cause mortality was determined during 2.9 ± 0.8 years of follow up. RESULTS:iECV demonstrated a good correlation with diffuse histological fibrosis on myocardial biopsies (r = 0.87; p < 0.001; n = 11) and was increased in patients with aortic stenosis (23.6 ± 7.2 ml/m2 vs. 16.1 ± 3.2 ml/m2 in control subjects; p < 0.001). iECV was used together with LGE to categorize patients with normal myocardium (iECV <22.5 ml/m2; 51% of patients), extracellular expansion (iECV ?22.5 ml/m2; 22%), and replacement fibrosis (presence of mid-wall LGE, 27%). There was evidence of increasing hypertrophy, myocardial injury, diastolic dysfunction, and longitudinal systolic dysfunction consistent with progressive left ventricular decompensation (all p < 0.05) across these groups. Moreover, this categorization was of prognostic value with stepwise increases in unadjusted all-cause mortality (8 deaths/1,000 patient-years vs. 36 deaths/1,000 patient-years vs. 71 deaths/1,000 patient-years, respectively; p = 0.009). CONCLUSIONS:CMR detects ventricular decompensation in aortic stenosis through the identification of myocardial extracellular expansion and replacement fibrosis. This holds major promise in tracking myocardial health in valve disease and for optimizing the timing of valve replacement. (The Role of Myocardial Fibrosis in Patients With Aortic Stenosis; NCT01755936).

SUBMITTER: Chin CWL

PROVIDER: S-EPMC5683736 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature

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Myocardial Fibrosis and Cardiac Decompensation in Aortic Stenosis.

Chin Calvin W L CWL Everett Russell J RJ Kwiecinski Jacek J Vesey Alex T AT Yeung Emily E Esson Gavin G Jenkins William W Koo Maria M Mirsadraee Saeed S White Audrey C AC Japp Alan G AG Prasad Sanjay K SK Semple Scott S Newby David E DE Dweck Marc R MR

JACC. Cardiovascular imaging 20161221 11

<h4>Objectives</h4>Cardiac magnetic resonance (CMR) was used to investigate the extracellular compartment and myocardial fibrosis in patients with aortic stenosis, as well as their association with other measures of left ventricular decompensation and mortality.<h4>Background</h4>Progressive myocardial fibrosis drives the transition from hypertrophy to heart failure in aortic stenosis. Diffuse fibrosis is associated with extracellular volume expansion that is detectable by T1 mapping, whereas la ...[more]

PMID: 28017384

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Project description:BackgroundAortic stenosis is accompanied by progressive left ventricular hypertrophy and fibrosis. We investigated the natural history of these processes in asymptomatic patients and their potential reversal post-aortic valve replacement (AVR).MethodsAsymptomatic and symptomatic patients with aortic stenosis underwent repeat echocardiography and magnetic resonance imaging. Changes in peak aortic-jet velocity, left ventricular mass index, diffuse fibrosis (indexed extracellular volume), and replacement fibrosis (late gadolinium enhancement [LGE]) were quantified.ResultsIn 61 asymptomatic patients (43% mild, 34% moderate, and 23% severe aortic stenosis), significant increases in peak aortic-jet velocity, left ventricular mass index, indexed extracellular volume, and LGE mass were observed after 2.1±0.7 years, with the most rapid progression observed in patients with most severe stenosis. Patients with baseline midwall LGE (n=16 [26%]; LGE mass, 2.5 g [0.8-4.8 g]) demonstrated particularly rapid increases in scar burden (78% [50%-158%] increase in LGE mass per year). In 38 symptomatic patients (age, 66±8 years; 76% men) who underwent AVR, there was a 19% (11%-25%) reduction in left ventricular mass index (P<0.0001) and an 11% (4%-16%) reduction in indexed extracellular volume (P=0.003) 0.9±0.3 years after surgery. By contrast midwall LGE (n=10 [26%]; mass, 3.3 g [2.6-8.0 g]) did not change post-AVR (n=10; 3.5 g [2.1-8.0 g]; P=0.23), with no evidence of regression even out to 2 years.ConclusionsIn patients with aortic stenosis, cellular hypertrophy and diffuse fibrosis progress in a rapid and balanced manner but are reversible after AVR. Once established, midwall LGE also accumulates rapidly but is irreversible post valve replacement. Given its adverse long-term prognosis, prompt AVR when midwall LGE is first identified may improve clinical outcomes.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifiers: NCT01755936 and NCT01679431.

Project description:PurposeTo use global longitudinal strain (GLS) as a marker of left ventricular decompensation in aortic stenosis and to investigate the relationship of GLS measured with cardiac MRI with markers of myocardial fibrosis, symptom development, remodeling, and clinical outcomes.Materials and methodsPatients with aortic stenosis and healthy control subjects were assessed. GLS was assessed by using cardiac MRI feature tracking, diffuse fibrosis by T1 mapping, and replacement fibrosis using late gadolinium enhancement. Follow-up was prospective for the primary endpoint of all-cause mortality.ResultsGLS was reduced in aortic stenosis (n = 159) compared with control subjects (n = 41) (-17.6% ± 3.1 [standard deviation] vs -18.9% ± 2.6, P = .02). GLS demonstrated weak associations with aortic stenosis severity (Vmax; r = 0.24, P = .0005) but showed moderate correlation with T1 mapping measures of myocardial fibrosis (eg, indexed extracellular volume [iECV]; r = 0.43, P < .0001). Moreover, GLS was reduced in patients with midwall fibrosis compared with control subjects (P < .001), although values were similar to those of patients with myocardial infarction (P = .25). In adjusted analyses, GLS was associated with total myocardial fibrosis burden (iECV) and ejection fraction (both P < .001). GLS offered poor discrimination between disease states, inability to distinguish between control subjects and patients (area under the curve [AUC], 0.60), presence or absence of fibrosis (AUC, 0.63), or symptomatic severity (left ventricular decompensation AUC, 0.64). At follow-up (median, 1466 days), 21 patients died. GLS did not independently predict clinical outcomes.ConclusionGLS correlates with established markers of myocardial fibrosis. However, widespread utility of single GLS measurements may be limited by overlap between disease states and its inability to predict clinical outcomes beyond current established markers.© RSNA, 2019Supplemental material is available for this article.

Dataset Information

Myocardial Fibrosis and Cardiac Decompensation in Aortic Stenosis.

Publications

Myocardial Fibrosis and Cardiac Decompensation in Aortic Stenosis.

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