Echocardiographic Global Longitudinal Strain Is Associated With Myocardial Fibrosis and Predicts Outcomes in Aortic Stenosis.
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SUBMITTER: Le TT
PROVIDER: S-EPMC8631398 | biostudies-literature |
REPOSITORIES: biostudies-literature
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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.
| S-EPMC7977929 | biostudies-literature
Project description:AimsMidwall myocardial fibrosis on cardiovascular magnetic resonance (CMR) is a marker of early ventricular decompensation and adverse outcomes in aortic stenosis (AS). We aimed to develop and validate a novel clinical score using variables associated with midwall fibrosis.Methods and resultsOne hundred forty-seven patients (peak aortic velocity (Vmax) 3.9 [3.2,4.4] m/s) underwent CMR to determine midwall fibrosis (CMR cohort). Routine clinical variables that demonstrated significant association with midwall fibrosis were included in a multivariate logistic score. We validated the prognostic value of the score in two separate outcome cohorts of asymptomatic patients (internal: n = 127, follow-up 10.3 [5.7,11.2] years; external: n = 289, follow-up 2.6 [1.6,4.5] years). Primary outcome was a composite of AS-related events (cardiovascular death, heart failure, and new angina, dyspnoea, or syncope). The final score consisted of age, sex, Vmax, high-sensitivity troponin I concentration, and electrocardiographic strain pattern [c-statistic 0.85 (95% confidence interval 0.78-0.91), P < 0.001; Hosmer-Lemeshow χ(2) = 7.33, P = 0.50]. Patients in the outcome cohorts were classified according to the sensitivity and specificity of this score (both at 98%): low risk (probability score <7%), intermediate risk (7-57%), and high risk (>57%). In the internal outcome cohort, AS-related event rates were >10-fold higher in high-risk patients compared with those at low risk (23.9 vs. 2.1 events/100 patient-years, respectively; log rank P < 0.001). Similar findings were observed in the external outcome cohort (31.6 vs. 4.6 events/100 patient-years, respectively; log rank P < 0.001).ConclusionWe propose a clinical score that predicts adverse outcomes in asymptomatic AS patients and potentially identifies high-risk patients who may benefit from early valve replacement.
| S-EPMC4761400 | biostudies-literature
Project description: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).
| S-EPMC5683736 | biostudies-literature
Project description:BackgroundMyocardial fibrosis is an important pathophysiologic mechanism of cardiac involvement that leads to increased mortality in patients with autoimmune diseases (AIDs). The aim of this study was to evaluate the association between myocardial strain from speckle-tracking echocardiography (STE) and fibrosis on cardiovascular magnetic resonance (CMR) and to further explore their prognostic implications in patients with AIDs.MethodsWe prospectively included 102 AIDs patients with clinically suspected cardiac involvement and 102 age- and sex-matched healthy individuals. Patients underwent CMR for evaluation of myocardial fibrosis by late gadolinium enhancement (LGE) and T1 mapping. A semiquantitative evaluation based on the extent of LGE was used to calculate the total (tLGEs) and segmental (sLGEs) LGE score. Global longitudinal strain (GLS) was evaluated by STE in all subjects. All patients were regularly followed up every 6 months. The primary endpoint was the composite incidence of all-cause death and cardiovascular hospitalization.ResultsCompared to healthy controls, AIDs patients had impaired GLS (-17.9 ± 5.1% vs. -21.2 ± 2.5%, p < 0.001). LGE was detected in 70% of patients. Patients with LGE presented worse GLS (-17.1 ± 5.3% vs. -19.6 ± 4.1%, p = 0.018) than those without LGE. On multivariate logistic analysis, GLS ≥ -15% was an independent predictor of LGE presence (OR = 4.98, 95%CI 1.35-18.33, p = 0.016). Moreover, a marked and stepwise impairment of segmental longitudinal strain (-19.3 ± 6.6 vs. -14.9 ± 6.5 vs. -8.9 ± 6.3, p < 0.001) was observed as sLGEs increased. During a median follow-up time of 25 months, 6 patients died, and 14 patients were hospitalized for cardiovascular reasons. Both GLS ≥ -15% (HR 3.56, 95%CI 1.28-9.86, p = 0.015) and tLGEs ≥ 6 (HR 4.13, 95%CI 1.43-11.92, p = 0.009) were independently associated with the primary endpoint.ConclusionsIn AIDs patients, impaired myocardial strain on STE could reflect the presence and extent of myocardial fibrosis and provide incremental prognostic value in addition to LGE in the prediction of adverse outcomes.
| S-EPMC8899104 | biostudies-literature
Project description:Sex differences in risk factors of aortic valve calcification (AVC) by echocardiography have not been reported from a large prospective study in aortic stenosis (AS).AVC was assessed using a prognostically validated visual score and grouped into none/mild or moderate/severe AVC in 1725 men and women with asymptomatic AS in the Simvastatin Ezetimibe in Aortic Stenosis study. The severity of AS was assessed by the energy loss index (ELI) taking pressure recovery in the aortic root into account.More men than women had moderate/severe AVC at baseline despite less severe AS by ELI (p<0.01). Moderate/severe AVC at baseline was independently associated with lower aortic compliance and more severe AS in both sexes, and with increased high-sensitive C reactive protein (hs-CRP) only in men (all p<0.01). In Cox regression analyses, moderate/severe AVC at baseline was associated with a 2.5-fold (95%?CI 1.64 to 3.80) higher hazard rate of major cardiovascular events in women, and a 2.2-fold higher hazard rate in men (95%?CI 1.54 to 3.17) (both p<0.001), after adjustment for age, hypertension, study treatment, aortic compliance, left ventricular (LV) mass and systolic function, AS severity and hs-CRP. Moderate/severe AVC at baseline also predicted a 1.8-fold higher hazard rate of all-cause mortality in men (95%?CI 1.04 to 3.06, p<0.05) independent of age, AS severity, LV mass and aortic compliance, but not in women.In conclusion, AVC scored by echocardiography has sex-specific characteristics in AS. Moderate/severe AVC is associated with higher cardiovascular morbidity in both sexes, and with higher all-cause mortality in men.ClinicalTrials.gov identifier: NCT00092677.
| S-EPMC5739834 | biostudies-literature
Project description:Left ventricular myocardial fibrosis in patients with aortic stenosis (AS) confers worse prognosis. Plasma osteoprotegerin (OPG), a cytokine from the TNF receptor family, correlates with the degree of valve calcification in AS, reflecting the activity of the tissue RANKL/RANK/OPG (receptor activator of nuclear factor ?? ligand/RANK/osteoprotegerin) axis, and is associated with poorer outcomes in AS. Its association with myocardial fibrosis is unknown. We hypothesised that OPG levels would reflect the extent of myocardial fibrosis in AS. We included 110 consecutive patients with AS who had undergone late-gadolinium contrast enhanced cardiovascular magnetic resonance (LGE-CMR). Patients were characterised according to pattern of fibrosis (no fibrosis, midwall fibrosis, or chronic myocardial infarction fibrosis). Serum OPG was measured with ELISA and compared between groups defined by valve stenosis severity. Some 36 patients had no fibrosis, 38 had midwall fibrosis, and 36 had chronic infarction. Patients with midwall fibrosis did not have higher levels of OPG compared to those without fibrosis (6.78 vs. 5.25 pmol/L, p?=?0.12). There was no difference between those with midwall or chronic myocardial infarction fibrosis (6.78 vs. 6.97 pmol/L, p?=?0.27). However, OPG levels in patients with chronic myocardial infarction fibrosis were significantly higher than those without fibrosis (p?=?0.005).
| S-EPMC6162228 | biostudies-literature
Project description:The pressure overload due to the progressive narrowing of the valve area determines the development of the left ventricular hypertrophy which characterizes aortic stenosis (AS). The onset of myocardial fibrosis marks the inexorable decline of an initially compensatory response towards heart failure. However, myocardial fibrosis does not yet represent a key element in the prognostic and therapeutic framework of AS. In this context, cardiac magnetic resonance imaging plays a major role by highlighting both the focal irreversible fibrotic replacement, using the late gadolinium enhancement (LGE) technique, and the earlier diffuse reversible interstitial fibrosis, using the T1 mapping techniques. For this reason, the presence of myocardial fibrosis would be useful to identify a subgroup of patients at greater risk of events among the subjects with severe AS. Actually, more and more evidences seem to identify the presence of LGE as a powerful prognostic factor to be used to optimize the timing of prosthetic valve replacement. Randomized clinical trials, such as the EVoLVeD trial currently underway, will be needed to better define the importance of myocardial fibrosis assessment in the management of patients with AS.
| S-EPMC8503407 | biostudies-literature
Project description:Aortic stenosis is characterized both by progressive valve narrowing and the left ventricular remodeling response that ensues. The only effective treatment is aortic valve replacement, which is usually recommended in patients with severe stenosis and evidence of left ventricular decompensation. At present, left ventricular decompensation is most frequently identified by the development of typical symptoms or a marked reduction in left ventricular ejection fraction <50%. However, there is growing interest in using the assessment of myocardial fibrosis as an earlier and more objective marker of left ventricular decompensation, particularly in asymptomatic patients, where guidelines currently rely on nonrandomized data and expert consensus. Myocardial fibrosis has major functional consequences, is the key pathological process driving left ventricular decompensation, and can be divided into 2 categories. Replacement fibrosis is irreversible and identified using late gadolinium enhancement on cardiac magnetic resonance, while diffuse fibrosis occurs earlier, is potentially reversible, and can be quantified with cardiac magnetic resonance T1 mapping techniques. There is a substantial body of observational data in this field, but there is now a need for randomized clinical trials of myocardial imaging in aortic stenosis to optimize patient management. This review will discuss the role that myocardial fibrosis plays in aortic stenosis, how it can be imaged, and how these approaches might be used to track myocardial health and improve the timing of aortic valve replacement.
| S-EPMC6361867 | biostudies-literature
Project description:BackgroundThe extent of myocardial fibrosis in patients with severe aortic stenosis might have an important prognostic value. Non-invasive imaging to quantify myocardial fibrosis by measuring extracellular volume fraction might have an important clinical utility prior to aortic valve intervention.MethodsSeventy-five consecutive patients with severe aortic stenosis, and 19 normal subjects were prospectively recruited and underwent pre- and post-contrast computed tomography for estimating myocardial extracellular volume fraction. Serum level of galectin-3 was measured and 2-dimensional echocardiography was performed to characterize the extent of cardiac damage using a recently published aortic stenosis staging classification.ResultsExtracellular volume fraction was higher in patients with aortic stenosis compared to normal subjects (40.0±11% vs. 21.6±5.6%; respectively, p<0.001). In patients with aortic stenosis, extracellular volume fraction correlated with markers of left ventricular decompensation including New York Heart Association functional class, left atrial volume, staging classification of aortic stenosis and lower left ventricular ejection fraction. Out of 75 patients in the AS group, 49 underwent TAVI, 6 surgical AVR, 2 balloon valvuloplasty, and 18 did not undergo any type of intervention. At 12-months after aortic valve intervention, extracellular volume fraction predicted the combined outcomes of stroke and hospitalization for heart failure with an area under the curve of 0.77 (95% confidence interval: 0.65-0.88). A trend for correlation between serum galectin-3 and extracellular volume was noted.ConclusionIn patients with severe aortic stenosis undergoing computed tomography before aortic valve intervention, quantification of extracellular volume fraction correlated with functional status and markers of left ventricular decompensation, and predicted the 12-months composite adverse clinical outcomes. Implementation of this novel technique might aid in the risk stratification process before aortic valve interventions.
| S-EPMC7946277 | biostudies-literature
Project description:BackgroundsThe presence of impaired global longitudinal strain (GLS) may be a valuable bio-marker in the early diagnosis for left ventricle (LV) impairment, which would help scrutinize asymptomatic aortic stenosis (AS) patients with high risk of adverse outcomes, such as major adverse cardiovascular events (MACE).MethodsThe study was prospectively registered in PROPSERO (CRD 42021223472). Databases, such as Pubmed, Embase, Cochrane Library, Web of science, and Scopus were searched for studies evaluating the impact of impaired GLS on MACE, all-cause mortality, and aortic valve replacement (AVR) in asymptomatic AS. Hazard ratios (HRs) with 95% CIs were calculated with meta-analysis for binary variants. Meta-regression, subgroup analysis, and sensitivity analyses were applied as needed to explore the heterogeneity.ResultsEventually, a total of nine studies reporting 1,512 patients were enrolled. Compared with the normal GLS group, impaired GLS significantly increased MACE (HR = 1.20, 95% CI: 1.10-1.30, I 2 = 79%) with evident heterogeneity, all-cause mortality (HR = 1.42, 95% CI: 1.24-1.63), and AVR (HR = 1.17, 95% CI: 1.07-1.28). Subgroup analyses stratified by left ventricular ejection fraction (LVEF) > 50% or LVEF without precise cut-off point found that compared with the normal GLS group, impaired GLS remarkably increased MACE both in two subgroups (LVEF > 50%: HR: 1.22, 95% CI: 1.05-1.50; LVEF without cutpoint: HR: 1.25, 95% CI: 1.05-1.50). The results stratified by AS severity (mild/moderate and severe) or follow-up time resembled those stratified by LVEF. In addition, when subgroup analysis was stratified by mean aortic valve pressure gradient (MG ≥ 40 mm Hg and MG <40 mm Hg), compared with normal GLS, impaired GLS significantly increased MACE both in two subgroups (MG ≥ 40 mm Hg: HR: 3.41, 95% CI: 1.64-7.09; MG below 40 mm Hg: HR: 3.17, 95% CI: 1.87-5.38). Moreover, the effect sizes here were substantially higher than those in the former two stratified factors.ConclusionsThe presence of impaired GLS substantially worsens the outcomes for adverse cardiovascular events in asymptomatic patients with AS regardless of LVEF or AS severity or follow-up time or mean aortic valve pressure gradient, which highlights the importance of incorporating impaired GLS into risk algorithms in asymptomatic AS.Systematic review registrationPROSPERO (registration number: CRD42021223472).
| S-EPMC8894446 | biostudies-literature