Background. Subclinical valvular alterations may trigger myocardial remodeling and fibrotic processes before overt symptoms of heart failure or diastolic dysfunction occur. However, the association of subclinical valvular disease and early detection of myocardial remodeling in a population-based setting is less-well studied. This study aims to identify the prevalence of early myocardial remodeling by imaging and biomarker parameters among individuals with subclinical left ventricular valvular heart disease (VHD).
Methods. We examined cross-sectional data from the first 10,000 participants enrolled in the large population-based Hamburg City Health Study cohort. We analyzed risk factors, dedicated cardiovascular examinations including biomarker profiles, electrocardiogram, echocardiography, and cardiac magnetic resonance tomography (CMR). VHD was defined as any echocardiographic or CMR evidence of aortic or mitral valve stenosis/regurgitation in the absence of VHD-history. Circulating biomarkers were measured to evaluate subclinical myocardial injury or stress.
Results. A total of 2,588 participants with available CMR imaging were included in the final analysis. The median age was 67 years and 41% were women. VHD was present in 988 (48%) participants and individuals with VHD were significantly older (69 vs. 64 years; p<0.001), showed higher rates of atrial fibrillation (8.3% vs. 3.3%; p<0.001; Fig. 1) and heart failure (4.9% vs. 1.8%; p<0.001), higher NTproBNP (107ng/l vs. 73ng/l; p<0.001; Fig. 1) as well as MRproANP concentrations (76pmol/L vs. 64pmol/l; p<0.001). Further, VHD participants exhibited significantly lower functional echocardiographic parameters, including left ventricular stroke volume (64ml vs. 68ml; p<0.001; Fig. 1), left ventricular end-diastolic (108ml vs. 117ml; p<0.001) and end-systolic volume (45ml vs. 49ml; p=0.007). Echocardiographic indices of diastolic dysfunction (E/E’ 7.63 vs. 7.39; p<0.001) were more frequent in VHD individuals. CMR imaging revealed myocardial changes in VHD participants with lower LVEF (69% vs. 71%; p<0.001) and higher rates of LV-hypertrophy (18% vs. 14%; p=0.047; Fig. 1). Within CMR mapping analysis, VHD was associated with native myocardial T1 levels (1,175ms vs. 1,173ms; p=0.042; Fig. 1), but not significantly linked to higher levels of extracellular volume fraction (ECV) (26.54% vs. 26.85%; p=0.2) or the presence of late gadolinium enhancement lesions (LGE) (11% vs. 12%; p=0.7; Fig. 1).
Conclusion. In this large, population-based cohort, subclinical VHD was associated with signs of early cardiac remodeling in multimodal imaging and higher natriuretic peptides. Higher native myocardial T1 times in the absence of elevated ECV or focal LGE suggest early diffuse myocardial fibrosis without manifest fibrotic transformation in subclinical VHD. The detection of subclinical valvular cardiovascular changes in the general population highlights the potential clinical relevance of identification of asymptomatic valve dysfunction.
