Multiparametric CMR and ECG features, including LGE volume >4%, discriminated hypertrophic cardiomyopathy from hypertensive heart disease with 74.1% sensitivity and 84.5% specificity (AUC 0.81).
Observational (n=150)
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Does multi-parametric CMR combined with ECG improve the differential diagnosis between hypertrophic cardiomyopathy and hypertensive heart disease in patients with septal left ventricular hypertrophy?
Multi-parametric CMR (specifically LGE volume and location, and torsion) combined with ECG repolarization abnormalities provides independent predictors that can reliably differentiate hypertrophic cardiomyopathy from hypertensive heart disease in patients with septal hypertrophy.
Odds Ratio: 0.63 (95% CI 0.42–0.85)
valor p: p=0.009
Abstract Background Septal left ventricular hypertrophy (LVH) can represent a diagnostic challenge, with hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD) being the most common differential diagnoses. Purpose To assess the ability of a multi-parametric cardiac magnetic resonance (CMR) evaluation, combined with electrocardiographic findings, to inform the differential diagnosis between HCM and HHD in patients presenting with septal LVH phenotype. Methods This two-center study enrolled consecutive patients with HCM (diagnosed as currently defined by guidelines) and HHD with septal LVH who underwent a clinically indicated CMR examination and ECG within 6 months. Patients with increased LV wall thickness in areas other than the basal and/or mid interventricular septum were excluded. A multi-parametric CMR protocol with cine, native T1 mapping, late gadolinium enhancement (LGE) imaging and feature-tracking strain analysis was performed. Results A total of 150 patients (86 HCM, 64 HHD) were included. HCM patients showed significantly greater septal maximal wall thickness (MWT) compared to HHD median (IQR); HCM: 16 (15, 19); HHD: 14 (13, 15); p0.001 and higher LGE volume percentage (p0.001). Conversely, the evidence of non-specific LGE limited to the LV/right ventricle insertion points was significantly more frequent in the HHD cohort (p0.001). Global HCM: -16.5 (-18.4, -4.1); HHD: -17.9 (-19.2, -15.7); p=0.009 and septal longitudinal strain HCM: -15.1 (-17.8, -12.0); HHD: -17.4 (-20.1, -15.4); p0.001 were more impaired in HCM vs HHD. Torsion was enhanced in HCM patients compared to HHD HCM: 1.8 (1.4-2.4); HHD: 1.5 (1.1-1.8); p=0.028. At the ECG, repolarization abnormalities were significantly more prevalent among HCM patients (62% vs 40%; p=0.011). Multivariable analysis identified LGE volume percentage (OR 0.63, 95% CI 0.42-0.85; p=0.009), septal LGE location (OR 0.17, 95% CI 0.04-0.73; p=0.019), enhanced torsion (OR 0.46, 95% CI 0.21-0.97, p=0.047), septal MWT (OR 0.42, 95% CI 0.20-0.69, p=0.005) and ECG repolarization abnormalities (OR 0.02, 95% CI 0.00-0.20, p=0.005) as independent predictors of HCM diagnosis. LGE volume4% discriminated HCM from HHD with 74.1% sensitivity and 84.5% specificity (AUC 0.81). In both groups, a mild but significant correlation was observed between septal MWT and septal longitudinal strain (HCM: R= 0.29, p=0.009; HHD: R= 0.37, p=0.002) while no correlation was observed between septal MWT and torsion (HCM: R= -0.13, p=0.23; HHD: R= -0.02, p=0.89). Conclusions In the challenging diagnostic scenario of septal LVH, multiparametric CMR and ECG aid to differentiate HCM versus HHD. Septal MWT, the percentage of LGE and its septal location, together with enhanced torsion and ECG repolarization abnormalities, are independent predictors of HCM. While strain impairment worsens with increasing LVH in both diseases, torsion is enhanced in HCM independently from LVH severity.
Malara et al. (Thu,) conducted a observational in Septal left ventricular hypertrophy (HCM vs HHD) (n=150). Multiparametric cardiac magnetic resonance (CMR) and ECG vs. Hypertensive heart disease (HHD) was evaluated on Diagnosis of hypertrophic cardiomyopathy (HCM) (OR 0.63, 95% CI 0.42-0.85, p=0.009). Multiparametric CMR and ECG features, including LGE volume >4%, discriminated hypertrophic cardiomyopathy from hypertensive heart disease with 74.1% sensitivity and 84.5% specificity (AUC 0.81).