Abstract Aims Hypertrophic cardiomyopathy (HCM) remains underdiagnosed due to limited access to expert imaging. We developed and validated a deep-learning (DL)-based echocardiographic model adaptable to point-of-care ultrasound (POCUS) for scalable HCM screening. Methods and results We retrospectively analysed 134 956 expert transthoracic echocardiograms (TTE) from 73 598 patients at Sheba Medical Center (2007–2022). A TTE-trained DL model integrating structural features and temporal motion patterns from parasternal long-axis and apical four-chamber views estimated HCM probability. Performance was evaluated in an independent test cohort and clinical subgroups. External validation used bedside POCUS studies from non-cardiologists with handheld devices. The test cohort included 12 096 patients with 119 confirmed HCM cases (prevalence 0.98%; median age 75 years, 57% male). HCM-positive patients showed increased expert TTE-measured septal (1.67 [1.5, 2.0] vs. 1.01 [0.9, 1.19] cm) and posterior wall thickness (1.1 [1.0, 1.3] vs. 0.9 [0.8, 1.0] cm) (P < 0.001). The model achieved excellent discrimination with an area under the curve of 0.982 (95% CI 0.966–0.993), sensitivity 88.2%, and specificity 97.3%, robust across subgroups. The POCUS cohort (n = 1047, median age 73 years, 55% male) represented multimorbid inpatients with 65 (6.2%) classified as screen-positive by the algorithm. These showed higher expert TTE-measured septal thickness (1.26 [1.07, 1.46] vs. 1.06 [0.9, 1.2] cm; 22% vs. 4% with IVS ≥1.5 cm; P ≤ 0.01). Among 49 (75%) POCUS-flagged positive patients with formal TTE and clinical data, 8 (16%) were confirmed by expert adjudication to have HCM. Specificity is limited by occasional confounding amyloidosis detection (4% of POCUS-flagged patients). Conclusion This DL-based model identifies HCM and demonstrates feasibility for POCUS screening, supporting earlier detection and broader diagnostic access.
N. Karra, Y. Klempfner, Viana Copeland et al.· European Heart Journal - Dig...· 0 citations
Atrial and ventricular ectopy are frequently encountered during ambulatory monitoring in asymptomatic adults; however, their independent long-term prognostic significance in low-risk populations without structural heart disease remains a subject of ongoing clinical debate.
To identify the distinct clinical and physiological determinants of atrial ectopic burden (AEB) and ventricular ectopic burden (VEB), and to evaluate their independent long-term associations with major adverse cardiovascular events (MACE) in a primary prevention cohort.
We evaluated 931 asymptomatic individuals (mean age 52 ± 7 years; 13% female) without structural heart disease who completed a baseline 24-hour Holter recording. High AEB and VEB were defined using cohort-specific medians and/or the presence of ambulatory arrhythmic complexity. Complete longitudinal tracking for MACE (composite of acute coronary syndrome, cerebrovascular accident, new-onset heart failure or cardiovascular mortality) was available for 840 participants over a median follow-up of 8 years (IQR 5-11 years). To evaluate the robustness of the atrial findings, a prespecified sensitivity analysis was performed by excluding patients with baseline atrial fibrillation (AF).
Over the follow-up period, the primary MACE endpoint occurred in 149 (18%) participants. In multivariable logistic regression models, high AEB was independently driven by older age (OR 1.09, 95% CI 1.06-1.12; p < 0.001), male sex (OR 1.60, 95% CI 1.02-2.52; p = 0.042), reduced eGFR (OR 0.98, 95% CI 0.97-0.99; p = 0.049), and low cardiorespiratory fitness (OR 1.38, 95% CI 1.01-1.92; p = 0.049). Conversely, high VEB was independently associated only with older age (OR 1.04, 95% CI 1.02-1.07; p < 0.001) and reduced eGFR (OR 0.98, 95% CI 0.97-0.99; p = 0.034). In fully adjusted multivariable Cox proportional hazards models, high VEB remained a robust independent predictor of MACE, conferring a three-fold increase in risk (HR 3.06, 95% CI 2.06-4.56; p < 0.001). In tertile-based analyses of pure ectopic burden, increasing VEB demonstrated a robust graded association with MACE after adjustment for age, sex, beta-blocker use and antiarrhythmic drug therapy (HR per tertile increase 2.02, 95% CI 1.60-2.53; p < 0.001), whereas AEB showed only a borderline association that did not reach statistical significance (HR per tertile increase 1.21, 95% CI 0.98-1.50; p = 0.076).
In asymptomatic adults without structural heart disease, the clinical determinants and long-term prognostic trajectories of ectopy exhibit a profound chamber-specific divergence. Ventricular ectopic burden stands out as a powerful, independent marker of intrinsic electrical vulnerability and long-term cardiovascular risk. Meanwhile, atrial ectopy is highly sensitive to systemic physiological fitness and carries a weaker prognostic signal that attenuates completely upon multivariate clinical and medication adjustment.
A. Moses, R. Givoli Vilensky, N. Makmal et al.· European Heart Journal Open· 0 citations
OBJECTIVE
To evaluate whether frailty modifies the association of multimorbidity in HF.
METHODS
A retrospective cohort study of HF patients. Multimorbidity was quantified using 26 conditions and categorized as low (≤4), intermediate (5-7), or high (>8). Frailty was defined using a multimodal construct integrating functional, nutritional, and biochemical domains. All-cause mortality was assessed using cox models with frailty-multimorbidity interaction testing. Charlson Comorbidity Index (CCI) was used for validation.
RESULTS
Among 18,058 patients (median age 74 years; 62% male; 64% frail), 57% died over a median follow-up of 4.0 years (IQR 1.3-7.7). Multimorbidity burden comprised 30.5% low, 48% intermediate, and 21.5% high. Frailty was associated with a 91% higher mortality risk (adjusted HR 1.91; 95% CI 1.85-2.00). Compared with low multimorbidity, intermediate and high burden were associated with an independent 8% and 20% higher mortality risks, respectively (95% CI 1.02-1.14 and 1.13-1.27; both p<.001). However, the association of multimorbidity differed by frailty such that among non-frail patients, intermediate and high multimorbidity increased mortality by 18% and 42% whereas in frail patients, the association was attenuated, with no excess risk for intermediate burden and only 13% increase for high burden (p-for-interaction <.001). CCI analyses was consistent, though differed among females and HFpEF.
CONCLUSION
Frailty fundamentally attenuates risk in HF, while multimorbidity stratifies prognosis only when physiological reserve is preserved.
Viana Copeland, Boris Fishman, S. Elimeleh et al.· Mayo Clinic proceedings· 0 citations
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