Key result
Impaired left ventricular torsion (OR 21.23) and increased late gadolinium enhancement (OR 1.17) were independently associated with the presence of apical aneurysms in patients with hypertrophic cardiomyopathy.
Why the study?
Apical aneurysm represents a high-risk subgroup in HCM, but the relationship of LV function changes and myocardial fibrosis to apical aneurysm formation is unclear.
Cross-Sectional (n=45)
No
Odds Ratio: 21.23 (95% CI 1.27–354.26)
p-value: p=0.03
Impaired left ventricular torsion and increased myocardial fibrosis are independent markers associated with the presence of apical aneurysms in patients with hypertrophic cardiomyopathy, providing incremental diagnostic value over standard clinical models.
May aid aneurysm detection in HCM beyond standard models; leaves open prospective validation and causal links.
Objectives：Apical aneurysm is a high-risk subgroup in hypertrophic cardiomyopathy (HCM). We aimed to explore the change of left ventricular (LV) function and myocardial fibrosis and the relationship between them and the formation of apical aneurysms in patients with HCM. Methods and results: The study enrolled 25 HCM patients without apical aneurysms and 20 HCM patients with apical aneurysms. The presence of an apical aneurysm was determined by echocardiography or CMR. LV function was assessed by speckle-tracking echocardiography and late gadolinium enhancement (LGE) was assessed by CMR. Patients with HCM in two groups had similar left ventricular ejection fraction (LVEF), global longitudinal strain (GLS), global circumferential strain (GCS), global radial strain (GRS), and global area strain (GAS). However, HCM patients with apical aneurysms had worse twist (7.49 ± 4.52° vs. 11.82 ± 5.55°, P=0.007), torsion (1.32 ± 0.81°/cm vs. 2.34 ± 0.98°/cm, P=0.001), and higher LGE than HCM patients without apical aneurysms. Multivariate analysis demonstrated that torsion (OR: 21.23; 95% CI: 1.27 to 354.26; P=0.03) and LGE (OR: 1.17; 95% CI: 1.01 to 1.36; P=0.03) were independent parameters of apical aneurysm events in patients with HCM. When applying a cutoff value of 1.25° for torsion and LGE into a baseline model with clinical and conventional echocardiographic parameters, the new model showed a significant incremental value of torsion and LGE (P<0.001) in identifying apical aneurysm events in HCM patients. The C-statistic for this model increased from 0.65 to 0.90 when adding torsion and LGE. Conclusion: HCM patients with apical aneurysms have impaired rotational mechanics and more pronounced fibrosis. Torsion and LGE are independent markers of apical aneurysm events in patients with HCM and could provide incremental value to baseline models in identifying apical aneurysms.
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Dai et al. (2023) conducted a cross-sectional in Hypertrophic cardiomyopathy (n=45). Left ventricular torsion vs. Preserved left ventricular torsion was evaluated on Apical aneurysm events (OR 21.23, 95% CI 1.27-354.26, p=0.03). Impaired left ventricular torsion (OR 21.23) and increased late gadolinium enhancement (OR 1.17) were independently associated with the presence of apical aneurysms in patients with hypertrophic cardiomyopathy.
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