Key result
LVOT obstruction in HCM is linked to ~10 mL/m2 higher minimum left atrial volume index.
Why the study?
The study aimed to compare left atrial structure and phasic function among healthy controls and patients with nonobstructive or obstructive HCM, and to assess their associations with left ventricular outflow tract obstruction.
Is left ventricular outflow tract obstruction associated with worsened left atrial structure and phasic function in patients with hypertrophic cardiomyopathy compared to nonobstructive HCM and healthy controls?
Cross-Sectional (n=140)
Is left ventricular outflow tract obstruction associated with worsened left atrial structure and phasic function in patients with hypertrophic cardiomyopathy compared to nonobstructive HCM and healthy controls?
Mean Difference: 10.03 (95% CI 6.71–13.36)
p-value: p=<0.001
In patients with hypertrophic cardiomyopathy, greater severity of left ventricular outflow tract obstruction is independently associated with increased minimum left atrial volume index and reduced left atrial reservoir strain.
May indicate greater LA impairment in obstructive HCM; hypothesis-generating for LA strain in risk models, pending prospective validation.
Purpose To compare left atrial (LA) structure and phasic function among healthy controls and patients with nonobstructive or obstructive hypertrophic cardiomyopathy (HCM), and assess their associations with left ventricular outflow tract obstruction (LVOTO). Methods We studied 90 patients with HCM and 50 healthy controls. Patients were classified by the highest resting or Valsalva‐provoked LVOT gradient (LVOTG) as nonobstructive (<30 mmHg; n = 50) or obstructive (≥30 mmHg; n = 40). Threedimensional echocardiography measured LA volumes, and two‐dimensional speckle tracking measured phasic strain. Multivariable linear regression examined prespecified echocardiographic outcomes by LVOTO status. Sensitivity analyses modeled LVOTG continuously and used a 50‐mmHg threshold. Results Both HCM groups had greater LA enlargement and dysfunction than controls, with the largest abnormalities in obstructive HCM. In the primary adjusted model, LVOTO was associated with higher LAVImin ( B = 10.03 mL/m 2 ; 95% CI, 6.71 to 13.36; p < 0.001) and lower LASr ( B = −2.72%; 95% CI, −4.17 to −1.28; p < 0.001). The associations remained when LVOTG was analyzed per 10 mmHg and with a threshold of ≥50 mmHg. E/e′ and TRV were not significantly associated with LVOTG in these sensitivity analyses. Conclusion In this cross‐sectional HCM cohort, greater obstruction severity was associated with higher LAVImin and lower LASr. Prospective studies are needed to determine whether these measures are associated with clinical outcomes.
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Lin et al. (2026) conducted a cross-sectional in Hypertrophic cardiomyopathy (HCM) (n=140). Left ventricular outflow tract obstruction (LVOTO, LVOT gradient >=30 mmHg) vs. Nonobstructive HCM (LVOT gradient <30 mmHg) and healthy controls was evaluated on Minimum left atrial volume index (LAVImin) and left atrial reservoir strain (LASr) (B = 10.03 mL/m2 for LAVImin; B = -2.72% for LASr, 95% CI 6.71 to 13.36, p=<0.001). Left ventricular outflow tract obstruction in HCM was associated with higher LAVImin (B=10.03 mL/m2; p<0.001) and lower LA reservoir strain (B=-2.72%; p<0.001).
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