To determine the prevalence and clinical correlates of a midsystolic Doppler signal void in patients with hypertrophic cardiomyopathy (HCM) and assess whether it identifies a distinct midapical obstructive phenotype beyond conventional gradient-based assessment.
Approach:
Study Population: Retrospective, single-center evaluation of 606 consecutive patients with HCM who underwent comprehensive transthoracic echocardiography at Zhejiang Provincial People’s Hospital from November 2021 through December 2024.
Echocardiographic Acquisition: Comprehensive transthoracic echocardiography was performed using a Vivid E95 system. Patients were stratified by the presence or absence of a midsystolic continuous-wave Doppler signal void reflecting systolic midapical cavity obliteration.
Quantitative Analysis: Left ventricular volumes were measured using the biplane Simpson method, and global longitudinal strain was quantified using 2-dimensional speckle-tracking echocardiography.
Assessment of Apical Morphology: Apical aneurysm was defined as a discrete apical outpouching with wall thinning and dyskinetic or akinetic motion, confirmed by contrast-enhanced echocardiography or, when available, cardiac CT or cardiac magnetic resonance.
Key Findings:
A midsystolic Doppler signal void was present in 142 patients (23.4%).
Patients with signal void had more pronounced midapical and papillary muscle hypertrophy, smaller indexed left ventricular end-diastolic volumes, lower absolute global longitudinal strain, higher cardiac troponin I levels, and a higher prevalence of apical aneurysm.
Apical aneurysm and lower absolute global longitudinal strain were independently associated with signal void.
The signal void may identify midapical obstruction not fully captured by peak Doppler gradients alone.
Interpretation:
A midsystolic Doppler signal void identifies a distinct midapical HCM phenotype associated with adverse structural remodeling and high-risk features. Its diagnostic and prognostic value requires prospective validation.
Limitations:
The retrospective, single-center design may introduce selection bias and limit external validity.
Genetic data, comprehensive medication exposure, and advanced imaging were not uniformly available.
Reproducibility testing was limited, and clinically selected use of contrast echocardiography or cardiac magnetic resonance may have introduced verification bias and underestimated apical aneurysm prevalence.
Longitudinal clinical outcomes were not evaluated.
Conclusion:
Systolic cavity obliteration manifested as a midsystolic Doppler signal void identifies a distinct midapical HCM phenotype and may complement conventional Doppler gradient assessment.
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