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[Midsystolic closure of the aortic valve in hypertrophic nonobstructive cardiomyopathy]
Insights
This study documents midsystolic cessation of left ventricular contraction in hypertrophic cardiomyopathy linked to Cushing's syndrome. This finding explains interrupted aortic flow and unique pulse patterns in affected patients.
Area of Science:
- Cardiology
- Endocrinology
- Physiology
Background:
- Hypertrophic nonobstructive cardiomyopathy (HCM) can present with complex hemodynamic patterns.
- Cushing's syndrome, caused by adrenal adenoma, can affect cardiovascular function.
- Understanding the interplay between endocrine disorders and cardiac mechanics is crucial.
Observation:
- A unique case of midsystolic cessation of left ventricular contraction was observed in a patient with HCM and Cushing's syndrome.
- Carotid pulse tracing revealed a bifid waveform with midsystolic decay.
- Echocardiography demonstrated midsystolic aortic valve closure coinciding with the pulse wave anomaly.
Findings:
- The left ventricle showed symmetrical hypertrophy (1.8 cm) and abnormal wall motion (trapezoidal pattern) with mid-systolic contraction arrest.
- Cardiac catheterization and left ventriculography confirmed no intraventricular pressure gradient and mid-systolic ejection completion.
- Systolic anterior motion of the mitral valve and mitral regurgitation were notably absent.
Implications:
- Midsystolic cessation of left ventricular contraction is identified as the cause of interrupted forward aortic flow in this patient.
- This phenomenon explains the observed bifid carotid pulse and midsystolic aortic valve closure.
- The findings highlight a specific cardiac manifestation of Cushing's syndrome in the context of HCM.
Abstract:
Midsystolic cessation of left ventricular contraction was documented in a patient with hypertrophic nonobstructive cardiomyopathy (HCM) associated with Cushing's syndrome (adrenal adenoma) without history of hypertension. The carotid pulse tracing showed a rapid upstroke with a prominent percussion wave which was rapidly decayed at midsystole followed by a tiny tidal wave. The decay of this percussion wave coincided in timing with midsystolic closure of the aortic valve in the echocardiogram. The left ventricle (LV) was symmetrically hypertrophied (wall thickness = 1.8 cm). The motion of the interventricular septum and LV posterior wall appeared trapezoid, and the contraction of these walls was normal in early-systole followed by the sudden cessation at midsystole till end-systole. Systolic anterior motion of the mitral valve was not observed. Cardiac catheterization revealed no pressure gradient in the LV even after the various provocative maneuvers. The left ventriculogram simultaneously recorded with LV pressure showed that LV ejection was completed at midsystole, when LV pressure fell from 98 to 83 mmHg. Mitral regurgitation was not observed. Midsystolic cessation of left ventricular contraction in this case is thought to be the cause of sudden interruption of forward aortic flow, resulting in a bifid carotid pulse and midsystolic closure of the aortic valve in the echocardiogram.