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[Transient obstruction of the left ventricular outflow tract induced by excessive alcohol intake: a case report]
Insights
Excessive alcohol intake can cause transient left ventricular outflow tract obstruction in susceptible individuals. This condition, linked to a hyperadrenergic state, resolved spontaneously within days.
Area of Science:
- Cardiology
- Internal Medicine
- Alcohol-Induced Conditions
Background:
- Alcohol consumption is a common factor in various health issues.
- Transient left ventricular outflow tract obstruction (LVOTO) is a rare cardiac event.
- Hyperadrenergic states can manifest with diverse cardiovascular symptoms.
Observation:
- A 41-year-old man presented with syncope after a week of excessive alcohol intake.
- Physical examination revealed a bifid carotid pulse, systolic ejection murmur, and paradoxical splitting of the second heart sound.
- Echocardiography demonstrated systolic anterior motion of the mitral valve (SAM) and thickened ventricular walls.
Findings:
- The patient exhibited signs of a hyperadrenergic state, including increased ejection fraction and prolonged corrected QT interval.
- LVOTO was attributed to the hyperadrenergic state and a redundant mitral apparatus causing SAM.
- All echocardiographic and clinical signs of LVOTO resolved within days of admission.
Implications:
- This case highlights a potential, reversible cause of LVOTO related to alcohol abuse.
- Understanding the link between hyperadrenergic states and mitral valve dynamics is crucial for diagnosis.
- Prompt recognition and supportive care can lead to complete recovery from alcohol-induced LVOTO.
Abstract:
A case of transient obstruction of the left ventricular outflow tract after excessive intake of alcohol was reported. This 41-year-old man was admitted to the Hiroo Hospital because of a syncopal attack experienced while walking. He had been drinking excessively for one week until the day before admission. On admission, physical examination revealed a bifid carotid pulse and a grade 3/6 systolic ejection murmur accentuated by Valsalva maneuvers and prompt standing. The second heart sound was paradoxically split. Echocardiography showed typical systolic anterior motion of the mitral valve (SAM). The interventricular septal and left ventricular posterior wall thicknesses were 13 mm and 11 mm, respectively. No enlargement or displacement of the papillary muscles was noted. The redundant mitral chordae tendineae protruded into the left ventricular outflow tract in systole, and both the anterior and posterior mitral valve leaflets were retracted upwards approximating the interventricular septum by these chordae, resulting in obstruction of the left ventricular outflow tract. All signs of left ventricular outflow obstruction, including SAM, disappeared within several days after admission, and prolapse of the anterior mitral leaflet became evident. Since ejection fraction was markedly increased and the corrected QT interval was prolonged on admission, this patient was considered to be in hyperadrenergic state induced by excessive alcohol intake. In this case, left ventricular outflow tract obstruction was attributed to hyperadrenergic state and a redundant mitral apparatus.