Key result
MAO isoforms are expressed in the severely impaired mitral valve of a patient with HOCM, with ROS production augmented by angiotensin II and reversed by MAO inhibitors ex vivo.
Why the study?
Monoamine oxidase is an important source of reactive oxygen species in the cardiovascular system, but literature data regarding its expression in valvular tissue is scarce.
Case Report (n=1)
MAO isoforms are expressed in the severely impaired mitral valve in HOCM and can be induced by angiotensin II, suggesting a potential role for MAO inhibitors in modulating valvular oxidative stress.
Hypertrophic obstructive cardiomyopathy (HOCM) is one of the most common hereditary heart diseases. The severely hypertrophied interventricular septum combined with the systolic anterior movement (SAM) of the mitral valve (MV) frequently cause a significant pressure gradient in the left ventricular outflow tract associated with varying degrees of mitral regurgitation (MR). We present the case of a 64-year-old female patient who was diagnosed with HOCM two years ago and was admitted to the Institute of Cardiovascular Disease with exertion dyspnea and fatigue. Transthoracic echocardiography revealed concentric, asymmetrical left ventricular hypertrophy, an elongated anterior mitral leaflet (AML) and a significant SAM causing severe regurgitation, with indication for valvular replacement Monoamine oxidase (MAO), a mitochondrial enzyme, with 2 isoforms, MAO-A and B, has emerged as an important source of reactive oxygen species (ROS) in the cardiovascular system, but literature data on its expression in valvular tissue is scarce. Therefore, we assessed MAO-A and B gene (qPCR) and protein (immune fluorescence) expression as well as ROS production (spectrophotometry and confocal microscopy) and in the explanted MV harvested during replacement surgery. MAO expression and ROS production (assessed by both methods) were further augmented following ex vivo incubation with angiotensin II, an effect that was reversed in the presence of either MAO-A (clorgyline) or B (selegiline) inhibitor, respectively. In conclusion, MAO isoforms are expressed at the level of severely impaired mitral valve in the setting of HOCM and can be induced in conditions that mimic the activation of renin-angiotensin-aldosterone system. The observation that the enzyme can be modulated by MAO inhibitors warrants further investigation in a patient cohort.
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Lascu et al. (2022) conducted a case report in Hypertrophic obstructive cardiomyopathy (HOCM) (n=1). Ex vivo angiotensin II and MAO inhibitors was evaluated on MAO expression and ROS production. MAO isoforms are expressed in the severely impaired mitral valve of a patient with HOCM, with ROS production augmented by angiotensin II and reversed by MAO inhibitors ex vivo.
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