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Case Reports
. 2022 Dec 15;58(12):1844.
doi: 10.3390/medicina58121844.

Monoamine Oxidase (MAO) Is Expressed at the Level of Mitral Valve with Severe Regurgitation in Hypertrophic Obstructive Cardiomyopathy: A Case Report

Ana Lascu  1   2 , Raluca Șoșdean  3   4 , Loredana Nicoleta Ionică  2   5 , Alexandru S Pescariu  3   4 , Lucian Petrescu  2   5 , Adina Ionac  3   4 , Constantin T Luca  3   4 , Adrian Sturza  1   2 , Horea B Feier  4   6
Affiliations
Case Reports

Monoamine Oxidase (MAO) Is Expressed at the Level of Mitral Valve with Severe Regurgitation in Hypertrophic Obstructive Cardiomyopathy: A Case Report

Ana Lascu et al. Medicina (Kaunas). .

Abstract

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.

Keywords: MAO inhibitors; hypertrophic obstructive cardiomyopathy; mitral valve regurgitation; monoamine oxidase; oxidative stress.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Transthoracic bidimensional echocardiography, 4 chamber view: a mitral valve with fibrosed leaflets, an elongated AML and SAM of both AML and PML, creating an anteriorly deviated “funnel”.
Figure 2
Figure 2
Transthoracic bidimensional echocardiography, four chamber view with color Doppler on the mitral valve: severe mitral valve regurgitation, with a central slightly posterolateral deviated jet. The regurgitant jet enters the pulmonary veins.
Figure 3
Figure 3
Expression of MAO-A and MAO-B in valvular tissue. (A) qRT-PCR for MAO-A and MAO-B mRNA expression (relative gene: GADPH), (B) DNA gel electrophoresis, (C) Immune-fluorescence for MAO-A and MAO-B protein expression. (CTL, control; AII, Angiotensin II).
Figure 4
Figure 4
Assessment of superoxide (bright red) in the explanted mitral valve by confocal microscopy (DHE staining) in the presence of AII, clorgyline, and selegiline.
See this image and copyright information in PMC

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