Nydia Ávila-Vanzzini1, Hector I Michelena2, Juan Francisco Fritche Salazar1, Héctor Herrera-Bello3, Silvia Siu Moguel4, Rubén Rafael Rodríguez Ocampo5, Diego Javier Oregel Camacho5, Nilda Espínola Zavaleta1. 1. Department of Out patients Care, Echocardiography, Nuclear medicine National Instituto of Cardiology Ignacio Chávez, Juan Badiano No.1, Colonia Sección XVI, Tlalpan, Mexico City 14080, Mexico. 2. Department of Cardiovascular Medicine, Mayo Clinic, 200 1st St Sw, Rochester, MN, USA. 3. Intermediate Care Unit Medica Sur Clinical Foundation, Puente de Piedra 150, Toriello Guerra, Delegación Tlalpan, Ciudad de México, Mexico City, Mexico. 4. Hospital Regional ISSSTE, Av Díaz Mirón SN Colonia, Moderno, 91910 Veracruz, Mexico. 5. Autonomous University of Nayarit, Edificio de la Unidad Academica de Medicina, Ciudad de la cultura "Amado Nervo" CP: 63000 Tepic Nayarit, Mexico.
Abstract
Aims: Ischaemic mitral regurgitation (IMR) is consequence of left ventricular (LV) remodelling after myocardial infarction. In some cases, the mitral valve enlarges to compensate for LV remodelling and tenting, improving its coaptation; a process termed 'plasticity'. We sought to identify clinical and echocardiographic factors associated with plasticity in patients with chronic inferior myocardial infarction (CII). Methods and results: This study included 91 revascularized CII patients and 46 controls. Plasticity and IMR severity were evaluated by 2D transthoracic echocardiography. Compared with controls, CII patients were older (59 vs. 25 years) and mostly men (80% vs. 46%), both P < 0.001. Chronic inferior myocardial infarction patients also had significant LV remodelling: larger LV volumes, larger mitral tenting areas, larger coaptation depths, longer mitral leaflets and chords, and worse mitral regurgitation (all P ≤ 0.03). Of 91 CII patients, 60 had mitral plasticity (longer anterior and posterior leaflets and longer posterior chords, all P < 0.001), despite not exhibiting significantly larger LV volumes, tenting area or coaptation depth, when compared with patients with no plasticity. Contralateral (anterior) papillary muscle-to-annulus length tended to be increased in CII plasticity patients (P = 0.05). Also they had less moderate and severe IMR (both P < 0.04) compared with non-plasticity CII patients. Multivariate analysis demonstrated independent associations between plasticity and smoking [odds ratio (OR) 0.03, 0.002-0.57; P = 0.019], duration of type-2 diabetes (OR 1.19, 1.007-1.42; P = 0.04) and haemoglobin (OR 2.17, 1.25-3.76; P = 0.005). Conclusion: Mitral plasticity results in less moderate and severe IMR. Longer time-duration of diabetes mellitus and higher haemoglobin level are independently associated with mitral plasticity, while smoking independently associates with no plasticity. Increased anterior papillary muscle-to-annulus length in CII patients with plasticity suggests complex LV remodelling mechanisms are involved in plasticity.
Aims: Ischaemic mitral regurgitation (IMR) is consequence of left ventricular (LV) remodelling after myocardial infarction. In some cases, the mitral valve enlarges to compensate for LV remodelling and tenting, improving its coaptation; a process termed 'plasticity'. We sought to identify clinical and echocardiographic factors associated with plasticity in patients with chronic inferior myocardial infarction (CII). Methods and results: This study included 91 revascularized CII patients and 46 controls. Plasticity and IMR severity were evaluated by 2D transthoracic echocardiography. Compared with controls, CII patients were older (59 vs. 25 years) and mostly men (80% vs. 46%), both P < 0.001. Chronic inferior myocardial infarctionpatients also had significant LV remodelling: larger LV volumes, larger mitral tenting areas, larger coaptation depths, longer mitral leaflets and chords, and worse mitral regurgitation (all P ≤ 0.03). Of 91 CII patients, 60 had mitral plasticity (longer anterior and posterior leaflets and longer posterior chords, all P < 0.001), despite not exhibiting significantly larger LV volumes, tenting area or coaptation depth, when compared with patients with no plasticity. Contralateral (anterior) papillary muscle-to-annulus length tended to be increased in CII plasticitypatients (P = 0.05). Also they had less moderate and severe IMR (both P < 0.04) compared with non-plasticity CII patients. Multivariate analysis demonstrated independent associations between plasticity and smoking [odds ratio (OR) 0.03, 0.002-0.57; P = 0.019], duration of type-2 diabetes (OR 1.19, 1.007-1.42; P = 0.04) and haemoglobin (OR 2.17, 1.25-3.76; P = 0.005). Conclusion: Mitral plasticity results in less moderate and severe IMR. Longer time-duration of diabetes mellitus and higher haemoglobin level are independently associated with mitral plasticity, while smoking independently associates with no plasticity. Increased anterior papillary muscle-to-annulus length in CII patients with plasticity suggests complex LV remodelling mechanisms are involved in plasticity.
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