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Post MI Remodeling of the Left Atrium: The contribution of Atrial Infarction and Ischemic Mitral Regurgitation

Reporter: Aviva Lev-Ari, PhD, RN

BACKGROUND Left atrial (LA) remodeling after an acute myocardial infarction (MI) is poorly characterized regarding its determinants or its effect on ischemic mitral regurgitation (MR) development.

OBJECTIVES The purpose of this study was: 1) to compare LA structural remodeling in experimental MI swine models recapitulating the effects of left ventricular (LV) dysfunction, ischemic MR, and left atrial infarction (LAI); and 2) to analyze how LA remodeling influences ischemic MR development.

METHODS Three models of MI were generated: 1) proximal left circumflex (LCx) coronary artery occlusion involving the LA branch (LAI group); 2) proximal LCx occlusion not involving the LA branch (LCx group); and 3) left anterior descending (LAD) occlusion (LAD group). Serial cardiac magnetic resonance scans were performed to define LA and LV remodeling and ischemic MR, and were correlated with histology.

RESULTS Occlusion of the LA branch (LAI group) induced a greater degree of LA dilation at 1 and 8 weeks post-MI than the LCx and LAD groups, along with early and severe impairment of LA function. In the LCx and LAD groups, LA dysfunction was less pronounced and not consistent. Development of ischemic MR was more pronounced in the LAI group than in the LCx group. Histology confirmed atrial infarction with extensive fibrosis in the LAI group and interstitial fibrosis in the LCx group. In the LAD group, LA remodeling was not observed by cardiac magnetic resonance or histology.

CONCLUSIONS

We provide the first experimental evidence of the deleterious effect of acute LAI on atrialstructural remodeling, characterized by early LA dilation, dysfunction, and fibrosis, and early occurrence
of ischemic MR. (J Am Coll Cardiol 2017;70:2878–89) © 2017 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.

Atrial Infarction and Ischemic Mitral Regurgitation Contribute to Post-MI Remodeling of the Left Atrium

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JaumeAgueroMD, PhD^abcCarlosGalan-ArriolaDVM^abRodrigoFernandez-JimenezMD^abdJavierSanchez-GonzalezPhD^eNinaAjmoneMD, PhD^fVictoriaDelgadoMD, PhD^fJorgeSolisMD, PhD^agGonzalo J.LopezRT^aAntoniode Molina-IrachetaPhD^aRoger J.HajjarMD^dJeroen J.BaxMD, PhD^fValentinFusterMD, PhD^adBorjaIbáñezMD, PhD^abha Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain ^b CIBER de enfermedades CardioVasculares, Madrid, Spain ^c Hospital Universitari i Politecnic La Fe, Valencia, Spain ^d The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York ^e Philips Healthcare, Madrid, Spain ^f Department of Cardiology, Heart Lung Center, Leiden University Medical Center, Leiden, the Netherlands ^g Hospital 12 de Octubre, Madrid, Spain ^h Cardiology Department, IIS-Fundación Jiménez Díaz Hospital, Madrid, Spain

Received 2 June 2017, Revised 28 September 2017, Accepted 5 October 2017, Available online 4 December 2017, Version of Record 4 December 2017.

This is an open access article under the CC BY-NC-ND license

(http://creativecommons.org/licenses/by-nc-nd/4.0/).
From the a Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain; bCIBER de enfermedades CardioVasculares, Madrid, Spain; cHospital Universitari i Politecnic La Fe, Valencia, Spain; dThe Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York; ePhilips Healthcare, Madrid, Spain;
fDepartment of Cardiology, Heart Lung Center, Leiden University Medical Center, Leiden, the Netherlands; gHospital 12 de
Octubre, Madrid, Spain; and the hCardiology Department, IIS-Fundación Jiménez Díaz Hospital, Madrid, Spain.

This study was supported by a competitive grant from the Carlos III Institute of Health-Fondo de Investigacion Sanitaria and the European Regional Development Fund (ERDF/FEDER) (PI13/01979 and PI16/02110); the Spanish Ministry of Economy, Industry, and Competitiveness (MEIC) and ERDF/FEDER (SAF2013-49663-EXP); and, in part, by the FP7-PEOPLE-2013-ITN Next Generation Training in Cardiovascular Research and Innovation (CARDIONEXT).

This research program is part of an institutional agreement between FIIIS-Fundación Jiménez Díaz and the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC). This study
forms part of a Master Research Agreement between the CNIC and Philips Healthcare. The CNIC is supported by the MEIC and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (MEIC award SEV-2015-0505). The Cardiology Department at Leiden University Medical Center has received unrestricted research grants from Medtronic, Biotronik, Boston Scientific, Edwards
Lifesciences, and General Electric Healthcare. Dr. Aguero is an FP7-PEOPLE-2013-ITN-Cardionext fellow. Dr. Fernández-Jiménez holds an FICNIC fellowship from the Fundació Jesús Serra, the Fundación Interhospitalaria de Investigación Cardiovascular (FIC),

Listen to this manuscript’s audio summary by JACC Editor-in-Chief Dr. Valentin Fuster.
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SOURCE

https://www.sciencedirect.com/science/article/pii/S073510971741103X