Author + information
- Fernanda Gallinaro Pessoa,
- Keila Fonseca,
- Charles Mady,
- Orlando N. Ribeiro,
- Adriana M. Oliveira-Fonoff,
- Vera Salemi,
- Paulo Saldiva,
- Fabio Fernandes and
- Felix Ramires
Background: We evaluated the role of particulate matter2.5 (PM2.5) in structural, geometric, and functional remodeling in hearts, using an experimental model of myocardial infarction.
Methods: 75 rats were divided into 5 groups: control (CG), CG exposed to PM2.5 pollution (CGP), myocardial infarcted group (MI), infarcted group immediately exposed to pollution (IGP-I), and infarcted group previously exposed to pollution and kept exposed after infarction (IGP-II). We used histology for morphometric analysis, infarct size and inflammatory infiltrates. Echocardiography was performed for cardiac geometry and function.
Results: Greater deposition of interstitial collagen occurred in the left ventricle in CGP, MI, IGP-I, and IGP-II compared with that in controls (p≤0.001). In the right ventricle, greater collagen deposition also occurred in CGP, MI, IGP-I, and IGP-II compared with that in CG (p≤0.002). Air pollution did not affect the size of the infarcted area (MI=27.30 ± 10.09%, IGP-I=24.50 ± 8.79%, and IGP-II=27.90 ± 11.97%; p=0.660). We found that all groups had greater inflammatory cell infiltration compared with CG, including CGP (p< 0.0001). However, PM2.5 exposure did not increase the inflammatory cell among infarcted groups. In fact, the MI had more inflammatory cells than exposed groups had (p< 0.001). Also IGP-II had more inflammatory cells than IGP-I (p< 0.001). Left ventricular systolic diameter was smaller in CG than in infarcted groups (p≤0.003), the same was observed in left ventricular diastolic diameter which IGP-II had larger than the CGP group (p≤0.002). Regarding left ventricular function, all groups, including CGP, had lower ejection fraction compared with control (p < 0.001).
Conclusions: PM2.5 stimulates the deposition of fibrosis in the myocardium of healthy hearts, but not in infarcted hearts. Air pollution did not affect the size of the infarcted area. PM2.5 did not modulate the inflammatory cell infiltration in infarcted groups. We also conclude that, PM2.5 plays a key role in structural myocardial remodeling resulting in the loss of heart function in healthy animals.
Poster Hall, Hall C
Friday, March 17, 2017, 10:00 a.m.-10:45 a.m.
Session Title: Population Specific Cardiomyopathies: From Exomes to Databases
Abstract Category: 12. Heart Failure and Cardiomyopathies: Basic
Presentation Number: 1122-263
- 2017 American College of Cardiology Foundation