P5251Prognostic value of unrecognized myocardial infarction detected by cardiac magnetic resonance imaging in patients presenting with first acute myocardial infarction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y Kanaji ◽  
T Sugiyama ◽  
M Hoshino ◽  
H Hirano ◽  
H Yuki ◽  
...  

Abstract Background Unrecognized myocardial infarction (UMI) has been reported to be strongly associated with worse outcome in patients with cardiovascular disease. Cardiac magnetic resonance (CMR) imaging is a useful instrument for the assessment of pathological and functional conditions. Purpose This study sought to evaluate the prognostic value of the presence of unrecognized non-infarct-related late gadolinium enhancement (non-IR LGE) evaluated by cardiac magnetic resonance imaging in patients presenting with a first acute myocardial infarction (AMI). Methods We studied 311 AMI patients including 213 STEMI and 98 NSTEMI patients without the history of prior MI who underwent uncomplicated primary or emergent PCI within 48 hours of symptom onset between October, 2012 and June, 2017. CMR images were acquired at 28 [21, 32] days after primary/emergent PCI. UMI was defined as having LGE separately in the different and remote area from the perfused territory by infarct-related artery. In case of multiple LGE areas of infarction, the coronary angiography findings were used to support identification of the area corresponding to the culprit artery of AMI. The association of CMR variables and other clinical characteristics with major adverse cardiac events (cardiac death, nonfatal myocardial infarction, nonfatal stroke) were investigated. Results Forty-six patients (14.8%) showed UMI defined by the presence of non-IR LGE (27 STEMI and 19 NSTEMI). During the follow up for 830 [385, 1309] days, cardiovascular death occurred in 7 patients (2.3%), and non-fatal MI and non-fatal stroke occurred in 10 and 1 patients, respectively (3.2%, 0.3%, respectively). There was no significant difference in the prevalence of UMI and incidence of MACE between the patients with STEMI and NSTEMI (p=0.13, p=0.11, respectively). Event-free survival was significantly worse in patients with UMI (log-rank χ2=16.3, P=0.001) in a total cohort. Cox proportional hazards analysis showed that UMI was independent predictors of adverse cardiac events during follow-up in patients with first MI (hazard ratio, 7.60, 95% confidence interval, 2.78–20.8, p=0.0001). Conclusions In first AMI patients, UMI defined by non-IR LGE obtained by noninvasive CMR provides significant prognostic information. Early detection of UMI by CMR may help risk stratification of patients with AMI and support adjunctive aggressive patient management such as strong statin therapy and life style intervention.

Author(s):  
Swati D. Sonkawade ◽  
Saraswati Pokharel ◽  
Badri Karthikeyan ◽  
Minhyung Kim ◽  
Shirley Xu ◽  
...  

Background: Myocardial Gal3 (galectin-3) expression is associated with cardiac inflammation and fibrosis. Increased Gal3 portends susceptibility to heart failure and death. There are no data reporting the causative role of Gal3 to mediate cardiac fibro-inflammatory response and heart failure. Methods: We developed a cardioselective Gal3 gain-of-function mouse ( Gal3+/+ ) using α-myosin heavy chain promotor. We confirmed Gal3-transgene expression with real-time polymerase chain reaction and quantified cardiac/circulating Gal3 with Western blot and immunoassays. We used echocardiogram and cardiac magnetic resonance imaging to measure cardiac volumes, function, and myocardial velocities. Ex vivo, we studied myocardial inflammation/fibrosis and downstream TGF (transforming growth factor) β1-mRNA expression. We examined the effects of acute myocardial ischemia in presence of excess Gal3 by inducing acute myocardial infarction in mice. Two subsets of mice including mice treated with N-acetyl-seryl-aspartyl-lysyl-proline (a Gal3-inhibitor) and mice with genetic Gal3 loss-of-function ( Gal3 −/−) were studied for comparative analysis of Gal3 function. Results: Gal3+/+ mice had increased cardiac/circulating Gal3. Gal3+/+ mice showed excess pericardial fat pad, dilated ventricles and cardiac dysfunction, which was partly normalized by N-acetyl-seryl-aspartyl-lysyl-proline. Cardiac magnetic resonance imaging showed reduced myocardial contractile velocities in Gal3+/+ . The majority of Gal3+/+ mice did not survive acute myocardial infarction, and the survivors had profound cardiac dysfunction. Myocardial histology of Gal3+/+ mice showed macrophage/mast-cell infiltration, fibrosis and higher TGFβ1-mRNA expression, which were mitigated by both Gal3 gene deletion and N-acetyl-seryl-aspartyl-lysyl-proline administration. Conclusions: Our study shows that cardioselective Gal3 overexpression leads to multiple cardiac phenotypic defects including ventricular dilation and cardiac dysfunction. Pharmacological Gal3 inhibition conferred protective effects with reduction of inflammation and fibrosis. Our study highlights the importance of translational studies to counteract Gal3 function and prevent cardiac dysfunction.


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