Key result
Acute MI elevates myocardial TSPO signal ~67% versus sham, predicting LV remodeling and concurrent neuroinflammation.
Why the study?
The local inflammatory response after acute myocardial infarction influences healing and may induce neuroinflammation as a precursor to neurodegeneration, but the heart-brain inflammatory interaction is not well characterized.
Does acute myocardial infarction induce cardiac and neuroinflammation measurable by TSPO PET imaging?
Does acute myocardial infarction induce cardiac and neuroinflammation measurable by TSPO PET imaging?
Acute myocardial infarction induces both local cardiac inflammation and systemic neuroinflammation that can be tracked via TSPO PET imaging and is attenuated by ACE inhibitor treatment.
Answers are grounded in this paper and cite their sources.
Post-MI TSPO PET should not yet change practice; leaves open heart-brain axis targeting to reduce remodeling.
BACKGROUND: The local inflammatory tissue response after acute myocardial infarction (MI) determines subsequent healing. Systemic interaction may induce neuroinflammation as a precursor to neurodegeneration. OBJECTIVES: This study sought to assess the influence of MI on cardiac and brain inflammation using noninvasive positron emission tomography (PET) of the heart-brain axis. METHODS: After coronary artery ligation or sham surgery, mice (n = 49) underwent serial whole-body PET imaging of the mitochondrial translocator protein (TSPO) as a marker of activated macrophages and microglia. Patients after acute MI (n = 3) were also compared to healthy controls (n = 9). RESULTS: Infarct mice exhibited elevated myocardial TSPO signal at 1 week versus sham (percent injected dose per gram: 8.0 ± 1.6 vs. 4.8 ± 0.9; p < 0.001), localized to activated CD68+ inflammatory cells in the infarct. Early TSPO signal predicted subsequent left ventricular remodeling at 8 weeks (rpartial = -0.687; p = 0.001). In parallel, brain TSPO signal was elevated at 1 week (1.7 ± 0.2 vs. 1.4 ± 0.2 for sham; p = 0.017), localized to activated microglia. After interval decline at 4 weeks, progressive heart failure precipitated a second wave of neuroinflammation (1.8 ± 0.2; p = 0.005). TSPO was concurrently up-regulated in remote cardiomyocytes at 8 weeks (8.8 ± 1.7, p < 0.001) without inflammatory cell infiltration, suggesting mitochondrial impairment. Angiotensin-converting enzyme inhibitor treatment lowered acute inflammation in the heart (p = 0.003) and brain (p = 0.06) and improved late cardiac function (p = 0.05). Patients also demonstrated elevation of cardiac TSPO signal in the infarct territory, paralleled by neuroinflammation versus controls. CONCLUSIONS: The brain is susceptible to acute MI and chronic heart failure. Immune activation may interconnect heart and brain dysfunction, a finding that provides a foundation for strategies to improve heart and brain outcomes.
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Thackeray et al. (2018) studied Acute myocardial infarction (n=61). Acute myocardial infarction vs. Sham surgery (mice) or healthy controls (humans) was evaluated on Myocardial TSPO signal at 1 week (percent injected dose per gram) (p=<0.001). Acute myocardial infarction induced elevated myocardial inflammation at 1 week compared to sham, predicting left ventricular remodeling and paralleling neuroinflammation.
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