Angiotensin-converting enzyme inhibitor treatment early after myocardial infarction attenuates acute cardiac and neuroinflammation without effect on chronic neuroinflammation.
Tobias BorchertAnnika HessMario LukačevićTobias L RossFrank M BengelJames T ThackerayPublished in: European journal of nuclear medicine and molecular imaging (2020)
Whole-body TSPO PET identifies myocardial macrophage infiltration and neuroinflammation after MI, and altered cardiomyocyte mitochondrial density in chronic heart failure. Improved chronic cardiac outcome by enalapril treatment derives partially from acute anti-inflammatory activity with complementary benefits in later stages. Whereas early ACE inhibitor therapy lowers acute neuroinflammation, chronic alleviation is not achieved by early or delayed ACE inhibitor therapy, suggesting a more complex mechanism underlying recurrent neuroinflammation in ischemic heart failure.
Keyphrases
- angiotensin converting enzyme
- lipopolysaccharide induced
- angiotensin ii
- liver failure
- lps induced
- traumatic brain injury
- cerebral ischemia
- drug induced
- heart failure
- left ventricular
- cognitive impairment
- respiratory failure
- inflammatory response
- aortic dissection
- computed tomography
- stem cells
- adipose tissue
- subarachnoid hemorrhage
- atrial fibrillation
- gene expression
- positron emission tomography
- combination therapy
- brain injury
- replacement therapy
- pet imaging
- blood brain barrier
- pet ct
- cardiac resynchronization therapy
- ischemia reperfusion injury
- endothelial cells
- acute respiratory distress syndrome
- mechanical ventilation