Dataset Information

Islet microangiopathy and augmented β-cell loss in Japanese non-obese type 2 diabetes patients who died of acute myocardial infarction.

ABSTRACT:

Aims/introduction

Islets have microvessels that might develop pathological alterations similar to microangiopathy in type 2 diabetes patients. It remains unclear, however, whether the changes correlate with endocrine cell deficits or whether the presence of macroangiopathy influences the islet microvasculature in Japanese type 2 diabetes patients. In this study, we characterized changes of the islet microvessels and endocrine cells in Japanese non-obese patients with type 2 diabetes who died of acute myocardial infarction (AMI).

Materials and methods

Clinical profiles and islet pathology were examined for 35 diabetes patients who died of AMI (DM + AMI) and 13 diabetes patients who were free from AMI (DM). A total of 13 age-matched, individuals without diabetes who died of AMI and 16 individuals without diabetes who were free from AMI were also studied. Pancreata were subjected to morphometric evaluation of islets, including microvascular alterations of immunostained sections.

Results

Body mass index in DM + AMI was comparable to those in DM. Compared with DM, DM + AMI showed greater glycated hemoglobin levels, higher prevalence of renal failure, hypertension, smaller β-cell volume density and greater amyloid area. DM + AMI showed an increased microvascular area and density compared with other groups. There was a significant increase in vascular basement membrane thickness and loss of pericytes in DM and DM + AMI compared with individuals without diabetes in each group, and the extent of thickening was correlated with the amyloid area and occurrence of β-cell loss in DM + AMI.

Conclusions

Islet microangiopathy was associated with augmented β-cell loss and amyloid deposition in non-obese Japanese type 2 diabetes patients who died of AMI.

SUBMITTER: Takahashi K

PROVIDER: S-EPMC8668063 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundPreclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans.Methods and resultsOverall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non-ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI.ConclusionsThe presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254.