Ischemic heart failure mortality is not predicted by cardiac insulin resistance but by diabetes per se and coronary flow reserve: A retrospective dynamic cardiac 18F-FDG PET study.

BACKGROUND & AIMS: The connection between peripheral insulin resistance (IR) and coronary artery disease is well-established. Both are major risk factors for the development of ischemic cardiomyopathy potentially leading to heart failure (HF). Whether cardiac IR also impacts overall survival and morbidity is still debated. We therefore aimed to test if cardiac IR predicts mortality and major cardiovascular events (MACE) in patients with HF scheduled for cardiac viability testing before revascularization. METHODS: This retrospective study included 131 patients with a clinical diagnosis of ischemic HF (114 (87%) male, 33 (25%) with diabetes) referred to a viability Rubidium-82 (perfusion) and dynamic 18F-Fluorodeoxyglucose (metabolism) positron emission tomography combined with computed tomography prior to a potential revascularization procedure. Cardiac IR was assessed by myocardial glucose uptake (MGU) in a remote (non-scarred) area of the left ventricle during a hyperinsulinemic-euglycemic clamp (1mIE/kg/min). RESULTS: MGU correlated with skeletal muscle glucose uptake (p < 0.001) and whole-body glucose uptake (M-value) (p < 0.001), whereas no association was observed for individuals with diabetes. MGU did not predict the risk of death or MACE. However, both overt diabetes and reduced coronary flow reserve predicted overall survival. CONCLUSION: Even though diabetes and related small-vessel disease is associated with increased mortality, cardiac IR per se does not predict cardiovascular morbidity and mortality.

Sudden death due to diabetic ketoacidosis following power failure of an insulin pump: Autopsy and pump data.

PURPOSE: To report a case in which autopsy findings and data from an insulin pump illustrate the course up to the death of a 31-year-old man with a history of type 1 diabetes mellitus who was found dead in his apartment with his insulin pump disassembled and placed in another room. METHODS: Autopsy findings including histological, toxicological and biochemical examination are presented. Postmortem download of data from the insulin pump gave the history of the pump, which included blood glucose, insulin bolus, carbohydrate intake and the time course in the days to death, and the pump settings were recorded. For this case report, police reports on the death as well as hospital records were also reviewed. RESULTS: At the patch for the insulin pump, nothing abnormal was found. Biochemical analysis showed glucose of 35 mmoL/L in vitreous humor fluid indicating antemortem hyperglycemia, and ketone bodies in the blood of 11.0 mmoL/L indicating ketoacidosis. Acute pulmonary hemostasis, chronic fat accumulation in the liver and acute fat accumulation in the kidneys were histological detected. There were no signs of late diabetic complications such as nephropathy or cardiovascular disease in the tissues. Insulin pump data showed that after three alarms, a power failure of the pump occurred leading to discontinuing insulin delivery, and about 48 h before the deceased was found dead, his body was depleted of insulin. CONCLUSION: The cause of death is believed to be diabetic ketoacidosis due to completely lack of insulin because of power failure of the insulin pump, which therefore has been a decisive factor in the cascade of events that led to death. The case is, to our knowledge, the first to illustrate a death caused by diabetic ketoacidosis which is supported by autopsy findings and by data of an insulin pump up to the time of power failure. It is a strong example of usefulness of postmortem download of data from insulin pumps to help determine the cause of death among diabetics. Forensic pathologists should therefore review data and history of the pump systematically.