Reactive Hyperglycaemia Connected with Low Glycated Haemoglobin – Risk Factor for Cardiovascular Adverse Events

Marek Andres^1*, Tomasz Rajs¹, Ewa Konduracka², Jacek Legutko¹, Janusz Andres³, Krzysztof Żmudka^1
1Department of Interventional Cardiology, John Paul II Hospital, Krakow, Poland
²Department of Coronary Diseaseand Heart Failure, John Paul II Hospital, Krakow, Poland
³Department of Anesthesiology and Intensive Care Medicine, Jagiellonian University Medical College, Krakow, Poland

Corresponding Author: Marek Andres MD, Ph.D. ^{ORCID iD}
Address: Department of Interventional Cardiology, John Paul II Hospital, Krakow, Poland.
Received date: 26 April 2021; Accepted date: 24 May 2021; Published date: 01 June 2021

Citation: Andres M, Rajs T, Konduracka E, Legutko J, Andres J, Żmudka K. Reactive Hyperglycaemia Connected with Low Glycated Haemoglobin - Risk Factor for Cardiovascular Adverse Events. J Health Care and Research. 2021 Jun 01;2(2):85-96.

Copyright © 2021 Andres M, Rajs T, Konduracka E, Legutko J, Andres J, Żmudka K. This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Keywords: Reactive Hyperglycaemia, Low Glycated Haemoglobin, Atherosclerosis, Cardiovascular Adverse Events, Segment Elevation Myocardial Infarction, Primary Percutaneous Coronary Intervention

Abstract

Introduction: Concomitance of glucose metabolism disturbances and ischemic heart disease is well known and connected to several times higher incidence of cardiovascular events resulted from atherosclerosis. Aim of this study was to assess impact of reactive hyperglycaemia accompanying chronic and not always optimally treated hyperglycaemia assessed with glycated haemoglobin level on cardiovascular prognosis among patient hospitalised in the course of acute myocardial infarction.
Methods: 92 patients diagnosed with ST – segment elevation myocardial infarction (STEMI) qualified to primary percutaneous coronary intervention (pPCI) was included in the study. Study population was divided into subgroups, depending glucose level on admission (reactive hyperglycaemia) and HbA1c concentration: subgroup A (HbA1c <6.5%, Glc<7.8 mmol/l: n = 37; 40,2%), subgroup B (HbA1c <6.5%, Glc ≥.,8 mmol/l: n = 27; 29,3%), subgroup C (HbA1c ≥6.5%, Glc ≥7.8 mmol/l: n = 20; 21,7%) and subgroup D (HbA1c ≥6.5% Glc<7.8 mmol/l: n = 8; 8.7%). Level of myocardium damage was assessed on the basis of concentration of myocardial necrosis enzymes: creatine kinase (CK) and creatine kinase MB fraction (CK-MB) in the 0 and 90^th minute and thereafter 8, 16, 24 and 48 hours after hospital admission and also echocardiographic examination. Prognosis in long and short term observation was assessed by major adverse cardiovascular events (MACE) such as death, myocardial infarction, stroke, heart failure requiring hospitalisation and repeated revascularisation and level of glucose metabolism disturbances in intrahospital phase, 4 months and 4 years follow up observation.
Results: Results in study population revealed significant change of average value of creatine kinase (p<0,001) and its MB fraction (p<0,001) during first 48 hours of hospitalisation in particular subgroups of patients. Mean values of CK and CK-MB assessed in subsequent hours of hospitalisation (1,5, 8, 16 and 48 hours) were significantly higher in subgroup B (CKp=0,034 and CK-MB p=0,01, respectively). It means that area under curve was significantly higher for subgroup B. In 4 months and 4 year follow up observation, statistically significant difference in frequency of MACE in particular subgroups of patients has been shown (p=0,016; p=0,01).
Conclusions: Patients with STEMI undergoing pPCI, who were diagnosed with disturbed carbohydrate metabolism, have inferior clinical outcomes in long term follow up observation. Noticeable difference was observed particularly in subgroup B (HbA1c <6.5%, Glc ≥7.8 mmol/l).