J. Heuser
19. June 2006
After the introduction of the universal definition of myocardial infarction, the incidence and diagnosis of type 2 myocardial infarction have risen dramatically, yet there are no clear guidelines on clinical management. Diabetic patients are at high risk for developing type 2 myocardial infarction when admitted in a decompensated state, and they are also at high risk for future cardiovascular events.
Methods
We performed a retrospective analysis of 1058 patients admitted with diabetic ketoacidosis or hyperosmolar hyperglycemic state between 2011 and 2016. Patients were included if they had cardiac troponin I measured within 24 hours of admission, were older than 18 years of age, and had no evidence of acute coronary syndrome on admission. Baseline characteristics, admission laboratory test results, major adverse cardiovascular events, cardiac stress testing, and coronary angiography data up to 1 year after admission were reviewed. Patients were categorized into 2 groups: those with and those without type 2 myocardial infarction. The study had 2 endpoints: mortality and major adverse cardiac events (MACE) at 1 year and an abnormal result on stress test or coronary angiography at 1 year.
Results
Of the 845 patients who met the inclusion criteria, 133 patients (15%) had type 2 myocardial infarction on admission. Patients with type 2 myocardial infarction were at a significantly higher risk for mortality and MACE at 1 year than those without. Patients with type 2 myocardial infarction were also at higher risk for developing an abnormal result on stress test or coronary angiography within 1 year of admission as compared with those without type 2 myocardial infarction (40% vs 24%; odds ratio 2; P = .0699).
Conclusion
Acutely decompensated diabetic patients with type 2 myocardial infarction are at increased risk for death and MACE. These patients may also be at risk for undiagnosed coronary artery disease.
Introduction
Acutely decompensated diabetes (diabetic ketoacidosis and hyperosmolar hyperglycemic state) is a potentially life-threatening and frequently encountered medical condition. It occurs when there is an acute insulin deficiency and low insulin/glucagon ratio in the liver. In response to the acute insulin deficiency, ketosis, and metabolic stress there is an increase in the levels of counterregulatory stress hormones, including glucagon, catecholamines, cortisol, growth hormone, and others.1
Type 2 myocardial infarction occurs when there is an imbalance between the myocardial oxygen supply and demand and is defined as myocardial necrosis in the absence of coronary plaque rupture or erosion.2 The high stress levels of acutely decompensated diabetes may lead to type 2 myocardial infarction in the presence or absence of underlying coronary artery disease.
Several small studies have demonstrated that type 2 myocardial infarction in patients hospitalized for acutely decompensated diabetes is associated with increased mortality and major adverse cardiovascular events (MACE).3, 4, 5 In the absence of established guidelines, management of such patients poses a medical conundrum and raises the question regarding the recognition of underlying obstructive coronary artery disease in this high-risk population.
Between the second (2007) and the third (2012) universal definitions of myocardial infarction, the incidence and diagnosis of type 2 myocardial infarction have doubled, but the guidelines on its management are still lacking.2, 6,7 In this study we sought to investigate 1) the clinical significance and prognosis of type 2 myocardial infarction; 2) the presence of underlying obstructive coronary artery disease; and 3) the subsequent need for risk stratification before discharge in acutely decompensated diabetic patients.
To our knowledge this is the largest observational study of type 2 myocardial infarction in patients with diabetic ketoacidosis and hyperosmolar hyperglycemic state.
You can read “Clinical Features and Prognosis of Type 2 Myocardial Infarction in Acutey Decompensated Diabetic Patients by Hritani et al ot our website.
This article originally appeared in the July 2018 issue of The American Journal of Medicine.
