Cardiac risk assessment in asymptomatic diabetes: Combing different imaging modalities and surrogate markers?

The growing number of patients who develop diabetes mellitus (DM) is a great concern for public health care. Type 2 DM comprises 90% of all diabetic patients worldwide, and is largely the result of excess body weight and physical inactivity. Long term complications of DM include microvascular damage and macrovascular injuries. These complications reduce life expectancy and quality of life, and significantly increase morbidity. Due to the often masked symptoms of DM, the disease may be diagnosed several years after onset when complications have already occurred. Often, the prognosis of patients with DM depends on the presence of cardiovascular disease. Coronary artery disease (CAD) is the leading cause of morbidity and mortality in individuals with type 2 DM. The 10-year mortality rate in patients with known CAD and diabetes exceeds 70%. Some studies suggest that the risk for future cardiac death in patients with diabetes without known CAD is similar to that in non-diabetic patients with overt clinical CAD. In addition, early and late outcomes of diabetic patients with acute coronary syndromes are worse than those of their non-diabetic counterparts. To compound the problem, myocardial ischemia is often asymptomatic in patients with DM, and CAD is frequently in an advanced state, when becoming clinically manifest. The previously described adverse clinical outcomes in patients with diabetes underscores the need to develop practical approaches to detect CAD in an early stage before clinical symptoms occur. Thus, early detection of CAD and myocardial ischemia appears to be important to reduce morbidity and mortality from cardiovascular disease in asymptomatic patients with type 2 DM. Identification of these asymptomatic diabetic patients might be important to intervene early and to increase long term survival. From a management perspective, patients with high risk characteristics on testing for myocardial ischemia may benefit from coronary revascularization. With regard to pharmacological therapy, the knowledge that a patient with diabetes has CAD may indicate the need to initiate or intensify pharmacological therapy with aspirins, statins, and angiotensin converting enzyme (ACE) inhibitors. Results from the BARI 2D trial showed no significantly differences in survival rates as well as in freedom from major cardiovascular events between optimal medical therapy and revascularization. So, it seems that testing for ischemia should be reserved for selected individuals with a strong suspicion of high risk CAD. Single photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) has been used extensively in the detection of (silent) myocardial ischemia in symptomatic as well as asymptomatic patients with DM. Several studies in the literature suggest a high prevalence of abnormal MPI in diabetic patients, ranging from 37% to 62%. The same studies furthermore demonstrate, in a mean follow-up of 24-70 months, a hard event rate of 3.6%-9.0% per year in diabetic patients with abnormal MPI. Retrospective database analysis reveals the same percentages of abnormal MPI and hard event rates in symptomatic and asymptomatic patients with diabetes. Prospective studies in asymptomatic patients with diabetes show a lower prevalence of silent myocardial ischemia ranging from 6% to 22%. Differences in design and stress testing methodology may explain these variations in prevalence. One of these prospective studies is the DIAD trial. The lessons learned from this important trial has been extensively described in this journal. The authors concluded that routine screening of asymptomatic patients with diabetes was not justified but they also speculated that other imaging studies might provide additional insights into models that might in combination with MPI From the Department of Cardiology, Leiden University Medical Center, RC, Leiden, The Netherlands. Reprint requests: Arthur J. H. A. Scholte, MD, PhD, Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300, RC, Leiden, The Netherlands; a.j.h.a.scholte@ lumc.nl. J Nucl Cardiol 2011;18:393–5. 1071-3581/$34.00 Copyright 2011 The Author(s). This article is published with open access at Springerlink.com doi:10.1007/s12350-011-9366-z