Silent myocardial infarction and ischaemia

In view of the increased prevalence of coronary artery disease (CAD) in diabetic patients, it is difficult to differentiate between the impact of coronary ischemia and CAN on cardiac autonomic function. In other words, silent ischemia in diabetic patients may either result from CAN or from autonomic dysfunction due to CAD itself, or both. In the Framingham study, the rates of unrecognised myocardial infarctions were 39 % in diabetic subjects and 22 % in non-diabetic subjects, but the difference was not significant (Margolis et al. 1973). In a survey from the National Registry of Myocardial Infarction 2 (NRMI-2), of 434,877 patients with myocardial infarction, 33 % did not have chest pain on presentation. The rates of patients with diabetes were 32.6 % among those presenting without chest pain vs 25.4 % among those with (Canto et al. 2000). It has been suggested that features such as sympathovagal balance (see below), impaired fibrinolysis and altered hemostasis, which are commonly clustered together, may trigger coronary plaque disruption and superimposed thrombosis in diabetic patients in a more unpredictable manner than they would in the absence of diabetes (Nesto 1999).

A meta-analysis including 12 studies (n = 1,468) revealed an increased risk of silent myocardial ischemia (SMI) during exercise of 1.96 (1.53-2.51) in diabetic patients with CAN, compared to those without CAN (Maser et al. 2003; Maser & Lenhard 2005). CAN is apredictor of cardiovascular events in diabetic patients, the risk being highest in those who have both CAN and SMI (Valensi et al. 2005). The DIAD study showed that SMI is encountered in 22 % of asymptomatic type 2 diabetic patients and correlates more strongly with reduced HRV than with male sex and the duration of diabetes (Wackers et al. 2004). In diabetic patients with exertional chest pain, a prolonged anginal perceptual threshold, i.e. the time from onset of 0.1 mV ST depression to the onset of angina pectoris during exercise ECG, has been demonstrated. This delay was associated with the presence of CAN (Ambepityia et al. 1990). Hence, patients with CAN and CAD are jeopardised, because the longer threshold permits them to continue exercising despite increasing ischaemia (Figure 16.2).

Figure 16.2 Anginal perceptual thresholds in diabetic and non-diabetic patients. Data points are the time from onset of 0.1 mV ST segment depression to onset of angina in individual patients during treadmill exercise.

Furthermore, it has been demonstrated that patients with silent ischaemia are more frequently diabetic, and impairment in several autonomic function tests including standard indices and 24-h HRV was not seen in the nondiabetic patients in the silent group but was confined to the diabetic patients with silent ischaemia (Marchant et al. 1993). These findings suggest CAN plays an important role in silent ischaemia in diabetic subjects. However, it has also been argued that the increased incidence of CAD in diabetes mainly reflects accelerated coronary atherosclerosis and that there is no convincing clinical and epidemiological evidence for CAN playing a major role in the lack of ischemic pain (Airaksinen 2001). Given the complex and controversial mechanisms of silent myocardial ischaemia even in the absence of diabetes, further studies are needed to clarify the exact role of CAN in this context.

A diagnostic algorithm for diabetic patients without ischemic symptoms published by Deutsche Diabetes-Gesellschaft (DDG) (Standl et al. 2001), according to the statements of the American Diabetes Association (ADA) (1998) and American Heart Association (AHA), (Grundy et al. 1999) is shown in Figure 16.3.

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