The present study demonstrated that patients with T2DM have subclinical myocardial injury as detected by elevated levels of hs-TnI. Arterial stiffness evaluated by ba-PWV was the only parameter associated with hs-TnI in patients with T2DM.
Previous studies have consistently demonstrated that subclinical myocardial necrosis detected by troponin I predicted adverse cardiovascular events in patients with T2DM [17, 18]. In addition to the prognostic value for future adverse cardiovascular events, the use of a high-sensitivity assay permits detection of minimally elevated troponin that represents subclinical myocardial damage [3, 7, 19, 20]. In a recent report from the Atherosclerosis Risk in Communities (ARIC) study (n = 9661), subclinical myocardial injury, detected by high-sensitivity troponin T, was closely associated with hyperglycemia in patients with no history of atherosclerotic disease . Similarly, this study demonstrates that patients with T2DM and no clinically relevant atherosclerotic disease had myocardial damage detected by hs-TnI. This suggests that T2DM contributes to subclinical myocardial injury, independent of clinically overt atherosclerotic disease.
Arterial stiffness measured by PWV (carotid to femoral) is a strong predictor for adverse cardiovascular events in community-based subjects . Studies have also demonstrated that T2DM is associated with increased arterial stiffness that may partly explain the increased cardiovascular risk . Although arterial stiffness has been postulated to act as a surrogate marker for underlying atherosclerosis and reflect clustering of cardiovascular risk factors, the exact mechanism of how this correlates with adverse cardiovascular outcome is uncertain. Studies have previously demonstrated that PWV was related with left ventricular diastolic dysfunction detected by echocardiography [23, 24]. Further, a recent report demonstrated that increased ba-PWV was associated with high-sensitivity troponin T level in a community-based subject aged over 60 (T2DM in 26%) . This suggests that arterial stiffening may cause subclinical myocardial injury, resulting in adverse cardiovascular events. The present study further demonstrated that arterial stiffness measured by ba-PWV was independently associated with elevated hs-TnI in patients with T2DM. The current results therefore suggest that increased arterial stiffness is related to subclinical myocardial injury and contribute to an adverse cardiovascular outcome in patients with T2DM.
Patients with T2DM have increased arterial stiffness due to multiple mechanisms including increased oxidative stress , accelerated endothelial cell apoptosis , endothelial dysfunction  and depletion of endothelial progenitor cells . Arterial stiffening may subsequently cause myocardial damage in several ways although the exact mechanism is uncertain. Decreased compliance of the aorta increases systolic pressure and left ventricular preload, resulting in elevated stress on the left ventricular myocardium during the systolic phase. This may predispose patients to develop left ventricular hypertrophy that is associated with an elevated high-sensitivity troponin level . Further, a reduction in diastolic pressure decreases coronary perfusion that may lead to myocardial ischemia, independent of underlying coronary atherosclerotic burden . Finally, increased arterial stiffness may be indirectly related to myocardial injury via such as clustering of adverse cardiovascular risk profiles and systemic inflammation. Nonetheless the means by which arterial stiffening relates to myocardial injury in patients with T2DM requires evaluation by further prospective study.
A number of further mechanisms have also been proposed to contribute to myocardial injury in patients with T2DM. The present study thus sought to identify any such additional mechanisms. Hyperglycaemia may induce impaired brachial FMD , which represents an early stage of atherosclerosis. Further, carotid IMT, a well validated surrogate for subclinical atherosclerosis, has been shown to be increased in patients with T2DM and its progression can be slowed by intensive treatment . The current study nonetheless demonstrated that only ba-PWV, not brachial FMD or carotid IMT, correlated with hs-TnI. A previous population-based study likewise was unable to demonstrate an association between elevated high-sensitivity troponin T level and atherosclerosis evaluated by coronary calcification . These findings thus suggest that troponin release in chronic setting differs from those in acute setting, and is not associated with subclinical atherosclerosis measured by brachial FMD and carotid IMT.
The present study had several limitations. A causal relationship between arterial stiffness and myocardial injury could not be established because of the cross-sectional nature of the study. Although patients with T2DM were all clinically free from overt cardiovascular complications, silent coronary artery disease could not be excluded. Further, this study did not replicate the previously demonstrated association of hs-TnI with hbA1c% , likely due to the small study population. The possibility of residual confounding factors could not be excluded even though the results were adjusted for multivariate covariates. The use of direct assessment of atherosclerosis, such as coronary angiography or coronary endothelial function assessment using intracoronary acetylcholine infusion may provide addition information regarding the relation between atherosclerosis and hs-TnI. However, these tests are invasive in nature and therefore may not be clinically feasible to perform for research purpose. Moreover, whether advanced glycation end products, an intermediate product that is elevated in patients with T2DM and an independent marker of post-infarction heart failure, would contribute to elevation of hs-TnI would require evaluation by future studies .