The main findings of this study in patients with type 2 diabetes and stable coronary artery disease are:
A decrease of both minimal and mean FCT is associated with increased LV-dilatation as characterized by CMR-derived LVEDV, LVESV and LVEDD.
Both minimal and mean FCT are associated with LV-dilatation independent of previous MIs.
LVEDD, LVEDV and LVESV predict plaque vulnerability with overall low or moderate diagnostic efficiency but considerate specificity at optimal cut-off values.
A minimal FCT ≤ 80 μm is an approved in vivo predictor of plaque rupture with subsequent acute coronary events . Patients with type 2 diabetes are prone to both, a high prevalence of vulnerable plaques as well as LV-dilatation [1–6]. However, to date nothing is known about the relationship between minimal and mean FCT on the one hand and LV-geometry on the other hand, neither in patients with type 2 diabetes nor in the general population. We extend the current knowledge by demonstrating an association between both minimal and mean FCT with CMR-derived LVEDV, LVESV and LVEDD as markers of LV-dilatation. In addition, we could demonstrate that a large variety of FCT values was present in patients with non-dilated LV, whereas in patients with dilated LV lesions were characterized by a smaller FCT. Thus, CMR-derived parameters at optimal cut-off values displayed low sensitivity in predicting FCT ≤ 80 μm but considerate specificity. Taken together, the data suggest that type 2 diabetic patients with dilated LV are at a particular high risk for vulnerable plaques whereas both vulnerable and stable plaques are present in patients with non-dilated LV.
Plaque rupture causes acute coronary events which subsequently result in ischemic cardiomyopathy with LV-dilatation. Thus, the relationship between FCT and LV-dilatation in patients with type 2 diabetes observed in this study may reflect the relationship between plaque vulnerability and previous MIs. However, although several cardiovascular risk factors including previous MI and HDL-cholesterol were different between patients with dilated versus non-dilated LV, multivariable regression analysis demonstrated that both minimal and mean FCT predict LV-dilatation independent of previous MIs. Moreover, minimal and mean FCT predicted LV-dilatation even when adjusted for further cardiovascular risk factors such as smoking and HDL-cholesterol which were different between patients with dilated versus non-dilated LV. As a direct causal relationship between both minimal and mean FCT on the one hand and LV-dilatation on the other hand seems unlikely, it is tempting to speculate that FCT and LV-dilatation may both be caused by a third pathophysiological entity. This may include microruptures and disturbances in microcirculation. Further candidates which are known to influence both LV-geometry and atherosclerosis include alterations in metabolism, adipokines and cytokines [24–28]. Future studies are needed to determine the underlying mechanisms linking plaque vulnerability and LV-dilatation.
To the best of our knowledge we are first to describe an association between plaque vulnerability as determined by OCT and left ventricular dilatation in patients with type 2 diabetes. However, the correlation between LV geometric parameters and atherosclerosis and the incidence of acute cardiovascular events is not a new concept. Specifically, Chahal et al. have demonstrated in 2279 patients without clinical cardiovascular disease that subclinical carotid plaque disease was related to LV systolic function and LV filling pressure, whereas no significant differences in LV systolic and diastolic volumes were observed between patients with compared to those without carotid disease . Madaj and colleagues have demonstrated an association between LV-mass and coronary artery calcification as determined by computed tomography . Furthermore, the Multiethnic Study of Atherosclerosis (MESA) has found several traditional risk factors of cardiovascular disease to be associated with LVEDV as determined by CMR . Our findings are in line with this study by demonstrating more classical cardiovascular risk factors including smoking, previous MI as well as a decreased HDL-cholesterol in diabetic patients with vs. without LV-dilatation.
Whereas stress-CMR reveals ischemia due to functionally relevant coronary stenosis , its diagnostic value in hemodynamically insignificant lesions remains insufficient. However, cardiac events frequently occur in angiographically insignificant stenoses  and usually arise from vulnerable lesions with a low FCT. In the light of our data it is tempting to speculate that CMR at rest with the assessment of LV-dilatation may add insights into plaque morphology and vulnerability in high risk patients with type 2 diabetes. Specifically, diagnostic efficiency and sensitivity of CMR-derived LVEDD, LVEDV and LVESV to predict plaque vulnerability was low to moderate with considerate specificity at optimal cut-off values. Thus, CMR-derived parameters of LV-dilatation may be valuable in identifying patients at risk for the presence of vulnerable plaques.
Echocardiography has the advantage of being widely available as well as time- and cost-effective. Moreover, it is the most commonly used imaging technique for the assessment of LV-dilatation. However, CMR for the assessment of LV-dilatation may be superior to echocardiography due to its higher resolution and exacter assessments particularly in overweight and obese patients with type 2 diabetes which is reflected in our own study population with a mean BMI of 29.70 kg/m2. It needs to be determined in future studies if our findings can be confirmed when echocardiography instead of CMR is used to assess LV-dilatation.
The present investigation is limited by a small sample size and in 15 patients the determination of a FCT was not possible due to the absence of a lipid-rich plaque. Therefore, for confirmation of our data a large-scale study is required. The sample size may be a limitation particularly for the presented multivariable regression analysis.
Second, patients with reduced kidney function were not included in the study due to ethical issues regarding additional contrast medium necessary for the OCT-investigation. However, a high percentage of those patients with reduced LV-function also have reduced kidney function and our findings may be biased by this fact.Third, although the relationship between LV-geometry and plaque vulnerability is particularly important in cardiovascular high-risk patients with type 2 diabetes, future studies are necessary to determine if the findings of this study can also be translated to patients without type 2 diabetes.
Furthermore, our findings are limited by the fact that in this study OCT was only used in the target vessel due to ethical issues in order to minimize complications associated with the use of OCT.
Moreover, we used the minimal FCT-threshold of 80 μm for defining plaque vulnerability. This value is above the currently accepted consensus of 65 μm that was based on post-mortem studies, where tissue-shrinkage may be a relevant issue . Therefore, we referred to a currently published OCT-investigation which demonstrated that 95% of ruptured lipid-rich plaques presented with a minimal FCT ≤ 80 μm in vivo .