Assessing culprit lesions and active complex lesions in patients with early acute myocardial infarction by multidetector computed tomography.

BACKGROUND: Accurate, non-invasive characterization of culprit lesions in patients after acute myocardial infarction (AMI) remains challenging. In this prospective study, multidetector row computed tomography (MDCT) is used to assess culprit and active complex lesions in patients early after AMI. METHODS AND RESULTS: We enrolled 103 patients with first non ST-elevation AMI who underwent 64-slices MDCT and conventional coronary angiography (CCAG). The definition of culprit lesion, stable non-culprit lesions and non-culprit active complex lesions was based on the findings of CCAG. The lesions were analyzed with MDCT data. In culprit lesions (n=103), luminal artery stenosis, remodeling index, plaque area and burden were significantly higher than non-culprit lesions (n=129). Multivariate discriminant analysis showed that MDCT density could discriminate culprit from non-culprit lesions. Receiver-operator characteristic curve analysis identified the optimal cutoff value of lesion density for discrimination between culprit and non-culprit lesion as 49.6 Hounsfield units (HU); this value was associated with a sensitivity, specificity and accuracy of 88.4%, 87.4%, and 87.9%, respectively. The MDCT in the stable non-culprit lesions (81.8+/-15.5 HU) was significantly higher than that in culprit lesions or non-culprit active complex lesions (33.2+/-13.8 and 48.3+/-15.7 HU, p<0.001). CONCLUSIONS: MDCT can predict culprit lesions in patients early after AMI, and identify multiple complex lesions.

Role of shortened QTc dispersion in in-hospital cardiac events in patients undergoing percutaneous coronary intervention for acute coronary syndrome.

BACKGROUND: QT dispersion (QTD) refers to the difference between maximal and minimal QT values on the electrocardiogram (ECG). QTD values are calculated and corrected with Bazett's formula (corrected QTD = QTcD = QTD/square root of RR). QTcD increases in patients with acute coronary syndrome (ACS). Recovery of increased QTcD (shortened QTcD) develops after successful revascularization, but prolonged QTcD occurs in certain patients. The aim of this study is to ascertain the clinical significance between shortened and prolonged QTcD groups after percutaneous coronary intervention (PCI). METHODS: We retrospectively enrolled 128 patients with ACS who had received PCI. The values of QTcD were measured manually on 12-lead standard ECGs obtained within 3 days before and after PCI (pre-PCI QTcD and post-PCI QTcD). All the patients were divided into 2 groups. The shortened QTcD group was defined as those patients with a decrease in QTcD after PCI and the prolonged QTcD group as those with an increase in QTcD after PCI. The underlying diseases, various clinical classifications and some prognostic factors were taken into comparison and statistical analysis between these 2 groups. RESULTS: The shortened QTcD group showed a significantly higher rate of in-hospital cardiac death (13% vs. 0%, p = 0.006) and a greater pre-PCI QTcD (100.8 +/- 39.5 vs. 61.3 +/- 24.1 ms, p < 0.001) than the prolonged QTcD group. There was a significantly greater pre-PCI QTcD in patients with cardiac death than those without cardiac death (111.6 +/- 38.3 vs. 83.3 +/- 38.3ms, p = 0.027). Furthermore, the patients with in-hospital cardiac death presented with a significantly more frequent occurrence of in-hospital ventricular arrhythmia, compared with those without cardiac death (30.0% vs. 4.0%, p = 0.014). CONCLUSION: Among the patients with ACS undergoing PCI, directly divided into shortened and prolonged QTcD groups regardless of initial pre-PCI QTcD, the shortened QTcD group showed a higher occurrence of in-hospital cardiac death and a greater pre-PCI QTcD. Shortened QTcD might be 1 risk factor for in-hospital cardiac death.