Impact of Multimodality Imaging on the Diagnosis of Left Ventricular Apical Thrombus in Patients After Anterior Myocardial Infarction.

BACKGROUND: The presence of the left ventricle (LV) apical thrombus is one of the most critical complications of anterior myocardial infarction (MI). Due to the high risk of systemic embolization, the determination of LV apical thrombus (LVAT) is essential. We aimed to compare the two-dimensional echocardiography (2DE), contrast-2DE and real-time three-dimensional echocardiography (RT-3DE) in the diagnosis of LVAT and determine which imaging modality is superior. METHODS: The study was designed as a prospective cohort study, and 161 patients were included. Patients with low ejection fraction (< 40%) and LV apical wall motion abnormality (severe hypokinetic, akinetic or dyskinetic) were included. 2DE, contrast-2DE, RT-3DE, and magnetic resonance imaging (MRI) were performed on all patients within one month after anterior MI. RESULTS: Transthoracic 2DE detected thrombi in 29 patients, contrast-2DE detected thrombi in 33 patients, RT-3DE detected thrombi in 32 patients, and MRI detected thrombi in 28 patients. While MRI is accepted as the gold standard for non-invasive imaging, the specificity of detecting thrombus with 2DE is 90%, and the sensitivity is 57%, contrast-2DE had 82% sensitivity and 92% specificity for the detection of LVAT. The specificity for detecting thrombus with RT-3DE is 93%, and the sensitivity is 85%. Accuracy was 84%, 90% and 92% with 2DE, contrast-2DE and RT-3DE, respectively. CONCLUSIONS: We found that RT-3DE was more sensitive and more specific than 2DE and contrast-2DE in the diagnosis of LVAT. The diagnostic accuracy of RT-3DE was higher than 2DE and contrast-2DE for LVAT.

Impaired endothelial function irrespective of systemic inflammation or atherosclerosis in mastocytosis.

BACKGROUND: Knowledge on endothelial dysfunction and its relation to atherosclerosis in mastocytosis is limited. OBJECTIVE: To investigate the endothelial function in mastocytosis by flow-mediated dilatation (FMD) and biomarkers related to vascular endothelia and to evaluate its relationship with the presence of subclinical atherosclerosis by carotid intima media thickness (CIMT). METHODS: A total of 49 patients with mastocytosis and 25 healthy controls (HCs) were included. The FMD and CIMT during transthoracic echocardiography biomarkers including endocan, endothelin-1, and vascular endothelial growth factor (VEGF) were measured in the sera of participants. Tumor necrosis factor-alpha, interleukin 6, and high-sensitive C-reactive protein were determined as inflammatory biomarkers. RESULTS: The mean FMD % was lower in the patients than HCs (11.26% ± 5.85% vs 17.84% ± 5.27% P < .001) and was the lowest in the advanced systemic mastocytosis and smoldering systemic mastocytosis group among the patients (P = .03). The median value of VEGF was considerably higher in patients than HCs (73.30 pg/mL; minimum-maximum 32.46-295.29 pg/mL vs 46.64 pg/mL; minimum-maximum, 11.09-99.86 pg/mL; P = .001) and it was the highest in the advanced systemic mastocytosis and smoldering systemic mastocytosis group (P = .01). The FMD was inversely correlated with endocan (r = -0.390; P = .006), endothelin-1 (r = -0.363; P = .01) and VEGF (r = -0.402; P = .004) but there were no correlations between FMD and tumor necrosis factor-alpha, interleukin 6, and high-sensitive C-reactive protein. No differences in CIMT values between patients and HCs and no correlation between CIMT and the biomarkers were observed. CONCLUSION: Endothelial dysfunction in mastocytosis becomes evident with decreased FMD and elevated serum VEGF in the absence of atherosclerosis or systemic inflammation and is related to disease severity.