Prediction of myocardial tissue loss by quantitative densitometric myocardial blush parameters following ST-elevation myocardial infarction.

UNLABELLED: Tissue level myocardial perfusion is one of the most important prognostic factors after successful recanalisation of the occluded coronary artery in patients suffering acute ST elevation myocardial infarction (STEMI). The primary objective of the present study was to examine the relationship between videodensitometric myocardial perfusion parameters as assessed on coronary angiograms directly following successful recanalization therapy and magnetic resonance imaging (MRI)-derived myocardial tissue loss late after STEMI. The study comprised 29 STEMI patients. Videodensitometric parameter G(max)/T(max) was calculated to characterize myocardial perfusion, derived from the plateau of grey-level intensity (G(max)), divided by the time-to-peak intensity (Tmax). Myocardial loss index (MLI) was assessed by cardiac MRI following 376 ± 254 days after PCI. RESULTS: Significant correlations could be demonstrated between MLI and G(max) (r = 0.36, p = 0.05) and G(max)/T(max) (r = 0.40, p = 0.03) using vessel masking. Using receiver operating characteristic curve analysis, G(max)/T(max) < 2.17 predicted best MLI = 0.3, 0.4, 0.5 and 0.6 with good sensitivity and specificity data, while G(max)/T(max) < 3.25 proved to have a prognostic role in the prediction of MLI = 0.7. CONCLUSIONS: Selective myocardial tissue level perfusion quantitative measurement method is feasible and can serve as a good predictor of myocardial tissue loss following STEMI and revascularization therapy.

Lipedema is associated with increased aortic stiffness.

Lipedema is a disproportional obesity due to unknown pathomechanism. Its major hallmark is frequent hematoma formation related to increased capillary fragility and reduced venoarterial reflex. Beyond microangiopathy, both venous and lymphatic dysfunction have also been documented. However, arterial circulation in lipedema has not been examined, and therefore we explored aortic elastic properties by echocardiography. Fourteen women with and 14 without lipedema were included in the study. Each subject consented to blood pressure measurement, physical examination, and transthoracic echocardiography. Aortic stiffness index (beta), distensibility, and strain were evaluated from aortic diameter and blood pressure data. Mean systolic (30.0 +/- 3.2 vs. 25.5 +/- 3.6, P < 0.05) and diastolic (27.8 +/- 3.3 vs. 22.3 +/- 3.1) aortic diameters (in mm) and aortic stiffness index (9.05 +/- 7.45 vs. 3.76 +/- 1.22, P < 0.05) were significantly higher, while aortic strain (0.082 +/- 0.04 vs. 0.143 +/- 0.038, P < 0.05) and distensibility (2.24 +/- 1.07 vs. 4.38 +/- 1.61, P < 0.05) were significantly lower in lipedematous patients compared to controls. Thus, lipedema is characterized with increased aortic stiffness.