Electrocardiogram patterns during hemodynamic instability in patients with acute pulmonary embolism.

BACKGROUND: We have previously described new electrocardiogram (ECG) findings for massive pulmonary embolism, namely ST-segment elevation in lead aVR with ST-segment depression in leads I and V4 -V6 . However, the ECG patterns of patients with acute pulmonary embolism during hemodynamic instability are not fully described. METHODS: We compared the differences between the ECG at baseline and after deterioration during hemodynamic instability in twenty patients with acute pulmonary embolism. RESULTS: Compared with the ECG at baseline, three ischemic ECG patterns were found during clinical deterioration with hemodynamic instability: ST-segment elevation in lead aVR with concomitant ST-segment depression in leads I and V4 -V6 , ST-segment elevation in leads V1 -V3 /V4 , and ST-segment elevation in leads III and/or V1 /V2 with concomitant ST-segment depression in leads V4 /V5 -V6 . Ischemic ECG patterns with concomitant S1Q3 and/or abnormal QRS morphology in lead V1 were more common (90%) during hemodynamic instability than at baseline (5%) (P = 0.001). CONCLUSIONS: Hemodynamic instability in acute pulmonary embolism is reflected by signs of myocardial ischemia combined with the right ventricular strain pattern in the 12-lead ECG.

In rats with myocardial infarction, interference by simvastatin with the TLR4 signal pathway attenuates ventricular remodelling.

OBJECTIVE: The objective of this study was to investigate the effect of simvastatin on TLR4,TNF-alpha and IL-6 expression in the myocardium and its relation to left ventricular (LV) remodelling in a rat model of myocardial infarction (MI) and to investigate the mechanism by which simvastatin improves LV remodelling in rats after MI. METHODS AND RESULTS: The rat MI models were established by ligation of the left anterior descending coronary artery and divided into three groups: (I) an untreated MI group; (2) a group treated with simvastatin [40 mg/(kg/d)] for 4 weeks; (3) the sham group. Cardiac geometry and function were determined by echocardiography and infarct size was determined by the histomorphometric analysis; the expression ofTLR4 in the myocardium was measured by RT-PCR and western blotting;TNF-alpha and IL-6 levels in myocardial homogenate and serum were measured by ELISA. LVEDD and LVESD significantly increased and fractional shortening (FS) markedly decreased in the MI group. It was clear that simvastatin inhibited LV dilation and improved LV function after MI without affecting infarct size. The expression of TLR4, TNF-alpha and IL-6 in the myocardium significantly increased in the MI group and simvastatin markedly inhibits the expression of TLR4, TNF-alpha, and IL-6 in the myocardium after MI. Serum TNF-alpha and IL-6 levels between the MI group and the simvastatin group remained unchanged. Both in the MI group and the simvastatin group,TLR4 protein positively related to LVEDD and to the levels of TNF-alpha and IL-6 in the myocardium, respectively. CONCLUSION: Amelioration of LV remodelling in rats after MI by simvastatin might be associated with its effect on the TLR4-mediated signalling pathway in the myocardium.

[Effects of MSCs on the progression of atherosclerosis plaque in ApoE-knock out mice].

AIM: To explore the effects of mesenchymal stem cells in the formation of atherosclerosis plaque in hypercholesterolemic apoliprotein (apo) E -/ - mice. METH-ODS: ApoE -- mice mesenchymal stem cells (MSCs)were isolated and identified. Thirty ApoE -/ - mice were divided into negative control group (Neg, n = 10), positive control group (Pos, n = 10) and MSCs group ( n = 10).MSCs were injected through caudal vein into the body ofPos and MSCs groups. The plaque area of all subjects were compared, the percentage of CD4 CD25' regulatory T cells in different tissues were analyzed by FACS, proliferation response of splenocytes to mesenchymal stem cells and cyto-kines in the supernatant were determined by ELISA. RE-SULTS: Compared with controls, MSCs resulted in a significant decrease of the atherosclerotic plaques size (P <0.05), and a significant increase of CD4 CD25 regulatory T cells in spleen (P<0.05). Specific proliferation response of CD4' CD25' regulatory T cells in splenocytes to MSCswas significantly suppressed. The supernatant levels ofTGF-f3 and IL-10 in MSCs group were increased while IFN-y decreased significantly. CONCLUSION: MSCs play an important role in regulating the inflammatory response and may significantly inhibit the formation of the atherosclerosis plaque in ApoE-'- mice.