Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts.

Urotensin II (UII) contributes to cardiovascular diseases by activating vasoactive peptides. The present study aimed to determine the effect of UII on aldosterone (ALD) and its receptor in cultured adventitial fibroblasts (AFs) and the tunica adventitia of rat vessels to explore the possible mechanisms underlying vascular remodeling. Expression levels of aldosterone and its receptor on tunica adventitia were determined using immunohistochemistry.

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.

Electrocardiographic characteristics in angiographically documented occlusion of the dominant left circumflex artery with acute inferior myocardial infarction: limitations of ST elevation III/II ratio and ST deviation in lateral limb leads.

Background: The prognosis of dominant left circumflex artery (LCx) occlusion-related inferior acute myocardial infarction (AMI) patients is poor, but the electrocardiographic (ECG) characteristics of this AMI entity have not been described.

Methods: One hundred thirty-five patients with first dominant right coronary artery (RCA) or dominant LCx-related inferior AMI were included. The characteristics of ECG obtained on admission for 55 patients with culprit lesions proximal to the first major right ventricular (RV) branch of dominant RCA (group proximal dominant RCA), 62 patients with culprit lesions distal to the first major RV branch of dominant RCA (group distal dominant RCA), and 18 patients with culprit lesions in dominant LCx (group dominant LCx) were compared.

Acute anterior wall myocardial infarction entailing ST-segment elevation in lead V3R, V1 or aVR: electrocardiographic and angiographic correlations.

Background: The correlation between ST-segment elevation (ST upward arrow) in lead V(3)R (ST upward arrow(V3R)), lead V(1) (ST upward arrow(V1)), and lead aVR (ST upward arrow(aVR)) during anterior wall acute myocardial infarction (AMI) and the culprit lesion site in the left anterior descending (LAD) coronary artery and the nature of the conal branch of the right coronary artery has not been thoroughly described.

Methods: One hundred forty-two patients with first anterior wall AMI were included. The 15-lead electrocardiogram with the standard 12 leads plus leads V(3)R through V(5)R showing the most pronounced ST-segment deviation before initiation of reperfusion therapy was evaluated and correlated with the exact LAD occlusion site in relation to the first septal perforator (S1) and the nature of the conal branch of the right coronary artery as determined by coronary angiography.