The external elastic lamina (EEL) serves as a barrier for cells and macromolecules between the media and adventitia in the vascular wall. We evaluated the morphological changes and quantitative assessments of the EEL architecture in the coronary circulation of pigs fed with a high cholesterol diet. Confocal microscopy analysis of the EEL from hypercholesterolemic coronary arteries revealed an altered pattern characterized by fragmentation and disorganization of the EEL associated with an increase in the thickness. Computerized digital analysis of the images obtained by confocal scanning microscopy demonstrated that compared to normal coronary arteries, the EEL of hypercholesterolemic coronary arteries decreased in the percentage of their elastin content (30.80 +/- 1.64% vs. 47.85 +/- 1.82%, p = 0.001). The percentage of elastin content was negatively correlated with the vessel wall area (r = -0.82, p = 0.001). The immunoreactivity for matrix metalloproteinase-3 (MMP-3) increased in cholesterol-fed coronary arteries, predominantly in the neointima and adventitia. This study demonstrates that experimental hypercholesterolemia induced ultrastructural changes of the EEL in coronary circulation. The EEL may also be an atherosclerosis-prone area compared with the intima. The EEL may play an important role in the development of structural changes which characterizes the early phase of coronary atherosclerosis and vascular remodeling.
Animal ; Arteries/ultrastructure ; Arteries/enzymology ; Coronary Vessels/ultrastructure* ; Coronary Vessels/enzymology ; Elastic Tissue/ultrastructure* ; Elastic Tissue/enzymology ; Female ; Hypercholesterolemia/pathology* ; Hypercholesterolemia/enzymology ; Stromelysin 1/metabolism ; Swine

OBJECTIVETo investigate electrocardiographic (ECG) and angiographic characteristics of patients with acute solitary posterior myocardial infarction. Patients complicated by inferior wall or right ventricular infarction were excluded.

METHODECG and angiographic changes in 11 patients with acute solitary posterior myocardial infarction admitted to our emergency room from 2001 to 2006 were analyzed.

RESULTSBesides typical ST segment elevation in V(7)-V(9) leads, other ECG manifestations in these patients included V(1)-V(2) R/S > or = 1 (9/11, 81.8%), 1 - 2 mm ST depression in V(1)-V(4) (5/11, 45.5%), 0.5 - 1.5 mm ST elevation in I, aVL leads (4/11, 36.4%) and 0.5 - 1.5 mm ST elevation in V(5)-V(6) leads (5/11, 45.5%). Coronary angiography showed that left circumflex artery (LCX) was the infarction related artery in all cases. The infarction area located before OM1 origination in 1 patient with a 95% pipe-like stenosis (1/11), after OM1 origination in 6 patients (6/11, 4 with total occlusion, 1 with sub-total occlusion and 1 with 90% long length stenosis), in OM1 in 4 patients (4/11, 2 with total occlusion, 1 with sub-total occlusion and 1 with 95% local stenosis). There were 3 patients (27.3%) with single vessel lesion, 4 patients (36.4%) combined with left anterior descending artery (LAD) lesion, 2 patients (18.2%) combined with right coronary artery (RCA) lesion and 2 patients (18.2%) combined with LAD and RCA lesions.

CONCLUSIONSAcute posterior myocardial infarction should be suspected with V(1)-V(2) R/S > or = 1 and V(1)-V(4) ST depression in standard 12 leads ECG. Besides symptoms and cardiac enzyme measurements, recording posterior leads electrocardiogram and performing coronary angiography will help to make the correct diagnosis.

Aged ; Coronary Angiography ; Coronary Vessels ; physiopathology ; Electrocardiography ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; diagnostic imaging ; physiopathology ; Myocardium ; enzymology

OBJECTIVEKawasaki disease (KD) is an acute and self-limited systemic vasculitis syndrome of unknown origin that mainly affects small and medium-sized arteries, particularly the coronary arteries, which is followed by aneurysm formation. Increased levels of matrix metalloproteinase-1 (MMP-1) have been detected in aortic aneurysms in adults, suggesting an important role of MMP-1 in arterial wall destruction and resultant aneurysm formation. The aim of this study was to investigate the potential role of MMP-1 in the pathogenesis of coronary artery lesions in patients with KD.

METHODSForty patients with KD, including 23 patients without coronary artery lesions (CAL) and 17 patients with CAL, as well as age-matched 10 febrile and 10 healthy afebrile controls were studied. The duration of KD was divided into three phases: the acute phase, the subacute phase and the convalescent phase. Enzyme-linked immunosorbent assay was used to detect the protein levels of MMP-1 in the sera. MMP-1 mRNA expression in the circulating leucocytes was studied using reverse transcription-polymerase chain reaction.

RESULTSLevels of MMP-1 protein in serum and MMP-1 mRNA expression in the leucocytes were significantly elevated at the acute phase in the two groups of KD patients (CAL group: 14.91 +/- 3.88 ng/ml and 0.89 +/- 0.15 ng/ml; NO-CAL group: 11.27 +/- 3.28 ng/ml and 0.77 +/- 0.14, respectively), compared with febrile (7.05 +/- 1.98 ng/ml and 0.45 +/- 0.12 ng/ml, respectively) and afebrile (5.13 +/- 1.20 ng/ml and 0.29 +/- 0.12 ng/ml, respectively) controls (P < 0.01). Furthermore, MMP-1 protein and MMP-1 mRNA levels were significantly higher in KD patients with CAL than in KD patients without CAL (P < 0.05). There was a significantly positive correlation between the serum protein level of MMP-1 at the acute phase of KD and the circulating leucocytes counts (r = 0.750, P < 0.01). The MMP-1 serum protein level and mRNA expression in the leucocytes at the acute phase of the two KD groups decreased obviously from the subacute through the convalescent phases (P < 0.05 or P < 0.01).

CONCLUSIONThe expression of MMP-1 at the acute phase of KD was significantly elevated, especially in KD patients with CAL. MMP-1 might be involved in the formation of coronary artery lesions and pathogenesis of KD.

Acute Disease ; Child, Preschool ; Coronary Aneurysm ; enzymology ; etiology ; pathology ; Coronary Vessels ; pathology ; Enzyme-Linked Immunosorbent Assay ; Fever ; etiology ; Humans ; Infant ; Leukocytes ; enzymology ; Male ; Matrix Metalloproteinase 1 ; blood ; genetics ; Mucocutaneous Lymph Node Syndrome ; complications ; diagnosis ; RNA, Messenger ; blood ; Reverse Transcriptase Polymerase Chain Reaction ; Severity of Illness Index

Polymorphism of angiotensin converting enzyme (ACE) gene is reported to be associated with ischemic heart disease, hypertrophic cardiomyopathy, and idiopathic dilated cardiomyopathy. In this study, we investigated the relationship between Kawasaki disease and insertion/deletion polymorphism of ACE gene. Fifty five Kawasaki disease patients and 43 healthy children were enrolled. ACE genotype was evaluated from each of the subjects' DNA fragments through polymerase chain reaction (PCR). Frequencies of ACE genotypes (DD, ID, II) were 12.7%, 60.0%, 27.3% in Kawasaki group, and 41.9%, 30.2%, 27.9% in control group respectively, indicating low rate of DD and high rate of ID genotype among Kawasaki patients (p<0.01). Comparing allelic (I, D) frequencies, I allele was more prevalent in Kawasaki group than in control group (57.3% vs. 43.0%, p<0.05). In Kawasaki group, both genotype and allelic frequencies were not statistically different between those with coronary dilatations and those without. ACE gene I/D polymorphism is thought to be associated with Kawasaki disease but not with the development of coronary dilatations.
*Polymorphism, Genetic ; Peptidyl-Dipeptidase A/*genetics ; Mucocutaneous Lymph Node Syndrome/*enzymology/*genetics/pathology ; Male ; Infant ; Humans ; Genotype ; Gene Frequency ; Female ; Dilatation, Pathologic ; Coronary Vessels/pathology ; Child, Preschool ; Case-Control Studies ; Alleles

BACKGROUNDSalvianolic acid B (Sal B) is a bioactive water-soluble compound of Salviae miltiorrhizae, a traditional herbal medicine that has been used clinically for the treatment of cardiovascular diseases. This study sought to evaluate the effect of Sal B on matrix metalloproteinase-9 (MMP-9) and on the underlying mechanisms in tumor necrosis factor-α± (TNF-α±)-activated human coronary artery endothelial cells (HCAECs), a cell model of Kawasaki disease.

METHODSHCAECs were pretreated with 1-10 αμmol/L of Sal B, and then stimulated by TNF-α± at different time points. The protein expression and activity of MMP-9 were determined by Western blot assay and gelatin zymogram assay, respectively. Nuclear factor-κB (NF-κB) activation was detected with immunofluorescence, electrophoretic mobility shift assay, and Western blot assay. Protein expression levels of mitogen-activated protein kinase (c-Jun N-terminal kinase [JNK], extra-cellular signal-regulated kinase [ERK], and p38) were determined by Western blot assay.

RESULTSAfter HCAECs were exposed to TNF-α±, 1-10 αμmol/L Sal B significantly inhibited TNF-α±-induced MMP-9 expression and activity. Furthermore, Sal B significantly decreased IκBα± phosphorylation and p65 nuclear translocation in HCAECs stimulated with TNF-α± for 30 min. In addition, Sal B decreased the phosphorylation of JNK and ERK1/2 proteins in cells treated with TNF-α± for 10 min.

CONCLUSIONSThe data suggested that Sal B suppressed TNF-α±-induced MMP-9 expression and activity by blocking the activation of NF-κB, JNK, and ERK1/2 signaling pathways.

Benzofurans ; pharmacology ; Blotting, Western ; Cell Line ; Cell Survival ; drug effects ; Coronary Vessels ; cytology ; Endothelial Cells ; drug effects ; enzymology ; Humans ; Matrix Metalloproteinase 9 ; metabolism ; NF-kappa B ; metabolism ; Tumor Necrosis Factor-alpha ; pharmacology