Acute myocardial infarction of the right coronary artery originating from the distal left circumflex artery.

A case of acute myocardial infarction (AMI) of the distal left circumflex, near the origin of an aberrant right coronary artery is presented. Coronary stenting was successfully performed. According to several reports, this anomaly is a common site for coronary atherosclerosis, but this is the first report of AMI.

Cross-over trial of intensive monotherapy with atorvastatin and combined therapy with atorvastatin and colestimide for Japanese familial hypercholesterolemia.

BACKGROUND: In familial hypercholesterolemia (FH), low-density lipoprotein-cholesterol (LDL-C)-lowering therapy is important to avoid predisposition to coronary artery disease. This study investigated the advantages of combined therapy with atorvastatin and colestimide vs intensive monotherapy with atorvastatin. METHODS AND RESULTS: The trial used a randomized cross-over design consisting of 2 16-week periods of open-label drug therapy. Among the 24 initial patients, 17 heterozygous FH patients (age: 54.1 years; 5 males) were enrolled after 20 mg/day atorvastatin failed to achieve their target level. The patients received 20 mg/day atorvastatin and 3 g/day colestimide or 40 mg/day atorvastatin. Fifteen patients completed the trial and their LDL-C reduced from 5.07 +/- 1.10 mmol/L to 3.76 +/- 0.90 mmol/L with the combined therapy and to 3.81 +/- 0.50 mmol/L with the intensive monotherapy. Although the 2 therapies showed comparable mean effects for decreasing LDL-C, similar adverse reaction and cost, each therapy was predominantly more effective in some patients than in others. The triglyceride and high-density lipoprotein cholesterol levels were similar in both therapies. CONCLUSIONS: To achieve the therapeutic target of LDL-C level for refractory FH, the LDL-C-lowering therapy selected can be either intensive monotherapy or combined therapy as the next to standard statin therapy.

Upregulation of vascular extracellular superoxide dismutase in patients with acute coronary syndromes.

OBJECTIVE: We examined the vascular expression levels of extracellular superoxide dismutase (EC-SOD), a major antioxidant enzyme in the cardiovascular system, in patients with acute coronary syndromes. METHODS AND RESULTS: Twenty-one consecutive patients with acute myocardial infarction (AMI), 14 patients with unstable angina, 11 patients with stable angina, and 20 control subjects were studied. The levels of vascular EC-SOD expression were assessed by the difference in plasma EC-SOD concentrations before and after intravenous heparan injection. In the patients with AMI, vascular EC-SOD expression (ng/mL) was significantly higher on day 1 after the onset of AMI (148+/-10) as compared with the control subjects (116+/-6, P<0.05). The vascular EC-SOD expression returned to the normal range on day 7 (104+/-8), and that level persisted thereafter. The vascular EC-SOD expression was also significantly higher in the patients with unstable angina (160+/-13) than in those with stable angina (122+/-10) or in the controls (116+/-6) (P<0.05 each). Moreover, in the patients with AMI, higher levels of vascular EC-SOD expression on day 1 were significantly associated with smaller myocardial infarct size (P<0.05). CONCLUSIONS: This is the first clinical demonstration showing that vascular EC-SOD may be upregulated in acute coronary syndromes in humans in vivo. EC-SOD may play an important protective role against increased oxidative stress during acute ischemic coronary events.

Plasma level of homocysteine is inversely-associated with the development of collateral circulation in patients with single-vessel coronary artery disease.

Homocysteine induces endothelial injury and inhibits endothelial cell proliferation, which is a key role in angiogenesis. The purpose of this study was to investigate whether the plasma level of homocysteine is associated with the development of collaterals in patients with single-vessel coronary artery disease (CAD). Among a series of 105 male patients with angiographic estimation, 49 with single-vessel CAD were intensively investigated. Development of collaterals was classified by Rentrop's method. Univariate and multivariate analyses revealed that hyperhomocysteinemia negatively affected the development of collaterals (p=0.0015 and 0.0011, odds ratio 0.69, 95% confidence interval 0.52-0.90), whereas the duration of angina and percent stenosis evaluated by quantitative coronary angiography had a positive affect. Moreover, the level of homocysteine in the group with poorly developed collaterals (n=7, Rentrop class 0 and 1) was significantly higher than that in the group with well-developed collaterals (n=12, Rentrop class 2 and 3) of the patients with single-vessel disease showing total occlusion (p=0.034). This study clearly demonstrates that the plasma level of homocysteine is independently and inversely associated with the development of collateral circulation in CAD patients. Homocysteine might be a new undesirable aspect of ischemic heart disease through its inhibition of collateral development.