No abstract

Background The lymphatic system has been suggested to play an important role in cholesterol metabolism and cardiovascular disease. However, the relationships of vascular endothelial growth factor‐C ( VEGF ‐C), a central player in lymphangiogenesis, with mortality and cardiovascular events in patients with suspected or known coronary artery disease are unknown. Methods and Results We performed a multicenter, prospective cohort study of 2418 patients with suspected or known coronary artery disease undergoing elective coronary angiography. The primary predictor was serum levels of VEGF ‐C. The primary outcome was all‐cause death. The secondary outcomes were cardiovascular death, and major adverse cardiovascular events defined as a composite of cardiovascular death, non‐fatal myocardial infarction, and non‐fatal stroke. During the 3‐year follow‐up, 254 patients died from any cause, 88 died from cardiovascular disease, and 165 developed major adverse cardiovascular events. After adjustment for established risk factors, VEGF ‐C levels were significantly and inversely associated with all‐cause death (hazard ratio for 1‐ SD increase, 0.69; 95% confidence interval, 0.60–0.80) and cardiovascular death (hazard ratio, 0.67; 95% confidence interval, 0.53–0.87), but not with major adverse cardiovascular events (hazard ratio, 0.85; 95% confidence interval, 0.72–1.01). Even after incorporation of N‐terminal pro‐brain natriuretic peptide, contemporary sensitive cardiac troponin‐I, and high‐sensitivity C‐reactive protein into a model with established risk factors, the addition of VEGF ‐C levels further improved the prediction of all‐cause death, but not that of cardiovascular death or major adverse cardiovascular events. Consistent results were observed within 1717 patients with suspected coronary artery disease. Conclusions In patients with suspected or known coronary artery disease, a low VEGF ‐C value may independently predict all‐cause mortality.

This study was designed to examined the effects of inhalation anaesthetics on function and metabolism in isolated ischaemic rat hearts. Four volatile anaesthetics in two different concentrations (1.0 to 1.5 MAC) were used before whole heart ischaemia was induced for 15 min followed by reperfusion for 30 min. The data were compared with a control group in which inhalation anaesthetics were not used. Before ischaemia, volatile anaesthetics depressed ventricular function. During reperfusion, ventricular function and coronary flow in both halothane groups were significantly lower than those in the control group. Myocardial ATP concentrations in the 1.0 MAC of enflurane and isoflurane groups were significantly higher than those in the control group. We conclude that halothane had more depressant effects than the other anaesthetics and that enflurane and isoflurane may enhance metabolic recovery in the ischaemic working rat heart.

Atherosclerosis is a dise ase characterized by inflammation in the arterial wall. Atherogenesis is dependent on the innate immune response involving activation of Toll-like receptors (TLRs) and the expression of inflammatory proteins, those may lead to acute coronary syndrome (ACS). We investigated the expression level of TLR-4 in ACS, as compared with TLR-2 and patients with stable angina. Fifty-eight consecutive patients who underwent primary percutaneous coronary intervention (PCI, n = 29) because of ACS and elective PCI (n = 29) because of stable angina using a filter-device distal protection device system were prospectively analyzed. mRNA levels of TLR-2 and TLR-4 in debris containing various inflammatory tissues entrapped in the filter device were altogether analyzed using real-time PCR. There were no significant differences in age, sex distribution, between stable angina and ACS groups. TLR-4 expression levels were higher in patients with ACS than in patients with stable angina. TLR-4 might play a more important role than TLR-2 in atherogenesis, especially in ACS.

Background and objective: To clarify the clinical features of coronary artery spasm (CAS) with no significant coronary stenosis in patients with suspected acute coronary syndrome (ACS) in real practice. Methods: This is a retrospective observational study of patients with suspected ACS (n = 645) based on symptoms, electrocardiographic changes, and/or positive cardiac biomarkers and vasospastic angina (VSA, n = 90). ACS patients were divided into two groups: (1) organic ACS (n = 515), culprit lesion ≥75% coronary stenosis with/without thrombosis; (2) spastic ACS (n = 70), coronary stenosis <75%, either with positive acetylcholine (ACh) test (n = 51) or without ACh test but verified spontaneous spasm (n = 19). The study compared clinical characteristics among organic ACS, spastic ACS, and VSA. Results: One hundred and thirty suspected ACS patients had a coronary organic stenosis <75% (130/645, 20%). Seventy of those patients (70/130, 54%) were confirmed to have CAS, and these accounted for 11% of all ACS patients (70/645). The rate of cigarette smoking was highest in the spastic ACS. No spastic ACS patients died during their hospital stay or after discharge, whereas acute myocardial infarction occurred in 19%, aborted sudden cardiac death in 6%, multivessel spasm was provoked in 78%, and diffuse spasm was more frequently provoked than in the VSA group (82% vs. 62%). Conclusions: CAS is not a rare cause of ACS. Although the prognosis of spastic ACS is good, there are occasional critical cases. An initial differential diagnosis including an ACh test is thus important to decide the treatment strategy of ACS.