The level of circulating soluble elastin (CSE) is reported to increase proportionally with the degree of clinical atherosclerosis; however, its diagnostic use is limited because CSE also increases with age. We aimed to investigate whether alterations in CSE concentrations are implicated in potential cardiovascular dysfunctions (indicated by standard physiological parameters) in medical check-up individuals, taking age into consideration.In a total of 531 individuals (age 20-89 years), CSE levels were correlated most significantly with age. The groups of male and female individuals were each further divided into two subgroups: those with higher and those with lower CSE levels than the reference values determined by polynomial regression.Male participants with lower CSE levels (n = 128) than the age-adjusted reference baseline levels showed higher serum glucose (P < 0.008), uric acid (P < 0.008) and triglyceride (P < 0.02) levels than those with higher CSE levels (n = 126). However, most of the parameters tested in female participants with lower CSE levels (n = 140) were statistically comparable to those with higher CSE levels (n = 137). The ratio of CSE level to the age-adjusted reference level was calculated in each of the male participants, and declines in the ratio were significantly correlated with increases of serum glucose, uric acid and triglyceride levels (P < 0.005, P < 0.02 and P < 0.006, respectively).The decrease in age-adjusted CSE levels is a potential indicator of eventual cardiovascular dysfunction in medical check-up individuals, as predicted by the risk factors dyslipidemia, hyperuricemia or diabetes.
1830 Objectives The presence, severity, and extent of left ventricular mechanical dyssynchrony (LVMD) have not been fully clarified in patients with end-stage renal disease (ESRD). Abnormal loading has capability to enhance Left ventricular mechanical dyssynchrony (LVMD) in patients with ESRD. The aim of this study was to assess the severity of LVMD and its relation to systolic function in ESRD. Methods A total of 219 patients (age 69 ± 10, 156 men) with chronic kidney disease (CKD) underwent stress/rest gated myocardial perfusion SPECT (GMPS). For the evaluation of LVMD, histogram bandwidth (HBW) and phase standard deviation (PSD) were determined by GMPS using phase analysis. LVMD was compared among three groups without ischemia (SSS > 3): 42 patients with CKD stage1 and 2, 54 patients with CKD stage 3 and 4, and 10 patients with CKD stage 5 defined as ESRD. Results Both HBW and PSD was significant negative correlated with LVEF in all 106 patients without ischemia. HBW in ESRD were significantly greater than those of CKD stage 1-2 and 3-4 (ESRD vs. CKD 1-2, p Conclusions LVMD was demonstrated to be enhancement in ESRD
We measured serial changes in myosin light chain-I (MLC-I) in 19 patients undergoing coronary recanalization for evolving myocardial infarction to elucidate whether analysis of MLC-I release kinetics is useful for the evaluation of myocardial salvage following coronary recanalization therapy.All patients had a left anterior descending artery lesion (#6 or #7 according to the American Heart Association classification) in the infarction related artery, and received intravenous or intracoronary administration of tissue plasminogen activator or urokinase within 6 hours after the onset except for 3 cases with spontaneous recanalization and 2 cases with direct percutaneus transluminal coronary angioplasty (PTCA). Six control patients with left anterior descending artery lesions in the infarction related artery were given conventional therapy using intravenous urokinase without emergent coronary angiography.The release kinetics of MLC-I following coronary recanalization therapy were divided into three patterns. Group A (n=7) showed two peaks with a larger first peak and a smaller second peak. Group B (n=5) showed two peaks with a smaller first peak and a larger second peak. Group C (n=7) showed a single late peak pattern of MLC-I release kinetics. The time need to obtain recanalization on coronary angiography was significantly longer in Group A compared to Groups B and C (5.72±1.11, n=6 vs 3.84+0.80 hours n=6, p<0.05). The left ventricular ejection fraction (LVEF) at the convalescent stage in Group A was significantly lower than that in Groups B and C (44.4+13 vs 62.0+15.0%, p<0.05).Patients showing a two-peaked pattern with a larger first peak were consistent with patients with late repertused, less salvaged, and more depressed left ventricular function at the convalescent stage. MLC-I release kinetics were influenced by the wash-out phenomenon in cases of late reperfusion.
Myocardial bridge (MB) is a congenital anomaly of the coronary artery and may occur in 5 to 12% of the human population. However, the mechanism of MB-induced myocardial ischemia is still speculative. We report 2 cases of variant form angina pectoris associated with MB in which myocardial ischemia seemed to be related to the interaction between coronary perfusion and MB. In case 1, electrocardiography during anginal attack at rest showed ST elevation in the inferior leads and MB was observed after percutaneous transluminal coronary angioplasty at the site of the right coronary artery lesion following successful dilatation. In case 2, MB of the left anterior descending coronary was located in the identical portion where coronary vasospasm was induced by intracoronary acetylcholine injection, although ischemia during the spontaneous anginal attack was limited to the inferior area of myocardium. These 2 cases suggest that MB can be, at least in some patients, one of the possible causes of the endothelial damage which seems to be related to coronary vasospasm; this was documented in both cases.
