Plasma levels of soluble thrombomodulin, C-reactive protein, and serum amyloid A protein in the atherosclerotic coronary circulation.

Plasma levels of C-reactive protein (CRP) and serum amyloid A protein (SAA), inflammatory markers, and soluble thrombomodulin (s-TM), a marker of endothelial damage. are thought to be related to coronary artery disease. However, the relationship between these inflammatory markers and endothelial injury in atherosclerotic coronary arteries is still unclear. Fifty-five patients who underwent coronary angiography were classified into 3 groups according to the severity of left coronary arterial atherosclerosis evaluated by the Gensini score (GS; normal: score = 0, n = 15; mild: 0 < score < 15, n = 29; severe: score > or = 15, n = 11). Blood samples were obtained from the aortic root (Ao) and coronary sinus (CS) and plasma CRP and SAA levels were measured by latex turbidimetric immunoassays, and s-TM levels were determined by an enzyme-linked immunosorbent assay. The difference between marker concentrations in the Ao and CS of the coronary circulation was expressed as the coronary sino-arterial (CS-Ao) difference. The CS-Ao differences of s-TM and SAA were significantly higher in patients with severe atherosclerosis than in normal patients (P < 0.01), and showed weak but significant positive correlations with the GS (r = 0.34, P < 0.01 and r = 0.33, P < 0.05, respectively). The CS-Ao differences in CRP did not differ among the three groups, and did not correlate with the GS. The results of our study reveal a possible relationship between endothelial cell injury and inflammation in atherosclerotic coronary arteries.

Pulse-spray thrombolysis in acute myocardial infarction caused by thrombotic occlusion of an ectatic coronary artery.

Pulse-spray thrombolysis was performed in 2 patients with acute myocardial infarction (AMI) caused by thrombotic occlusion of coronary artery ectasia. Case 1, a 66-year-old woman with an inferior AMI underwent emergency coronary arteriography, which revealed occlusion of an ectatic right coronary artery. Primary balloon angioplasty failed to reestablish distal flow. Urokinase was administered through the pulse-spray infusion catheter (UltraFuse) and intravenous recombinant tissue plasminogen activator was also administered. Angiographic disappearance of the thrombus was observed within 30 min of starting the infusion, and there was only mild irregularity in the ectatic coronary artery. Case 2, a 45-year-old man with an inferior AMI underwent emergency coronary arteriography, which revealed occlusion of an ectatic right coronary artery. TIMI-3 flow was soon obtained after administration of 480,000 units of urokinase through the pulse-spray infusion catheter. There was diffuse right coronary ectasia without angiographic evidence of coronary stenosis. Coronary ectasia sometimes develops into AMI without the coexistence of coronary stenosis. Because a massive thrombus plays a major role, pulse-spray thrombolysis is a possible treatment in coronary artery ectasia with thrombotic occlusion.

Levels of soluble E-selectin and ICAM-1 in the coronary circulation of patients with stable coronary artery disease: association with the severity of coronary atherosclerosis.

The recruitment of circulating leukocytes to atherosclerotic sites is mediated by a family of adhesion molecules. The objective of the present study was to evaluate the relationship between circulating adhesion molecule levels in the coronary circulation and the severity of coronary atherosclerosis in patients with stable coronary artery disease. The subjects were 79 patients undergoing coronary angiography. According to the severity of coronary atherosclerosis as assessed by the Gensini Score (GS) of the left coronary artery, they were classified into three groups: group C (no organic stenosis, score 0, n = 14), group M (mild organic stenosis, score 1-13, n = 39) and group S (severe organic stenosis, score > or = 14, n = 26). Blood samples were taken from the aorta (Ao) and coronary sinus (CS), and plasma levels of soluble E-selectin (sE-selectin) and soluble intercellular adhesion molecule-1 (sICAM-1) were measured by enzyme-linked immunosorbent assay. These levels were then compared between groups. There were no significant differences in plasma sICAM-1 levels in the Ao or CS between the three groups. The difference in sICAM-1 levels between the CS and Ao (CS-Ao) also showed no significant difference. Plasma sE-selectin levels in both the Ao and CS were significantly higher in group S than in groups C and M (p < 0.05), but there were no significant differences in CS-Ao. There was a weak but significant correlation between the plasma levels of these adhesion molecules and the number of coronary risk factors present. Multivariate analysis showed that the number of coronary risk factors was the only positive predictor (p = 0.0048) of the GS; there was no association between the plasma level of either adhesion molecule and the GS. In patients with stable coronary artery disease, sICAM-1 plasma levels do not indicate the severity of coronary atherosclerosis, while sE-selectin plasma levels appear to reflect the severity of systemic rather than coronary atherosclerosis.

Hemodynamic basis of the reduced oxygen uptake relative to work rate during incremental exercise in patients with chronic heart failure.

BACKGROUND: The ratio of the increase in oxygen uptake to the increase in work rate (DeltaVO2/DeltaWR) during incremental exercise is reduced in patients with severe chronic heart failure (CHF). However, the pathophysiological basis of the reduced O2 uptake relative to work rate has not been elucidated. METHODS: To elucidate the hemodynamic basis of the reduced ratio of DeltaVO2/DeltaWR during exercise in severe CHF, 48 patients with CHF (15 patients in class I, 21 in class II and 12 in class III) performed maximal ergometer exercise with respiratory gas analysis. Cardiac output and systemic O2 extraction were measured at 1-min intervals during exercise. RESULTS: Both peak VO2 and peak cardiac output decreased as the severity of CHF advanced. Patients in class III showed significantly reduced DeltaVO2/DeltaWR than those in class I (8.2+/-0.9 vs. 9.8+/-1.5 ml/min/W, P<0.01). Cardiac output at rest was significantly lower, and O2 extraction at rest was significantly higher in class III than class I. The ratio of the increase in cardiac output to the increase in work rate (DeltaCO/DeltaWR) was significantly lower in class III than class I (42.5+/-14.5 vs. 60.6+/-10.3 ml/min/W), and the ratio of the increase in O2 extraction to the increase in work rate (DeltaO2 extraction/DeltaWR) was significantly higher in class III than class I (0.45+/-0.13 vs. 0.34+/-0.08%/W). The DeltaVO2/DeltaWR was significantly correlated with the DeltaCO/DeltaWR (r=0.67, P<0.01), and the DeltaCO/DeltaWR was inversely correlated with DeltaO2 extraction/DeltaWR (r=-0.65, P<0.01). CONCLUSIONS: Decreased O2 supply due to reduced cardiac output was not fully compensated by the increased O2 extraction. Reduced ratio of DeltaVO2/DeltaWR in advanced CHF reflected the severely attenuated cardiac output response to exercise.

Limited role of coronary angioplasty and stenting in coronary spastic angina with organic stenosis.

OBJECTIVES: We investigated the efficacy of percutaneous coronary intervention (PCI) in patients with coronary spastic angina (CSA) and severe organic stenosis. BACKGROUND: Coronary spasm occurs at the site of organic stenosis in most patients with CSA and severe stenosis, whereas multivessel spasm occurs frequently in those with normal coronary arteries. The incidence of multivessel spasm and the efficacy of PCI in patients with CSA and severe stenosis have not been fully elucidated. METHODS: Forty-five patients with CSA and severe stenosis underwent spasm provocative testing with intracoronary acetylcholine before and 7 +/- 3 months after PCI (20 patients had angioplasty and 25 patients had stenting), when all patients were free of restenosis. RESULTS: Spasm was induced at the site of severe stenosis in 30 patients (66.7%) with (n = 12) or without (n = 18) spasm induced in another vessel. In the remaining 15 patients, spasm was induced at a different site in the stenotic vessel and/or in another vessel. Repeat provocative tests were performed in 43 of 45 patients. Although spasm was never induced at exactly the same site of the initial stenosis that had been dilated, spasm was induced at a different site in the dilated vessel and/or in another vessel, in 33 (76.7%) of 43 patients. Multivessel spasm occurred in 28 (62.2%) of 45 patients on one or both provocations. CONCLUSIONS: Spasm was frequently induced at a site different from the initial stenosis, even in the absence of restenosis after PCI. Calcium antagonists should be continued in most patients with CSA who show no restenosis after PCI.