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Aim: To evaluate the additional benefit of visual and quantitative perfusion measurements compared with conventional real-time myocardial contrast echocardiography (MCE) in the detection of CAV., Methods and Results: Thirty patients (26 males, age 58 +/- 9.6 years) underwent dobutamine stress echocardiography (DSE) and myocardial perfusion imaging (MPI) as well as coronary angiography (CA) with intravascular ultrasound (IVUS). Ultrasound images were analysed off-line, evaluating (1) wall motion and thickening at high mechanical index ('conventional evaluation'), (2) the MCE loops stored during continuous infusion of contrast agent with regard to visual changes (stress vs. rest, 'visual grading'), and (3) the replenishment curves of the contrast agent at low mechanical index after bubble destruction ('quantitative grading'). CA/IVUS plus MPI showed ischaemia in seven and myocardial scars in nine patients. Sensitivity, specificity, NPV, PPV and accuracy for the detection of ischaemia representing functionally relevant CAV were, respectively, 0.71, 0.83, 0.90, 0.55 and 0.80 for the conventional evaluation alone, 0.71, 0.91, 0.91, 0.71 and 0.87 for additional visual grading and 0.86, 0.91, 0.95, 0.75 and 0.90 for additional quantitative grading., Conclusion: Real-time MCE including visual and quantitative analysis is feasible for screening patients after HTX and is highly accurate in the diagnosis of haemodynamically relevant CAV.

Ischemia -modified albumin was regarded as an early marker of cardiac ischemia. On the other hand, it has been reported that increased ischemia-modified albumin levels are associated with unstable plaque processes like percutaneous coronary intervention, acute coronary syndrome or myocardial infarction. This prospective study aimed to investigate the role of ischemia-modified albumin in patients with peripheral vascular disease undergoing peripheral vascular intervention, a plaque-altering procedure without evidence of tissue ischemia. Peripheral vascular intervention was performed in 21 consecutive patients (68.2+/-13.3 years) with typical leg claudication and documented peripheral vascular disease. Additionally, 96 consecutive patients (66+/-12.0 years) undergoing routine exercise stress test for the exclusion of functionally relevant coronary artery disease were defined as controls. It was assumed that in the latter patients no unstable plaque-altering processes were present. Blood samples were drawn before, and 30 min and 3 h after, revascularization in the peripheral vascular intervention group, as well as before, and 30 min and 3 h after, maximum stress testing in the control group, respectively. Ischemia-modified albumin levels were analyzed using the albumin cobalt-binding test. In patients undergoing peripheral vascular intervention, ischemia-modified albumin increased from 116.6+/-19.1 U/ml at baseline to 132.0+/-19.3 U/ml 30 min after intervention (+14.4+/-15.7%, P<0.001) and decreased to 123.5+/-17.8 U/ml 3 h later (-5.7+/-10.5%, P<0.001 compared with postintervention, P<0.001 compared with baseline). The control group showed a slight but significant decrease in ischemia-modified albumin from 103.0+/-11.0 to 100.2+/-11.6 U/ml poststress (-2.2+/-11.5%, P<0.05) and returned close to baseline 3 h later (101.8+/-10.3 U/ml, +2.4+/-10.9%, P=NS, compared with poststress and with baseline). For both groups, ischemia-modified albumin showed no correlation with albumin (at baseline P=0.62) and total protein (P=0.67), but significant correlation with creatinine (P=0.04) and C-reactive protein (P=0.02). In addition, ischemia-modified albumin was independent of age, sex, alanine aminotransferase, aspartate aminotransferase, creatine kinase, creatine kinase-MB, cholesterol, and triglycerides. This study showed an increased basal ischemia-modified albumin level in patients with peripheral vascular disease undergoing peripheral vascular intervention. Ischemia-modified albumin levels transiently increased shortly after peripheral vascular intervention, indicating a strong correlation between serum concentration of ischemia-modified albumin and processes associated with acute plaque disruption/rupture.