A comparative approach of four different image registration techniques for quantitative assessment of coronary artery calcium lesions using intravascular ultrasound.

In IVUS imaging, constant linear velocity and a constant angular velocity of 1800 rev/min causes displacement of the calcium in subsequent image frames. To overcome this error in intravascular ultrasound video, IVUS image frames must be registered prior to the lesion quantification. This paper presents a comprehensive comparison of four registration methods, namely: Rigid, Affine, B-Splines and Demons on five set of calcium lesion quantification parameters namely: (i) the mean lesion area, (ii) mean lesion arc, (iii) mean lesion span, (iv) mean lesion length, and (v) mean lesion distance from catheter. Using our IRB approved data of 100 patient volumes, our results shows that all four registrations showed a decrease in five calcium lesion parameters as follows: for Rigid registration, the values were: 4.92%, 5.84%, 5.89%, 5.27%, and 4.57%, respectively, for Affine registration the values were: 6.06%, 6.51%, 7.28%, 6.50%, and 5.94%, respectively, for B-Splines registration the values were: 7.35%, 8.03%, 9.54%, 8.18%, and 7.62%, respectively, and for Demons registration the five parameters were 7.32%, 8.02%, 10.11%, 7.94%, and 8.92% respectively. The relative overlap of identified lesions decreased by 5.91% in case of Rigid registration, 6.23% in case of Affine registration, 4.48% for Demons registration, whereas it increased by 3.05% in case of B-Splines registration. Rigid and Affine transformation-based registration took only 0.1936 and 0.2893 s per frame, respectively. Demons and B-Splines framework took only 0.5705 and 0.9405 s per frame, respectively, which were significantly slower than Rigid and Affine transformation based image registration.

Assessment of coronary risk based on cumulative exposure to lipids in systemic lupus erythematosus.

OBJECTIVE: To quantify the independent role of each of low-density lipoprotein cholesterol (LDL-C), total cholesterol:high-density lipoprotein cholesterol ratio (TC:HDL-C), triglyceride (TG) level, and HDL-C as a marker of coronary risk in systemic lupus erythematosus (SLE). METHODS: Patients with lipid measurements taken before a coronary event (or last clinic visit) were included. Mean and time-adjusted mean (TAM) levels were calculated for each lipid variable in each patient. Time-dependent proportional hazards regression models were used to quantify the risk of coronary event [myocardial infarction (MI) or angina], after adjustment for age. RESULTS: Among 384 patients, over a mean (SD) followup of 3.81 (2.58) years, there were 21 "first" coronary events (6 MI, 15 angina). Mean and TAM LDL-C (HR 1.83, 95% CI 1.19-2.81, p = 0.006), TC:HDL ratio (HR 1.43, 95% CI 1.02-2.00, p = 0.04), and TG (HR 2.11, 95% CI 1.32-3.39, p = 0.0019) were predictive of coronary event at subsequent visits. In contingency table analysis, TAM LDL-C cutpoint of 2.0 mmol/l had a sensitivity and negative predictive value for coronary event of 85.7% (95% CI 63.7-97.0) and 93.9% (95% CI 83.1-98.7), respectively. However, at this cutpoint the specificity was only 12.7% (95% CI 9.4-16.5). CONCLUSION: This study links LDL-C, TC:HDL-C ratio, and TG to coronary risk in patients with SLE and quantifies the magnitude of this risk. SLE-specific risk assessment levels for lipids may be selected to optimize positive or negative predictive values.

Enhanced Rho-kinase activity in circulating neutrophils of patients with vasospastic angina: a possible biomarker for diagnosis and disease activity assessment.

OBJECTIVES: The aim of this study was to examine whether Rho-kinase activity is systemically enhanced in patients with vasospastic angina (VSA) and, if so, whether a noninvasive diagnostic method could be developed to improve practice. BACKGROUND: The activated Rho-kinase pathway plays a central role in the molecular mechanism of coronary vasospasm in animal models and patients with VSA. Recently, it has been reported that Rho-kinase activity in circulating leukocytes is associated with various diseases. METHODS: Fifty-three consecutive patients with chest pain who underwent acetylcholine provocation testing for coronary spasm were examined. Patients were divided into 2 groups depending on their response to the test: VSA (n = 33) and non-VSA (n = 20) groups. Venous blood samples were collected to measure Rho-kinase activity in circulating neutrophils, determined by the extent of phosphorylation of myosin-binding subunit (MBS), a substrate of Rho-kinase. RESULTS: Rho-kinase activity was significantly higher in the VSA group than in the non-VSA group (phosphorylated MBS/total MBS ratio 1.33 ± 0.37 vs. 0.95 ± 0.22, p < 0.001). In the VSA group, no correlation was noted between Rho-kinase activity and high-sensitivity C-reactive protein, smoking, or accumulated number of coronary risk factors. After the 3-month medical treatment, Rho-kinase activity in the VSA group was significantly decreased to 1.08 ± 0.31 (p < 0.001). On receiver-operating characteristic curve analysis, a phosphorylated MBS ratio of 1.18 was identified as the best cutoff level to predict the diagnosis of VSA. CONCLUSIONS: These results indicate that Rho-kinase activity in circulating neutrophils is enhanced in patients with VSA and may be a useful biomarker for diagnosis and disease activity assessment of the vasospastic disorder.

[Assessment of myocardial fatty acid metabolism in patients with angina pectoris and diabetes mellitus using 123I-BMIPP myocardial scintigraphy].

PURPOSE: We studied the effect of myocardial ischemia and diabetes mellitus (DM) on the myocardial fatty acid metabolism using 123I-BMIPP myocardial scintigraphy. METHODS: We performed 123I-BMIPP myocardial scintigraphy in 50 patients with myocardial ischemia and without DM (AP), in 30 patients with myocardial ischemia and DM (AP + DM), 12 patients with DM and without myocardial ischemia (DM), and in 10 normal subjects (N). Myocardial uptake rate of 123I-BMIPP was obtained using the time activity curve. Myocardial washout rate of 123I-BMIPP was calculated using the polar images of early and delayed SPECT images. RESULTS: Myocardial uptake rate of 123I-BMIPP (%) were AP: 4.9 +/- 0.6, AP + DM: 5.5 +/- 0.5, DM 5.7 +/- 0.5 and N: 5.0 +/- 0.4. 123I-BMIPP myocardial uptake rate was increased in AP + DM and DM. 123I-BMIPP myocardial washout rate (%) were AP: 30.2 +/- 4.3, AP + DM: 24.5 +/- 3.9, DM: 16.1 +/- 2.8 and N: 19.4 +/- 3.2. 123I-BMIPP myocardial washout rate was increased in AP and AP + DM. 123I-BMIPP myocardial washout rate was increased particularly in patients with multi-vessels disease. 123I-BMIPP myocardial washout rate was decreased in DM. CONCLUSION: The present study suggested that diabetes mellitus increased myocardial fatty acid uptake and decreased myocardial fatty acid washout, and that myocardial ischemia increased myocardial fatty acid washout.

Delayed metabolic recovery of hibernating myocardium after percutaneous transluminal coronary angioplasty: assessment with iodine-123-betamethyl-p-iodophenyl-pentadecanoic acid imaging.

The time course of improvement in fatty acid metabolism after percutaneous transluminal coronary angioplasty (PTCA) was investigated using echocardiography and fatty acid metabolic imaging with iodine-123-betamethyl-p-iodophenyl-pentadecanoic acid (123I-BMIPP) before, 1 week and 3 months after PTCA in 31 patients with angina pectoris. Decreased left ventricular wall motion before PTCA improved 1 week after PTCA in 13 of 31 patients. 123I-BMIPP uptake was reduced in these 13 patients before PTCA, and did not improve 1 week after PTCA. Decreased myocardial uptake of 123I-BMIPP improved 1 week after PTCA in eight of 23 patients (group A). Thirteen patients in whom 123I-BMIPP uptake had not improved 1 week after PTCA showed a delayed recovery of 3 months after PTCA (group B). All patients in groups A and B showed improvement in wall motion 1 week after PTCA. Patients in group B had a higher incidence of unstable angina (77% vs 25%, p < 0.01), 99% or 100% stenosis (62% vs 13%, p < 0.01) and collateral vessels (46% vs 13%, p < 0.05) than those in group A. Serial fatty acid metabolic imaging with 123I-BMIPP after PTCA showed delayed metabolic recovery after improvement in wall motion in 13 of 23 patients. The presence of severe myocardial ischemia before PTCA enhanced the chronological discrepancies between the recovery of wall motion and fatty acid metabolism.

Effect of intracoronary nitroglycerin on myocardial blood flow and distribution in pacing-induced angina pectoris. Quantitative assessment by single-photon emission tomography.

Changes in regional coronary flow after administration of intracoronary nitroglycerin were assessed by measuring total coronary blood flow (using coronary sinus flow catheters) and its regional distribution (by quantitative single-photon emission tomography of injected radioactive microspheres). After pacing to angina, 10 patients with coronary artery disease received serial selective left coronary injections of technetium-99m microspheres, 40 micrograms of nitroglycerin, and indium-111 microspheres. Significant changes in coronary flow distribution were determined by subtracting prenitroglycerin from postnitroglycerin tomographic profiles. Perfusion of each myocardial segment was classified as normal mildly, moderately or severely compromised, based on upstream coronary anatomy. The overall increase in coronary flow was 23% in the normal territories and 33%, 44% and 15% (p less than 0.05), in the mildly, moderately and severely compromised territories, respectively, compared with control values. Thus, intracoronary nitroglycerin increased coronary blood flow to all perfusion territories. The increase in distribution of coronary flow was greatest in the mildly and moderately compromised regions and the least in the most severely compromised regions; this is probably a reflection of the underlying coronary reserve.