Feasibility of ultra low-dose coronary computed tomography angiography.

There is an urgent need to develop new protocols to reduce radiation dose of coronary computed tomography angiography (CTA). The aim of this pilot study was to demonstrate the feasibility of an ultra-low dose CTA scanning.

Impact of Stress Cardiac Magnetic Resonance Imaging on Clinical Care.

Given the rising costs of imaging, there is increasing pressure to provide evidence for direct additive impact on clinical care. Appropriate use criteria (AUC) were developed to optimize test-patient selection and are increasingly used by payers to assess reimbursement. However, these criteria were created by expert consensus with limited systematic validation. The aims of this study were therefore to determine (1) rates of active clinical change resulting from stress cardiovascular magnetic resonance (CMR) imaging and (2) whether the AUC can predict these changes. We prospectively enrolled 350 consecutive outpatients referred for stress CMR. Categories of "active changes in clinical care" due to stress CMR were predefined. Appropriateness was classified according to the 2013 AUC. Multivariate logistic regression analysis was used to identify factors independently associated with active change. Overall, stress CMR led to an active change in clinical care in about 70% of patients. Rates of change in clinical care did not vary significantly across AUC categories (p = 0.767). In a multivariate model adjusting for clinical variables and AUC, only ischemia (odds ratio [OR] 6.896, 95% CI 2.637 to 18.032, p <0.001), known coronary artery disease (OR 0.300, 95% CI 0.161 to 0.559, p <0.001), and age (OR 0.977, 95% CI 0.954 to 1.000, p = 0.050) independently predicted significant clinical change. In conclusion, stress CMR made a significant impact on clinical management, resulting in active change in clinical care in about 70% of patients. AUC categories were not an independent predictor of clinical change. Clinical change was independently associated with the presence of ischemia, absence of known coronary artery disease, and younger age.

Downstream clinical consequences of stress cardiovascular magnetic resonance based on appropriate use criteria.

BACKGROUND: Appropriate use criteria (AUC) have been developed by professional organizations as a response to the rising costs of imaging, with the goal of optimizing test-patient selection. Consequently, the AUC are now increasingly used by third-party-payers to assess reimbursement. However, these criteria were created by expert consensus and have not been systematically assessed for CMR. The aim of this study was to determine the rates of abnormal stress-CMR and subsequent downstream utilization of angiography and revascularization procedures based on the most recent AUC. METHODS: 300 consecutive patients referred for CMR-stress testing were prospectively enrolled. Two cardiologists reviewed all clinical information before the CMR-stress test and classified the test as "appropriate', "maybe appropriate" or "rarely appropriate" according to the 2013 AUC. Patients were followed for 2 months for the primary outcomes of coronary angiography and/or revascularization. RESULTS: 49.7% of stress CMRs were appropriate, 36.7% maybe appropriate, and 13.6% rarely appropriate. Ischemia was significantly more likely to be seen in the appropriate (18.8%) or maybe appropriate groups (21.8%) than the rarely appropriate group (4.8%) (p = 0.030 and p = 0.014 respectively). Referral for cardiac catheterization was not significantly different in the appropriate (10.1%) and maybe appropriate groups (10.0%) compared to the rarely appropriate group (2.4%) (p = 0.119 and p = 0.127 respectively). No patients undergoing catheterization in the rarely appropriate group went on to require revascularization, in contrast to 53.3% of the appropriate vs 36.4% of the maybe appropriate patients (p = 0.391). Presence of ischemia led to referral for cardiac catheterization in 50.0% of the appropriate group vs 33.3% of the maybe appropriate group (p = 0.225); in contrast to none of the rarely appropriate group. CONCLUSIONS: The great majority of tests were classified as appropriate or maybe appropriate. Downstream cardiac catheterization rates were similar in all 3 groups. However, rarely appropriate studies never required revascularization, suggesting suboptimal resource utilization. Studies classified as maybe appropriate had similar rates of abnormal findings and led to similar rates of downstream catheterization and revascularization as those that were deemed appropriate. This suggests that consideration could be given to upgrading some of the common maybe appropriate indications to the appropriate category.

The effects of modulating eNOS activity and coupling in ischemia/reperfusion (I/R).

The in vivo role of endothelial nitric oxide synthase (eNOS) uncoupling mediating oxidative stress in ischemia/reperfusion (I/R) injury has not been well established. In vitro, eNOS coupling refers to the reduction of molecular oxygen to L-arginine oxidation and generation of L-citrulline and nitric oxide NO synthesis in the presence of an essential cofactor, tetrahydrobiopterin (BH(4)). Whereas uncoupled eNOS refers to that the electron transfer becomes uncoupled to L-arginine oxidation and superoxide is generated when the dihydrobiopterin (BH(2)) to BH(4) ratio is increased. Superoxide is subsequently converted to hydrogen peroxide (H(2)O(2)). We tested the hypothesis that promoting eNOS coupling or attenuating uncoupling after I/R would decrease H(2)O(2)/increase NO release in blood and restore postreperfused cardiac function. We combined BH(4) or BH(2) with eNOS activity enhancer, protein kinase C epsilon (PKC ε) activator, or eNOS activity reducer, PKC ε inhibitor, in isolated rat hearts (ex vivo) and femoral arteries/veins (in vivo) subjected to I(20 min)/R(45 min). When given during reperfusion, PKC ε activator combined with BH(4), not BH(2), significantly restored postreperfused cardiac function and decreased leukocyte infiltration (p < 0.01) while increasing NO (p < 0.05) and reducing H(2)O(2) (p < 0.01) release in femoral I/R veins. These results provide indirect evidence suggesting that PKC ε activator combined with BH(4) enhances coupled eNOS activity, whereas it enhanced uncoupled eNOS activity when combined with BH(2). By contrast, the cardioprotective and anti-oxidative effects of the PKC ε inhibitor were unaffected by BH(4) or BH(2) suggesting that inhibition of eNOS uncoupling during reperfusion following sustained ischemia may be an important mechanism.

Inguinal lymph node metastasis of colon cancer.

We present a case of adenocarcinoma of colon with unusual metastasis to inguinal lymph nodes. Our patient is a young male with bilateral inguinal lymphadenopathy, bone pains, and jaundice who presented as carcinoma of unknown primary. He was diagnosed as widely metastatic adenocarcinoma of colon for which he received chemotherapy and has had a good response to the treatment.

The role of tetrahydrobiopterin and dihydrobiopterin in ischemia/reperfusion injury when given at reperfusion.

Reduced nitric oxide (NO) bioavailability and increased oxidative stress are major factors mediating ischemia/reperfusion (I/R) injury. Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury. The effects of BH(4) and BH(2) on oxidative stress and postreperfused cardiac functions were examined in ex vivo myocardial and in vivo femoral I (20 min)/R (45 min) models. In femoral I/R, BH(4) increased NO and decreased H(2)O(2) releases relative to saline control, and these effects correlated with improved postreperfused cardiac function. By contrast, BH(2) decreased NO release relative to the saline control, but increased H(2)O(2) release similar to the saline control, and these effects correlated with compromised postreperfused cardiac function. In conclusion, these results suggest that promoting eNOS coupling to produce NO and decrease H(2)O(2) may be a key mechanism to restore postreperfused organ function during early reperfusion.