Faculty Bibliography

BACKGROUND: : In November 2005, a new automated distal anastomotic device (C-Port) for coronary artery bypass grafting (CABG) was cleared by the FDA for use in the United States. This study represents a prospective evaluation of our early experience using the device with graft patency assessment determined by 64 slice multidetector row computed tomography angiography (64CT). MATERIALS AND METHODS: : Patients undergoing coronary artery bypass were evaluated preoperatively by cine angiography for possible use of the C-Port system. A final decision for its use was made clinically at operation based on target vessel and vein graft specifications. Patency of the grafts was evaluated at 1 to 7 months (average 91 days) by 64CT with IRB approval and signed informed consent. RESULTS: : The C-Port device was used to form 69 distal anastomoses in 50 patients (46 CABG were performed off pump). There were eight misfires with no adverse effects for an immediate success rate of 88.4%. Thirty-five of 41 patients were available postoperatively for evaluation by 64CT (85.4% follow-up). There was one postoperative death. Seventeen sequential anastomoses were excluded because of inability to reliably evaluate patency by 64CT. Four 64CT scans were uninterpretable. For the remaining 31 patients, 64CT scans were used to evaluate for graft patency. The overall patency rate for all anastomoses was 94.5% (86/91) with selected patency for internal mammary artery of 100% (28/28), for C-Port connectors of 93.3% (42/45), and for hand-sewn venous end-to-side anastomosis of 88.9% (16/18). The difference in patency between C-Port anastomoses and hand sewn was not statistically significant (P = 0.62). CONCLUSIONS: : The C-Port system provides reliable and reproducible compliant automated distal venous anastomoses, which results in acceptable patency at intermediate follow-up. With proper training, the learning curve for using this connector system is relatively short and the need to abandon the procedure is low. 64CT is an excellent noninvasive method for cardiac surgeons and their institutions to accurately evaluate their actual surgical results.

Using cardiac magnetic resonance, the presence of myocardial delayed contrast enhancement (DCE) has been described in the ventricular septum at the level of the right ventricular insertion points in patients with pulmonary hypertension (PH). The aim of this study was to investigate the prevalence, extent, and correlates of this finding. Septal DCE was evaluated in 55 patients with known or suspected PH of various causes. The extent of DCE was estimated visually with an insertion enhancement score (range 0 to 4) and quantified as DCE mass. The results were correlated with cine magnetic resonance and right-sided cardiac catheterization. Predictors of DCE were investigated using multivariate analysis. PH at rest was present in 42 patients (group 1) and absent in 13 (group 2). DCE was noted in 41 patients (97%) in group 1 and 3 (23%) in group 2 (p <0.0001). The extent of DCE was higher in group 1 than group 2 (median insertion enhancement score 3 vs 0, median DCE mass 8.7 vs 0 g, respectively; p <0.0001 for both). The extent of DCE showed moderate to good univariate correlations (r = 0.5 to 0.73) with pulmonary pressures and with right ventricular volumes, mass, and ejection fractions. In multivariate analysis, systolic pulmonary pressure was the only predictor of DCE. In conclusion, the presence of septal DCE at the right ventricular insertion points is common in PH of different causes, and the level of systolic pulmonary pressure elevation appears to be the main determinant of this finding.

PURPOSE: To retrospectively identify pulmonary arterial (PA) flow parameters measured with phase-contrast magnetic resonance (MR) imaging that allow noninvasive diagnosis of chronic PA hypertension (PAH). MATERIALS AND METHODS: The study was HIPAA compliant and was approved by the institutional review board; a waiver of informed consent was obtained. Fifty-nine patients (49 female patients; mean age, 46 years; range, 16-85 years) known to have or suspected of having PAH underwent breath-hold phase-contrast MR imaging and right-sided heart catheterization (RHC). The presence of PAH (mean pulmonary artery pressure [mPAP], >25 mm Hg) was confirmed in 42 patients. Parameters, including PA areas, PA strain, average velocity, peak velocity, acceleration time, and ejection time, were measured in each patient by investigators blinded to RHC results. These measurements were correlated with mPAP, systolic pulmonary artery pressure (sPAP), and pulmonary vascular resistance index (PVRI). The diagnostic ability of phase-contrast MR imaging to depict PAH was quantified. Statistical tests included Spearman rho coefficients, receiver operating characteristic curve analysis, and Bland-Altman plots. RESULTS: Results showed average velocity to have the best correlation with mPAP, sPAP, and PVRI (r = -0.73, -0.76, and -0.86, respectively; P < .001). Average velocity (cutoff value = 11.7 cm/sec) revealed PAH with a sensitivity of 92.9% (39 of 42) and a specificity of 82.4% (14 of 17). Sensitivity and specificity for the minimum PA area (cutoff value = 6.6 cm(2)) were 92.9% (39 of 42) and 88.2% (15 of 17), respectively. CONCLUSION: The average blood velocity throughout the cardiac cycle is strongly correlated with pulmonary pressures and resistance.

PURPOSE: To retrospectively evaluate the accuracy and reproducibility of the cardiac magnetic resonance (MR) imaging-derived left ventricular septal-to-free wall curvature ratio for prediction of the right ventricular systolic pressure (RVSP) in patients clinically known to have or suspected of having pulmonary hypertension (PH), with same-day right-side heart catheterization (RHC) as the reference standard. MATERIALS AND METHODS: Institutional review board approval was received for this HIPAA-compliant study. Sixty-one patients clinically known or suspected of having PH underwent cardiac MR and RHC on the same day. Interventricular septal curvature (C(IVS)) and left ventricular free wall curvature (C(FW)) measured at end systole were used to derive the curvature ratio (C(IVS)/C(FW)). Effective distending transmural pressure (dP(FW)) and transseptal pressure gradient (dP(IVS)) were assumed to be equivalent, respectively, to the systolic blood pressure (SBP) and the difference between SBP and RVSP. Curvature ratio and SBP were used to noninvasively estimate RVSP. Linear regression analysis was performed to assess the difference between curvature ratio and rate of pressure rise (dP) ratio (dP(IVS)/dP(FW)). The accuracy of the dichotomized curvature ratio in PH detection was analyzed by using receiver operating characteristic (ROC) curves. RESULTS: PH, defined as RVSP higher than 40 mm Hg, was confirmed with RHC in 46 patients. A direct linear correlation between dP ratio and curvature ratio was observed (r = 0.85, P < .001). Bland-Altman analysis revealed moderate agreement between cardiac MR- and RHC-derived RVSPs (mean difference, -1.1 mm Hg +/- 15.9 [standard deviation]). ROC analysis of the accuracy of the curvature ratio for detection of increased RVSP revealed 87% sensitivity and 100% specificity (area under ROC curve, 0.95; P < .001). Intraobserver (r = 0.97) and interobserver (r = 0.95) curvature ratio measurements were closely correlated. CONCLUSION: In patients clinically known to have or suspected of having PH, cardiac MR-derived curvature ratio, as compared with RHC measurement, was an accurate and reproducible index for estimation of RVSP.

Decreased myocardial attenuation on contrast-enhanced multidetector computed tomography (MDCT) images can be observed in subjects with myocardial infarctions (MIs). It was hypothesized that myocardial hypoattenuation in MDCT can accurately detect the presence of a healed MI as determined by cardiac magnetic resonance delayed hyperenhancement (CMR-DH). Coronary MDCT and CMR-DH were performed in 42 subjects. Pre- and postcontrast MDCT images were analyzed for the presence of myocardial hypoattenuation, and volumes of MIs were quantified on MDCT and CMR-DH images in a blinded manner. The sensitivity, specificity, and negative and positive predictive values of postcontrast MDCT for the detection of MI were 91%, 81%, 83%, and 90%, respectively. MI sizes by postcontrast MDCT and by CMR-DH were strongly correlated (r=0.87, p<0.0001), although MDCT systematically underestimated MI volume (2.7+/-2.5 vs 25.9+/-19.9 ml, p<0.0001). MI size by MDCT was correlated negatively with the left ventricular ejection fraction (r=-0.62, p=0.03) and positively with left ventricular volumes (r=0.68 to 0.72, p<0.01). In 71% of subjects with MIs by CMR-DH, corresponding areas of hypoattenuation were noted also in precontrast MDCT. In conclusion, healed MIs can be detected as areas of myocardial hypoattenuation on MDCT images with high diagnostic accuracy, although their sizes are largely underestimated compared with CMR-DH. The presence of precontrast hypoattenuation suggests that mechanisms independent of reduced contrast delivery contribute to this finding.

Platelet-derived growth factor (PDGF) has protean manifestations, including the regulation of growth and migration, in many cell types. We have previously reported that PDGF-BB induces the accumulation of monocyte chemoattractant protein (MCP)-1 mRNA in smooth muscle cells (SMC), in large part due to an increase in mRNA stability. To elucidate the mechanism by which PDGF-BB stabilizes MCP-1 mRNA, we have employed in vitro RNA gel mobility shift and decay assays. Cytoplasmic extracts from PDGF-BB-treated SMC increased the half-life of in vitro transcribed MCP-1 mRNA from approximately 45 min to >2 h. PDGF-BB-inhibitable degradation was not dependent on specific regions of the MCP-1 mRNA and was equally effective on a variety of in vitro transcribed mRNAs. Angiotensin II had a similar effect on MCP-1 mRNA stability, whereas tumor necrosis factor-alpha and basic fibroblast growth factor did not. The PDGF-BB-inhibitable RNAse activity was active at pH 6.6 and heat stable, but was sensitive to proteinase K. Extracts from PDGF-BB- or angiotensin II-treated cells inhibited the RNAse activity of control extracts, suggesting that the effect of PDGF-BB and angiotensin II are due to activation of a soluble inhibitor of the RNAse. The effect of PDGF-BB was blocked by inhibitors of tyrosine phosphorylation, but not by inhibitors of phosphatidylinositol 3-kinase or mitogen-activated protein kinases. These studies provide new insights into the mechanisms by which PDGF-BB enhances mRNA accumulation.