Citations

Background Experiments were designed to define cardiac function in dogs with single lung allografts during acute rejection of the allografted lung. Methods and Results Left lungs were either autotransplanted (n=4) or allotransplanted (n=8) in adult male mongrel dogs. All allotransplanted animals were maintained on triple-drug immunosuppression (cyclosporine, azathioprine, and steroids) for 5 days after the operation. In 4 allotransplanted animals, treatment was discontinued, allowing the animals to reject (usually after a further 3 days; rejecting group); 4 other allotransplanted animals were maintained on immunosuppression for an additional 3 days (immunosuppressed group). Another group of dogs were not operated on but were maintained on the same immunosuppression as the rejecting group (controls). All experimental animals underwent fast computed tomographic scanning with measurement of left ventricular pressure and calculation of ventricular chamber volumes, cross-sectional areas of coronary arteries, myocardial perfusion, and intramyocardial blood volume. Neither cardiac output, left ventricular mass, left ventricular pressure, nor myocardial oxygen consumption was altered during acute rejection of lung allografts. However, left ventricular contractility (systolic elastance, E max ) and ejection fraction were depressed to approximately one half ( P <.05) in acutely rejecting animals compared with other groups. The cross-sectional area of the coronary arteries was less in autotransplanted and allotransplanted treated animals than in animals that were not operated on. Cross-sectional area of the coronary arteries was decreased by an additional 30% in the rejecting group ( P <.05). Conclusions The results of this study indicate that acute rejection of a single lung allograft decreases cardiac performance and reduces diameter of coronary arteries in the recipient. Alterations of circulating humoral factors and activated leukocytes may contribute to these changes.

We report a case of transcatheter valve‐in‐valve therapy performed on an 85‐year‐old man with severe mitral bioprosthetic valve dysfunction. He was a high risk candidate for conventional surgery and he underwent placement of the Melody transcatheter heart valve into the mitral bioprosthesis via the right femoral vein.© 2012 Wiley Periodicals, Inc.

Abstract We tested whether the association between bone mineral density (BMD) and coronary artery calcification (CAC) varies according to dyslipidemia in community-living individuals. Between 2002 and 2005, 305 women and 631 men (mean age of 64 years), who were not taking lipid-lowering medications or estrogen were assessed for spine BMD, CAC, and total (TC), HDL- and LDL-cholesterol and triglycerides. Participants were a random sample from the Multi-Ethnic Study of Atherosclerosis (MESA) without clinical cardiovascular disease. Spine BMD at the L3 vertebrate was performed by computer tomography (CT). CAC prevalence was measured by CT. The total cholesterol to HDL ratio (TC:HDL) ≥ 5.0 was used as the primary marker of hyperlipidemia. The association of BMD with CAC differed in women with TC:HDL &lt; 5.0 versus higher (p-interaction = 0.01). In age- and race-adjusted models, among women with TC:HDL &lt; 5.0, each SD (43.4 mg/cc) greater BMD was associated with a 25% lower prevalence of CAC (prevalence ratio [PR] 0.75, 95% confidence interval [CI] 0.63–0.89), whereas among women with higher TC:HDL, higher BMD was not significantly associated with CAC (PR 1.22, 95% CI 0.82–1.82). Results were similar using other definitions of hyperlipidemia. In contrast, no consistent association was observed between BMD and CAC in men, irrespective of the TC:HDL ratio (p interaction 0.54). The inverse association of BMD with CAC is stronger in women without dyslipidemia. These data argue against the hypothesis that dyslipidemia is the key factor responsible for the inverse association of BMD with atherosclerosis. © 2011 American Society for Bone and Mineral Research

Background— Percutaneous repair has emerged as a potential therapy for patients with prosthetic paravalvular regurgitation. However, there is a relative paucity of data on the feasibility and outcome of this procedure. Methods and Results— All patients in whom percutaneous paravalvular regurgitation closure was attempted at our hospital were identified and included. Under echocardiographic and fluoroscopic guidance, patients underwent implantation of ≥1 an Amplatzer Septal Occluder, Duct Occluder, Muscular Ventricular Septal Defect Occluder, or Vascular Plug II. Percutaneous repair of 141 paravalvular defects was attempted in 115 patients (age, 67±12 years; men, 53%) with heart failure, hemolytic anemia, or both and who were at high risk of open surgery (mean estimated Society of Thoracic Surgeons mortality, 6.9%). Devices were implanted in 125 defects (89% of total defects), including in 19 patients with multiple defects. Because of the complexity of the procedures, wire exteriorization was required in 29 patients. Overall, successful percutaneous closure (defined as ≤1+ residual regurgitation) was achieved in 88 (77%) patients. Procedural time decreased with increasing case experience for percutaneous repair of both perimitral and periaortic defects. Overall, the 30-day complication rate was 8.7% (sudden and unexplained death, 1.7%; stroke, 2.6%; emergency surgery, 0.9%; bleeding, 5.2%). Two devices embolized during the procedure and were retrieved without sequelae. No procedural deaths occurred, but 2 (1.7%) patients died by 30 days. Conclusions— Percutaneous repair of paravalvular prosthetic regurgitation can be performed with a reasonable rate of procedural success and may be an initial therapeutic option, particularly in patients at significant risk for open surgery. Increased case experience is associated with shorter procedural time.

Although the Fontan procedure has been enormously successful in palliation of single-ventricle patients, many seem to experience progressive failure of the Fontan circulation over time. Ventricular assist devices (VADs) have developed into stable platforms for long-term support of adult patients with heart failure. Given the success of axial flow devices, it was hypothesized that the technology could provide clinical benefit to failing Fontan patients. The aim of this study was to use a computer model to evaluate VAD support in failing Fontan physiology. A computer model of Fontan circulation with heart failure was developed and the HeartMate II (HM II) (Thoratec Corp) axial flow ventricular assist device was connected to this model in a systemic configuration to examine its impact. Cardiac catheterization data from 7 patients (8 catheterization studies) with failing Fontan physiology were applied to this model to evaluate the impact of using the HM II in this manner. When the HM II was used in a systemic configuration at 8000 rpm, there was a 35% decrease in the systemic venous pressure in the Fontan circuit and a 63% decrease in pulmonary capillary wedge pressure with a resultant 41% increase in CI. The model also predicted patient-specific parameters where the VAD may not benefit the patient, such as fixed elevated pulmonary vascular resistance, low systemic ventricular end-diastolic pressure, and high unresponsive systemic vascular resistance. These data suggest a potential benefit from application of axial flow VAD technology in the management of failing Fontan physiology. Clinical correlation will allow for refinement of this model as a predictive tool in discerning which patients may benefit from placement of a VAD and what issues must be addressed prior to implanting the device.