An isolated working heart system for large animal models.

Since its introduction in the late 19(th) century, the Langendorff isolated heart perfusion apparatus, and the subsequent development of the working heart model, have been invaluable tools for studying cardiovascular function and disease(1-15). Although the Langendorff heart preparation can be used for any mammalian heart, most studies involving this apparatus use small animal models (e.g., mouse, rat, and rabbit) due to the increased complexity of systems for larger mammals(1,3,11). One major difficulty is ensuring a constant coronary perfusion pressure over a range of different heart sizes - a key component of any experiment utilizing this device(1,11). By replacing the classic hydrostatic afterload column with a centrifugal pump, the Langendorff working heart apparatus described below allows for easy adjustment and tight regulation of perfusion pressures, meaning the same set-up can be used for various species or heart sizes. Furthermore, this configuration can also seamlessly switch between constant pressure or constant flow during reperfusion, depending on the user's preferences. The open nature of this setup, despite making temperature regulation more difficult than other designs, allows for easy collection of effluent and ventricular pressure-volume data.

Impact of major bleeding on long-term mortality in anemic versus nonanemic patients undergoing percutaneous coronary intervention using bivalirudin.

Bleeding complications after percutaneous coronary intervention (PCI) have been associated with higher short and long-term mortality. Bivalirudin has been shown to reduce bleeding complications in patients who underwent PCI; however, the impact of anemia on bleeding complications and long-term mortality has not been studied. A total of 11,991 patients who underwent PCI over a period of 8 years with bivalirudin as the primary antithrombotic agent were included. Anemia was defined according to the World Health Organization definition. Bleeding complications were prospectively collected. Survival analysis was performed using multivariable Cox proportional hazards models. Of the 11,991 patients, 4,815 patients (40%) had baseline anemia. Major bleeding occurred in 3.3% of patients with anemia compared with 0.7% of patients without anemia (p <0.001) driven largely by transfusion events. In the overall study population, major bleeding was a significant predictor of mortality (hazard ratio [HR] 1.4, 95% confidence interval [CI] 1.04 to 1.8, p = 0.027) at a mean follow-up of 2.6 years (interquartile range 1.4 to 3.5). In patients with anemia, major bleeding remained an independent predictor of mortality (HR 1.5, 95% CI 1.1 to 2.0, p = 0.008); however, in patients without anemia, it did not (HR 1.25, 95% CI 0.52 to 3.03, p = 0.62). In patients who underwent PCI with bivalirudin therapy, major bleeding is associated with early and long-term mortality, which is more pronounced in patients with baseline anemia.

Rat model of veno-arterial extracorporeal membrane oxygenation.

BACKGROUND: We aim to develop a rat model of veno-arterial extracorporeal membrane oxygenation (VA-ECMO). METHODS: VA-ECMO was established in twelve Male Sprague-Dawley rats (250-350 g) through cannulation of the right jugular vein for venous drainage and the right femoral artery for arterial reinfusion. Arterial blood pressure was measured using a conductance catheter through cannulation of the left carotid artery. Heart rate was monitored by electrocardiography and arterial blood gas parameters with a blood gas analyzer. The VA-ECMO circuit was tested by subjecting the rats to hypoxic cardiac arrest with resuscitation using VA-ECMO. Both load-dependent and load-independent measures of myocardial contractility were measured using pressure-volume loop analysis to confirm restoration of myocardial function post-resuscitation. RESULTS: Following hypoxic cardiac arrest VA-ECMO provided sufficient oxygenation to support the circulation. The haemodynamic and blood gas parameters were maintained at transition and during ECMO. All animals were resuscitated, regained cardiac function and were able to be weaned off ECMO post-resuscitation. CONCLUSION: We have established a safe, high-throughput, economical, functioning rat model of VA-ECMO.

Impact of donor cardiac arrest on heart transplantation.

BACKGROUND: Cardiac transplantation is an effective therapy for patients with end-stage heart failure, but it is still hindered by the lack of donor organs. A history of donor cardiac arrest raises trepidation regarding the possibility of poor post-transplant outcomes. The impact of donor cardiac arrest following successful cardiopulmonary resuscitation on heart transplant outcomes is unknown. Therefore, we sought to evaluate the impact of donor cardiac arrest on orthotropic heart transplantation using the United Network for Organ Sharing database. METHODS: We performed a secondary longitudinal analysis of all cardiac transplants performed between April 1994 and December 2011 through the United Network for Organ Sharing registry. Multiorgan transplants, repeat transplants, and pediatric recipients were excluded. Survival analyses were performed using Kaplan-Meier methods as well as multivariate adjusted logistic regression and Cox proportional hazard models. RESULTS: A total of 19,980 patients were analyzed. In 856 cases, the donors had histories of cardiac arrest, and in the remaining 19,124 cases, there was no history of donor cardiac arrest. The unadjusted 1-, 5-, and 10-year actuarial survival rates between the arrest and the nonarrest groups were not significantly different. Multivariate logistic regression demonstrated no difference in survival in the donor arrest group at 30 days, 1 year, or 3 years. Furthermore, the adjusted Cox proportional hazard model for cumulative survival also showed no survival difference between the 2 groups. CONCLUSION: If standard recipient and donor transplantation criteria are met, a history of donor cardiac arrest should not prohibit the potential consideration of an organ for transplantation.

Remote ischemic preconditioning reduces myocardial and renal injury after elective abdominal aortic aneurysm repair: a randomized controlled trial.

BACKGROUND: Myocardial and renal injury commonly contribute to perioperative morbidity and mortality after abdominal aortic aneurysm repair. Remote ischemic preconditioning (RIPC) is a phenomenon whereby brief periods of ischemia followed by reperfusion in one organ provide systemic protection from prolonged ischemia. To investigate whether remote preconditioning reduces the incidence of myocardial and renal injury in patients undergoing elective open abdominal aortic aneurysm repair, we performed a randomized trial. METHOD AND RESULTS; Eighty-two patients were randomized to abdominal aortic aneurysm repair with RIPC or conventional abdominal aortic aneurysm repair (control). Two cycles of intermittent crossclamping of the common iliac artery with 10 minutes ischemia followed by 10 minutes reperfusion served as the RIPC stimulus. Myocardial injury was assessed by cardiac troponin I (>0.40 ng/mL), myocardial infarction by the American College of Cardiology/American Heart Association definition and renal injury by serum creatinine (>177 micromol/L) according to American Heart Association guidelines for risk stratification in major vascular surgery. The groups were well matched for baseline characteristics. RIPC reduced the incidence of myocardial injury by 27% (39% versus 12% [95% CI: 8.8% to 45%]; P=0.005), myocardial infarction by 22% (27% versus 5% [95% CI: 7.3% to 38%]; P=0.006), and renal impairment by 23% (30% versus 7%; [95% CI: 6.4 to 39]; P=0.009). Multivariable analysis revealed the protective effect of RIPC on myocardial injury (OR: 0.22, 95% CI: 0.07 to 0.67; P=0.008), myocardial infarction (OR: 0.18, 95% CI: 0.04 to 0.75; P=0.006) and renal impairment were independent of other covariables. CONCLUSIONS: In patients undergoing elective open abdominal aortic aneurysm repair, RIPC reduces the incidence of postoperative myocardial injury, myocardial infarction, and renal impairment.

Cardiac arrest in the organ donor does not negatively influence recipient survival after heart transplantation.

OBJECTIVE: Cardiac arrest in the organ donor raises concerns about the possibility of ischemic cardiac damage. We evaluated the outcome of heart transplantation in patients receiving an organ from donors who had suffered a period of cardiac arrest. METHODS: Demographics, operative details and outcome data were obtained retrospectively. Actuarial survival was reported using Kaplan-Meier analysis and compared with the log rank test. Cox proportional hazards regression was used to model risk adjusted survival. RESULTS: Between 1 January 1991 and 1 November 2004 38 patients were transplanted with hearts from multiorgan donors who were resuscitated after a cardiac arrest. The mean (standard deviation) duration of cardiac arrest was 15 (8)min. The interval between donor cardiac arrest and organ excision was 69 (5)h. The 30-day mortality was 2.6% (1/38). In the same interim 566 patients underwent cardiac transplantation with hearts from organ donors without a cardiac arrest. Median time to follow up was 61 months (IQR 15-166). One and 5-year survival comparing the arrest and non-arrest groups was 94.2% versus 83.6% and 79.8% versus 74.5%, respectively, p=0.35. Donor cardiac arrest was not an adverse predictor of mortality on multivariate analysis, the adjusted odds ratio was 0.86 (95% CI 0.60-1.25, p=0.42). CONCLUSIONS: With careful case selection, there was no evidence that survival after cardiac transplantation was worse following a period of cardiac arrest in the organ donor. A history of cardiac arrest in the organ donor should not exclude an organ from being considered for transplantation.

Pulmonary and paradoxical embolism in protein C and S deficient patient.

We document the case of a 67-year-old woman who presented with a history of right upper quadrant anopia, dyspnea, hypoxemia, and a systolic murmur. An intracardiac embolus wedged at a patent foramen ovale was successfully removed by resecting the atrial septum along with a pulmonary embolectomy on cardiopulmonary bypass. We review the literature with specific focus on the pathogenesis and acute treatment options of this life-threatening occurrence.

Allogenic blood transfusion does not predispose to infection after cardiac surgery.

BACKGROUND: Many retrospective studies report increased postoperative infection after allogenic blood transfusion. To investigate this phenomenon, we prospectively studied 232 patients undergoing cardiac surgery. METHODS: Patients were screened daily for evidence of culture positive infections. Wounds were examined daily and defined on the ASEPSIS score. Chest radiographs and white cell counts and differentials were recorded on days 1, 2, and 4. The use of blood products was monitored blindly and independently. Patients were grouped according to transfusion status and compared using chi2 or Fisher's test. Logistic regression analyses were performed to identify predictors of transfusion and infection. RESULTS: Of 232 patients, 116 (50%) received blood product transfusion. Patients receiving blood had lower preoperative hemoglobin, were older, with a greater proportion of urgent/emergency or revision surgery, and were higher risk. Despite this, there were no differences in the frequency of chest infection (20% versus 15%, p = 0.38), urinary infection (3.5% versus 5.3%, p = 0 0.75), wound infection (3.5% versus 8.0%, p = 0.16), or overall infection (28% versus 30%, p = 0.89) comparing the transfused versus untransfused groups. There was no evidence to suggest that administration of blood products was associated with infection (odds ratio 0.92, p = 0.77). CONCLUSIONS: The administration of blood per se did not lead to increased postoperative infection. Clinicians should reconsider withholding blood transfusion in patients solely owing to concerns of predisposition to infection.

Replacement of a regurgitant pulmonary valve with a stentless bioprosthesis.

Acquired surgical disease of the pulmonary valve is rare. We report a 72-year-old man who presented with subacute endocarditic pulmonary regurgitation. This lesion was surgically corrected with a stentless bioprosthesis. Previously, homografts and various xenografts have been used for replacement of the pulmonary valve both in the pediatric population and in adult patients with congenital heart disease. Pulmonary regurgitation is a rare lesion, but if it is encountered our case demonstrates that it can be successfully and easily treated with pulmonary valve replacement by using a stentless bioprosthesis.