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Background-Adverse events (AEs), such as intracranial hemorrhage, thromboembolic event, and progressive aortic insufficiency, create substantial morbidity and mortality during continuous flow left ventricular assist device support yet their relation to blood pressure control is underexplored.

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Heart failure is epidemic in the United States with a prevalence of over 5 million. The diagnosis carries a mortality risk of 50% at 5 years rivaling many diagnoses of cancer. Heart transplantation, long the “gold standard” treatment for end stage heart failure unresponsive to maximal medical therapy falls way short of meeting the need with only about 2,000 transplants performed annually in the United States due to donor limitation. Left ventricular devices have emerged as a viable option for patients as both a “bridge to transplantation” and as a final “destination therapy”.

Background and Purpose-The goals of this study were to compare the ability of statewide and institutional models of stroke risk after coronary artery bypass (CAB) to predict institution-specific results and to examine the potential additive stroke risk of combined CAB and carotid endarterectomy (CEA) with these predictive models. Methods-An institution-specific model of stroke risk after CAB was developed from 1975 consecutive patients who underwent nonemergent CAB from 1994 to 1999 in whom severe carotid stenosis was excluded by preoperative duplex screening. Variables recorded in the New York State Cardiac Surgery Program database were analyzed. This model (model I) was compared with a published model (model II) derived from analysis of the same variables using New York statewide data from 1995. Predicted and observed stroke risks were compared. These formulas were applied to 154 consecutive combined CAB/CEA patients operated on between 1994 and 1999 to determine the predicted stroke risk from CAB alone and thereby deduce the maximal added risk imputed to CEA. Results-Risk factors common to both models included age, peripheral vascular disease, cardiopulmonary bypass time, and calcified aorta. Additional risk factors in model I also included left ventricular hypertrophy and hypertension. Risk factors exclusive to model II included diabetes, renal failure, smoking, and prior cerebrovascular disease. Our observed stroke rate for isolated CAB was 1.7% compared with a rate predicted with model II (statewide data) of 1.56%. The observed stroke rate for combined CEA/CAB was 3.9%. When the Stony Brook model (model I) based on patients without carotid stenosis was used, the predicted stroke rate was 2.8%. When the statewide model (model II), which included some patients with extracranial vascular disease, was used, the predicted stroke rate was 3.4%. The differences between observed and predicted stroke rates were not statistically significant. Conclusions-Estimation of stroke risk after CAB was similar whether statewide data or institution-specific data were used. The statewide model was applicable to institution-specific data collected over several years. Common risk factors included age, aortic calcification, and peripheral vascular disease. The observed differences in the predicted stroke rates between models I and II may be due to the fact that carotid stenosis was specifically excluded by duplex ultrasound from the patient population used to develop model I. Modeling stroke risk after CAB is possible. When these models were applied to patients undergoing combined CAB/CEA, no additional stroke risk could be ascribed to the addition of CEA. Such models may be used to identify groups at increased risk for stroke after both CAB and combined CAB/CEA. The ultimate place for CEA in patients undergoing CAB will be defined by prospective randomized trials. (Stroke. 2003; 34:1212-1217.)

Simulated laparoscopic sigmoidectomy training affected responsiveness in surgery residents with significantly decreased operating time and anastomotic leak rate.

BackgroundThere are no evidence based guidelines for the surveillance of patients with moderate-sized (<5 cm) thoracic aortic aneurysms (MTAA), who do not warrant surgical intervention. The purpose of this study was to review the MTAA patient surveillance strategy used currently at the Northport Veterans Affairs Medical Center, to assess outcomes over time and accrue data to develop guidelines to optimize MTAA patients’ follow-up.MethodsThe study group included veterans referred to the Thoracic Surgery clinic for the management of moderate-sized (<5 cm) thoracic aortic aneurysms (MTAA) not warranting immediate surgical repair.As a pilot study, all MTAA patients’ charts from 2005–2013 were reviewed to describe imaging practices and evaluate patient-specific long-term outcomes. An adverse composite endpoint was defined if a patient’s aneurysm grew substantially (≥0.5 cm/year or reached 5.5 cm) or a MTAA-related event (surgery or death) occurred.Additionally, number of CT scans obtained during the follow up period were documented.ResultsFor 110 MTAA patients, the average presenting index size was 4.45 ± 0.4 cm with average growth of 0.04 cm total (0.03 cm/year). Fourteen (13%) patients met the adverse composite endpoint, with no MTAA-related deaths. Patients achieving the adverse composite endpoint had higher index sizes (4.81 vs. 4.40 cm, p = 0.001) and higher average growth rates as compared to non-endpoint patients (0.16 vs. 0.01 cm, p = 0.0009). Optimizing the negative likelihood ratio defined a new “not-at-risk” population with aneurysm index size < 4.3 cm. A shorter time to adverse event for “at-risk” patients was found versus “not-at-risk” patients (p = 0.02). On average, there were 4.8 CT scans/patient and estimated cumulative radiation dose of 34 mSv/patient. Only one “not-at-risk” patient had substantive MTAA growth (≥0.5 cm/year) over the 8 year follow-up period.Conclusion and relevanceAnnual imaging of MTAA “not-at-risk” patients appears unwarranted, resulting in potentially excessive radiation exposure. Although additional research is necessary for validation, longer surveillance imaging intervals (beyond one year) seem appropriate for MTAA patients presenting with < 4.3 cm index aneurysms.

Ventricular assist devices (VAD) became in recent years the standard of care therapy for advanced heart failure with hemodynamic compromise. With the steadily growing population of device recipients, various post-implant complications have been reported, mostly associated with the hyper-shear generated by VADs that enhance their thrombogenicity by activating platelets. While VAD design optimization can significantly improve its thromboresistance, the implanted VAD need to be evaluated as part of a system. Several clinical studies indicated that variability in implantation configurations may contribute to the overall system thrombogenicity. Numerical simulations were conducted in the HeartAssist 5 (HA5) and HeartMate II (HMII) VADs in the following implantation configurations: (i) Inflow cannula angles – 115° and 140° (HA5); (ii) three VAD circumferential orientations: 0°, 30° and 60° (HA5 and HMII); and (iii) 60° and 90° outflow graft anastomotic angles (AA) with respect to the ascending aorta (HA5). The stress accumulation of the platelets was calculated along flow trajectories and collapsed into a probability density function (PDF), representing the “thrombogenic footprint” (TF) of each configuration- a proxy to its thrombogenic potential (TP). The 140° HA5 cannula generated lower TP independent of the circumferential orientation of the VAD. 60° orientation generated the lowest TP for the HA5 versus 0° for the HMII. An AA of 60° resulted in lower TP for HA5. These results demonstrate that optimizing the implantation configuration reduces the overall system TP. Thromboresistance can be enhanced by combining VAD design optimization with the surgical implantation configurations for achieving better clinical outcomes of implanted VADs.