Experimental stent-graft treatment of ascending aortic dissection.

BACKGROUND: This study assessed the feasibility of stent graft treatment of ascending aortic dissections in a porcine in vitro model. METHODS: The entire thoracic aortic aorta including the supraaortic branches was harvested from 12 adult pigs and an intimal tear was artificially created. The aortic annulus was then sewn into a silicon ring of a driving chamber. The distal aorta was connected to tubing with adjustable resistance elements. The circulation was driven by a hydraulic motor piston pump to mimic aortic flow and pressure. After creating a dissection by elevating the systolic aortic pressure to 180 mm Hg, a 2- x 2.6-cm covered stent graft was inserted through the brachiocephalic trunk using a specially designed delivery system. Stent graft placement was performed under continuous ultrasound control. RESULTS: The longitudinal length of the created ascending aortic dissection was 1.8 +/- 0.39 cm. Ultrasound studies revealed successful deployment of the stent graft and closure of the false lumen in all 12 cases. Diameter and area of the true lumen increased from 0.52 +/- 0.15 cm to 2.54 +/- 0.36 cm (p < 0.05) and from 0.78 +/- 0.27 cm2 to 5.13 +/- 1.35 cm2 (p < 0.05), respectively. The circumference of the true lumen increased from 4.50 +/- 0.52 cm to 7.96 +/- 1.2 cm (p < 0.05). Ultrasound studies also revealed uncompromised function of the aortic valve in all cases. No dislodging of stent grafts was observed. CONCLUSIONS: Given ideal anatomy, experimental stent graft placement for ascending aortic dissection is feasible and achieves complete closure of the false lumen.

Post-transplant survival after lowering fixed pulmonary hypertension using left ventricular assist devices.

OBJECTIVE: We have previously shown that fixed pulmonary hypertension in cardiac transplant candidates can be lowered using left ventricular assist devices (LVADs). The post-transplant survival of these patients is uncertain as pulmonary hypertension may reappear, possibly affecting post-transplant survival. MATERIALS AND METHODS: Between 01/2000 and 01/2005 a total of 26 cardiac transplant candidates (92% male; mean age 56.2 years) in whom fixed pulmonary hypertension was lowered by LVAD implantation (pulmonary vascular resistance (PVR) before implantation: 5.1+/-2.8wood units (WU); PVR before cardiac transplantation: 2.0+/-.9WU) underwent cardiac transplantation at our institution. These patients were age and sex matched with 52 cardiac transplant candidates without pulmonary hypertension undergoing cardiac transplantation during the same time period. Study endpoints were peri-transplant complications and long-term survival. Mean follow-up was 36+/-14 months. RESULTS: Peri-transplant mortality was 5% in patients after LVAD therapy and 7% in patients without prior LVAD therapy (p=.089). We observed 2 cases (4%) of acute right heart failure requiring mechanical support in patients without prior LVAD therapy. None of the patients with LVAD therapy developed peri-transplant right heart failure requiring mechanical support. Incidence of other peri-transplant complications was comparable between the two groups. Log-rank (p=.124) revealed comparable long-term survival between patients with (1 year: 85%, 2 year: 85%, 3 year: 85%) and without (1 year: 90%, 2 year 82%, 3 year prior 79%) prior LVAD therapy. CONCLUSION: LVAD therapy lowers fixed pulmonary hypertension in cardiac transplant candidates with fixed pulmonary hypertension. Thereafter, long-term post-transplant survival is comparable to cardiac transplant recipients without pulmonary hypertension.

Left ventricular assist devices decrease fixed pulmonary hypertension in cardiac transplant candidates.

OBJECTIVE: Fixed pulmonary hypertension is a contraindication for cardiac transplantation because of the increased risk of donor heart failure. We sought to determine whether left ventricular assist devices improve fixed pulmonary hypertension in cardiac transplant candidates to enable safe cardiac transplantation. METHODS: Thirty-five consecutive cardiac transplant candidates (age 56 +/- 6 years, 88.5% were men) with fixed pulmonary hypertension (5.1 +/- 2.6 Wood units) resistant to medical treatment received a left ventricular assist device as a bridge to transplantation. Three left ventricular assist device systems were used (pulsatile blood flow: Novacor [World Heart Inc, Oakland, Calif] n = 8; continuous blood flow: MicroMed DeBakey [MicroMed Technology Inc, Houston, Tex] n = 24, DuraHeart [Terumo Heart Inc, Ann Arbor, Mich] n = 3). Right-sided heart catheter data were obtained before left ventricular assist device implantation at 3-day and 6-week follow-ups. Clinical data and complications were recorded. RESULTS: Before left ventricular assist device implantation, the pulmonary vascular resistance was 5.1 +/- 2.8 Wood units. Values were comparable in patients receiving pulsatile (5.1 +/- 3.4 Wood units) or continuous blood flow left ventricular assist devices (5.1 +/- 2.7 Wood units, P = .976). Left ventricular assist device implantation decreased pulmonary vascular resistance at 3-day (2.9 +/- 1.3 Wood units, P < .0001) and 6-week (2.0 +/- 0.8 Wood units, P < .0001) follow-ups compared with before implantation. This effect was independent of the type of left ventricular assist device system used (3-day follow-up: pulsatile flow: 3.2 +/- 1.3 Wood units vs continuous flow: 2.7 +/- 1.2 Wood units; P = .310 and 6-week follow-up: pulsatile flow: 1.9 +/- 0.9 Wood units vs continuous flow: 2.1 +/- 0.8 Wood units; P = .905). Twenty-four patients had successful bridges to transplantation (69%, mean time on left ventricular assist device 210 +/- 83 days), and 11 patients died before transplantation (31%, mean time on left ventricular assist device 67 +/- 30 days). The 1-year survival after transplantation was 95%. CONCLUSION: Left ventricular assist devices decrease fixed pulmonary hypertension in cardiac transplant candidates and allow patients to overcome a contraindication for cardiac transplantation. Therefore, left ventricular assist devices should be considered in all cardiac transplant candidates with fixed pulmonary hypertension.

Neurocognitive function in patients with ventricular assist devices: a comparison of pulsatile and continuous blood flow devices.

The effect of successful ventricular assist device (VAD) implantation on neurocognitive function in terminal heart failure is uncertain. Additionally, the different impact of continuous versus pulsatile blood flow devices is unknown. A total of 29 patients (mean age 53 years), surviving implantation of a ventricular assist device as bridge to transplantation were prospectively followed (continuous flow: Micromed DeBakey, n = 11; pulsatile flow: Thoratec and Novacor, n = 18). Normative data were obtained in 40 age- and sex-matched healthy subjects (mean age 54 years). Neurocognitive function was objectively measured by means of cognitive P300 auditory evoked potentials before operation (baseline), at intensive care unit (ICU) discharge, and at the 8-week and 12-week follow-up. Before implantation of the VAD, cognitive P300 evoked potentials were impaired (prolonged) compared with age- and sex-matched healthy subjects (p < 0.001). After successful VAD implantation, P300 evoked potentials markedly improved compared with before operation (ICU discharge, p = 0.007; 8-week follow-up, p = 0.022; 12-week follow-up, p < 0.0001). Importantly, there was no difference between continuous and pulsatile VADs (before operation, p = 0.676; ICU discharge, p = 0.736; 8-week follow-up, p = 0.911 and 12-week follow-up, p = 0.397; respectively). Nevertheless, P300 peak latencies did not fully normalize at 12-week follow-up compared with healthy subjects (p = 0.012). Successful VAD implantation improves neurocognitive impairment in patients with terminal heart failure. Importantly, this effect is independent of the type of VAD (pulsatile vs. continuous blood flow).

Prosthetic replacement of the aorta is a risk factor for aortic root aneurysm development.

BACKGROUND: Noncompliant prostheses are used in aortic replacement. We hypothesized that this leads to increased distension and wall stress in the aortic root because of the loss of ventriculo arterial coupling. METHODS: Pressure relations in the aortic root caused by changes of aortic elasticity simulating prosthetic aortic replacement were tested in a computer model. We then developed an in vitro model using porcine aortas and performed in vivo validation. RESULTS: Findings in vitro and in vivo confirmed the predicted changes of the computer model. Pressure amplitude increased significantly by 17% after prosthetic replacement (p < 0.01). Pressure-time differential (Dp/dt) and dicrotic notch pressure amplitude both increased significantly. Echocardiography demonstrated systolic aortic root distension with percentage area change increasing in vitro from 28.2%+/-9.7% to 35.9%+/-10% (p < 0.05) and in vivo from 13.3%+/-3.1% to 24.3%+/-3.1% (p < 0.0001). Aortic root wall stress increased markedly. CONCLUSIONS: Replacement of the aorta with vascular prostheses causes important negative alterations of hemodynamics and increases in wall stress.