The use of risk scores failed to predict the need of RV support after LVAD. Stratification of the hazard with these scores should occur with extreme caution.
A commonly heard concern in the Ross procedure, where a diseased aortic valve is replaced by the patient's own pulmonary valve, is the possibility of pulmonary autograft dilatation. We performed a biomechanical investigation of the use of a personalized external aortic root support or exostent as a possibility for supporting the autograft. In ten sheep a short length of pulmonary artery was interposed in the descending aorta, serving as a simplified version of the Ross procedure. In seven of these cases, the autograft was supported by an external mesh or so-called exostent. Three sheep served as control, of which one was excluded from the mechanical testing. The sheep were sacrificed six months after the procedure. Samples of the relevant tissues were obtained for subsequent mechanical testing: normal aorta, normal pulmonary artery, aorta with exostent, pulmonary artery with exostent, and pulmonary artery in aortic position for six months. After mechanical testing, the material parameters of the Gasser-Ogden-Holzapfel model were determined for the different tissue types. Stress-strain curves of the different tissue types show significantly different mechanical behavior. At baseline, stress-strain curves of the pulmonary artery are lower than aortic stress-strain curves, but at the strain levels at which the collagen fibers are recruited, the pulmonary artery behaves stiffer than the aorta. After being in aortic position for six months, the pulmonary artery tends towards aorta-like behavior, indicating that growth and remodeling processes have taken place. When adding an exostent around the pulmonary autograft, the mechanical behavior of the composite artery (exostent + artery) differs from the artery alone, the non-linearity being more evident in the former.
NM can simulate the effect of a VAD in complex physiopathologies, with the inclusion of changes in circulatory parameters during the acute phase and at FUP. The simulation of differently assisted physiopathologies offers a useful support for clinicians.
The aim of this study is to investigate the intravascular application of a micro-electro-mechanical system (MEMS) pressure sensor to directly measure the hemodynamic characteristics of a ventricular assist device (VAD). A bio- and hemo-compatible packaging strategy is implemented, based on a ceramic thick film process. A commercial sub-millimeter piezoresistive sensor is attached to an alumina substrate, and a double coating of polydimethylsiloxane (PDMS) and parylene-C is applied. The final size of the packaged device is 2.6 mm by 3.6 mm by 1.8 mm. A prototype electronic circuit for conditioning and read-out of the pressure signal is developed, satisfying the VAD-specific requirements of low power consumption (less than 14.5 mW in continuous mode) and small form factor. The packaged sensor has been submitted to extensive in vitro tests. The device displayed a temperature-independent sensitivity (12 μV/V/mmHg) and good in vitro stability when exposed to the continuous flow of saline solution (less than 0.05 mmHg/day drift after 50 h). During in vivo validation, the transducer has been successfully used to record the arterial pressure waveform of a female sheep. A small, intravascular sensor to continuously register the blood pressure at the inflow and the outflow of a VAD is developed and successfully validated in vivo.
Background: Exertional intolerance is a limiting and often crippling symptom in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Traditionally the etiology has been attributed to central factors, including ventilation-perfusion mismatch, increased pulmonary vascular resistance and right heart dysfunction and uncoupling. Pulmonary endarterectomy and, balloon pulmonary angioplasty provide substantial improvement of functional status and hemodynamics. However, despite normalization of pulmonary hemodynamics, exercise capacity often does not return to age-predicted. By systematically evaluating the oxygen (O 2 ) pathway we aimed to elucidate the cause/s of functional limitations in CTEPH patients before and after pulmonary vascular intervention. Methods: Using exercise cardiac magnetic resonance (CMR) imaging with simultaneous invasive hemodynamic monitoring, we sought to quantify the steps of the O2 transport cascade from the mouth to the mitochondria in patients with CTEPH (n=20) as compared to healthy subjects (n=10). Furthermore we evaluated the effect of pulmonary vascular intervention (pulmonary endarterectomy or balloon angioplasty) on the individual components of the cascade (n=10). Results: Peak VO2 was significantly reduced in CTEPH patients relative to controls (56±17 vs 112±20% of predicted, p<0.0001). The difference was due to impairments in multiple steps of the O 2 cascade, including O 2 delivery (product of cardiac output and arterial O 2 content), skeletal muscle diffusion capacity, and pulmonary diffusion. The total O 2 extracted in the periphery, i.e. ΔAVO 2 , was not different. Following pulmonary vascular intervention, peak VO 2 increased significantly (12.5±4.0 to 17.8±7.5 ml/kg/min, p=0.036) but remained below age-predicted (70±11%). The O 2 delivery was improved due to an increase in peak cardiac output and lung diffusion capacity. However, peak exercise ΔAVO2 was unchanged, as was skeletal muscle diffusion capacity. Conclusions: We demonstrated that CTEPH patients have significant impairment of all steps in the O 2 utilisation cascade resulting in markedly impaired exercise capacity. Pulmonary vascular intervention increased peak VO 2 , by partly correcting O 2 delivery but having no impact on abnormalities in peripheral O 2 extraction. This suggests that current interventions only partially address patients' limitations and that additional therapies may improve functional capacity.
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