The pulmonary venous systolic flow wave has been attributed both to left heart phenomena, such as left atrial relaxation and descent of the mitral annulus, and to propagation of the pulmonary artery pressure pulse through the pulmonary bed from the right ventricle. In this study we hypothesized that all waves in the pulmonary veins originate in the left heart, and that the gross wave features observed in measurements can be explained simply by wave propagation and reflection. A mathematical model of the pulmonary vein was developed; the pulmonary vein was modeled as a lossless transmission line and the pulmonary bed by a three-element lumped parameter model accounting for viscous losses, compliance, and inertia. We assumed that all pulsations originate in the left atrium (LA), the pressure in the pulmonary bed being constant. The model was validated using pulmonary vein pressure and flow recorded 1 cm proximal to the junction of the vein with the left atrium during aortocoronary bypass surgery. For a pressure drop of 6 mmHg across the pulmonary bed, we found a transit time from the left atrium to the pulmonary bed of tau approximately 150ms, a compliance of the pulmonary bed of C approximately 0.4 ml/mmHg, and an inertance of the pulmonary bed of 1.1 mmHgs2/ml. The pulse wave velocity of the pulmonary vein was estimated to be c approximately 1m/s. Waves, however, travel both towards the left atrium and towards the pulmonary bed. Waves traveling towards the left atrium are attributed to the reflections caused by the mismatch of impedance of line (pulmonary vein) and load (pulmonary bed). Wave intensity analysis was used to identify a period in systole of net wave propagation towards the left atrium for both measurements and model. The linear separation technique was used to split the pressure into one component traveling from the left atrium to the pulmonary bed and a reflected component propagating from the pulmonary bed to the left atrium. The peak of the reflected pressure wave corresponded well with the positive peak in wave intensity in systole. We conclude that the gross features of the pressure and flow waves in the pulmonary vein can be explained in the following manner: the waves originate in the LA and travel towards the pulmonary bed, where reflections give rise to waves traveling back to the LA. Although the gross features of the measured pressure were captured well by the model predicted pressure, there was still some discrepancy between the two. Thus, other factors initiating or influencing waves traveling towards the LA cannot be excluded.
The Carpentier‐Edwards standard porcine bioprosthesis was implanted in 1,195 patients in 1,213 operative procedures between 1975 and 1987, with the majority of implants performed prior to 1982 at the University of British Columbia. The mean age of the patient population was 57.2 years (range 8 to 85 years). The mean follow‐up was 7.4 years per patient. The freedom from the combination of thromboemboiism and antithromboembolic therapy‐related hemorrhage at 15 years was 79.5% for aortic valve replacement (AVR), 72% for mitral valve replacement (MVR), and 84% for multiple valve replacement (MR) (p < 0.05, AVR > MR > MVR). The freedom from structural valve deterioration at 15 years was 71% for AVR, 41% for MVR, and 41% for MR (14 years) (p < 0.05, AVR > MVR > MR). The freedom from nonstructural dysfunction and prosthetic valve endocarditis did not distinguish the valve positions (p = NS). The freedom from valve‐related mortality from all causes including reoperation was 92% for AVR, 78% for MVR, and 77% for MR at 15 years (p < 0.05, AVR > MVR > MR). The freedom from residual morbidity was not significantly different between valve positions (p = NS). The freedom from treatment failure (valve‐related mortality and residual morbidity) at 15 years was 87% for AVR, 72% for MVR, and 75% for MR (p < 0.05, AVR > MR > MVR). The freedom from all complications at 14 years was 50% for AVR, 25% for MVR, and 27% for MR (p < 0.05, AVR > MR > MVR). The Carpentier‐Edwards standard porcine bloprosthesis has provided satisfactory clinical performance in a valve replacement population essentially receiving only biological prostheses.
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