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Background Thrombolysis (T) is an effective therapy for prosthetic valve thrombosis (PVT). Debate still exists as to which clinical or noninvasive finding best predict the result of T. The aim of the study was to investigate the role of fluoroscopy (F) to predict efficacy of T in pts with mitral PVT. Methods We evaluated 17 consecutive pts with bileaflet mitral PVT. F criteria for PVT were: abnormal disc motion and calculated opening angle >25°. T was carried out with tissue-type plasminogen activator (tPA; 100 mg over 3 hours followed by heparin infusion for 24 hours) and was considered successful when normalization of leaflet motion and opening angle occurred. Results were evaluated according to symptom duration (21 days, late PVT) and to F pattern of PVT (blocked leaflet versus hypomobile leaflet). Results F showed disc motion alteration in 24 of 34 leaflets: 8 leaflets were blocked, whereas 16 were hypomobile. Early (12.7±6.1 days, range 3–21) and late (113±114 days, range 28–365) PVT was present in 8 and 7 pts, respectively. Thrombolysis was successful in 20 of 24 leaflets. Blocked leaflet fully recovered only in early PVT (n=4) pts, whereas they remained blocked in late PVT (n=4). On the contrary, in all of the cases with hypomobile leaflet, disc motion normalized regardless duration of symptoms and extent of disc motion reduction. Interestingly, 4 leaflets with late PVT was diagnosed as blocked by trans-thoracic (TTE). F showed a residual disc movement in all: they fully recovered after T. Two pts with late PVT had both leaflets affected (1 blocked +1 hypomobile); although blocked leaflet did not respond to T, the normalization of hypomobile significantly improved clinical condition. Conclusions F can predict result of T in mitral PVT. PVT with F evidence of hypomobile leaflet always recovers regardless of symptom duration and extent of disc motion reduction, suggesting that the small amount of thrombus needed to interfere with discs motion in bileaflet prostheses remains sensitive to T even after a long time. PVT with F evidence of blocked leaflet has a favorable response to T only in case of early PVT. Late PVT with blocked leaflet does not respond to T, suggesting a larger and stratified thrombus and the coexistence of pannus and, in our series, always required surgery. However, if a hypomobile leaflet coexists, T may be used to restore normal movement of hypomobile leaflet so that to improve patient clinical and hemodynamic condition before operation.

In this study, we tested the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension. The hypothesis took origin from the following two considerations: alveolar hypoxia constricts the pulmonary vessels by enhancing the Ca2+ penetration across sarcolemma of the smooth muscle cells and systemic high blood pressure is associated with an elevation of tone and reactivity of the lung vessels, which seems to depend on an excessive cytosol free Ca2+ concentration due to alterations in sodium handling and in the Na+-Ca2+ exchange system. These considerations suggest the possibility that the disorders in the biochemistry of smooth muscle contraction in hypertension facilitate the rise of cytosol Ca2+ concentration during alveolar hypoxia, thus resulting in a potentiation of the vasoconstrictor properties of this stimulus. In 43 hypertensive and 17 normotensive men, pulmonary arteriolar resistance has been evaluated during air respiration and after 15 minutes of breathing 17%, 15%, and 12% oxygen in nitrogen. Curves relating changes in pulmonary arteriolar resistance to oxygen breathing contents had similar configuration in the two populations but in hypertension were steeper and significantly shifted to the left, reflecting a lower threshold and an enhanced reactivity. This pattern was not related to differences in severity of the hypoxic stimulus, plasma catecholamine concentration, or hypocapnia and respiratory alkalosis induced by hypoxia and probably was not mediated through alpha-receptor activation. Calcium channel blockade with nifedipine was able to almost abolish both the normotensive and the hypertensive pulmonary vasoconstriction reaction. These findings support the hypothesis that hypoxic pulmonary vasoconstriction may be enhanced in systemic hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)