Background: Platypnea-orthodeoxia syndrome (POS) is a rare clinical phenomenon, associating normal oxygen saturation in a supine position and arterial hypoxemia in an upright position. This pathology can be secondary to an intracardiac shunt, a pulmonary vascular shunt or a ventilation-perfusion mismatch. Cardiac POS occurs in the presence of a right-to-left cardiac shunt, most commonly through a patent foramen ovale (PFO). Methods and results: From our single-center prospective database of percutaneous PFO closure we identified five patients (4 females, mean age: 77 ± 11 years) out of 224 (2.2%) patients with a PFO who presented with a POS of cardiac origin. Transthoracic and transoesophageal echocardiographic examinations revealed the underlying mechanisms of POS and the diagnosis was confirmed by right-and-left cardiac catheterization (RLC) and by measuring serial blood oxygen saturation in the pulmonary veins and left atrium in supine and upright positions. PFO was associated with atrial septal aneurysm and a persistent prominent Eustachian valve in 3 patients. All patients underwent a successful percutaneous PFO closure without any immediate or subsequent complications (mean follow-up of 24 ± 18 months). Immediately after the procedure, mean arterial oxygen saturation improved from 83% ± 3 to 93% ± 2 in an upright position and symptoms disappeared. Conclusion: POS is a rare and under-diagnosed pathology that must be actively investigated in the presence of position-dependent hypoxemia. The diagnostic work-up must exclude other causes of hypoxemia and confirm the intracardiac shunt using either contrast echocardiography or RLC. For cardiac POS, percutaneous PFO closure is a safe and effective technique that immediately relieves orthodeoxia and patient symptoms.
The embolization of side branches arising from an infrarenal aortic aneurysm before endovascular repair is feasible, with a high success rate; this maneuver may play a relevant role in reducing the rate of type II endoleak, improving long-term outcome.
Currently, angiography is still considered to be the gold standard for the diagnosis of a renal artery stenosis (RAS). However, angiography is invasive and carries the potential risk of haematoma, pseudoaneurysm, contrast agent induced nephropathy, and athermanous embolization. Color-coded duplex ultrasound is a noninvasive frequently repeatable bed-side examination and is currently the only diagnostic method to reliably differentiate between a hemodynamically relevant or irrelevant stenosis using the side-to-side difference of the intrarenal resistance index (RI). There is a highly specific correlation between a side difference of the RI of >0.05 and an at least 70% angiographic diameter stenosis. All other duplex parameters like a peak systolic flow velocity >200 cm/sec or a renal aortic flow velocity ratio >3.5 are correlated to a 50 or 60% angiographic diameter stenosis and offer therefore indeed a high sensitivity in terms of detecting a RAS; however, the specificity detecting a hemodynamically relevant RAS is low. Provided that duplex ultrasound is performed by an experienced physician with an adequate machine it should be the preferred imaging method. The present article gives an overview about the literature related to duplex based diagnosis of RAS and as a follow-up diagnostic procedure following RAS revascularization.
Managing bleeding in patients receiving P2Y12 inhibitors is challenging. Few data are available regarding the efficacy of platelet transfusion in patients treated with prasugrel or ticagrelor. The aim of this study was to evaluate the minimal amount of platelet supplementation (in terms of ratio of non-inhibited platelets to inhibited platelets) necessary to restore platelet reactivity in platelet-rich plasma (PRP) of patients treated with aspirin and a prasugrel or ticagrelor loading dose for an acute coronary syndrome. PRP samples from patients were mixed ex vivo with increasing proportions of pooled PRP from healthy volunteers. Platelet reactivity was challenged with adenosine diphosphate (ADP), arachidonic acid, collagen or thrombin receptor activating peptide using light transmission aggregometry. The primary endpoint was the proportion of patient samples recovering an ADP-induced maximal aggregation (ADP-Aggmax) value above 40%. In patients treated with prasugrel (n = 32), ADP-Aggmax increased progressively with supplements of pooled PRP, with an average increase of 7.9% (95% CI [7.1; 8.8], p < 0.001) per each 20% increase in the ratio of non-inhibited platelets to inhibited platelets. A ratio of 60% was associated with 90% of patients reaching the primary endpoint. In patients treated with ticagrelor (n = 15), ADP-Aggmax did not significantly increase with any level of supplements. In conclusions, ex vivo addition of non-inhibited platelets significantly improved ADP-Aggmax in patients treated with prasugrel with a dose-dependent effect. There was no evidence of such a reversal in patients treated with ticagrelor. These results suggest that platelet transfusion may be more effective in blunting bleeding in patients treated with prasugrel, than those treated with ticagrelor.
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