Aims: Smoking is linked to disease and survival in the general and transplant population. We studied the smoking history, disease and survival of patients after heart transplantation.Methods: A total of 130 patients who underwent heart transplantation between 1995 and 2019 received a questionnaire to document their smoking history. We assessed patient characteristics, comorbidities and survival.Results: Sixty-five percent of patients were active or former smokers prior to heart transplantation. All patients stopped smoking; 26% of the former smokers resumed smoking after transplantation.Patients who resumed smoking were younger at the time of transplantation, used fewer statins and were more likely to be treated with azathioprine after transplantation. The mean follow-up for all patients was 11±5.5 years. Patients who resumed smoking were more likely to develop solid organ cancers (45%) compared to those who remained abstinent (23%) and those who never smoked (13%) (p 0.014). A Cox proportional hazards regression analysis identified smoking resumption, with an RR of 2.31 (1.14-4.68, p 0.02), and age at transplantation, with an RR of 1.03 (1-1.06, p 0.034), as significant for survival. Patients resuming smoking after transplantation had a significantly higher risk of dying from solid organ cancer, with an RR of 2.54 (1.03, 6.28; p 0.04) with a short median survival time (25 th -75 th percentile) of (1 (0-5) months, p 0.007).Conclusion: Patients who resume smoking after heart transplantation have worse survival and are at higher risk of dying from solid organ cancer. Implementing a smoking cessation plan throughout the post-transplant period is important.
The authors report a case of thoracic splenosis, which is the autotransplantation of splenic tissue into the pleural cavity. Splenosis in the chest is a rare entity and most often an incidental finding on chest computed tomography, typically showing solitary or multiple well-defined, noncalcified pleural nodules of variable size in the left hemithorax. It is important to include this benign pathology in the differential diagnosis among other, generally malignant, pleural lesions. Imaging clues to the diagnosis are absence of the spleen and/or associated rib fractures. Early identification of thoracic splenosis as a cause of pleural nodules can prevent unnecessary and risky invasive procedures, such as biopsy or surgery.
The effects of the heparin (H)-Urokinase (UK) treatment on pulmonary emboli (PE) are limited by the rapid disappearance of the plasminogen (Pig) contained in the clots. Two groups of patients with recent PE (less than 8 days) of equal severity (as judged by angiography) have been studied: Group I (15 patients) treated by H(500 IU/kg/24h) and UK (i.v. bolus 15,000 u. CTA/kg/20min) and Group II (15 patients) receiving H and a sequential treatment with a bolus of UK followed by Lysyl-Plg infusion (300 UI/kg/6h), then by a 2nd bolus of UK and finally by a Pig loading. Angiography and catheterization were performed before and 24 hours after the treatment. The vascular obstruction (VO%) was appreciated by the UPET method. In Group II, the values before treatment were : VO 57±11% ; mean pulmonary arterial pressure (PAP) : 30±5 torrs ; cardiac index (CI) ; 2.0±0.6 I/min/m2 ; pulmonary arterial resistances (PAR) 8.4±2.7 torrs/I/min/m2 ; PaO2 : 56±7 tors. The UK + Pig treatment elicited significant changes : 50% decrease in VO and PAR, 33% decrease in PAP and 30% increase in PaO2 and CI in 24 hours. One month later, hemodynamic was normal and the residual VO was less than 15%. In Croup I the initial hemodynamic values were similar but the 24 hours decrease in VO, PAP and FAR were respectively of 30, 22 and 29%, differing significantly of the Group II (F test). After one month, the residual VO was 25%. These observations suggest that Lys-Plg loading increases significantly the efficacy of thrombolytic treatment of massive and recent PE.
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