Pulmonary complications of solid organ and hematopoietic stem cell transplantation

The ability to successfully transplant solid organs and hematopoietic stem cells represents one of the landmark medical achievements of the twentieth century. Solid organ transplantation has emerged as the standard of care for select patients with severe vital organ dysfunction and hematopoietic stem cell transplantation has become an important treatment option for patients with a wide spectrum of nonmalignant and malignant hematologic disorders, genetic disorders, and solid tumors. Although advances in surgical techniques, immunosuppressive management, and prophylaxis and treatment of infectious diseases have made long-term survival an achievable goal, transplant recipients remain at high risk for developing a myriad of serious and often life-threatening complications. Paramount among these are pulmonary complications, which arise as a consequence of the immunosuppressed status of the recipient as well as from such factors as the initial surgical insult of organ transplantation, the chemotherapy and radiation conditioning regimens that precede hematopoietic stem cell transplantation, and alloimmune mechanisms mediating host-versus-graft and graft-versus-host responses. As the population of transplant recipients continues to grow and as their care progressively shifts from the university hospital to the community setting, knowledge of the pulmonary complications of transplantation is increasingly germane to the contemporary practice of pulmonary medicine.     

Vascular stiffness is related to superoxide generation in the vessel wall

OBJECTIVES: Oxidative stress causes endothelial dysfunction and plays a major role in the pathogenesis of cardiovascular disease. Increased vascular stiffness is an intermediate phenotype in the development of cardiovascular disease. We hypothesized that vascular stiffness is partially determined by oxidative stress. METHODS: We examined 163 participants out of whom 80 had coronary artery disease. Vascular stiffness was assessed by pulse wave analysis, pulse wave velocity and measurement of aortic compliance by cardiac MRI. Circulating markers of oxidative stress and vascular superoxide generation in saphenous vein were measured. RESULTS: After adjustment for age, sex, BMI, heart rate, blood pressure and lipids only carotid-femoral pulse wave velocity and aortic compliance were different between patients and control group. Aortic compliance was reduced (11.4 +/- 6.3 vs. 13.9 +/- 7.3 ml x 10(-3) per mmHg; P = 0.035) and vascular superoxide generation increased (1.01 +/- 0.45 vs. 0.76 +/- 0.44 nmol/mg per min; P = 0.035) in patients with coronary artery disease compared with those without. In a multiple stepwise regression analysis, aortic compliance was determined by age (P < 0.001) and vascular superoxide production (P = 0.033). CYBA C242T and NOS3 G894T polymorphisms had additive effects on vascular superoxide generation (P = 0.026) and xanthine oxidase activity was increased in patients with CAD (P = 0.043). Genetic factors (P = 0.033) and xanthine oxidase activity (P < 0.001) were also related to aortic compliance. CONCLUSION: By measuring vascular superoxide generation and aortic compliance using cardiac MRI, we demonstrated a functional relationship between oxidative stress and vascular stiffness. Patients identified with high levels of vascular stiffness are most likely to benefit from strategies to reduce vascular oxidative stress.     

Increased incidence of subacute lead perforation noted with one implantable cardioverter-defibrillator.

BACKGROUND: The rapid evolution of implantable cardioverter-defibrillator (ICD) leads has resulted in thinner active fixation leads. While these advances have made the leads more versatile, new configurations may be associated with unforeseen complications. OBJECTIVE: The purpose of this study was to determine the incidence of perforation and dislodgement of defibrillator leads in a single center in the year 2005. METHODS: All patients who underwent percutaneous ICD implantation at the Massachusetts General Hospital using an endocardial right ventricular lead were included in this study. The specific leads analyzed were the Riata (1580/1581 and 1590/1591, St. Jude Medical, St Paul, Minnesota, USA;) and Sprint Fidelis (6949-65, Medtronic, Minneapolis, Minnesota, USA.). Information was collected retrospectively. RESULTS: A total of 130 Riata leads and 111 Sprint Fidelis leads were implanted at the Massachusetts General Hospital during this time period. A total of five lead perforations occurred in patients implanted with the Riata lead as compared with none with the Sprint Fidelis lead (3.8% vs. 0%, respectively; P <.05). Two of the five patients with perforation required pericardiocentesis for tamponade. Clinical symptoms of perforation developed 1-10 days after implant. Moreover, there were five additional lead revisions in the Riata group, which were likely due to dislodgement and/or microperforation, as compared with none in the Sprint Fidelis group (7.7% vs. 0%, respectively; P <.005). CONCLUSIONS: In 2005, at one institution, there were significantly more cardiac perforations and lead revisions with the Riata lead as compared with the Sprint Fidelis right ventricular defibrillator lead. Further data are required to determine whether certain lead characteristics are responsible for this observation.