Faculty Bibliography

BACKGROUND: Inadequate data exist regarding the management of acute major pulmonary embolism. Various modalities that are used, including thrombolytics and embolectomy, have not been shown to conclusively improve mortality when compared to heparin. In the past, open pulmonary embolectomy was reserved for patients with severe hemodynamic instability because of its high mortality rate. Our objective was to analyze our experience with early embolectomy as an alternative for the treatment of major pulmonary embolism. METHODS: A retrospective review of charts of all patients undergoing pulmonary embolectomy at our institution over the last two years was performed. Patients were followed until their discharge from hospital. RESULTS: There were 13 patients (7 women and 6 men). Four had massive and 9 had submassive pulmonary embolism. There was one mortality. Postoperative echocardiography showed no evidence of pulmonary hypertension in 7. CONCLUSIONS: Open pulmonary embolectomy can be performed in patients with major pulmonary embolism with minimal mortality and morbidity. It may prevent the development of chronic thromboembolic pulmonary hypertension and should be a part of the algorithm in the treatment of major pulmonary embolism

Penetrating aortic ulcers (PAUs) are rare exotic pathological entities, classically located in the descending thoracic aorta. Their association with syphilis has never been reported. We describe a first case of a patient with cardiovascular syphilis presenting as PAU in the ascending aorta

To determine whether cellular aging leads to a cardiomyopathy and heart failure, markers of cellular senescence, cell death, telomerase activity, telomere integrity, and cell regeneration were measured in myocytes of aging wild-type mice (WT). These parameters were similarly studied in insulin-like growth factor-1 (IGF-1) transgenic mice (TG) because IGF-1 promotes cell growth and survival and may delay cellular aging. Importantly, the consequences of aging on cardiac stem cell (CSC) growth and senescence were evaluated. Gene products implicated in growth arrest and senescence, such as p27Kip1, p53, p16INK4a, and p19ARF, were detected in myocytes of young WT mice, and their expression increased with age. IGF-1 attenuated the levels of these proteins at all ages. Telomerase activity decreased in aging WT myocytes but increased in TG, paralleling the changes in Akt phosphorylation. Reduction in nuclear phospho-Akt and telomerase resulted in telomere shortening and uncapping in WT myocytes. Senescence and death of CSCs increased with age in WT impairing the growth and turnover of cells in the heart. DNA damage and myocyte death exceeded cell formation in old WT, leading to a decreased number of myocytes and heart failure. This did not occur in TG in which CSC-mediated myocyte regeneration compensated for the extent of cell death preventing ventricular dysfunction. IGF-1 enhanced nuclear phospho-Akt and telomerase delaying cellular aging and death. The differential response of TG mice to chronological age may result from preservation of functional CSCs undergoing myocyte commitment. In conclusion, senescence of CSCs and myocytes conditions the development of an aging myopathy

The effects of hypoxia-reoxygenation on internal mammary (IMA) and radial (RA) arteries used for coronary artery bypass grafting (CABG) were examined to identify mechanisms regulating contractile function and differences that could contribute to vasospasm. Isolated endothelium-intact IMA and RA rings precontracted with KCl (30 mM) rapidly dilated to hypoxia (95% N(2)/5% CO(2)) with a greater relaxation in RA than IMA. Inhibitors of cyclooxygenase (10 microM indomethacin) and the thromboxane A(2) (TxA)(2) receptor [1 microM [1S-[1alpha,2alpha(Z),3alpha,4alpha]]-7-[3-[2-(phenylamino)carbonyl]hydraz ine]methyl]-7-oxabicyclo[2.2.1]hept-2-yl]-5-heptenoic acid (SQ-29548)] potentiated the relaxation to hypoxia in IMA, but not RA, a response associated with increases in TxA(2). Relaxation of IMA and RA to hypoxia appears to involve a calcium-reuptake mechanism inhibited by cyclopiazonic acid (0.2 mM), and it was not attenuated by a blocker of potassium channels (10 mM TEA). The recovery of force generation of IMA, but not RA, upon reoxygenation after 30 min of hypoxia was significantly reduced in the initial phase of reoxygenation by indomethacin and SQ-29548 and by endothelin receptor blocker BQ-123 [cyclo(l-Leu-d-Trp-d-Asp-l-Pro-d-Val)]. Thus, hypoxia relaxes IMA and RA by a prostaglandin-independent mechanism potentially involving enhanced intracellular calcium reuptake. The prostaglandin-mediated alterations of responses to hypoxia-reoxygenation seen in IMA, but not in RA, may predispose IMA to vasospasm-related complications of CABG