Isolated blunt abdominal aortic injury without concomitant abdominal injuries treated with endovascular stent grafting.

Blunt injury of the abdominal aorta is a rare event, seen in only 0.07% to 0.17% of all blunt traumas. These injuries are frequently associated with other intra-abdominal injuries, with high rates of morbidity and mortality. We present a case of isolated blunt abdominal aortic trauma to the infrarenal aorta without concomitant abdominal or spinal injuries. The patient was treated with endovascular aortic stent grafting and is without complications 12 months after the procedure.

Capsaicin blocks HIV protease inhibitor ritonavir-induced vascular dysfunction in porcine pulmonary arteries.

BACKGROUND: Highly active antiretroviral therapy (HAART) including HIV protease inhibitor ritonavir may be associated with the clinical complications including accelerated atherosclerosis and pulmonary artery hypertension. The objective of this study was to determine whether capsaicin, a major ingredient of hot pepper with antioxidative property, could effectively inhibit ritonavir-induced oxidative injury in porcine pulmonary arteries. MATERIAL/METHODS: Fresh porcine pulmonary artery rings were treated with ritonavir (15 microM), capsaicin (50 microM) or both for 24 hours and, then, subjected to myograph analysis in response to vasoactive drugs including thromboxane A2 analog U-46619, bradykinin, and sodium nitroprusside (SNP). RESULTS: In response to U-46619 (3x10(-8) M), ritonavir-treated porcine pulmonary artery rings reduced the contraction by 15% compared with control rings. In response to bradykinin (10(-6) M), ritonavir-treated rings showed a significant reduction of endothelium-dependent vasorelaxation by 32% compared with untreated control vessels (P<0.05, n=5, Student t-test). However, ritonavir treatment did not change endothelium-independent vasorelaxation in response to SNP (10(-6) M). Capsaicin-treated vessel rings did not show any significant changes in response to U-46619, bradykinin, and SNP compared with untreated control vessels. More importantly, capsaicin co-cultured with ritonavir significantly blocked ritonavir-induced inhibition of endothelium-dependent vasorelaxation and contraction compared with ritonavir alone treatment in porcine pulmonary artery rings (P<0.05, n=5, Student t-test). CONCLUSIONS: Capsaicin effectively inhibits the detrimental effects of HIV protease inhibitor ritonavir on vasomotor functions of porcine pulmonary arteries. These findings may suggest that capsaicin could have clinical applications to prevent vascular and pulmonary complications of HAART drugs in HIV patients.

Lipid laden macrophage indices and reflux finding score in canine gastroesophageal reflux model.

UNLABELLED: Laryngeal exposure to acid and aspiration of gastric contents may lead to severe respiratory disorders. This study utilizes the canine model of Gastroesophageal reflux (GER) to identify whether lower esophageal dysfunction is associated with upper and lower airway pathology. MATERIALS AND METHODS: Five mongrel dogs underwent GER-creating surgery (partial cardiomyectomy). Laryngeal reflux finding score (RFS), lipid-laden macrophage index (LLMI) and BAL fluid cell differential were obtained before and after surgery. RESULTS: Partial cardiomyectomy in dogs significantly increased the Reflux index (RI) from 0.38 +/- 0.21% to 7.56 +/- 2.89% (P = 0.048), the duration of the longest reflux episode (DLRE) from 1.22 +/- 1.19 min to 66.2 +/- 42.03 min postoperatively (P = 0.049) and the total number of episodes in 24 hr from 2.06 +/- 1.03 to a postoperative value of 19.24 +/- 4.79. There was no statistically significant change in values for RFS, LLMI, and BAL fluid cell differential after the induction of GER. CONCLUSIONS: Acid reflux to the proximal esophagus of this animal model did not cause laryngeal exposure to acid or aspiration of gastric content. The results of this study suggest that presence of GER, secondary to lower esophageal dysfunction is not necessarily associated with upper and lower airway pathology.

Circadian rhythm has no effect on mortality in coronary artery bypass surgery.

BACKGROUND: The circadian variation that affects atherosclerosis has not been studied in the surgical patient. The circadian variation in mortality dependent on the time of surgery was examined in patients undergoing coronary artery bypass graft (CABG) surgery. METHODS: A 4-year retrospective review of all CABG patients (n = 3140) from 1999 to 2002 was undertaken. The patients were divided into elective, urgent, and emergency cases. The cases were subdivided according to the start time of the operation as morning (7 AM to 2 PM = AM), afternoon (2 PM to 8 PM = AF), and night (8 PM to 7 AM = NT). The outcome was mortality within 30 days and compared for three different time frames: (1) AM versus AF (2) AM versus NT (3) AF versus NT for each prioritized group. Risk factors and number of anastamoses were compared for each group. Sigma Statistical package and Z-test for two group comparison were used for analysis. t-Test was used to compare age and ejection fraction. RESULTS: No statistically significant difference in mortality was observed for the elective and urgent groups for each of the time periods compared. The emergency cases had significantly increased deaths in the AM and NT compared to the AF (p < 0.01 and p < 0.05, respectively). There was no statistically significant difference with respect to age, gender, number of anastamoses performed, ejection fraction, and preoperative risk factors between groups. CONCLUSIONS: The mortality for nonemergent CABG is independent of the timing of surgery. Circadian variation does not influence the outcome in cardiac surgical patients.

Pseudoaneurysms of the ascending aorta following coronary artery bypass surgery.

BACKGROUND: Ascending aortic pseudoaneurysms following prior cardiac procedures are a rare entity. We reviewed our institutional experience given the isolated case reports in the literature. METHODS: A 10-year retrospective review identified 5 patients who underwent ascending aorta pseudoaneurysm repair. There were 3 women and 2 men with a median age of 70 years (range 63 to 79 years). Median duration from initial CABG to pseudoaneurysm repair was 5 years (range 5 months to 18 years). The clinical presentations included dyspnoea (2 patients), chest pain, fever of unknown origin, and a pulsatile mass. Four patients underwent urgent investigation and surgery. Diagnosis was established via CT scan (3 patients), transesophageal echocardiogram (1 patient), and MRA (1 patient). Two patients had a prior history of sternal wound infection. RESULTS: Mortality was 60%. One survivor experienced a stroke. The etiology was prior cannulation site in 4 cases and vein graft anastamotic site in 1. Necrotic aortic tissue was noticed in 2 cases. Aortic tissue cultures were negative in all the patients. Cardiopulmonary bypass was established prior to sternotomy in 4 cases and 1 case was performed off-pump. Inadvertent rupture of the pseudoaneurysm (without exsanguination) occurred in 2 cases following sternotomy. Repair was performed with bovine pericardial patch in 2 cases and plication in 3 cases. CONCLUSION: This highlights the varied presentation, necessity for urgent diagnosis and repair with a high operative mortality due to the late presentation. Aggressive diagnosis should be sought and consideration should be given to catheter-based interventions for initial treatment.

Nicotine induces mitogen-activated protein kinase dependent vascular smooth muscle cell migration.

Cigarette smoke, specifically the nicotine contained within, has been shown to cause ultrastructural changes in vascular endothelium resulting in the development of atherosclerosis. Our study examines the effects of nicotine on vascular smooth muscle cell (VSMC) migration and attempts to eludicidate the cellular mechanisms governing those effects. Bovine aortic VSMC were cultured in 10% fetal bovine serum (FBS) growth media and exposed to 10(-8) nicotine for varying periods of time. Boyden chamber chemotaxis assays and a scrape injury model using confluent cells were used to assess cell motility. Activation of the mitogen-activated protein kinases (MAPK), p38 and p44/42, was assessed using Western blotting methods. Nicotine, itself, did not cause significant VSMC migration. However, augmented migration was seen in nicotine-treated VSMCs (16.6+/-3-fold) and media (17.0+/-4-fold) with 10% FBS as chemoattractant. Inhibitors of p38 and p44/42 diminished this migration by 48.5+/-6% and 29.4+/-2%, respectively. Immunoblotting verified p38 and p44/42 activation with nicotine and inhibition with inhibitors of p38 and p44/42. Nicotine-treated endothelial cell (EC) conditioned media (CM) was shown to increase migration 20.3+/-l.l-fold. This chemotactic effect was diminished both with heat treatment and serial dilution. In conclusion, nicotine enhances the chemoatactiveness of VSMC. This migration is mediated via the MAPKs p38 and p44/42. Nicotine causes EC production of a chemoattractant molecule that enhances VSMC migration.