Carbon monoxide induces relaxation of human internal thoracic and radial arterial grafts.

Carbon monoxide is produced by the degradation of heme by intracellular heme-oxygenase. The aim of our study was to evaluate, in vitro, the vasodilating effect of carbon monoxide and its mechanisms of action on human internal thoracic and radial artery grafts. Segments of human internal thoracic artery and radial artery, obtained from isolated coronary artery bypass surgery patients, were studied in organ chambers. The arterial rings were precontracted with norepinephrine then submitted to carbon monoxide. Inhibitors of nitric oxide synthase and of soluble guanylate cyclase were added to some arterial rings. Carbon monoxide induced significant relaxation in precontracted human internal thoracic artery and radial artery rings. This relaxation was independent of the presence of functional endothelium in internal thoracic artery. Blocking soluble guanylate cyclase partially inhibited this relaxation, while blocking nitric oxide synthase had no effect. Carbon monoxide has a relaxing effect on human internal thoracic artery and radial artery grafts in vitro, partially via cyclic guanylate monophosphate (cGMP) pathway activation. Inducing carbon monoxide production at the cellular level in vivo in human arterial grafts might help prevent vasospasm.

Outcomes of delayed sternal closure after complex aortic surgery.

OBJECTIVE: Open chest management during complex proximal aortic surgery may sometimes be necessary. Infectious complications such as mediastinitis and late aortic graft infection remain a concern. The objective of this study was to report our experience with open chest management and delayed sternal closure after complex proximal aortic surgery. METHODS: Between 1991 and 2007, 12 patients (1.2%, 12/1011) required open chest management and delayed sternal closure. Eight patients were men (67%), with a mean age of 56 years (range 28-83 years). Four cases involved redo-median sternotomy (33%) and seven cases (58%) involved acute dissection. All procedures were performed using total cardiopulmonary bypass with profound hypothermic circulatory arrest. Reasons for open chest management included hemodynamic instability, mediastinal edema, bleeding, and respiratory compromise. RESULTS: In-hospital mortality was 16.7% (2/12). Delayed sternal closure was achieved in 92% of patients (11/12). Mean time to closure was 3 days (range 1-9 days). Five patients (42%) required one or more mediastinal explorations prior to final closure. Mean length of stay was 51 days (range 1-186 days). Significant predictors of open chest management were pump time (p<0.0001) and intra-operative blood transfusions (p<0.002). Mean follow-up was 60 months (range 8-106 months). No patients developed mediastinitis or aortic graft infection during postoperative follow-up. CONCLUSIONS: Open chest management with delayed sternal closure after complex aortic repairs may be performed with acceptable mortality. Open chest management does not appear to increase the risk of infectious complications (mediastinitis or graft infections) during complex proximal aortic replacement.

Role of somatosensory evoked potentials in predicting outcome during thoracoabdominal aortic repair.

BACKGROUND: Clinical utility of somatosensory evoked potentials (SSEP) in descending thoracic and thoracoabdominal aortic repair is debated. We reviewed our practical experience with SSEP in descending thoracic and thoracoabdominal aortic repairs. METHODS: Between January 2000 and April 2005, we used SSEP monitoring in 444 patients (270 thoracoabdominal aorta and 174 descending thoracic aorta). Median age was 68 years; 36% were female. Only changes of spinal origin were analyzed. Changes were classified as (1) no change, (2) transient changes that returned to baseline by the end of the procedure, or (3) persistent changes that did not return to baseline by the end of the procedure. RESULTS: Somatosensory evoked potential changes occurred in 87 (19.6%) patients; 22 (25%) of these did not return to baseline. Immediate neurologic deficit occurred in 8 of 444 patients (1.8%); five deficits (5 of 87; 5.8%) occurred in patients with SSEP changes, compared with three deficits (3 of 357; 0.8%) in patients without changes. Odds ratio for this comparison was 7.2 (p < 0.002). Somatosensory evoked potential was a poor screening tool for neurologic deficit, with a sensitivity of 62.5% and specificity 81.2%. Negative predictive value was 99.2%, indicating a very low event probability in the absence of SSEP changes. Delayed neurologic deficit occurred in 3.2% and was not related to SSEP changes. Somatosensory evoked potential changes were also associated with increased 30-day mortality and low glomerular filtration rate. CONCLUSIONS: Intraoperative SSEP monitoring was reliable in ruling out spinal injury in descending thoracic and thoracoabdominal aortic repair, but had a low sensitivity. It did not predict delayed neurologic deficit. Spinal SSEP change was an independent predictor of mortality and correlated with low preoperative glomerular filtration rate.

Update on outcomes of acute type B aortic dissection.

BACKGROUND: The optimal treatment of acute type B aortic dissection remains controversial. This study reports early clinical outcomes of medical management for acute type B aortic dissection. METHODS: Between January 2001 and April 2006, data on 159 consecutive patients (55 women [35%]) with the confirmed diagnosis of acute type B aortic dissection were prospectively collected and analyzed. Mean age was 62 years (range, 29 to 94). On admission, all patients were initiated on an acute type B aortic dissection protocol with the intent to manage all patients medically. Indications for surgical intervention included rupture, aortic expansion, retrograde dissection, malperfusion (visceral, peripheral), and intractable pain. All patients were followed up after discharge with serial clinical and radiographic examinations. RESULTS: Overall hospital mortality was 8.8% (14/159): 17% (4/23) with procedural intervention, and 7.4% (10/136) when medical management was maintained. Early intervention was required in 23 patients (14.5%), of which 21 (13.2%) were open vascular/aortic procedures, and two (1.3%) were percutaneous aortic interventions. Morbidity included rupture (5.0%), stroke (5.0%), paraplegia (8.2%), bowel ischemia (5.7%), acute renal failure (20.1%), dialysis requirement (13.8%), and peripheral ischemia (3.8%). Mortality associated with complicated dissection (74/159) was 17%, and mortality associated with uncomplicated dissection (85/159) was 1.2% (p < 0.0003). Late vascular related procedures were performed in 11 (7.6%) of 144 cases (9 aortic, 2 peripheral vascular). The only independent risk factors for hospital mortality by multiple logistic regression analysis was rupture (p < 0.0009). Independent risk factors for mid-term death were history of chronic obstructive pulmonary disease (p < 0.002) and glomerular filtration rate at admission (p < 0.0001). CONCLUSIONS: Medical management, especially for uncomplicated acute type B aortic dissection, is associated acceptable outcomes. This study provides current data for initial medical management of acute type B aortic dissection. Alternative strategies for the treatment of acute Type B aortic dissection should be compared with these results.

Acute type A aortic dissection complicated by stroke: can immediate repair be performed safely?

OBJECTIVE: Emergency surgical intervention for acute type A aortic dissection complicated by stroke remains controversial. The urgency of immediate repair in this setting is tempered by the concern that cerebral reperfusion may worsen neurologic outcome. The purpose of this study was to report and analyze our results with acute type A aortic dissection complicated by stroke. METHODS: Between September 1999 and March 2005, 151 consecutive patients presented with acute type A aortic dissection. Of this group, 16 (10.6%) patients had sustained a preoperative stroke. Mean age was 56 years (range 43-73 years), with 6 (38%) women. Right hemispheric, left hemispheric, and bilateral strokes occurred in 81%, 13%, and 6%, respectively. Computed tomographic scan or transesophageal echocardiography diagnosed aortic dissection; clinical examination, computed tomographic scan, or transcranial Doppler ultrasound diagnosed stroke. Aortic repair was performed with cardiopulmonary bypass, profound hypothermic circulatory arrest, and retrograde cerebral perfusion. One patient with complete neurologic devastation (coma) was not operated on. RESULTS: Overall hospital mortality was 18.8% (3/16). Mortality in 2 patients who did not undergo surgery (1 patient who was neurologically devastated, and 1 patient whose aorta ruptured while awaiting surgery) was 100% (2/2). Operative mortality was 7% (1/14). Among patients undergoing surgery, neurologic status completely recovered in 2 (14%) patients, improved in 6 (43%) patients, remained the same in 6 (43%) patients, and worsened in none. Median time from onset of stroke to surgery was 9 hours (range 1-240 hours). Eighty percent of patients who underwent surgical repair within 10 hours had improvement in neurologic status, where as none operated on beyond 10 hours improved (P < .02). CONCLUSIONS: In our experience, surgical repair of acute type A aortic dissection can be performed in the setting of preoperative stroke with acceptable mortality. Moreover, no worsening of neurologic condition was observed after surgical repair. Immediate surgical repair is warranted even if acute type A aortic dissection is complicated by stroke.

Gastrointestinal complications after descending thoracic and thoracoabdominal aortic repairs: a 14-year experience.

OBJECTIVE: There is a paucity of data regarding gastrointestinal (GI) complications after descending thoracic and thoracoabdominal aortic (DTA/TAA) surgical repairs. We examined our 14-year experience with these repairs to determine the incidence, outcomes, and risk factors for postoperative GI complications. METHODS: Between February 1991 and February 2005, we repaired 1,159 DTA/TAA. Data were prospectively collected. The mean patient age was 68 years and 36% were women. Complications were classified as biliary disease, hepatic dysfunction, pancreatitis, GI bleeding, peptic ulcer disease, bowel ischemia, and ileus. Risk factors for the occurrence of GI complications were ascertained by univariate and multivariable analysis. RESULTS: Of the 1,159 patients, 81 had 109 GI complications, for a 7% incidence. The mortality associated with GI complications was 39.5% compared with 13.5% (P < .0001) in patients without GI complications. The incidences of complications were bowel ischemia, 2.5% with 62% mortality; biliary disease, 0.3% with 75% mortality; hepatic dysfunction, 1.6% with 38% mortality; acute pancreatitis, 0.3% with 20% mortality; GI bleeding, 1.5% with 29% mortality; peptic ulcer disease, 0.9% with 30% mortality; and ileus, 2.2% with 26% mortality. Postoperative biliary disease (odds ratio [OR], 16.58; P = .001), hepatic dysfunction (OR, 3.58; P = .006), and bowel ischemia (OR, 10.03; P = .0001) were significantly associated with an increased postoperative mortality. Risk factors for the occurrence of GI complications were visceral involvement of the aortic repair (TAA extent II, III, and IV) (OR, 2.08; P = .002) and low preoperative glomerular filtration rate (OR, .98; P = .0002). CONCLUSION: Biliary disease, hepatic dysfunction, and bowel ischemia after DTA/TAA surgical repairs were associated with an increased mortality. Visceral involvement and preoperative renal insufficiency were risk factors for the occurrence of GI complications.

Outcomes of medical management of acute type B aortic dissection.

BACKGROUND: Currently, the optimal treatment of acute type B aortic dissection remains controversial. The purpose of this study was to report early clinical outcomes of medical management for acute type B aortic dissection. METHODS AND RESULTS: Between January 2001 and March 2005, 129 consecutive patients with the confirmed diagnosis of acute type B aortic dissection were studied. Mean age was 61 years (range, 29 to 94), with 33.3% (43/129) female. Acute type B aortic dissection protocol was instituted with the intent to manage all patients medically. Indications for surgical intervention included rupture, aortic expansion, malperfusion, and intractable pain. All patients were followed-up after discharge. Hospital mortality was 10.1% (13/129), 19% (4/21) when vascular intervention was required, and 8.3% (9/108) when medical management was maintained. Early intervention was required in 21 cases (16.2%), 19 (14.7%) open vascular/aortic cases and 2 cases (1.6%) of percutaneous aortic interventions. Morbidity included rupture (4.7%), stroke (4.7%), paraplegia (8.5%), bowel ischemia (7%), acute renal failure (21%), dialysis requirement (13%), and peripheral ischemia (4.7%). Late vascular-related procedures were performed in 5.2% (6/116) of cases. Univariate risk factors for early mortality were rupture (P<0.0001), need for laparotomy (P<0.008), acute renal failure (P<0.0001), need for dialysis (P<0.0001), and lower extremity ischemia (P<0.0004). The only independent risk factors for hospital mortality by multiple logistic regression was rupture (P<0.0009), and independent risk factors for midterm death were history of chronic obstructive pulmonary disease (P<0.002) and low glomerular filtration rate (<57 mL/min; P<0.0001). CONCLUSIONS: Medical management for acute type B aortic dissection is associated acceptable outcomes. Outcomes of other management strategies, eg, endovascular stenting, for acute type B aortic dissection need to be compared with these results.

Postoperative intravenous iron used alone or in combination with low-dose erythropoietin is not effective for correction of anemia after cardiac surgery.

OBJECTIVES: The aim of this study was to examine whether intravenous iron III-hydroxide sucrose complex (IHSC) used alone was sufficient to provide rapid correction of anemia after cardiac surgery and whether additional stimulation of erythropoiesis is possible by means of a single low dose of recombinant-human erythropoietin (r-HuEPO) administration. DESIGN: Prospective, randomized, double-blind study. SETTING: The study was conducted in a university hospital. PARTICIPANTS: One hundred twenty American Society of Anesthesiologists II or III patients, who underwent elective cardiac surgery using cardiopulmonary bypass and in whom postpump hemoglobin ranged between 7 and 10 g/dL. INTERVENTIONS: Patients were divided into 3 groups: group I = control; group II received postoperative intravenous iron supplementation with an iron III-hydroxide sucrose complex (IHSC); and group III received IV iron and a single dose of r-HuEPO (300 U/kg). MEASUREMENTS AND RESULTS: No significant difference in transfusion needs was observed among the 3 groups (22%, 25%, and 17% of patients transfused in groups I, II, and III, respectively). Hemoglobin levels, reticulocyte counts, and serum ferritin levels were evaluated at different time intervals (until day 30 postoperatively). No side effects because of iron administration were noted in the study. Reticulocyte counts increased rapidly at day 5 (2.24% +/- 1.11%, 1.99% +/- 1.44%, and 3.84% +/- 2.02% in groups I, II, and III, respectively) and decreased after day 15 in the 3 groups. Ferritin levels increased significantly at day 5 in the 2 treated groups (899.33 +/- 321.55 ng/mL in group II, 845.75 +/- 289.96 ng/mL in group III v 463.15 +/- 227.74 ng/mL in group I). In group I, ferritin levels, after a slight elevation on day 5, decreased at day 15 to lower than baseline levels. No significant difference in hemoglobin increase was noted among the 3 groups. CONCLUSION: Postoperative intravenous iron supplementation alone or in combination with a single dose of r-HuEPO (300 U/kg) is not effective in correcting anemia after cardiac surgery.

Recurrence of left ventricular outflow tract obstruction after left anterior descending coronary artery revascularization in a patient with hypertrophic obstructive cardiomyopathy.

A patient with known hypertrophic obstructive cardiomyopathy presented with an anteroseptal myocardial infarction which resulted in the disappearance of his subaortic pressure gradient. Surgical revascularization of his left anterior descending coronary artery after the viability of his myocardium had been documented led to the recurrence of his left ventricular outflow tract obstruction and subaortic pressure gradient.