Which factors have a great impact on coagulopathy and hemostatic impairment after cardiopulmonary bypass in cardiovascular surgery? An analysis based on rotational thromboelastometry.

OBJECTIVES: This study aimed to investigate which factors have a great impact on coagulopathy after cardiopulmonary bypass (CPB) using rotational thromboelastometry (ROTEM). METHODS: Ninety-eight patients undergoing cardiovascular surgery using CPB were enrolled. Data of amplitude 10 min after clotting time (A10) of ROTEM measured routinely before and after CPB were retrospectively collected. ROTEM has some assays by which we can evaluate the capacity of extrinsic coagulation (EXTEM), intrinsic coagulation (INTEM), fibrin polymerization (FIBTEM), and the effect of heparin (HEPTEM). The platelet component, defined as PLTEM, can be calculated by subtracting FIBTEM from EXTEM. Age, sex, total plasma volume, pre-CPB A10, lowest body temperature, in-out balance during CPB, intraoperative bleeding amount, and type of pumps were considered as possible factors. Univariate and multivariate analyses were performed for the rate of change of A10. RESULTS: The change rate of each A10 had a significant negative correlation with bleeding amount (p < 0.01 for EXTEM, p < 0.01 for INTEM, p = 0.02 for FIBTEM, p < 0.01 for PLTEM). Female sex was a significant contributive predictor for the greater decline of EXTEM (p < 0.01) and INTEM (p < 0.01), positive balance for EXTEM (p < 0.01), FIBTEM (p = 0.01), and PLTEM (p < 0.01), long CPB time for INTEM (p = 0.01), centrifugal pump for FIBTEM (p < 0.01), and large pre-CPB A10 for PLTEM (p < 0.01). CONCLUSION: In perioperative hemostatic management using ROTEM, attention should be given to the effects of these multiple factors.

Successful cardiac surgery in a patient with Evans syndrome.

Evans syndrome is a rare haematological disease that may cause several complications during heart surgery. Herein we documented heart valve surgery in a patient with Evans syndrome who was receiving monoclonal antibody therapy, and valve replacement was successfully performed via prophylactic measures against haemolysis.

Traumatic right common femoral artery occlusion caused by blunt bicycle handlebar injury: a case report.

BACKGROUND: Traumatic femoral artery occlusion caused by blunt impact to the groin is rare; this condition is called the "motor-scooter handlebar syndrome." We herein report a case of traumatic femoral artery occlusion and performed a literature review on its diagnosis and treatment. CASE PRESENTATION: An 18-year-old man visited our hospital complaining of pain and swelling in his right groin and numbness in his right leg after a bicycle collision accident. Contrast computed tomography revealed an occlusion extending from the right external iliac artery to the common femoral artery. The right ankle-brachial index (ABI) was 0.50. We performed thrombectomy and femoral artery repair with a saphenous vein patch. The postoperative course was good, and the right ABI improved to 1.05. CONCLUSIONS: Motor-scooter handlebar syndrome is a rare complication of traumatic injury. The presence of vascular injury should be considered in patients with groin or lower abdomen injuries following an impact with handlebars or similar hard objects. This injury often needs surgical treatment; therefore, prompt diagnosis is the key to successful treatment.

Targeted regional injection of biocomposite microspheres alters post-myocardial infarction remodeling and matrix proteolytic pathways.

BACKGROUND: Although localized delivery of biocomposite materials, such as calcium hydroxyapatite (CHAM), have been demonstrated to potentially attenuate adverse left ventricular (LV) remodeling after myocardial infarction (MI), the underlying biological mechanisms for this effect remain unclear. This study tested the hypothesis that targeted CHAM injections would alter proteolytic pathways (matrix metalloproteinases [MMPs] and tissue inhibitors of MMPs [TIMPs]) and would be associated with parameters of post-MI LV remodeling. METHODS AND RESULTS: MI was induced in adult sheep followed by 20 targeted injections of a total volume of 1.3 mL (n=6) or 2.6 mL of CHAM (n=5) or saline (n=13) and LV end-diastolic volume (EDV) and MMP/TIMP profiles in the MI region were measured at 8 weeks after MI. LV EDV decreased with 2.6 mL CHAM versus MI only (105.4 ± 7.5 versus 80.6 ± 4.2 respectively, P<0.05) but not with 1.3 mL CHAM (94.5 ± 5.0, P=0.32). However, MI thickness increased by 2-fold in both CHAM groups compared with MI only (P<0.05). MMP-13 increased 40-fold in the MI only group (P<0.05) but fell by >6-fold in both CHAM groups (P<0.05). MMP-7 increased approximately 1.5-fold in the MI only group (P<0.05) but decreased to referent control values in both CHAM groups in the MI region (P<0.05). Collagen content was reduced by approximately 30% in the CHAM groups compared with MI only (P<0.05). CONCLUSIONS: Differential effects on LV remodeling and MMP/TIMP profiles occurred with CHAM. Thus, targeted injection of a biocomposite material can favorably affect the post-MI remodeling process and therefore holds promise as a treatment strategy in and of itself, or as a matrix with potentially synergistic effects with localized pharmacological or cellular therapies.

Elimination of ischemic mitral regurgitation does not alter long-term left ventricular remodeling in the ovine model.

BACKGROUND: The efficacy of annuloplasty for ischemic mitral regurgitation (IMR) has been difficult to establish. Using an established ovine model of IMR, we tested the ability of ring annuloplasty to durably relieve IMR and reverse or limit progression of left ventricular (LV) remodeling during a clinically relevant follow-up period. METHODS: A posterolateral infarction known to result in chronic IMR was initiated in 33 sheep. Echocardiography was used to assess LV end diastolic and systolic volumes and IMR (0 to 4 scale) before and 8 weeks after infarction. Eight weeks after infarction, 20 surviving animals with > or = 2+ IMR were randomized (1:1) to no treatment or undersized, semi-rigid, complete ring annuloplasty placement. LV remodeling and IMR were assessed at 4 and 6 months after infarction. RESULTS: All animals had similarly sized LV volumes at baseline (end systolic, 27.8 +/- 4.6 mL; end diastolic, 53.5 +/- 6.4 mL). The 20 randomized animals survived to complete the study. The degree of IMR before randomization was similar in treatment (2.6 +/- 0.4) and control (2.8 +/- 0.3) groups. At the 6-month follow-up, the degree of IMR was significantly less in the annuloplasty group (0.3 +/- 0.1 vs 3.4 +/- 0.6); however, LV volumes in the treatment group were not significantly different from the control group (end systolic, 82.1 +/- 15.6 vs 81.1 +/- 8.6 mL; end diastolic, 110.4 +/- 22.1 vs 111.1 +/- 16.5 mL). CONCLUSIONS: In a clinically relevant ovine model of IMR, annuloplasty provides durable relief from IMR during an extended follow-up period but does not significantly influence LV remodeling.

Intraoperative bronchoscopic resection of a papillary fibroelastoma in the left ventricular outflow tract after aortic mechanical valve replacement.

We report the case of an 80-year-old man who 11 years previously had undergone aortic valve replacement (St. Jude Medical mechanical heart valve 23 mm) because of aortic stenosis. At the current presentation, a 7-mm pedunculated tumor was discovered along the septal wall in the left ventricular outflow tract. In an attempt to perform a less invasive procedure because of the patient's advanced age, transaortic valve bronchoscopic resection was undertaken. A bronchoscope (Olympus BF P-200) was fed through a gap in the mechanical aortic valve. The entire tumor was removed using biopsy forceps, with histology revealing a papillary fibroelastoma. By using a bronchoscope, we avoided a second valve replacement.

Allogeneic mesenchymal precursor cell therapy to limit remodeling after myocardial infarction: the effect of cell dosage.

BACKGROUND: This experiment assessed the dose-dependent effect of a unique allogeneic STRO-3-positive mesenchymal precursor cell (MPC) on postinfarction left ventricular (LV) remodeling. The MPCs were administered in a manner that would simulate an off-the-self, early postinfarction, preventative approach to cardiac cell therapy in a sheep transmural myocardial infarct (MI) model. METHODS: Allogeneic MPCs were isolated from male crossbred sheep. Forty-six female sheep underwent coronary ligation to produce a transmural LV anteroapical infarction. One hour after infarction, the borderzone myocardium received an injection of 25, 75, 225, or 450 x 10(6) MPCs, or cell medium. Echocardiography was performed at 4 and 8 weeks after MI to quantify LV end-diastolic (LVEDV) and end-systolic volumes (LVESV), ejection fraction (EF), and infarct expansion. CD31 and smooth muscle actin (SMA) immunohistochemical staining was performed on infarct and borderzone specimens to quantify vascular density. RESULTS: Compared with controls, low-dose (25 and 75 x 10(6) cells) MPC treatment significantly attenuated infarct expansion and increases in LVEDV and LVESV. EF was improved at all cell doses. CD31 and SMA immunohistochemical staining demonstrated increased vascular density in the borderzone only at the lower cell doses. There was no evidence of myocardial regeneration within the infarct. CONCLUSION: Allogeneic STRO-3 positive MPCs attenuate the remodeling response to transmural MI in a clinically relevant large-animal model. This effect is associated with vasculogenesis and arteriogenesis within the borderzone and infarct and is most pronounced at lower cell doses.

Mild hypothermia to limit myocardial ischemia-reperfusion injury: importance of timing.

BACKGROUND: Hypothermia during ischemia has been shown to reduce myocardial reperfusion injury. We sought to establish the cardioprotective effect of very mild total-body hypothermia (

Regional heterogeneity of myocardial reperfusion injury: effect of mild hypothermia.

BACKGROUND: Mild hypothermia confers a myocardial protective effect that may make it a useful adjunct to reperfusion therapy for myocardial infarction (MI). The effect of temperature on the extent and distribution of myocardial reperfusion injury in a collateral deficient ovine model was studied. METHODS: Topical cooling maintained left atrial temperature at 39.5 degrees C (n = 8), 38.5 degrees C (n = 5), 37.5 degrees C (n = 6), 36.5 degrees C (n = 6), or 35.5 degrees C (n = 5) in sheep prior to 1 hour of coronary occlusion to produce an anteroapical myocardial risk area (AR) followed by 3 hours of reperfusion. A dual staining and planimetry technique was used to assess infarct size as a percentage of the AR in 3 myocardial short axis slices that included the entire AR (slice 1= most apical; slice 3= most basal). The subendocardial, midmyocardial, and subepicardial extent in short axis of the infarct was also assessed in each slice. Microspheres assessed transmural blood flow. RESULTS: At 39.5 degrees C there was a long-axis gradient in myocardial injury that was most severe at the apex and lessened toward the base. The midmyocardial region was most susceptible to injury at all long axis levels. Temperature reduction (as little as 1 degrees C) was associated with improved salvage that was most pronounced in the apical subendocardium and least in the basilar midmyocardium. Reperfusion at 39.5 degrees C resulted in severe transmural microvascular injury (no-reflow) that was completely obviated at temperatures below 38.5 degrees C. CONCLUSIONS: Myocardial reperfusion injury varies over the long and short LV axes. Mild hypothermia preferentially improves myocardial salvage at the LV apex. Small temperature changes can dramatically affect microvascular integrity.

Very mild hypothermia during ischemia and reperfusion improves postinfarction ventricular remodeling.

BACKGROUND: Mild hypothermia (< 4 degrees C) improves myocardial salvage after infarct reperfusion in animals and in early clinical studies. In this experiment the effect of mild hypothermia during ischemia and early reperfusion on long-term postinfarction left ventricular (LV) remodeling was assessed in an ovine infarct model. METHODS: In the initial phase of the experiment the effect of progressive degrees of hypothermia on infarct size was quantified. Thirty-eight male sheep were subjected to 1 hour of ischemia using a standardized anteroapical infarct followed by 3 hours of reperfusion. Temperature was maintained at either 39.5 degrees C (n = 11), 38.5 degrees C (n = 7), 37.5 degrees C (n = 7), 36.5 degrees C (n = 7), or 35.5 degrees C (n = 6) for the entire period of ischemia and reperfusion. The area at risk (AR) and infarct size as a percentage of AR (I/AR) were determined with a double staining and planimetry technique. In the second phase of the study, chronic post-infarction remodeling was assessed in animals with nonreperfused infarcts (n = 6), 1 hour of ischemia followed by reperfusion at 39.5 degrees C (n = 6) and 1 hour of ischemia followed by reperfusion at 37.5 degrees C (n = 6). Remodeling was determined at 8 weeks after infarction using echocardiography. RESULTS: The I/AR in the 39.5 degrees C, 38.5 degrees C, 37.5 degrees C, 36.5 degrees C, and the 35.5 degrees C groups was 71.8 +/- 3.0%, 63.1 +/- 1.9%, 49.4 +/- 1.4%, 38.7 +/- 1.4%, and 21.7 +/- 2.2%, respectively (p < 0.05 between all groups). In the chronic study LV end systolic volume at 8 weeks after infarction was 81 +/- 8 mL in the nonreperfused group, 57 +/- 4 mL in the 39.5 degrees C reperfusion group, and 41 +/- 3 mL in the 37.5 degrees C reperfusion group (p < 0.05 for between group differences). CONCLUSIONS: Subtle degrees of hypothermia can significantly improve immediate myocardial salvage and long-term LV remodeling after infarct reperfusion.

Effect of reperfusion on left ventricular regional remodeling strains after myocardial infarction.

BACKGROUND: Reperfusion therapy for myocardial infarction is currently the most effective means for limiting early and late mortality. We sought to elucidate how reperfusion influences remodeling strains in the infarct, borderzone, and remote myocardial regions. Understanding the effects of reperfusion on regional remodeling will help to evaluate and optimize emerging treatments for patients who do not achieve effective reperfusion after myocardial infarction. METHODS: An ovine infarct model (n = 13) was used to assess the effect of 1 hour of ischemia followed by reperfusion on regional and global myocardial geometry, function, and perfusion using sonomicrometry, echocardiography, and microspheres. Thirteen additional animals were assessed chronically (8 weeks) with echocardiography and postmortem analysis after either reperfusion (n = 5) or untreated infarction (n = 8). RESULTS: During ischemia the area at risk thinned, stretched, and became dyskinetic. The normally perfused borderzone also stretched, and contraction decreased by 40% during ischemia. Reperfusion increased area at risk wall thickness and reduced area at risk stretching but did not restore contractile function. Borderzone stretching was reduced and contractile function improved by reperfusion. Contractile function of remote regions was also improved with reperfusion. Ventricular dilatation after ischemia was reversed within 180 minutes of reperfusion. Chronically, reperfusion significantly improved global remodeling when compared with nonreperfused controls. Reperfused animals had thicker infarcts and akinetic rather than dyskinetic apical segments. CONCLUSIONS: Reperfusion acutely increases area at risk wall thickness, reduces area at risk and borderzone stretching, and improves borderzone and remote function. Reperfusion increases mature scar thickness and improves chronic global remodeling. These beneficial effects of reperfusion result primarily from reduced infarct expansion (stretching).

In vivo biomechanical assessment of triglycidylamine crosslinked pericardium.

While glutaraldehyde crosslinking is most often used to fabricate bioprosthetic heart valves (BHV) using heterograft tissues, it predisposes BHV to calcification and dramatically stiffens the heterograft tissues. Our group previously reported the synthesis and characterization of a novel epoxy-crosslinker, triglycidylamine (TGA). TGA pretreatment of BHV tissues compared to glutaraldehyde results in both calcification resistance in subdermal implants and improved leaflet compliance. In these prior studies, optimal calcification inhibition was noted with the combined use of TGA with mercapto-aminobisphosphonate (MABP). In the present study, we investigated the hypothesis that bovine pericardium cross-linked with TGA-MABP retains these beneficial biomechanical properties in vivo using a novel mitral valve anterior leaflet (MVAL) ovine valvuloplasty model. Bovine pericardial specimens were crosslinked with either glutaraldehyde or TGA-MABP, from which 1cm2 sections were implanted in the ovine MVAL after removal of the original tissue of the same size. An array of four sonomicrometry transducers were implanted on the corners and used to compute the complete in-surface strain tensor cardiac cycle over the cardiac cycle at 0 and 4 weeks. Following explant samples were fixed in formalin for histology studies. At 4 weeks both treatment groups experienced no dimensional changes in the unloaded state, indicating no shrinkage. When fully loaded during peak systolic ejection, TGA-MABP valvuloplasty patches were significantly more compliant, which did not change at 4 weeks. In contrast, the glutaraldehyde areal strain increased significantly by 4 weeks. Estimated implant stresses for both treatment groups, based on previously measured biomechanical properties [Connolly JM, Alferiev I, Clark-Gruel JN, Eidelman N, Sacks M, Palmatory E, et al. Triglycidylamine crosslinking of porcine aortic valve cusps or bovine pericardium results in improved biocompatibility, biomechanics, and calcification resistance: chemical and biological mechanisms. Am J Pathol 2005;166(1):1-13], were 40 and 250 kPa in the circumferential and radial directions, respectively, which are comparable to predicted BHV peak stress levels. We conclude that TGA-MABP crosslinked bovine pericardium, when subjected to in vivo BHV stress levels in a blood-contacting environment, maintains stable functionality.

Progression of myocardial injury during coronary occlusion in the collateral-deficient heart: a non-wavefront phenomenon.

It is widely accepted that, during acute coronary occlusion, ischemic cell death progresses from the subendocardium to the subepicardium in a wavefront fashion. This concept, which implies that the subendocardium is the most susceptible myocardial region to ischemic injury, was established using a canine model with an extensive system of subepicardial coronary collaterals. In humans, particularly in those with coronary artery disease, there is a wide range in the distribution and functional capacity of the collateral circulation, which may affect the pattern of infarct evolution. Using an ovine model with a limited system of preformed subendocardial coronary collaterals, we characterized the effect of increasing lengths of ischemia on regional blood flow and infarct size in three regions of the ventricular wall: subendocardium, midmyocardium, and subepicardium. Our results demonstrate that the myocardium and microvasculature in these three regions are equally susceptible to injury after 45 min of ischemia. When ischemic time is increased to 1 h, infarct size in the midmyocardium (90 +/- 2%) is greater than in the subendocardium (76 +/- 4%, P = 0.004) and subepicardium (84 +/- 3%, P = 0.13). Microvascular dysfunction as assessed as a percentage of baseline flow is also greater in the midmyocardium (14 +/- 5%) compared with the subendocardium (20 +/- 3%, P = 0.23) and subepicardium (51 +/- 9%, P = 0.007). These findings suggest that, in subjects with a limited system of coronary collateral circulation, the midmyocardium is the most susceptible myocardial region to ischemia and the subendocardium is the most resistant. Myocardial viability during coronary occlusion appears to be primarily determined by the distribution and functional capacity of the collateral circulation.

Aortic root subadventitial hematoma.

A 51-year-old woman was operated on for aortic valve regurgitation 3 months after experiencing chest tightness awakening her from sleep. Intraoperative findings included turbid dark brown pericardial fluid and a nipple-shaped protrusion on the external aspect of the noncoronary sinus of Valsalva. Histologically, the lesion was enclosed by intact media and adventitia, and represented an organized hematoma. Dilated venules noted adjacent to the lesion were suggestive of an intramural hemangioma. The etiology of this lesion is unclear, but it might be an unusual type of intramural hematoma (IMH) and gives us a hint of an origin of IMH.

Effects of hemodynamic alterations on anterior mitral leaflet curvature during systole.

OBJECTIVES: The application of repair techniques to treat mitral valve incompetence has increased progressively during the past 20 years. Unfortunately, recent reports have demonstrated the longevity of these repairs to be less than previously believed. Most repair failures are stress related. Computational models to optimize valve repair are in development, but to be brought to fruition, a better understanding of dynamic leaflet geometry is necessary. In this study, sonomicrometry was used in an ovine model to compute systolic leaflet curvature at varying afterloads and states of contractility. METHODS: The anterior leaflet of 12 sheep was instrumented with 5 piezoelectric transducers in a cruciate array. Systolic blood pressure ranged from 90 to 200 mm Hg with increasing phenylephrine hydrochloride infusion. Epinephrine was used to vary contractile state. Leaflet curvature was calculated continuously (200 Hz) during systole. RESULTS: Anterior leaflet curvature in the septolateral direction was double that in the intercommisural direction. There were also significant changes in leaflet curvature during systole. Curvature in neither direction was affected by afterload. Epinephrine augmented intercommisural curvature in a dose-independent fashion, whereas it had no effect on curvature in the septolateral direction. CONCLUSIONS: Dynamic mitral anterior leaflet geometry was found to be amazingly constant over a wide range of hemodynamic conditions. These data provide information about leaflet geometry that will aid in the construction of realistic computational models. Such models may facilitate the design of annuloplasty rings and surgical techniques that minimize leaflet stress and increase mitral valve repair longevity.

Effect of prostaglandin E1 on ischemia-reperfusion injury during abdominal aortic aneurysm surgery.

OBJECTIVE: Abdominal aortic aneurysm (AAA) surgery subjects the lower extremities to ischemia and reperfusion. Although it is not extensive or prolonged, ischemia of the lower extremities during aortic cross-clamping is gradually and steadily induced. We studied the effects of prostaglandin E1 (PGE1) on ischemia-reperfusion injury of the lower extremities during AAA repair. METHODS: During AAA surgery, two near-infrared spectroscopy probes were positioned on each calf muscle to monitor oxygen metabolism in the lower extremities. We also measured lactate concentration in both iliac veins. RESULTS: Near-infrared spectroscopy signals responded sensitively to aortic cross-clamping and declamping. Lactate increased time-dependently during aortic cross-clamping. The continuous venous administration of PGE1 (20 ng/kg per minute) inhibited the accumulation of lactate during aortic cross-clamping. Declamping of the first iliac artery resulted in a further but transient increase in ipsilateral venous lactate, which may be one component in the mechanism of declamping shock. Prostaglandin E1 eliminated the transient increase in ipsilateral lactate. The administration of PGE1 inhibited the contralateral accumulation of lactate after first declamping, and the lactate level decreased gradually before the second declamping. CONCLUSIONS: Prostaglandin E1 seems to have a protective effect against ischemia-reperfusion injury of the lower extremities during AAA surgery.

MRSA aortic valve endocarditis treated by pericardium-lined Dacron patch and vancomycin-containing fibrin glue.

A 40-year-old man was admitted with a diagnosis of MRSA aortic valve endocarditis. He was treated conservatively with clindamycin and vancomycin for three days, but embolism occurred into the brain and the right lower limb, and urgent aortic valve replacement was performed. Resecting an aortic annular abscess resulted in a huge defect of the root. The defect was reconstructed with a combined patch: a Dacron graft lined with pericardium using vancomycin-containing fibrin glue. Although complete healing of the infected leg wound was slow, no prosthetic valve endocarditis has been detected in the 11 months since operation.

Limb ischemia and reperfusion during abdominal aortic aneurysm surgery.

PURPOSE: Abdominal aortic aneurysm (AAA) surgery involves ischemia and reperfusion of the lower extremities, but assessing the pathophysiological changes is difficult. We evaluated the extent and time course of ischemia-reperfusion injury of the lower extremities during AAA surgery. METHODS: To monitor oxygen metabolism, two near-infrared spectroscopy (NIRS) probes were positioned on each calf muscle of nine patients undergoing AAA surgery. Lactate and pH were also measured in both iliac veins. RESULTS: Near-infrared spectroscopy signals responded sensitively to aortic cross-clamping and declamping. Lactate increased gradually and exponentially during aortic cross-clamping, and reconstruction of the first iliac artery resulted in a further but transient increase in ipsilateral venous lactate. The time course of the pH level after declamping was almost a mirror image of that of lactate. Reconstruction of the first iliac artery did not affect the contralateral NIRS signals, lactate, or pH. CONCLUSIONS: Near-infrared spectroscopy may be useful for monitoring limb ischemia during AAA surgery. The transient increase in lactate and the transient decrease in pH after first declamping may contribute to the mechanism of declamping shock. The fact that first declamping did not affect measurements on the other side shows that contralateral ischemia progresses steadily after reconstruction of the first iliac artery. Therefore, reconstruction of the second iliac artery should be done as soon as possible.

An implantation of DDD epicardial pacemaker through ministernotomy in a patient with a superior vena cava occlusion.

We successfully implanted a DDD epicardial pacemaker through a limited lower sternotomy in a patient whose superior vena cava had been occluded. Both epicardial leads were connected to the generator placed in the existing subcutaneous pocket on the left pectoral region through the second intercostal space. This approach provided excellent exposure and easy access to both the right appendage and the right ventricle. The combined procedure of epicardial DDD pacemaker implantation through a limited lower sternotomy with placement of the generator in the pectoral subcutaneous pocket is one of the better methods when intravenous lead implantation is difficult.

Successful treatment of a Salmonella aortic arch aneurysm.

A 52-year-old man hospitalized for hoarseness and chest pain was found in chest computed tomography to have an impending aortic arch aneurysm rupture. Laboratory studies showed the presence of severe inflammation. Based on a clinical diagnosis of infected aortic arch aneurysm, we conducted total arch replacement. Salmonella was identified in the aneurismal wall and antibiotics were administered long-term. The postoperative course was uneventful. The patient was discharged on postoperative day 48. He has remained afebrile and asymptomatic in the 10 months since surgery but continues to take 300 mg/d of oral levofloxacin.