Biomedical subjects

R C McIntyre

Publications and source records attributed to R C McIntyre.

At least 73 records · Page 4Linked to original sources

PubMed1996

Adenosine is a selective pulmonary vasodilator in cardiac surgical patients.

OBJECTIVE: The purpose of this study was to examine and compare the systemic and pulmonary hemodynamic effects of a central venous infusion of adenosine in cardiac surgical patients. DESIGN: Prospective; each subject served as his/her own control. SETTING: University Hospital and Veteran's Affairs Medical Center. PATIENTS: Ten cardiac surgical patients (age 56 +/- 6 years) were studied in the operating room under general anesthesia after weaning from cardiopulmonary bypass. Pulmonary vascular resistance (PVR), systemic vascular resistance (SVR), mean pulmonary arterial pressure (MPAP), and mean systemic arterial pressure (MAP) were determined before, during, and after central venous infusion of adenosine (50 micrograms/kg/min) for 15 min. Statistical analysis was by analysis of variance; significance was accepted at p < 0.05. RESULTS: Adenosine produced selective vasodilation of the pulmonary vascular bed: both PVR and MPAP were significantly reduced during adenosine infusion without changes in either SVR or MAP. PVR and MPAP returned to preinfusion levels after cessation of the infusion. Adenosine effectively reduced PVR and pulmonary arterial pressure without decreasing SVR or systemic arterial pressure. CONCLUSIONS: Adenosine may be used clinically as a selective pulmonary vasodilator to optimize pulmonary hemodynamics without adverse systemic hemodynamic effects in cardiac surgical patients. It may be particularly valuable in patients with right heart dysfunction by selectively lowering right ventricular afterload.

Adenosine↗

PubMed1996

Adenosine for refractory pulmonary hypertension.

We report 2 patients with refractory acute pulmonary hypertension. In both, a central venous infusion of adenosine into the circulation effectively lowered pulmonary arterial pressure when standard treatment measures had failed, and reversed the clinical state of shock by achieving pulmonary vasodilatation. We conclude that adenosine may help lower pulmonary arterial pressure without lowering systemic arterial pressure in the setting of acute pulmonary hypertension when standard measures have failed.

Adenosine↗

PubMed1995

Pulmonary hypertension in acute lung injury is due to impaired vasodilation with intact vascular contractility.

The major hemodynamic feature of acute lung injury (ALI) is pulmonary hypertension. Both endothelial-dependent and -independent pulmonary vasorelaxation is impaired in ALI due to endotoxemia. We hypothesized that endotoxemia selectively impairs relaxation of the pulmonary artery but does not impair contractility of pulmonary vascular smooth muscle (VSM). Our purpose was to determine the effect of endotoxemia (ETX) on the contractile response of pulmonary VSM to (1) tubular depolarization (KCl), (2) alpha 1-adrenoreceptor stimulation (phenylephrine, PE), (3) 5HT2 receptor stimulation (serotonin, 5HT), and (4) prostaglandin F2 alpha receptor stimulation. Pulmonary artery rings were isolated from rats 6 hr after injection of ETX, 20 mg/kg ip (n > or = 6), or saline (n > or = 6) and suspended on tensiometers in individual organ baths. Endothelial-dependent cGMP-mediated relaxation was determined using the receptor agonist acetylcholine (ACh) in rings preconstricted with PE. Dose-response curves were generated to each contractile agonist. Statistical comparison was performed using one-way ANOVA with post hoc Bonferonni-Dunn, P < 0.05 accepted as significant. Relaxation to ACh was 96.4 +/- 1.3% in controls vs 21.4 +/- 3.1% (P < 0.05) in endotoxin-treated rats. Endotoxin did not affect the maximal tension in response to the contractile agonists nor did it change the concentration required to produce 50% contraction (EC50). From these data we conclude that endotoxemia causes a decrease in vasorelaxation to the endothelial-dependent receptor agonist acetylcholine but does not impair agonist-induced contractility of pulmonary VSM. This suggests that pulmonary hypertension in ALI is mediated by impairment of pulmonary vasodilation with preservation of VSM contractility.

Acute Disease↗

PubMed1995

Laparoscopic ultrasonography as compared with static or dynamic cholangiography at laparoscopic cholecystectomy. A prospective multicenter trial.

We compared laparoscopic ultrasonography (LICU) with static (S) or dynamic (D) cholangiography (IOC) for assessment of duct anatomy an calculi in 209 patients. LICU visualized ducts in 88% compared with 93% for IOC (P = 0.046). Nineteen patients (9%) had stones: 17 were found by LICU (89%) and 10 (53%) by IOC (P = 0.032). Time to perform LICU (7 +/- 3 min) was less than IOC (13 +/- 6 min) (P < 0.0001). Time to perform SIOC (12 +/- 5 min) and DIOC (14 +/- 6 min) did not differ (P = 0.48), nor did these tests differ in accuracy. LICU provided useful anatomical information but IOC better defined anatomic anomalies. LICU required less time but was less reliable at defining anatomy and complete duct visualization. LICU was more sensitive for stones. SIOC and DIOC did not differ objectively. LICU and IOC are complementary.

Bile Duct Diseases↗

PubMed1995

Are corticosteroids salvage therapy for refractory acute respiratory distress syndrome?

BACKGROUND: Late acute respiratory distress syndrome (ARDS), characterized by progressive pulmonary interstitial fibroproliferation, is associated with mortality > 80%. Although previous large prospective trials failed to show a benefit of steroids in early ARDS, recent small reports describe improved survival in patients with late ARDS. Recognizing the pathogenetic differences between early and late ARDS, we employed steroid therapy in patients with refractory late ARDS. PATIENTS AND METHODS: Over a 5-year period, we treated 6 patients who were dying of isolated refractory ARDS with methylprednisolone sodium succinate (1 to 2 mg/kg every 6 hours). Ventilatory parameters and lung injury scores were serially recorded, and steroids were weaned based on clinical response. RESULTS: Steroids were instituted after 16 days of advanced mechanical ventilatory support. By day 7 of steroid therapy, there was clinically significant improvement in PaO2/FiO2 ratios (84 to 172) and lung injury scores (3.6 to 2.9); 5 patients (83%) survived. CONCLUSIONS: Steroid therapy appears to be effective in patients with refractory late ARDS. Prospective trials are needed to define the indications, timing of intervention, dose and duration, and precautions of steroid therapy.

Acute Disease↗

PubMed1995

Modified ilioinguinal node dissection for metastatic melanoma.

BACKGROUND: Standard ilioinguinal node dissection for melanoma has substantial cost and morbidity. Beginning in 1988, we modified the procedure in hopes of reducing side effects without compromising survival. PATIENTS AND METHODS: Dissection was standard except for preservation of saphenous vein and femoral sheath and omission of sartorius muscle transfer. To date, 19 patients with recurrent melanoma in the groin have had the procedure, 6 for N1 disease and 13 for N2, M1 metastases. RESULTS: Average hospital stay was 4.5 days (range 3 to 7). Postoperative edema occurred in 1 (5%) patient. Disease-free survival at 40 months was 66% for N1 disease and 26% for N2, M1 metastases. CONCLUSION: Modified ilioinguinal node dissection appears to reduce cost and morbidity of treating recurrent melanoma in the groin without compromising survival.

Adolescent↗

PubMed1995

Lung transplantation with cardiopulmonary bypass exaggerates pulmonary vasomotor dysfunction in the transplanted lung.

Pulmonary vascular resistance is significantly increased in the transplanted lung. If cardiopulmonary bypass is required, the transplanted lung is reperfused with activated blood elements, which might exacerbate the reperfusion injury. The purpose of this study was to examine the influence of cardiopulmonary bypass on the following mechanisms of pulmonary vasomotor control in a dog model of autologous lung transplantation: (1) endothelium-dependent cyclic guanosine monophosphate-mediated relaxation (response to acetylcholine), (2) endothelium-independent cyclic guanosine monophosphate-mediated relaxation (response to nitroprusside), and (3) beta-adrenergic cyclic adenosine monophosphate-mediated relaxation (response to isoproterenol). Autologous right lung transplants were performed with (n = 4 dogs) and without (n = 5 dogs) bypass. Lungs were stored in cold saline solution (4 degrees C, 3 hours) before reimplantation. Pulmonary vasomotor control mechanisms were studied in isolated pulmonary arterial rings immediately after harvest and 1 hour after reimplantation. Ten rings were studied in each group at each time. Statistical analysis was by analysis of variance. Without bypass, endothelium-dependent cyclic guanosine monophosphate-mediated relaxation and beta-adrenergic cyclic adenosine monophosphate-mediated relaxation were significantly impaired, although endothelium-independent cyclic guanosine monophosphate-mediated relaxation was not. Use of bypass produced significantly greater impairment of both endothelium-dependent cyclic guanosine monophosphate-mediated relaxation and beta-adrenergic cyclic adenosine monophosphate-mediated relaxation. In addition, use of bypass produced significant dysfunction of endothelium-independent cyclic guanosine monophosphate-mediated relaxation as well. We conclude that using cardiopulmonary bypass to perform lung transplantation greatly exaggerates pulmonary vasomotor dysfunction in the transplanted lung. This dysfunction may contribute to significantly higher pulmonary vascular resistance in the transplanted lung if cardiopulmonary bypass is used.

Acetylcholine↗

PubMed1995

Selective inhibition of cyclic adenosine monophosphate-mediated pulmonary vasodilation by acute hypoxia.

BACKGROUND: Adult respiratory distress syndrome is characterized by hypoxia and acute pulmonary hypertension. Therefore we examined the effect of acute hypoxia on the mechanisms of pulmonary vasodilation. METHODS: Isolated rat pulmonary artery rings were suspended on tensiometers in a balanced salt solution. A normoxic gas mixture was bubbled through the solution (21% O2, 5% CO2, 74% N2). Rings were preconstricted with phenylephrine, and the following mechanisms of pulmonary vascular smooth muscle relaxation were studied in a random order: (1) endothelial-dependent cyclic guanosine monophosphate-mediated (acetylcholine, 10(-9) to 10(-6) mol/L), (2) endothelial-independent cyclic guanosine monophosphate-mediated (nitroprusside, 10(-9) to 10(-6) mol/L), and (3) beta-adrenergic receptor cyclic adenine monophosphate-mediated (isoproterenol, 10(-9) to 10(-6) mol/L). Separate rings were preconstricted with phenylephrine, and the gas was switched to a hypoxic mixture (0% O2, 5% CO2, 95% N2). After vasoconstriction to hypoxia reached a plateau, the response to the maximal effective dose of the above vasodilators (10(-6) mol/L) was determined in a random order. Statistical analysis was done with one-way analysis of variance with post hoc Bonferroni-Dunn correction. A p value of less than 0.05 was accepted as significant. RESULTS: Endothelial-dependent and -independent cyclic guanosine monophosphate-mediated relaxation was the same in normoxia and hypoxia. On the other hand, hypoxia inhibited beta-adrenergic receptor cyclic adenine monophosphate-mediated pulmonary vasorelaxation (97.5% +/- 2.5% versus 71.5% +/- 2.3% in hypoxia; p < 0.01). CONCLUSIONS: These data suggest that hypoxia selectively inhibits beta-adrenergic cyclic adenine monophosphate-mediated pulmonary vasorelaxation. This dysfunction of the normal mechanism of pulmonary vasodilation may contribute to the pulmonary hypertension seen in adult respiratory distress syndrome.

Acetylcholine↗

PubMed1995

Inhaled nitric oxide variably improves oxygenation and pulmonary hypertension in patients with acute respiratory distress syndrome.

OBJECTIVE: The purpose of this study was to determine the effect of inhaled nitric oxide (NO) on oxygenation, hemodynamics, and ventilation in patients with adult respiratory distress syndrome (ARDS). METHODS: Sixteen trials of inhaled NO were performed in 14 ARDS patients (age 42.9 +/- 6) who had significant pulmonary hypertension (mean pulmonary artery pressure > 30 mm Hg). Patients were monitored with arterial and pulmonary artery catheters. Volume ventilation was performed by a strict protocol. Data were collected at baseline and 30 minutes after 20 and 40 ppm NO. RESULTS: Overall, the Pao2/FIO2 ratio increased from 69.5 +/- 3.9 to 100.8 +/- 9.5 at 20 ppm, a 42.9 +/- 8.7% increase, and to 97.7 +/- 13.1 at 40 ppm, a 44.1 +/- 14.2% increase over baseline (p = 0.001). However, 5/16 trials demonstrated minimal improvement (Pao2/FIO2 ratio increase < 20%), 5 moderate improvement (20-50%), and 6 marked improvement (> 50%). Overall the mean pulmonary artery pressure (MPAP) decreased from 41.1 +/- 1.8 mm Hg to 34.3 +/- 1.3 at 20 ppm and 33.5 +/- 1.8 mm Hg at 40 ppm, a 15.0 +/- 3.7% decrease, p = 0.002. However, 5/16 trials demonstrated minimal improvement (MPAP decrease < 10%), 7 moderate improvement (10-20%), and 4 marked improvement (> 20%). At 40 ppm NO, 4 patients with moderate improvement in MPAP at 20 ppm NO had marked improvement. There were no changes in systemic oxygen delivery and consumption, intrapulmonary shunt, or lung compliance at 20 or 40 ppm (p > 0.05). Following collection of these data, prolonged NO inhalation (2-20 ppm) was done in 10 of 14 patients for 4.5 +/- 0.7 days (range 1-10 days). Overall, there were 7 deaths (mortality 50%). In patients receiving prolonged NO, there were 3 deaths (mortality 30%). All 4 patients who failed to respond to inhaled NO subsequently died (mortality 100%). CONCLUSIONS: Inhaled NO improves oxygenation and pulmonary hemodynamics in patients with ARDS. However, the improvement to NO is variable.

Adolescent↗

PubMed1995

Role of bradykinin in cardiac functional protection after global ischemia-reperfusion in rat heart.

We have reported that cardiac preconditioning against ischemia-reperfusion (IR) can be induced by transient ischemia (TI) and alpha 1-adrenoreceptor stimulation, both mediated by protein kinase C (PKC) (Mitchell, M., X. Meng, C. Parker, E. Brew, A. Harken, and A. Banerjee. Circ. Res. 76: 73-81, 1995). Our study objective was to explore the mechanism of endogenous preconditioning and address the role of PKC activation in bradykinin-mediated cardiac functional protection. Isolated rat heart was used to assess the effects of exogenous bradykinin, TI, selective B2-receptor blocker, and PKC antagonism on cardiac functional recovery after a global IR injury. Final recovery of developed pressure was improved in hearts treated with bradykinin and TI compared with controls. Bradykinin- and TI-mediated preconditioning was eliminated with coinfusion of the B2-receptor antagonist. Further evaluation of bradykinin-mediated preconditioning revealed that PKC blockade also eliminated functional protection. Immunofluorescent stains of bradykinin-treated hearts demonstrated translocation and activation of specific PKC isoforms in the preconditioned heart. We conclude that TI-mediated preconditioning involves intrinsic cardiac bradykinin receptor stimulation. Bradykinin, through the B2 receptor, initiates a series of intracellular events culminating in the activation of PKC.

Animals↗

PubMed1995

Dysfunction of cGMP-mediated pulmonary vasorelaxation in endotoxin-induced acute lung injury.

Endothelial-dependent and -independent cGMP-mediated mechanisms of pulmonary vasorelaxation were studied in endotoxin-induced acute lung injury in the rat. Concentration-response curves were generated (10(-9) to 10(-6) M) for acetylcholine (ACh), A23187, and sodium nitroprusside (SNP) and for 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) (10(-9) to 10(-4) M) in isolated pulmonary arterial rings preconstricted with phenylephrine 6 h after endotoxin treatment (20 mg/kg ip). Endotoxin treatment produced significantly increased lung neutrophil accumulation (myeloperoxidase assay, 28 +/- 6 units/g lung tissue vs. 1.8 +/- 1 in controls) and lung leakage (lung/blood 125I-labeled albumin ratio, 0.06 +/- 0.01 vs. 0.028 +/- 0.01 in controls) as well as histological evidence of pulmonary vascular endothelial damage. The concentration-response curves demonstrated that pulmonary vasorelaxation by mechanisms that require generation of cGMP by either endothelial-dependent (both receptor-dependent, ACh, and receptor-independent, A23187) or endothelial-independent (SNP) pathways were significantly impaired after endotoxin treatment. Relaxation by stimulation with the cGMP analogue 8-BrcGMP was not different from control. Pulmonary vascular smooth muscle is able to relax in response to cGMP after endotoxin treatment, but relaxation by endothelial-dependent and -independent pathways that require generation of cGMP is significantly impaired.

Acetylcholine↗

PubMed1995

Laparoscopic ultrasonography. Has it extended the horizon?

Laparoscopic ultrasonography complements conventional radiologic evaluation of the biliary system at cholecystectomy. Addition of laparoscopic ultrasonography for staging patients with hepatic and pancreatic cancer improves accuracy and minimizes futile laparotomy. Dedicated laparoscopic ultrasound-guided biopsy devices facilitate tissue sampling. Ultrasonography will play an increasingly important role in laparoscopic diagnosis and treatment.

Abdomen↗

PubMed1994

Endotoxin disrupts beta-adrenergic signal transduction in the heart.

BACKGROUND: Nonsurvivors of septic shock demonstrate impaired myocardial function refractory to the administration of beta-agonists. METHODS: Using the isolated rat heart preparation, the integrity of the beta-adrenergic transduction pathway was tested (rate pressure product, rate of contraction, rate of relaxation, and cyclic adenosine monophosphate content) using isoproterenol hydrochloride (beta-receptor agonist) or colforsin (forskolin) (adenylyl cyclase activator) stimulation following intracoronary endotoxin infusion. RESULTS: Basal rate pressure product, rate of contraction, rate of relaxation, and cyclic adenosine monophosphate concentrations were unaffected by endotoxin infusion. Endotoxin impaired, increases in rate pressure product, rates of contraction and relaxation, and cyclic adenosine monophosphate to isoproterenol (P < .05), but the response to colforsin was unaffected by endotoxin. CONCLUSIONS: Endotoxin disrupts the myocardial response to direct beta-receptor stimulation but not to adenylyl cyclase stimulation in the isolated rat heart. CLINICAL RELEVANCE: Alteration of the proximal beta-adrenoreceptor complex by endotoxin suggests that therapy of the failing heart during refractory septic shock may be directed to intact sites distal in the beta-adrenergic pathway.

Adenylyl Cyclases↗

PubMed1994

Reexploration and angiographic ablation for hyperparathyroidism.

OBJECTIVE: Persistent and recurrent hyperparathyroidism remains a challenging clinical problem. The purposes of this study were to determine the causes of initial failure, the accuracy of preoperative localization tests, the role of angiographic parathyroid ablation, and the safety and efficacy of reexploration for hyperparathyroidism. DESIGN: A retrospective review of 42 patients undergoing reexploration or angiographic ablation for hyperparathyroidism was done, with a mean follow-up of 3 years, 7 months (range, 1 month to 13 years). SETTING: This study was carried out in a university medical center and a Veterans Affairs hospital. PATIENTS: All patients who underwent reexploration or angiographic ablation for hyperparathyroidism were included. INTERVENTION: All patients underwent preoperative localization studies. The cervical approach was used when the abnormal gland was suspected to be in the neck or the mediastinum superior to the aortic arch; sternotomy was used for deeper mediastinal glands not resectable through a cervical approach. Angiographic ablation of mediastinal glands was performed using contrast administration after a catheter was wedged into the selective feeding artery. MAIN OUTCOME MEASURES: End points included causes of initial treatment failure, accuracy of preoperative localization studies, long-term correction of hypercalcemia with repeated treatment, need for subsequent intervention for hypercalcemia, and complications of therapy. RESULTS: The most common reasons for initial failure were mediastinal glands (18 patients), surgeon's inexperience (12 patients), supernumerary glands (six patients), and other anatomic anomalies. Hyperplasia accounted for hyperparathyroidism in 11 patients (26%) and adenomas in 31 patients (74%). Preoperative localization studies included technetium-Tc-99m-sestamibi scanning (sensitivity, 86%), technetium-thallium scanning (67%), arteriography (63%), venous sampling (52%), computed tomography (42%), magnetic resonance imaging (33%), and ultrasonography (27%). Thirty-three (89%) of 37 patients who underwent reexploration had resolution of hypercalcemia. Localization study results were negative in all four patients who experienced failure. Angiographic ablation was successful in four (67%) of six patients. One of the patients with a failed ablation had successful mediastinal exploration. Hypoparathyroidism occurred in six patients (14.3%) and there was no instance of recurrent nerve injury. CONCLUSIONS: The most common causes of initial failure were ectopic mediastinal glands and incomplete surgical exploration; the most sensitive preoperative localization study is the technetium-Tc-99m-sestamibi scan; angiographic ablation of parathyroid tissue is most useful for poor-risk surgical patients or to avoid median sternotomy; and reexploration and angiographic ablation yield a high success rate with acceptable morbidity and mortality.

Adenoma↗

PubMed1994

Laparoscopic intracorporeal ultrasound. An alternative to cholangiography?

The purpose of this study was to compare laparoscopic intracorporeal ultrasound (LICU) examination of the biliary duct system with cholangiography for delineation of duct anatomy and determination of presence or absence of ductal calculi. Thirty-one patients had LICU examination of the extrahepatic bile ducts after exposure of the gallbladder but prior to dissection of the cystic duct. After LICU examination, cystic duct dissection and cholangiography were done. Evaluation of duct anatomy and decision for duct exploration were based on findings of both tests. All patients had successful LICU examination and 30 had successful cholangiography. Duct size as determined by LICU corresponded precisely with cholangiography. LICU provided useful anatomical information in two patients with aberrant anatomy and detected cholangiogram. LICU aids in delineation of biliary duct anatomy and accurately determines presence or absence of duct calculi.

Adolescent↗

PubMed1994

Mechanisms of coronary vasomotor dysfunction in the transplanted heart.

The transplanted heart sustains both cold ischemic and reperfusion injuries. These can produce coronary vascular endothelial or smooth muscle injury or both, which, in turn, can produce coronary vasomotor dysfunction. Using a canine model of autologous heart transplantation, we examined the following coronary vasomotor control mechanisms in isolated coronary artery rings: (1) endothelial-dependent cyclic guanosine monophosphate (cGMP)-mediated vasorelaxation (response to acetylcholine); (2) endothelial-independent cGMP-mediated vasorelaxation (response to sodium nitroprusside); and (3) beta-adrenergic cyclic adenosine monophosphate (cAMP)-mediated vasorelaxation (response to isoproterenol hydrochloride). Further, these mechanisms were related to 3 hours of cold ischemia alone and to 3 hours of cold ischemia plus 1 hour of reperfusion. Autologous heart transplantation was performed in dogs, and isolated distal left anterior descending coronary artery rings were studied in individual organ chambers. Cold ischemia alone produced significant dysfunction of beta-adrenergic cAMP-mediated vasorelaxation, which was exacerbated after reperfusion. Neither endothelial-dependent nor endothelial-independent cGMP-mediated vasorelaxation was dysfunctional after cold ischemia alone, but both were significantly impaired after reperfusion. We conclude that cold ischemia and reperfusion each produce coronary vasomotor dysfunction in the transplanted heart. Cumulatively, such coronary vasomotor dysfunction can acutely impair coronary vasodilatation and potentially jeopardize myocardial blood flow in the transplanted heart.

Acetylcholine↗

PubMed1994

A critical analysis of acutely injured children managed in an adult level I trauma center.

The triage of all injured children to regional pediatric trauma centers may be impractical and unnecessarily exclude adult level I trauma centers from the care of the acutely injured child. The purpose of this study was to critically evaluate the outcome of injured children treated in an adult level I trauma center by adult trauma surgeons. The records of 410 consecutively treated children (age < or = 15 years) and 188 young adults (age 16 to 18 years) admitted to the trauma service during a 2-year period (ending December 1991) were studied. The probability of survival was calculated using TRISS methodology. Results were analyzed using the Z statistic, permitting objective comparison with national norms (Major Trauma Outcome Study). Severity of injury (RTS and ISS) was equivalent (P > .05) in children and young adults. The observed survival (98.0%) in children compared favorably with the predicted survival (TRISS) of 97.7%. Calculation of the Z statistic showed no difference in outcomes of acutely injured children (+0.47) relative to young adults (+0.45) or national norms (MTOS). The triage of injured children to an adult level I trauma center does not adversely affect outcome. Subset analysis of injured children showed no differences in observed outcome relative to predicted outcome (national control) or outcome in young adults (institutional control). These data support the continued triage of acutely injured children to regional trauma centers regardless of pediatric or adult designation.

Acute Disease↗

PubMed1994

Transesophageal echocardiography in the evaluation of a transmediastinal gunshot wound: case report.

Transesophageal echocardiography is a safe, minimally invasive imaging modality that may be useful in the evaluation of transmediastinal gunshot wounds. In this report, we describe a hemodynamically stable patient who sustained a gunshot wound to the ascending aorta. Routine diagnostic evaluation, including aortography, failed to confirm the suspected diagnosis. Transesophageal echocardiography definitively detailed the injury to the aorta enabling definitive surgical repair.

Adult↗