Spinal Cord Infarction With Prolonged Femoral Venoarterial Extracorporeal Membrane Oxygenation.

OBJECTIVES: There have been sporadic reports of ischemic spinal cord injury (SCI) during venoarterial extracorporeal membrane oxygenation (VA-ECMO) support. The authors observed a troubling pattern of this catastrophic complication and evaluated the potential mechanisms of SCI related to ECMO. DESIGN: This study was a case series. SETTING: This study was performed at a single institution in a University setting. PARTICIPANTS: Patients requiring prolonged VA-ECMO were included. INTERVENTIONS: No interventions were done. This was an observational study. MEASUREMENTS AND MAIN RESULTS: Four hypotheses of etiology were considered: (1) hypercoagulable state/thromboembolism, (2) regional hypoxia/hypocarbia, (3) hyperperfusion and spinal cord edema, and (4) mechanical coverage of spinal arteries. The SCI involved the lower thoracic (T7-T12 level) spinal cord to the cauda equina in all patients. Seven out of 132 (5.3%) patients with prolonged VA-ECMO support developed SCI. The median time from ECMO cannulation to SCI was 7 (range: 6-17) days.There was no evidence of embolic SCI or extended regional hypoxia or hypocarbia. A unilateral, internal iliac artery was covered by the arterial cannula in 6/7 86%) patients, but flow into the internal iliac was demonstrated on imaging in all available patients. The median total flow (ECMO + intrinsic cardiac output) was 8.5 L/min (LPM), and indexed flow was 4.1 LPM/m2. The median central venous oxygen saturation was 88%, and intracranial pressure was measured at 30 mmHg in one patient, suggestive of hyperperfusion and spinal cord edema. CONCLUSIONS: An SCI is a serious complication of extended peripheral VA-ECMO support. Its etiology remains uncertain, but the authors' preliminary data suggested that spinal cord edema from hyperperfusion or venous congestion could contribute.

Case Report: An Atypical Case of Carney Complex.

BACKGROUND Intracardiac tumors are a rare entity, with myxomas being the most common among them (approximately 50% of intracardiac tumors). Up to 80% of myxomas originate within the left atrium and while most are incidental or isolated findings in asymptomatic patients, others may result in clinical manifestations of heart failure or emboli. Moreover, in some cases, myxomas can be part of a genetically inherited syndrome known as Carney complex (CNC), and present with varied phenotypes, including skin, endocrine, and neuroendocrine tumors. CASE REPORT We present a case of a 54-year-old male patient who presented with a several-month history of non-specific cough, dyspnea on exertion, and palpitations along with several skin tags, nevi, and nodules. He was found to have a retrocardiac density on chest X-ray, which was revealed to be a large left atrial myxoma on echocardiography. The myxoma was surgically excised and genetic testing for a mutation of the PRKAR1A gene (the most common mutation underlying CNC) was negative. However, 2 major clinical criteria for diagnosis of CNC were fulfilled based on cardiac myxoma and spotty skin pigmentation. In this report, we focus on the clinical manifestations of CNC, including guidance on tumor surveillance and genetic variants of CNC. CONCLUSIONS While CNC is most commonly associated with an inactivating mutation of the PRKAR1A gene, it can be diagnosed clinically in the absence of an identifiable genetic mutation. In patients presenting with atypical cardiac tumors, the early recognition of cutaneous manifestations can raise the index of suspicion for CNC, which can facilitate early diagnosis, treatment, and initiation of surveillance for neoplasia development.

Mitral Valve Translocation: A Novel Operation for the Treatment of Secondary Mitral Regurgitation.

BACKGROUND: Conventional annuloplasty repair of secondary (functional) ischemic mitral regurgitation (IMR) is associated with a 60% recurrence of moderate or greater mitral regurgitation at 2 years. We developed a novel repair technique for IMR that addresses the underlying geometric alterations of the mitral valve apparatus and compared outcomes with those of conventional repair in a swine model. METHODS: Chronic IMR was induced by percutaneous embolization of the circumflex artery. Swine with severe IMR (median 9 weeks after infarction) underwent undersized rigid annuloplasty (n = 5) or translocation repair (n = 6). Translocation repair consisted of detaching the mitral valve en bloc at the annulus, creating a 1 cm wide frustum-shaped pericardial patch, and suturing the outer circumference of the patch to the annulus and inner circumference to the mitral valve. RESULTS: Operative survival was 92% (11 of 12). All animals had none/trace residual central mitral regurgitation, and mean inflow gradients were similar (1 mm Hg [interquartile range, 1 to 2] vs 2 mm Hg [interquartile range, 1 to 2]; P = .75) in the annuloplasty and translocation groups, respectively. Median coaptation length marginally improved in conventional swine (3 to 4 mm, P = .05), but dramatically improved in translocation swine (3 to 8 mm, P = .003). Posterior leaflet angle increased from 39 to 80 degrees (P = .05) in annuloplasty swine but decreased from 50 to 31 degrees (P = .03) in translocation swine. The posterior leaflet was immobile after annuloplasty but had preserved motion after translocation (excursion, 1 degree vs 24 degrees; P = .045). CONCLUSIONS: Mitral valve translocation effectively treats mitral regurgitation by relieving leaflet tethering. Compared with annuloplasty, mitral valve translocation creates a larger surface of coaptation and preserves leaflet mobility without compromising diastolic function.

Development of a Reproducible Swine Model of Chronic Ischemic Mitral Regurgitation: Lessons Learned.

BACKGROUND: Durability of mitral valve repair for ischemic mitral regurgitation (IMR) remains poor. We established a swine model of chronic IMR, and describe the methods and lessons learned from this model. METHODS: Thirty-five swine underwent percutaneous myocardial infarction with ethanol ablation of the circumflex or obtuse marginal (OM) arteries. Swine were followed with routine echocardiography for the development of severe IMR. Once severe IMR was established, swine underwent mitral valve operations on cardiopulmonary bypass. After operation, swine were survived up to 7 weeks. Angiographic and echocardiographic features of swine who developed severe IMR (IMR swine) and those who did not (non-IMR swine) were compared. RESULTS: The median number of OM arteries was 3, with 2 OM arteries infarcted. Acute survival after the myocardial infarction was 74% (26 of 35) with 3 (9%) early, postoperative deaths. Among the 23 swine with follow-up to determine IMR status, 14 of 23 (61%) developed significant IMR. Among IMR pigs, left ventricular (LV) ejection fraction decreased from 65% pre-myocardial infarction to 45% pre-mitral valve intervention (P < .001). Among non-IMR swine, LV ejection fraction decreased nonsignificantly from baseline (60%) to latest follow-up (55%) (P = .443). LV end-diastolic dimension (P = .039), wall motion score (P = .027), global circumferential strain (P = .014), and global longitudinal strain (P = .023) were significantly worse in IMR compared with non-IMR swine. CONCLUSIONS: A reproducible percutaneous model of severe IMR in swine is feasible with a guided anesthetic and perioperative approach. This model can serve as a platform to better understand the mechanism of IMR and subsequently to test novel repair techniques.

Echo is a good, not perfect, measure of cardiac output in critically ill surgical patients.

BACKGROUND: Compared with a pulmonary artery catheter (PAC), transthoracic echocardiography (TTE) has been shown to have good agreement in cardiac output (CO) measurement in nonsurgical populations. Our hypothesis is that the feasibility and accuracy of CO measured by TTE (CO-TTE), relative to CO measured by PAC thermodilution (CO-PAC), is different in surgical intensive care unit patients (SP) and nonsurgical patients (NSP). METHODS: Surgical patients with PAC for hemodynamic monitoring and NSP undergoing right heart catheterization were prospectively enrolled. Cardiac output was measured by CO-PAC and CO-TTE. Pearson coefficients were used to assess correlation. Bland-Altman analysis was used to determine agreement. RESULTS: Over 18 months, 84 patients were enrolled (51 SP, 33 NSP). Cardiac output TTE could be measured in 65% (33/51) of SP versus 79% (26/33) of NSP; p = 0.17. Inability to measure the left ventricular outflow tract diameter was the primary reason for failure in both groups; 94% (17/18) in SP versus 86% (6/7) NSP; p = 0.47. Velocity time integral could be measured in all patients. In both groups, correlation between PAC and TTE measurement was strong; SP (r = 0.76; p < 0.0001), NSP (r = 0.86; p < 0.0001). Bland-Altman analysis demonstrated bias of -0.1 L/min, limits of agreement of -2.5 and +2.3 L/min, percentage error (PE) of 40% for SP, and bias of +0.4 L/min, limits of agreement of -1.8 and +2.5 L/min, and PE of 40% for NSP. CONCLUSION: There was strong correlation and moderate agreement between TTE and PAC in both SP and NSP. In both patient populations, inability to measure the left ventricular outflow tract diameter was a limiting factor. LEVEL OF EVIDENCE: Diagnostic tests or criteria, level III.