[Ventricular Pseudoaneurysm after Sutureless Repair of Postinfarction Free Wall Rupture of the Left Ventricle:Report of a Case].

We herein report a case of a left ventricular pseudoaneurysm following sutureless repair for left ventricular free wall rupture. A 78-year-old woman underwent emergency sutureless repair for left ventricular free wall rupture following acute myocardial infarction. Three months later, echocardiography revealed an aneurysm in the postero-lateral wall of the left ventricle. The ventricular aneurysm was incised during reoperation, and defect in the left ventricular wall was closed with a bovine pericardial patch. Histopathologically, the aneurysm wall did not contain any myocardium, confirming the diagnosis of pseudoaneurysm. Although sutureless repair is a simple and highly effective method for oozing-type left ventricular free wall rupture, post-procedural pseudoaneurysm can develop both in acute and chronic phases. Consequently, long-term follow-up is mandatory.

[Successful Use of Left Ventricular Support Device (Impella 5.0) for Ischemic Heart Disease with Cardiogenic Shock:Report of a Case].

Postoperative hemodynamic support with an Impella 5.0 was effective in an obese man who underwent coronary artery bypass grafting (CABG) for ischemic heart disease and cardiogenic shock. A 43-year-old obese man presented to our hospital complaining severe chest pain. Coronary angiography revealed acute coronary syndrome due to severe triple-vessel disease, and the patient fell into a state of shock, which required veno-arterial extracorporeal membrane oxygenation (VA-ECMO) support. The patient subsequently underwent CABG, but he was unable to be separated from VA-ECMO. Impella 5.0 was introduced through right axillary artery on the next day. VA-ECMO was converted to veno-venous (VV)-ECMO on the 3rd postoperative day to enable respiratory rehabilitation in a sitting posi-tion;his respiratory status gradually improved. VV-ECMO and the Impella 5.0 were discontinued on the 6th and 7th postoperative days, respectively. He was eventually transferred to nearby facility for further rehabilitation three months later. As of two years, his cardiac function has improved and he is doing well at home.

[Mitral Valve and Tricuspid Valve Regurgitation in a Patient with Dextrocardia and Absence of the Inferior Vena Cava].

Dextrocardia is a rare condition frequently associated with multiple and complex cardiovascular abnormalities. A 66-year-old woman, who had been diagnosed with dextrocardia at young age, was referred to our hospital with complaint of increasing dyspnea. Severe mitral regurgitation, moderate tricuspid regurgitation, and atrial fibrillation were detected. The multi detector-row computed tomography(MDCT) revealed absence of the inferior vena cava, and the hepatic vein connected directly with the right atrium. The venous cannulae were inserted into the superior vena cava directly and into the hepatic vein from the right atrium. Mitral valve repair, tricuspid valve repair, and maze procedure were successfully performed. MDCT is useful for detecting abnormality of vena cava in a cases of dextrocardia.

[Dual Left Anterior Descending Coronary Artery;Report of a Case].

A 77-year-old male presented with angina pectoris. On coronary angiography, the left anterior descending artery(LAD) was obstructed after branching the second septal branch. Three-dimensional (3D) images constructed with 64-slice computed tomography (CT) showed type I dual LAD. The short LAD, which had been erroneously recognized as a septal branch on coronary angiography, ran on the anterior interventricular sulcus (AIVS) where it then terminated. The long LAD, which was obstructed at its origin, ran on the left ventricular side of the AIVS, and entered the distal part of the AIVS. Coronary artery bypass grafting including a bypass to the long LAD was successfully performed. Recognition of the dual LAD, a rare coronary artery anomaly regarding its origin and course, is import ant in performing successful myocardial revascularization procedures. The 3D-CT images are extremely useful in demonstrating dual LAD, especially in cases where there is occlusion of the LAD.

Age influences inflammatory responses, hemodynamics, and cardiac proteasome activation during acute lung injury.

BACKGROUND: Acute lung injury (ALI) is a significant source of morbidity and mortality in critically ill patients. Age is a major determinant of clinical outcome in ALI. The increased ALI-associated mortality in the older population suggests that there are age-dependent alterations in the responses to pulmonary challenge. The objective of this observational study was to evaluate age-dependent differences in the acute (within 6 hours) immunological and physiological responses of the heart and lung, to pulmonary challenge, that could result in increased severity. METHODS: Male C57Bl/6 mice (young: 2-3 months, old: 18-20 months) were challenged intratracheally with cell wall components from Gram-positive bacteria (lipoteichoic acid and peptidoglycan). After 6 hours, both biochemical and physiological consequences of the challenge were assessed. Alveolar infiltration of inflammatory cells and protein, airspace and blood cytokines, cardiac function and myocardial proteasome activity were determined. RESULTS: In young mice, there was a dose-dependent response to pulmonary challenge resulting in increased airspace neutrophil counts, lung permeability, and concentrations of cytokines in bronchoalveolar lavage fluid and plasma. A midrange dose was then selected to compare the responses in young and old animals. In comparison, the old animals displayed increased neutrophil accumulation in the airspaces, decreased arterial oxygen saturation, body temperatures, plasma cytokine concentrations, and a lack of myocardial proteasome response, following challenge. CONCLUSIONS: Age-dependent differences in the onset of systemic response and in maintenance of vital functions, including temperature control, oxygen saturation, and myocardial proteasome activation, are evident. We believe a better understanding of these age-related consequences of ALI can lead to more appropriate treatments in the elderly patient population.

Macrophage migration inhibitory factor antagonizes pressure overload-induced cardiac hypertrophy.

Macrophage migration inhibitory factor (MIF) functions as a proinflammatory cytokine when secreted from the cell, but it also exhibits antioxidant properties by virtue of its intrinsic oxidoreductase activity. Since increased production of ROS is implicated in the development of left ventricular hypertrophy, we hypothesized that the redox activity of MIF protects the myocardium when exposed to hemodynamic stress. In a mouse model of myocardial hypertrophy induced by transverse aortic coarctation (TAC) for 10 days, we showed that growth of the MIF-deficient heart was significantly greater by 32% compared with wild-type (WT) TAC hearts and that fibrosis was increased by fourfold (2.62 ± 0.2% vs. 0.6 ± 0.1%). Circulating MIF was increased in TAC animals, and expression of MIF receptor, CD74, was increased in the hypertrophic myocardium. Gene expression analysis showed a 10-fold increase (P < 0.01) in ROS-generating mitochondrial NADPH oxidase and 2- to 3-fold reductions (P < 0.01) in mitochondrial SOD2 and mitochondrial aconitase activities, indicating enhanced oxidative injury in the hypertrophied MIF-deficient ventricle. Hypertrophic signaling pathways showed that phosphorylation of cytosolic glycogen synthase kinase-3α was greater (P < 0.05) at baseline in MIF-deficient hearts than in WT hearts and remained elevated after 10-day TAC. In the hemodynamically stressed MIF-deficient heart, nuclear p21(CIP1) increased sevenfold (P < 0.01), and the cytosolic increase of phospho-p21(CIP1) was significantly greater than in WT TAC hearts. We conclude that MIF antagonizes myocardial hypertrophy and fibrosis in response to hemodynamic stress by maintaining a redox homeostatic phenotype and attenuating stress-induced activation of hypertrophic signaling pathways.

Late outcomes of the frozen elephant trunk technique for acute and chronic aortic dissection: the angle change of the FROZENIX by "spring-back" force.

OBJECTIVES: To evaluate the outcomes of total arch replacement using the frozen elephant trunk technique with a FROZENIX® J Graft for patients with either acute or chronic aortic dissection, and to evaluate the late-phase outcomes. METHODS: Between January 2015 and December 2020, we used the frozen elephant trunk technique in 47 patients with acute aortic dissection and 12 patients with chronic aortic dissection. The primary endpoints were 30-day mortality, late aorta-related death and late aortic events. The secondary endpoints included early surgical complications and any aortic events (e.g. stent graft-induced new entry, frozen elephant trunk angle change). RESULTS: In the acute group, there were no aorta-related deaths, although 13 patients (27.7%) experienced an aortic event; stent graft-induced new entry occurred in 6 patients (12.8%). In the chronic group, 1 patient (9.1%) experienced aorta-related death, and 9 (81.8%) experienced an aortic event; stent graft-induced new entry occurred in 4 patients (36.4%). During the late phase after surgery, there was a significant increase in the frozen elephant trunk angle in both groups. In the AAD group, both the FET angle and spring-back angle were significantly enlarged in the late phase. There were no significant differences between groups in the degree of angle change, the overall survival, or aortic event-free survival. CONCLUSIONS: Total arch replacement using the frozen elephant trunk technique affords good early-stage results for both acute and chronic aortic dissection. During follow-up, careful monitoring for aortic events and appropriate therapeutic interventions are required. If surgeons are to use this device, they must have a thorough understanding of its spring back force and other features.

Strain differences in alveolar neutrophil infiltration and macrophage phenotypes in an acute lung inflammation model.

Pulmonary infection is a major cause of mortality and morbidity, and the magnitude of the lung inflammatory response correlates with patient survival. Previously, we have shown that neutrophil migration into joints is regulated by arthritis severity quantitative trait loci (QTLs). However, it is unclear whether these QTLs contribute to the regulation of lung inflammation in pneumonias. Therefore, to more clearly define the factors regulating acute inflammatory responses in the lung, we examined two inbred rat strains, DA and F344, that differ in these QTLs and their susceptibility to joint inflammation. Staphylococcal cell wall components lipoteichoic acid (LTA) and peptidoglycan (PGN), administered intratracheally, significantly increased the numbers of neutrophils retrieved in the bronchoalveolar lavage fluid (BALF). F344 had approximately 10-fold more neutrophils in the BALF compared with DA (P < 0.001) and higher BALF concentrations of total protein, tumor necrosis factor-α and macrophage inflammatory protein 2. LTA/PGN administration in DA×F344 congenic strains (Cia3d, Cia4, Cia5a, and Cia6) resulted in inflammation similar to that in DA, demonstrating that the genes responsible for the differences in pulmonary inflammation are not contained within the chromosomal intervals carried by these congenic strains. Alveolar macrophages (AMs) isolated from naïve F344 stimulated in vitro with LTA/PGN produced significantly higher levels of keratinocyte-derived chemokine and macrophage inflammatory protein 2 than alveolar macrophages from DA rats. The differences were related to differential mitogen-activated protein kinase phosphorylation. We conclude that the factors contributing to inflammation can be site and challenge dependent. A better understanding of site-specific inflammation may lead to more effective treatment of acute lung inflammation and injury.

Macrophage CD74 contributes to MIF-induced pulmonary inflammation.

BACKGROUND: MIF is a critical mediator of the host defense, and is involved in both acute and chronic responses in the lung. Neutralization of MIF reduces neutrophil accumulation into the lung in animal models. We hypothesized that MIF, in the alveolar space, promotes neutrophil accumulation via activation of the CD74 receptor on macrophages. METHODS: To determine whether macrophage CD74 surface expression contributes MIF-induced neutrophil accumulation, we instilled recombinant MIF (r-MIF) into the trachea of mice in the presence or absence of anti-CD74 antibody or the MIF specific inhibitor, ISO-1. Using macrophage culture, we examined the downstream pathways of MIF-induced activation that lead to neutrophil accumulation. RESULTS: Intratracheal instillation of r-MIF increased the number of neutrophils as well as the concentration of macrophage inflammatory protein 2 (MIP-2) and keratinocyte-derived chemokine (KC) in BAL fluids. CD74 was found to be expressed on the surface of alveolar macrophages, and MIF-induced MIP-2 accumulation was dependent on p44/p42 MAPK in macrophages. Anti-CD74 antibody inhibited MIF-induced p44/p42 MAPK phosphorylation and MIP-2 release by macrophages. Furthermore, we show that anti-CD74 antibody inhibits MIF-induced alveolar accumulation of MIP-2 (control IgG vs. CD74 Ab; 477.1 +/- 136.7 vs. 242.2 +/- 102.2 pg/ml, p < 0.05), KC (1796.2 +/- 436.1 vs. 1138.2 +/- 310.2 pg/ml, p < 0.05) and neutrophils (total number of neutrophils, 3.33 +/- 0.93 x 104 vs. 1.90 +/- 0.61 x 104, p < 0.05) in our mouse model. CONCLUSION: MIF-induced neutrophil accumulation in the alveolar space results from interaction with CD74 expressed on the surface of alveolar macrophage cells. This interaction induces p44/p42 MAPK activation and chemokine release. The data suggest that MIF and its receptor, CD74, may be useful targets to reduce neutrophilic lung inflammation, and acute lung injury.

Leaflet escape in an Edwards TEKNA mitral prosthesis.

In almost every type of artificial valve, structural failure has been described. We are reporting on a case of a sudden leaflet escape of an Edwards TEKNA mitral valve prosthesis 12 years after implantation. The patient had a sudden onset of dyspnea and severe pulmonary edema with subsequent cardiogenic shock. An emergency mitral replacement was successfully performed. A multi-detector computed tomography scanning and three-dimensional imaging showed two fragments that had embolized in the terminal aorta and the left common iliac artery. The patient presented visual field abnormality, and postoperative head computed tomography showed watershed cerebral infarction. The escaped leaflet that fractured transversely was removed, following the patient's recovery, during cardiac surgery.

Very rare case of large obstructive myxofibrosarcoma of the right ventricle assessed with multi-diagnostic imaging techniques.

Primary myxofibrosarcoma of the heart is quite rare. We herein present the case of a 56-year-old man who presented with large obstructive myxofibrosarcoma of the right ventricle (RV), as assessed on multi-diagnostic imaging techniques (multidetector row computed tomography, magnetic resonance imaging and positron emission tomography). Most previous cases of cardiac myxofibrosarcoma have been reported in the left atrium and ventricle. In this report, we describe a very rare case of large obstructive myxofibrosarcoma of the RV.

Macrophage migration inhibitory factor provides cardioprotection during ischemia/reperfusion by reducing oxidative stress.

Macrophage migration inhibitory factor (MIF) is a multifunctional protein that exhibits an intrinsic thiol protein oxidoreductase activity and proinflammatory activities. In the present study to examine intracellular MIF redox function, exposure of MIF-deficient cardiac fibroblasts to oxidizing conditions resulted in a 2.3-fold increase (p < 0.001) in intracellular ROS that could be significantly reduced by adenoviral-mediated reexpression of recombinant MIF. In an animal model of myocardial injury by ischemia/reperfusion (I/R), MIF-deficient hearts exhibited higher levels of oxidative stress than did wild-type hearts, as measured by significantly higher oxidized glutathione levels (decreased GSH/GSSG ratio), increased protein oxidation, reduced aconitase activity, and increased mitochondrial injury (increased cytochrome c release). The increased myocardial oxidative stress after I/R was reflected by larger infarct size (INF) in MIF-deficient hearts versus wild-type (WT) hearts (21 ± 6% vs. 8 ± 3% INF/LV; p < 0.05). In vivo hemodynamic measurements showed that left ventricular (LV) contractile function of MIF-deficient hearts subjected to 15-min ischemia failed to recover during reperfusion compared with WT hearts (LV developed pressure and ± dP/dt; p = 0.02). These data represent the first in vivo evidence in support of a cardioprotective role of MIF in the postischemic heart by reducing oxidative stress.