Post-Thoracic Endovascular Aortic Repair Complicated with Mycotic Aneurysm Rupture, Repaired by Redo Thoracic Endovascular Aortic Repair.

Mycotic aneurysms although rare can be devastating. We encountered a dialysis patient with rapidly expanding distal aortic arch aneurysm who underwent axilloaxillary bypass and thoracic endovascular aortic repair (TEVAR). Three months later, he suffered mycotic aneurysm rupture for which redo TEVAR was performed. Antibiotic therapy was discontinued 16 weeks after the second operation, and renal transplantation was performed 6 months later. Dialysis was discontinued in the patient without infection recurrence.

[Effectiveness of tolvaptan for postoperative heart failure in a patient with combined valvular disease and pulmonary hypertension].

We report a case of a 60-year-old man with postoperative congestive heart failure( CHF) successfully treated with tolvaptan. The patient was diagnosed with pulmonary hypertension due to mitral stenosis and regurgitation combined with tricuspid regurgitation. He underwent mitral and tricuspid valvuloplasty. His postoperative course was uneventful until CHF symptoms secondary to volume overload appeared on the 4th day. Congestion with pulmonary hypertension was treated with 0.042 µg/kg/min of intravenous human atrial natriuretic peptide (hANP). His condition improved, and on the 11th postoperative day, he was weaned off hANP;oral administration of 40 mg per day of furosemide was initiated. However, 2 days after discontinuation of intravenous hANP, CHF recurred and serum sodium decreased to 128 mEq/l. Oral tolvaptan 7.5 mg per day was added to the furosemide, and CHF and hyponatremia subsequently improved. In this case, oral tolvaptan was effective for the treatment of refractory CHF with pulmonary hypertension after cardiac surgery.

[Redo coronary artery bypass grafting after pneumonectomy].

A 77-year-old man who had undergone left pneumonectomy 16 years and quadruple coronary artery bypass grafting (CABG) 4 years previously presented with unstable angina pectoris. Coronary angiography revealed severe stenosis of the left main trunk and the proximal left anterior descending artery(LAD), and the severely narrowed left internal thoracic artery (LITA)-LAD graft. Computed tomography(CT) presented a marked shift of the heart and great vessels into the left hemithorax with a hyperinflated right lung crossing the midline. The LAD would not seem to be accessible by median sternotomy. Off-pump coronary artery bypass grafting (OPCAB) with a saphenous vein graft to LAD was performed through a rib-cross left thoracotomy. The patient's postoperative course was uneventful, and postoperative CT revealed a patent graft. OPCAB through rib-cross thoracotomy is safe and useful and can be an option for redo CABG, particularly in instances of previous pneumonectomy.

[Management of cardiopulmonary bypass during cardiac surgery for patients with heparin-induced thrombocytopenia].

We experienced 4 cases of open heart surgeries under preoperative diagnosis of heparin-induced thrombocytopenia(HIT). We performed operation with argatroban instead of heparin. The argatroban was administered intravenously with a bolus of 100 µg/kg. After activated clotting time(ACT)reached over 200 seconds, continuous infusion of argatroban was started, 1~2 µg/kg/min until the level of ACT over 250 in the case of off-pump coronary artery bypass grafting(OPCAB), with 6~10 µg/kg/min, or the level of ACT over 400 with the use of cardiopulmonary bypass (CPB). All cases required more than 60 minutes to achieve the target ACT level after starting the argatroban. In 1 case it was impossible to achieve target level of ACT by argatroban alone, and heparin was used concomitantly. In 1 case there was a complication of membrane occlusion of CPB. Open cardiac surgery with the use of argatroban required specific care for coagulation to complete operation.

[Preserving autologous heart operation for dilated cardiomyopathy].

OBJECTIVE: We report non transplant surgical procedure (preserving autologous heart operation) for the patients with dilated cardiomyopathy( DCM), clinical outcomes, and the factor of predict prognosis. PATIENT AND METHOD: Since May 2000, 258 patients received surgical procedure for 11 years. SURGICAL PROCEDURES: We performed mitral surgery (plasty or replacement) for the patients with more than mild mitral regurgitation (MR). We performed papirally muscule plication since 2005, and we performed 2nd chordal cutting since 2008, for the patients with MR due to mitral tethering. The surgical left ventricular reconstruction( SVR) was performed for the patients with dilated left ventricular. We use spackle tracking echocardiography to decide the type of SVR since 2008. RESULT: Hospital death was 18.2%, and late cardiac death was 27.5%.Almost the cause of death was congestive heart failure and ventricular arrhythmia. Five years survival was 58%, 10 years survival was 39%. Preoperative condition, emergent operation, inotropic support, intra aortic balloon pumping(IABP),affect the prognosis. But left ventricular size did not affect it. CONCLUSION: Surgical treatment for the patient with DCM should be performed with stable preoperative condition.

[Acute Type A aortic dissection with superior mesenteric arterial dissection; report of a case].

We report a case of acute type A dissection with acute abdomen due to blood flow insufficiency in the superior mesenteric artery. A 73-year-old man was presented to hospital complaining sudden onset of chest pain. Contrast-enhanced computed tomography revealed a type A aortic dissection, that extended from the ascending aorta to the left common iliac atery. Superior mesenteric artery was compressed by the thrombosed false lumen. Epigastric pain was exacerbated acutely, we decided to treat the bowel ischemia 1st, and after that, if bowel ischemia was reversible, central repair operation performed. Emergent saphenous vein bypass was performed from the right external iliac artery to the superior mesenteric artery. Then total arch replacement was performed using cardiopulmonary bypass. The patient complicated with postoperative paralytic ileus, he completely recovered without bowel resection.

[Non-occlusive mesenteric ischemia after off-pump coronary artery bypass grafting].

Non-occlusive mesenteric ischemia( NOMI) after cardiac surgery is a rare but catastrophic complication. Although NOMI is generally recognized to be associated with extracorporeal circulation, we present a fatal case of a patient who developed NOMI after off-pump coronary artery bypass grafting (OPCAB). An 85-year-old man with left main trunk and triple vessel disease underwent OPCAB. He developed severe abdominal pain with metabolic acidosis 9 hours postoperatively. Selective angiography of the superior mesenteric artery( SMA) showed narrow and spastic branches of the SMA. A continuous intra-arterial perfusion with papaverine was started, but he died of multiple organ failure on the 3rd postoperative day. We emphasize the importance of early diagnosis and adequate treatment of NOMI including prompt exploratory laparotomy.

Multicenter randomized study evaluating the outcome of ganglionated plexi ablation in maze procedure.

OBJECTIVE: The benefit of adding ganglionated plexi ablation to the maze procedure remains controversial. This study aims to compare the outcomes of the maze procedure with and without ganglionated plexi ablation. METHODS: This multicenter randomized study included 74 patients with atrial fibrillation associated with structural heart disease. Patients were randomly allocated to the ganglionated plexi ablation group (maze with ganglionated plexi ablation) or the maze group (maze without ganglionated plexi ablation). The lesion sets in the maze procedure were unified in all patients. High-frequency stimulation was applied to clearly identify and perform ganglionated plexi ablation. Patients were followed up for at least 6 months. The primary endpoint was a recurrence of atrial fibrillation. RESULTS: The intention-to-treat analysis included 69 patients (34 in the ganglionated plexi ablation group and 35 in the maze group). No surgical mortality was observed in either group. After a mean follow-up period of 16.3 ± 7.9 months, 86.8% of patients in the ganglionated plexi ablation group and 91.4% of those in the maze group did not experience atrial fibrillation recurrence. Kaplan-Meier atrial fibrillation-free curves showed no significant difference between the two groups (P = .685). Cox proportional hazards regression analysis indicated that left atrial dimension was the only risk factor for atrial fibrillation recurrence (hazard ratio: 1.106, 95% confidence interval 1.017-1.024, P = .019). CONCLUSION: The addition of ganglionated plexi ablation to the maze procedure does not improve early outcome when treating atrial fibrillation associated with structural heart disease.

Ablation of C/EBP homologous protein attenuates endoplasmic reticulum-mediated apoptosis and cardiac dysfunction induced by pressure overload.

BACKGROUND: Apoptosis may contribute to the development of heart failure, but the role of apoptotic signaling initiated by the endoplasmic reticulum in this condition has not been well clarified. METHODS AND RESULTS: In myocardial samples from patients with heart failure, quantitative real-time polymerase chain reaction revealed an increase in messenger RNA for C/EBP homologous protein (CHOP), a transcriptional factor that mediates endoplasmic reticulum-initiated apoptotic cell death. We performed transverse aortic constriction or sham operation on wild-type (WT) and CHOP-deficient mice. The CHOP-deficient mice showed less cardiac hypertrophy, fibrosis, and cardiac dysfunction compared with WT mice at 4 weeks after transverse aortic constriction, although the contractility of isolated cardiomyocytes from CHOP-deficient mice was not significantly different from that in the WT mice. In the hearts of CHOP-deficient mice, phosphorylation of eukaryotic translation initiation factor 2alpha, which may reduce protein translation, was enhanced compared with WT mice. In the hearts of WT mice, CHOP-increased apoptotic cell death with activation of caspase-3 was observed at 4 weeks after transverse aortic constriction. In contrast, CHOP-deficient mice had less apoptotic cell death and lower caspase-3 activation at 4 weeks after transverse aortic constriction. Furthermore, the Bcl2/Bax ratio was decreased in WT mice, whereas this change was significantly blunted in CHOP-deficient mice. Real-time polymerase chain reaction microarray analysis revealed that CHOP could regulate several Bcl2 family members in failing hearts. CONCLUSIONS: We propose the novel concept that CHOP, which may modify protein translation and mediate endoplasmic reticulum-initiated apoptotic cell death, contributes to development of cardiac hypertrophy and failure induced by pressure overload.

[Repented Bentall operation for the case of aortitis with totally calcified ascending aortic allograft].

A 49-year-old male underwent re-do root Bentall operation with aortic allograft for the prosthetic valve detouchment due to aortitis syndrome 15 years ago (reported in 1998). He was presented with the hemolytic anemia due to severe aortic stenosis. The totally calcified aortic allograft was found by the computed tomography and chest X-ray. The allograft severely migrated to the sternum was approached by re-sternotomy under the circulatory arrest following the establishment of cardiopulmonary circulation and the 2nd-re-operation of root replacement was performed with composite graft with mechanical heart valve. He was discharged on foot on the 46th postoperative day. A tight follow-up is necessary for such a case of aortitis syndrome.

[Preserving autologous heart operation for ischemic cardiomyopathy].

OBJECTIVE: We report our surgical procedure (preserving autologous heart operation) for the patients with ischemic cardiomyopathy (ICM), and the results. PATIENT AND METHOD: Since May 2000, 212 patients received surgical procedure for ten years. SURGICAL PROCEDURES: We performed complete coronary artery bypass grafting (CABG), mitral surgery (plasty or replacement) for the patients with more than mild mitral regurgitation. We performed papirally muscle plication since 2005, and we performed 2nd chordal cutting since 2008, for the patients with mitral regurgitation (MR) due to severe mitral tethering. The surgical left ventricular reconstruction (SVR) was performed for the patients with dilated left ventricular. We use speckle tracking echocardiography to decide the type of the procedure of surgical left ventricular reconstruction since 2008. RESULT: Hospital death was 8.0%, and late death was 9.9%. Almost of the cause of death was congestive heart failure and ventricular arrhythmia. Five years survival was 78%, 10 years survival was 73%. CONCLUSION: The non transplant surgery for the patient with ICM was effective with the combination of CABG, mitral valve plasty (MVP) or mitral valve replacement (MVR), SVR. The size of left ventricle (LV) after SVR seemed to be a factor for late outcome of the surgery.

Paraplegia After Valvular Surgery After Remote Thoracoabdominal Aortic Aneurysm Repair.

Neurological disorders are the most unpredictable and feared complications after open surgery or endovascular aortic repair. Paraplegia because of spinal cord injury is well known after thoracoabdominal aortic surgery but not after valvular surgery. We herein present a case of paraplegia after mitral and tricuspid valve surgery in a patient with a history of surgery involving the thoracoabdominal and abdominal aorta. The paraplegia was likely caused by temporary postoperative hypotension as low as 40 mm Hg for more than 10 minutes with decreased spinal perfusion in the intensive care unit.

Minimally Invasive Multiple Coronary Artery Bypass Grafting with Composite Graft Using in situ Right Gastroepiploic and Radial Arteries.

Minimally invasive surgery/coronary artery bypass grafting (MICS CABG) via left thoracotomy and multiple CABG is a reported alternative to the standard sternotomy approach. However, harvesting the right internal thoracic artery (RITA) under direct vision requires high surgical skill. We describe MICS CABG with the left internal thoracic artery (LITA) and a composite graft using the in situ right gastroepiploic artery (GEA) and radial artery (RA) to achieve complete coronary revascularization. No complications occurred, and postoperative computed tomography showed patency of all grafts. Our experience suggests that this composite graft can be used safely and effectively in MICS CABG for complete arterial revascularization without difficulty.

The Growth Potential and Patency of Free Right Internal Thoracic Arteries Verified by Computed Tomography Angiography.

BACKGROUND: The use of the left internal thoracic artery (LITA) is the gold standard in coronary artery bypass graft surgery (CABG). Multiarterial grafting for CABG is being increasingly emphasized. This study aimed to resolve the utility of the right internal thoracic artery (RITA) for multiple CABG as "free" RITA and described new evidence. METHODS: One hundred sixty-three patients received solo CABG with bilateral internal thoracic arteries between 2005 and 2018. The RITA was used as in situ RITA, group A (n = 62), and the composite graft created with saphenous vein graft (SVG), group B (n = 101). The patency rate and graft size of the composite free RITA and SVG were examined by coronary computed tomography angiography. RESULTS: The average number of distal anastomoses per patient was 3.4 ± 1.0 in group A, and 4.2 ± 1.1 in group B (P < .001). The sequential grafting with free RITA was in 86 patients. The patency rate of both LITA and RITA was similar in both groups. In group B, 40 patients received late computed tomography angiography at a mean of 46 months (range, 17 to 175). The late patency rate was 95.1% in LITA and 96.9% in free RITA. The diameter of free RITA increased from 2.06 ± 0.34 mm to 2.37 ± 0.23 mm (P = .036); that of in situ LITA increased from 2.08 ± 0.51 mm to 2.44 ± 0.49 mm (P = .047); and that of composite SVG decreased from 4.1 ± 0.9 mm to 2.6 ± 0.7 mm (P < .001). CONCLUSIONS: Multiple bypass grafting can be sufficiently achieved with LITA and free RITA. The growth potential of free RITA and in situ LITA might play the important role of expected long-term patency.

X-box binding protein 1 regulates brain natriuretic peptide through a novel AP1/CRE-like element in cardiomyocytes.

The unfolded protein response (UPR) is triggered to assist protein folding when endoplasmic reticulum (ER) function is impaired. Recent studies demonstrated that ER stress can also induce cell-specific genes. In this study, we examined whether X-box binding protein 1 (XBP1), a major UPR-linked transcriptional factor, regulates the expression of brain natriuretic peptide (BNP) in cardiomyocytes. In samples from failing human hearts, extensive splicing of XBP1 was observed along with increased expression of glucose-regulated protein of 78 kDa (GRP78), a target of spliced XBP1 (sXBP1), suggesting that the UPR was induced in heart failure in humans. Interestingly, quantitative real-time PCR revealed a positive correlation between cardiac expression of GRP78 and BNP, leading us to test the hypothesis that sXBP1 regulates BNP as well as GRP78 in cardiomyocytes. A pharmacological ER stressor caused a dose-dependent increase in the expression of sXBP1 and BNP by cultured cardiomyocytes. Short interfering RNA targeting XBP1 suppressed the induction of BNP expression by a pharmacological ER stressor or norepinephrine, which was rescued by the adenovirus-mediated overexpression of sXBP1. The promoter assay with overexpression of sXBP1 or norepinephrine showed that the proximal AP1/CRE-like element in the promoter region of BNP was critical for transcriptional regulation of BNP by sXBP1. Direct binding of sXBP1 to this element was confirmed by the chromatin immunoprecipitation assay. These findings suggest that ER stress observed in failing hearts regulates cardiac BNP expression through a novel promoter region of the AP1/CRE-like element.

A cardiac myosin light chain kinase regulates sarcomere assembly in the vertebrate heart.

Marked sarcomere disorganization is a well-documented characteristic of cardiomyocytes in the failing human myocardium. Myosin regulatory light chain 2, ventricular/cardiac muscle isoform (MLC2v), which is involved in the development of human cardiomyopathy, is an important structural protein that affects physiologic cardiac sarcomere formation and heart development. Integrated cDNA expression analysis of failing human myocardia uncovered a novel protein kinase, cardiac-specific myosin light chain kinase (cardiac-MLCK), which acts on MLC2v. Expression levels of cardiac-MLCK were well correlated with the pulmonary arterial pressure of patients with heart failure. In cultured cardiomyocytes, knockdown of cardiac-MLCK by specific siRNAs decreased MLC2v phosphorylation and impaired epinephrine-induced activation of sarcomere reassembly. To further clarify the physiologic roles of cardiac-MLCK in vivo, we cloned the zebrafish ortholog z-cardiac-MLCK. Knockdown of z-cardiac-MLCK expression using morpholino antisense oligonucleotides resulted in dilated cardiac ventricles and immature sarcomere structures. These results suggest a significant role for cardiac-MLCK in cardiogenesis.

Identification of genes related to heart failure using global gene expression profiling of human failing myocardium.

Although various management methods have been developed for heart failure, it is necessary to investigate the diagnostic or therapeutic targets of heart failure. Accordingly, we have developed different approaches for managing heart failure by using conventional microarray analyses. We analyzed gene expression profiles of myocardial samples from 12 patients with heart failure and constructed datasets of heart failure-associated genes using clinical parameters such as pulmonary artery pressure (PAP) and ejection fraction (EF). From these 12 genes, we selected four genes with high expression levels in the heart, and examined their novelty by performing a literature-based search. In addition, we included four G-protein-coupled receptor (GPCR)-encoding genes, three enzyme-encoding genes, and one ion-channel protein-encoding gene to identify a drug target for heart failure using in silico microarray database. After the in vitro functional screening using adenovirus transfections of 12 genes into rat cardiomyocytes, we generated gene-targeting mice of five candidate genes, namely, MYLK3, GPR37L1, GPR35, MMP23, and NBC1. The results revealed that systolic blood pressure differed significantly between GPR35-KO and GPR35-WT mice as well as between GPR37L1-Tg and GPR37L1-KO mice. Further, the heart weight/body weight ratio between MYLK3-Tg and MYLK3-WT mice and between GPR37L1-Tg and GPR37L1-KO mice differed significantly. Hence, microarray analysis combined with clinical parameters can be an effective method to identify novel therapeutic targets for the prevention or management of heart failure.

Genome-wide histone methylation profile for heart failure.

Epigenetic alterations are implicated in the development of cardiac hypertrophy and heart failure, but little is known of which epigenetic changes in which regions of the genome play such a role. We now show that trimethylation of histone H3 on lysine-4 (K4TM) or lysine-9 (K9TM) is markedly affected in cardiomyocytes in association with the development of heart failure in a rat disease model. High-throughput pyrosequencing performed with ChIP products for K4TM or K9TM prepared from human left ventricular tissue with retained or damaged function also revealed that protein-coding genes located in the vicinity of K4TM marks differ between functional and disabled myocytes, yet both sets of genes encode proteins that function in the same signal transduction pathways for cardiac function, indicative of differential K4TM marking during the development of heart failure. However, K9TM mark-profile was less dependent on the disease status compared to that of K4TM. Our data collectively reveal global epigenetic changes in cardiac myocytes associated with heart failure.

Enhanced expression of the ubiquitin-proteasome system in the myocardium from patients with dilated cardiomyopathy referred for left ventriculoplasty: an immunohistochemical study with special reference to oxidative stress.

The ubiquitin (Ub)-proteasome system (UPS) is an important proteolytic mechanism for selecting and digesting cytotoxic proteins. The aim of this study is to elucidate expression and in situ localization of the UPS in the myocardium from patients with dilated cardiomyopathy (DCM) with refractory heart failure. The expression profile of the oxidative stress-induced cytotoxic proteins was also examined. Myocardium was obtained from 26 patients with DCM at the left ventriculoplasty. Ten normal autopsied hearts served as controls. Myocardial expressions of Ub and proteasomes were studied immunohistochemically. Oxidative stresses were examined in point of localization of the oxidation-induced modifier molecules (OMM). The relationship between immunohistochemical results and clinical parameters was also evaluated. Both Ub and proteasomes were stained positive in granular structures accumulating between the myofibrils and adjacent to nuclei in cardiomyocytes. The OMMs were also positive in the same Ub-positive granular structures. The area fraction of Ub, proteasomes and OMM was significantly higher in DCM hearts than in normal controls. Significant positive correlation was observed between the area fractions of Ub and plasma levels of brain natriuretic peptide (p = 0.046) in DCM hearts. In conclusion, enhanced expression of the UPS colocalized with OMM in cardiomyocytes may be involved in the pathophysiology of DCM hearts.

[Saphenous vein graft aneurysm after coronary artery bypass grafting surgery presenting with chronic heart failure].

An 82-year-old woman with a history of a coronary artery bypass grafting (CABG) 10 years prior was admitted because of general fatigue, appetite loss and systemic edema. She presented with a right pericardial mass on chest radiography. Echocardiogram and computed tomography (CT) revealed a 6.0 x 7.0 cm saphenous vein graft aneurysm (SVGA) compressing both right atrium and the right ventricle. She was successfully treated with the aneurysmal resection and postoperative course was uneventful. Although SVGA is an unusual complication after CABG, we recommend that any patient with a history of previous CABG who presents with a mediastinal mass should be evaluated for possibility of SVGA.