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BACKGROUND: Multisystem inflammatory syndrome in children (MIS-C) is a rare syndrome temporally related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). MIS-C shares similarities with Kawasaki disease, but left ventricular dysfunction is more common in MIS-C.Methods and Results:This study reports the case of a 16-year-old Japanese male patient with MIS-C. Although the initial presentation was severe with circulatory and respiratory failure, the patient recovered completely. Endomyocardial biopsy showed active myocarditis with fibrosis. Immunoglobulin treatment was useful for recovery. CONCLUSIONS: This is the first reported case of MIS-C in Japan. Cardiologists should be aware of MIS-C, a new disease, occurring during the global SARS-CoV-2 pandemic.

Background Ventilator weaning protocols have been shown to reduce the duration of mechanical ventilation (MV), intensive care unit length of stay, and resource use. However, weaning protocols have not significantly affected mortality or reintubation rates. The extubation process is a critical component of respiratory care in patients who receive MV. Post-extubation respiratory failure (PERF) is a common event associated with significant morbidity and mortality. We hypothesized that a comprehensive protocol for ventilator weaning and extubation would be effective for preventing PERF and reintubation and reducing mortality in critically ill patients. Methods A ventilator weaning and extubation protocol was developed. The protocol consisted of checklists across four evaluations: spontaneous breathing trial, extubation, prophylactic non-invasive positive pressure ventilation (NPPV), and evaluation after extubation. Observational data were collected after implementing the protocol in patients admitted to the Advanced Emergency and Critical Care Center of Shinshu University Hospital. Not only outcomes of patients but also influences of each component of the protocol on the clinical decision-making process were investigated. Further, a comparison between PERF and non-PERF patients was performed. Results A total of 464 consecutive patients received MV for more than 48 h, and 248 (77 women; mean age, 65 ± 17 years) were deemed eligible. The overall PERF and reintubation rates were 9.7% and 5.2%, respectively. Overall, 54.1% of patients with PERF received reintubation. Hospital stay and mortality were not significantly different between PERF and non-PERF patients (p = 0.16 and 0.057, respectively). As a result, the 28-day and hospital mortality were 1.2% and 6.9%, respectively. Conclusions We found that the rates of PERF, reintubation, and hospital mortality were lower than those in previous reports even with nearly the same degree of severity at extubation. The comprehensive protocol for ventilator weaning and extubation may prevent PERF and reintubation and reduce mortality in critically ill patients.

Malignant lymphoma sometimes manifests with septic‐like shock symptoms. We report a case of peripheral T‐cell lymphoma presenting with unexplained recurrent shock in absence of apparent lymphadenopathy. The patient also experienced varied symptoms, including severe chest and back pain, respiratory distress due to tracheobronchomalacia, skin rash, and fever., Malignant lymphoma sometimes manifests with septic‐like shock symptoms. We report a case of peripheral T‐cell lymphoma presenting with unexplained recurrent shock in the absence of apparent lymphadenopathy.

A 42-year-old woman presented with fever, dyspnea, lower-leg edema, significant pulmonary congestion, pleural effusion, and severely reduced left ventricular contractions. She was resistant to treatment for heart failure, including catecholamines, furosemide, phosphodiesterase III inhibitors, and human atrial natriuretic peptide, and antibiotics failed to reduce her inflammation. She had renal dysfunction and hypocomplementemia and was positive for anti-nuclear and anti-ds-DNA antibodies. The patient was diagnosed with myocarditis and pleurisy associated with systemic lupus erythematosus (SLE). Prednisolone administration improved her general condition, reducing inflammation and improving left ventricular function. On day 1, an electrocardiography (ECG) revealed a T-wave inversion similar to a T-U complex configuration in leads II, aVF, and V3-6. By day 8, however, ECG showed prolonged corrected QT (QTc) and T-wave alternans (alternating beat-to-beat T-wave patterns) in lead V3-6. Careful ECG monitoring should be used to identify potentially fatal ventricular arrhythmias during the recovery phase of SLE-related myocarditis. .

Background D-dimer shows high sensitivity but low specificity for the diagnosis of acute aortic dissection (AAD). Previous reports indicated that negative D-dimer patients have shorter dissection length. However, whether patients with negative D-dimer results have a good prognosis is unknown. This study aimed to elucidate the clinical characteristics and implications of a negative D-dimer result on AAD diagnosis. Methods The study group comprised 126 patients (71 males, 55 females; mean age, 69 ± 11 years) with AAD admitted to our hospital between April 2009 and March 2015. Blood samples on presentation were used for D-dimer measurement. Clinical characteristics and outcomes were assessed. Results Nine (7.1%) and 117 (92.9%) exhibited negative and positive D-dimer results, respectively. The negative group showed a significantly lower extension score and a higher platelet count than the positive group. Multivariate analysis demonstrated that platelet count (odds ratio, 1.31 (1.09–1.58), p = 0.003) and extension score (odds ratio, 0.56 (0.33–0.96), p = 0.03) were significantly related to a negative result. Notably, 44% of patients in the negative group had type A dissection and 33% underwent an emergency operation due to cardiac tamponade. Conclusion We found that high platelet count and low extension score were independent factors related to a negative D-dimer result. Even if the length of the dissection is short, an emergency operation is necessary in some patients with a negative D-dimer result. Physicians should recognize that a negative D-dimer result alone cannot exclude patients with fatal AAD conditions.

Background: Spontaneous spinal epidural hematoma (SSEH) is a rare disease. Despite numerous case reports, the clinical characteristics and prognosis of patients with SSEH in the contemporary aging population are unknown. The purpose of this study was to clarify the clinical characteristics, prognostic factors, and optimal management of SSEH. Methods: We retrospectively reviewed and analyzed patients with SSEH who were admitted to Shinshu University Hospital between July 2009 and October 2019. The modified Rankin Scale (mRS) was used to measure the degree of disability in patients with SSEH at discharge as a functional outcome and patients were classified accordingly. Clinical variables of patients with good (mRS 0–2) and poor (mRS > 2) outcomes were compared. Results: We identified 30 patients with SSEH (17 men and 13 women) aged 36–89 years (median age, 67 years). Twelve patients had hypertension. Surgical treatment was performed in 11 patients. The number of patients who had taken anticoagulants was higher in the poor outcome group than in the good outcome group (p = 0.01). The poor outcome group were older (p = 0.048), had a higher operation rate (p = 0.04) and longer lengths of hospitalization (p

Case A 72-year-old man with hypertension was admitted with acute-onset chest and back pain followed by epigastralgia. He was transported by helicopter due to suspected acute aortic dissection. Systolic blood pressures were equal in both arms. Physical examination showed epigastric tenderness without rebound. Blood tests showed leukocytosis. Electrocardiogram and echocardiogram were normal. Abdominal radiography showed acute gastric dilatation with an air-outlined large mass-like shadow. Abdominal computed tomography revealed a 6-cm exophytic mass and large intramural hematoma in the lesser curvature of the gastric body. Outcome The patient underwent urgent laparotomy with total gastrectomy. The resected tumor showed positivity for CD117 and CD34 but negativity for S100, indicating a gastrointestinal stromal tumor. Fourteen days after the surgery, the patient was uneventfully discharged. Conclusion Intramural bleeding of submucosal tumors including gastrointestinal stromal tumor should be considered in cases of acute gastric dilatation. Abdominal radiography may be a clue regarding the presence of this condition.

Inflammatory biomarkers have been proposed for use in the risk stratification of patients with acute myocardial infarction (AMI). We examined the value of inflammatory biomarkers over clinical features for predicting cardiovascular (CV) events in stable outpatients with MI. We enrolled 430 post-MI patients and measured their levels of high-sensitivity C reactive protein (hs-CRP), growth differentiation factor-15 (GDF-15), and the interleukin-1 receptor family member called ST2 (ST2), one month after AMI. Patients were prospectively followed for 3 years. In our study cohort (mean age, 66 ± 12 years; left ventricular ejection fraction, 55 ± 13%), CV events were observed in 39 patients (9.1%). Kaplan- Meier analysis revealed that patients with high levels of GDF-15 (≥ 1221.0 ng/L) showed poorer prognoses than those with low levels of GDF-15 (< 1221.0 ng/L) (20.4% versus 3.6%, P < 0.001); hs-CRP and ST2 did not show a similar correlation with prognoses. GDF-15 remained associated with CV events after adjusting for age, chronic kidney disease, and B-type natriuretic peptide (hazard ratio, 1.001; 95% confidence interval, 1.000 - 1.001; P = 0.046). GDF-15 provided an incremental predictive value for CV events over clinical features (incremental value in global χ(2) = 43.81, P < 0.001). In outpatients with prior MI, GDF-15 was an independent indicator of CV events, unlike hs-CRP and ST2. GDF15 provided an incremental prognostic value over clinical features.

Hyaluronan (HA), a primary component of the extracellular matrix, is associated with several cardiovascular diseases. However, its precise cardiac origin and role in atrial fibrillation (AF) remain unclear. We investigated chamber-specific HA levels in patients with paroxysmal AF (PAF) or persistent AF (PSAF). The levels of HA, a diacron-reactive oxygen metabolite (dROM) as a marker for oxidative stress, at different cardiac sites, and peripheral brain natriuretic peptide (BNP) levels were measured in patients with PAF (n = 50) or PSAF (n = 35). HA levels in the coronary sinus (CS-HA) were significantly higher than those other sites, in both PAF and PSAF patients, and CS-HA levels were significantly higher in PSAF patients than in PAF patients [37.1 (interquartile range, 31.2–48.3) vs. 30.6 (23.7–40.2) pg/mL, P

Several literatures have reported that the elimination of autoantibodies by immunoadsorption (IA) therapy induced short- and long-term improvements in cardiac function of patients with dilated cardiomyopathy (DCM). We assessed whether reduction in oxidative stress was related to the mechanism underlying left ventricular functional benefit from IA. We studied 7 patients with DCM (New York Heart Association (NYHA) functional class III/IV). Autoantibodies were removed with IA by passing patients’ plasma over tryptophan columns. The level of anti-β1-adrenoreceptor (AR) autoantibodies was measured by enzyme- linked immunosorbent assay. The level of diacron- reactive oxygen metabolite (d-ROM) was determined as a marker of oxidative stress. During IA, the anti- β1-AR autoantibodies titers of all the patients decreased significantly from 27.8 ± 5.0 to 18.7 ± 5.5 U/ml (p < 0.01). IA induced the following hemodynamic improvements: cardiac index increased from 1.71 ± 0.40 to 1.97 ± 0.41 l/min/m2 and left ventricular ejection fraction (LVEF) increased from 22.8 ± 6.1 to 29.1±9.1% (p < 0.05). d-ROM level decreased significantly from 392.7 ±17.0 to 314.1 ± 22.0 Carratelli units (p < 0.05), and was negatively correlated with LVEF before and after IA therapy (r = －0.601, p < 0.05). The anti-β1-AR autoantibodies, LVEF and d- ROM returned to the baseline levels at 12 months after IA. In conclusion, oxidative stress reduction may be responsible for the beneficial effect of IA therapy in patients with DCM.

Background— Inflammation plays a key role in the pathophysiology of myocardial ischemia/reperfusion (I/R) injury; however, the mechanism by which myocardial I/R induces inflammation remains unclear. Recent evidence indicates that a sterile inflammatory response triggered by tissue damage is mediated through a multiple-protein complex called the inflammasome. Therefore, we hypothesized that the inflammasome is an initial sensor for danger signal(s) in myocardial I/R injury. Methods and Results— We demonstrate that inflammasome activation in cardiac fibroblasts, but not in cardiomyocytes, is crucially involved in the initial inflammatory response after myocardial I/R injury. We found that inflammasomes are formed by I/R and that its subsequent activation of inflammasomes leads to interleukin-1β production, resulting in inflammatory responses such as inflammatory cell infiltration and cytokine expression in the heart. In mice deficient for apoptosis-associated speck-like adaptor protein and caspase-1, these inflammatory responses and subsequent injuries, including infarct development and myocardial fibrosis and dysfunction, were markedly diminished. Bone marrow transplantation experiments with apoptosis-associated speck-like adaptor protein–deficient mice revealed that inflammasome activation in bone marrow cells and myocardial resident cells such as cardiomyocytes or cardiac fibroblasts plays an important role in myocardial I/R injury. In vitro experiments revealed that hypoxia/reoxygenation stimulated inflammasome activation in cardiac fibroblasts, but not in cardiomyocytes, and that hypoxia/reoxygenation–induced activation was mediated through reactive oxygen species production and potassium efflux. Conclusions— Our results demonstrate the molecular basis for the initial inflammatory response after I/R and suggest that the inflammasome is a potential novel therapeutic target for preventing myocardial I/R injury.

BACKGROUND The dysregulation of systemic blood pressure (BP) variation or cardiac neuroadrenergic dysfunction is associated with adverse cardiovascular events. We aimed to clarify the prognostic significance of neuroadrenergic dysfunction for cardiovascular events in patients with acute myocardial infarction (AMI). METHODS AND RESULTS We enrolled 63 AMI patients (mean age, 67±12 years) underwent ambulatory BP monitoring (ABPM) and cardiac iodine-(123)metaiodobenzylguanidine (MIBG) imaging within 4 weeks after AMI onset. We analyzed the circadian BP pattern and heart-to-mediastinum (H/M) MIBG uptake ratio. All the patients were followed for 2 years. The study endpoint was a composite of major adverse cardiovascular events, including all-cause death, MI, coronary revascularization except for the MI culprit lesion, and stroke. Patients with a non-dipper pattern (n=29) or an H/M ratio

Background Little is known concerning the effect of ezetimibe for secondary prevention in post-myocardial infarction (MI) patients. In this study, we investigated the secondary prevention effect of ezetimibe for post-MI patients. Methods This study is a retrospective analysis of Assessing Lipophilic vs. hydrophilic Statin therapy for Acute MI (ALPS-AMI study). The patients were divided into two groups: those administered a statin to control low density lipoprotein-cholesterol (LDL-C), the ezetimibe(−) group, and those administered ezetimibe in addition to a statin to control LDL-C, the ezetimibe(+) group. The endpoints were Major Adverse Cardiac and Cerebrovascular Event (MACCE), including all-cause death, recurrence of MI, stroke, and heart failure requiring hospitalization, and MACCE with revascularization. Results The ezetimibe(+) and ezetimibe(−) groups contained 113 and 337 patients, respectively. Incidences of MACCE and MACCE with revascularization were lower in the ezetimibe(+) group than in the ezetimibe(−) group (2.6% vs. 11.5%, p = 0.002; 23.0% vs. 36.7%, p = 0.014, respectively). Moreover, logistic regression analysis revealed ezetimibe(+) was a significant negative predictor of MACCE (OR 0.208, 95% CI 0.048 to 0.903, p = 0.047) and MACCE with revascularization (OR 0.463, 95% CI 0.258 to 0.831, p = 0.008). The preventive effect of ezetimibe against MACCE was observed in both moderate- and high-intensity lipid lowering treatment groups (0% vs. 17%; p = 0.077, 3.1% vs. 9.4%; p = 0.033). Conclusions In lipid-lowering therapy post-MI, ezetimibe and statin combination therapy improved MACCE with or without revascularization compared with statin monotherapy. These findings suggest that post-MI secondary prevention should be more intensive.

Background The optimal period to achieve target percent reduction of low-density lipoprotein cholesterol (LDL-C) level for secondary prevention of acute myocardial infarction (AMI) is not well established. Methods The Assessment of Lipophilic vs. Hydrophilic Statin Therapy in AMI (ALPS-AMI) study enrolled 508 patients (mean age, 66.0± 11.6 years; 80.6% male) who were hospitalized for AMI and underwent percutaneous coronary intervention (PCI). Of these patients, 81 were excluded because of the absence of LDL-C measurements at 4 weeks after randomization. In the remaining 427 patients, the target LDL-C level reduction of ≥30% was achieved and not reached within 4 weeks after randomization in 204 cases (early reduction group) and 223 cases (late reduction group). The groups were formed prospectively and analyzed with regard to the composite end point (major adverse cardiovascular event [MACE]: all-cause death, myocardial infarction, and stroke) and clinical outcomes. Results MACE were significantly more frequent in the late reduction group compared to the early reduction group (9.4% vs. 3.4%, P = 0.013). The incidence of cardiac deaths was also significantly higher in the late reduction group (3.1% vs. 0.5%, P = 0.044). On age-adjusted Cox proportional hazards analysis in statin-naive patients, percent reduction of LDL-C level during the initial 4 weeks (HR, 0.98; 95% CI: 0.97–0.99, P = 0.042) and baseline LDL-C level (HR, 0.98; 95% CI: 0.97–0.99, P = 0.033) predicted adverse events. Conclusions Rapid reduction of LDL-C level is strongly associated with favorable outcome in patients with AMI.

Background: In terms of secondary prevention of acute myocardial infarction (AMI), optimal period for achievement of target percent reduction of LDL-C level has not yet been well established. Methods: The Assessment of Lipophilic vs. Hydrophilic Statin Therapy in AMI (ALPS-AMI) study enrolled a total of 508 patients (mean age, 66.0±11.6 years, 80.6% male) hospitalized for AMI. Of these patients, 248 patients achieved percent reduction of LDL-C ≧ 30% until 8 week after randomization, 204 patients achieved at 4 week (early reduction group), 44 patients achieved at 8week (late reduction group). The two groups were identified prospectively and analyzed with regard to the composite end point (MACE: all-cause death, myocardial infarction, stroke). We evaluated long term clinical outcomes of AMI patients after PCI in terms of the period for achievement of target percent reductions in LDL-C. Results: MACE were significantly higher in the late reduction group compared to early reduction group (20.5% vs. 3.9 %, P Conclusions: The earlier reduction of LDL-C level is important for the patients with AMI in terms of reduction of ischemic events. We should reduce LDL-C level to target percent reductions for at least moderate-intensity statin therapy as early as 4 weeks after primary PCI in patients with AMI.

Background:Statins reduce the incidence of cardiovascular events, but no randomized trial has investigated the best statins for secondary prevention. We compared the efficacy of hydrophilic pravastatin with that of lipophilic atorvastatin in patients with acute myocardial infarction (AMI).Methods and Results:A prospective, multicenter study enrolled 508 patients (410 men; mean age, 66.0±11.6 years) with AMI who were randomly assigned to atorvastatin (n=255) or pravastatin (n=253). The target control level of low-density lipoprotein cholesterol (LDL-C) was

This report concerns two patients with severe protein losing enteropathy and refractory diarrhea due to AA amyloidosis who were successfully treated with corticosteroid and octreotide. In these patients, biopsied tissues from the gastrointestinal (GI) tract showed extensive deposition of AA amyloid, which was caused by rheumatoid arthritis in one case and was of unidentified etiology in the other. Both patients manifested severe diarrhea unresponsive to conventional treatment with hypoproteinemia, and protein leakage from the small intestine to the ascending colon was confirmed by 99mTc-diethylene triamine pentaacetic acid human serum albumin (HSA-D) scintigraphy. Soon after starting a long-acting somatostatin analogue, octreotide, with co-administration of oral prednisolone, their general status improved in parallel with a rapid decrease in the volume of watery diarrhea and an increase in serum levels of albumin and IgG. Also on 99mTc-HSA-D scintigraphy protein leakage from the GI tract was apparently decreased in both patients. Combination therapy with a somatostatin analogue and corticosteroid may be effective for protein losing enteropathy with intractable diarrhea ascribable to GI amyloidosis. Because of the lack of specific therapies in this serious clinical situation, the described therapy should actively be considered as a therapeutic option not only in AA amyloidosis, but also in other types of systemic amyloidosis.

We sought to determine whether serial measurements of oxidative stress levels could serve as a predictive marker for cardiovascular (CV) events in patients with ST-segment elevation myocardial infarction (STEMI). Biological antioxidant potential (BAP) levels were measured at admission and at 6, 12, and 24 months in 69 patients with STEMI. The CV events abruptly increased 6 to 10 months after successful percutaneous coronary intervention in patients with STEMI, and the 6-month BAP levels were significantly lower in patients with CV events (2456 μmol/L [interquartile range: 2237-2615 μmol/L]) than in those without (2849 μmol/L [2575-2987 μmol/L], P < .001). A decreased 6-month BAP level was an independent and significant predictor of long-term CV events (hazard ratio = 2.45; 95% confidence intervals 1.10-5.78; P = .04). Our findings suggest that serial changes in antioxidant capacity, assessed by BAP levels, may serve as a predictive marker for CV events after STEMI.

Atrial fibrillation (AF) is associated with oxidative stress and elevated brain natriuretic peptide (BNP) levels. However, the exact cardiac origin of oxidative stress and its association with BNP levels in AF patients remain unclear. Therefore, we investigated the chamber-specific plasma oxidative stress levels in patients with paroxysmal AF (PAF) and persistent AF (PSAF). Diacron-reactive oxygen metabolite (dROM) levels were measured in patients with PAF (n = 50) and PSAF (n = 35) at different cardiac sites before ablation and in peripheral vein 3 months after ablation. For all sites, dROM levels were higher in PSAF patients than in PAF patients; the levels were the highest in the coronary sinus at 429.0 (interquartile range: 392.0-449.0) vs. 374.0 (357.0-397.8) Carratelli units (P < 0.05). dROM levels in the coronary sinus were related to the BNP levels (r = 0.436, P < 0.001). Furthermore, the reduction in the peripheral dROM levels was related to that in the peripheral BNP levels in patients with symptomatic improvement (r = 0.473, P < 0.001). Cardiac oxidative stress may either be a cause or consequence of prolonged AF, and cardiac oxidative stress levels correlated with BNP levels, though a possible source of oxidative stress in AF patients may be systemic circulation.

Aims Increasing evidence suggests that CD4+ T cells contribute to neovascularization in ischaemic tissue. However, the T cell subset responsible for neovascularization after ischaemia remains to be determined. Here, we investigated the role of Th17 cells secreting interleukin (IL)-17, a newly identified subset of CD4+ T cells, in the neovascularization after murine hindlimb ischaemia. Methods and results Unilateral hindlimb ischaemia was produced in wild-type (WT) C57BL/6 mice. Depletion of CD4+ T cells resulted in significantly reduced blood flow perfusion in the ischaemic limbs. The expression of IL-17 and retinoic acid receptor-related orphan receptor γt (RORγt) was up-regulated in the ischaemic limbs. IL-17-deficient mice showed a significant reduction in blood flow perfusion, inflammatory cell infiltration, and production of angiogenic cytokines in the ischaemic limbs compared with WT mice. In bone marrow transplantation experiments, the absence of IL-17 specifically in bone marrow cells diminished the neovascularization after ischaemia. Furthermore, IL-17-deficient CD4+ T cells transferred into the ischaemic limbs of T cell-deficient athymic nude mice evoked a significantly limited neovascularization compared with WT CD4+ T cells. Conclusion These findings identify Th17 cells as a new angiogenic T cell subset and provide new insight into the mechanism by which T cells promote neovascularization after ischaemia.

Background: Accumulating evidence indicates that CD4 + T cells contribute to the development of collateral vesssels in ischemic tissue; however, little is known about the responsible subset of CD4 + T cells in the induction of angiogenesis. Th17 cells are recently identified as a new subset of CD4 + T cells and have been associated with the pathogenesis of certain autoimmune diseases. Th17 cells specifically secrete interleukin-17 (IL-17) and regulate various biological functions. The purpose of this study is to investigate the role of CD4 + T and Th17 cells in angiogenic response to hindlimb ischemia. Methods and Results: Unilateral hindlimb ischemia was produced in wild-type (WT: C57BL/6, 8- to 10-week-old) mice treated with or without a neutralizing antibody against CD4. Blood flow perfusion and capillary formation were assessed by using a laser Doppler perfusion imaging (LDPI) and CD31 immunostaining, respectively. Well-developed collateral vessels and capillary formation were observed in WT mice in response to hindlimb ischemia. Treatment with a neutralizing anti-CD4 antibody resulted in almost complete CD4 + T cell depletion (flow cytometry analysis, control: 45.4% vs. antibody: 1.0%) and a significant decrease in angiogenesis after the induction of hindlimb ischemia (LDPI, 21 days, control: 0.61 ± 0.1 vs. antibody: 0.41 ± 0.1, p−/− ) mice also showed a significant reduction of blood flow perfusion, compared with WT mice (LDPI, day 14: 0.56 ± 0.3 vs. 0.31 ± 0.2, p−/− mice had severe ischemic damage of the limb and resulted in a 25% incidence of autoamputation by day 21 (no limb loss in WT mice). Furthermore, capillary formation was also decreased significantly in IL-17 −/− mice (692.9 ± 165.6/mm 2 vs. 1223.3 ± 267.3/mm 2 , p Conclusion : These findings demonstrate that Th17 cells, a new subset of CD4 + T cells, contribute to the angiogenic response to hindlimb ischemia and provide new insights into the mechanism by which T cells promote collateral development and angiogenesis.

This report describes a case of traumatic incomplete rupture of the ventricular septum, a rare complication caused by blunt chest trauma. Although a serial ECG progressed its course similar to acute anteroseptal myocardial infarction in this case, there was little clinical clue of septal tear. The diagnosis was established by transthoracic echocardiography. The authors chose a conservative line of management rather than surgical repair for incomplete septal rupture because of the patent’s stable clinical course and hemodynamic status. A sequence of echocardiography during a 32-day stay in the hospital showed no change in the extent of incomplete septal rupture, septal structure, systolic function, and shape of left ventricle and also obtained no evidence of shunting through the rupture. In conclusion, echocardiography is a useful investigation to make a diagnosis as well as for follow-up in case of incomplete ventricular septal rupture. A close follow-up of incomplete septal rupture with serial echocardiography should be performed, because several cases of delayed ventricular septal rupture following blunt chest trauma have been reported.

Background Hyaluronan (HA) is a primary component of the extracellular matrix of cells, and it is involved in the pathogenesis of atherosclerosis. The purpose of this study was to investigate the role of HA in neointimal formation after vascular injury and determine its tissue-specific role in vascular smooth muscle cells (VSMCs) by using a cre-lox conditional transgenic (cTg) strategy. Methods and Results HA was found to be expressed in neointimal lesions in humans with atherosclerosis and after wire-mediated vascular injury in mice. Inhibition of HA synthesis using 4-methylumbelliferone markedly inhibited neointimal formation after injury. In vitro experiments revealed that low-molecular-weight HA (LMW-HA) induced VSMC activation, including migration, proliferation, and production of inflammatory cytokines, and reactive oxygen species (ROS). The migration and proliferation of VSMCs were mediated by the CD44/RhoA and CD44/ERK1/2 pathways, respectively. Because HA synthase 2 (HAS2) is predominantly expressed in injured arteries, we generated cTg mice that overexpress the murine HAS2 gene specifically in VSMCs (cHAS2/CreSM22α mice) and showed that HA overexpression markedly enhanced neointimal formation after cuff-mediated vascular injury. Further, HA-overexpressing VSMCs isolated from cHAS2/CreSM22α mice showed augmented migration, proliferation, and production of inflammatory cytokines and ROS. Conclusion VSMC-derived HA promotes neointimal formation after vascular injury, and HA may be a potential therapeutic target for cardiovascular disease.

Summary Background: Statins reduce the incidence of cardiovascular events in patients with acute myocardial infarction (AMI). Although all statins are equally effective in secondary prevention, there might be certain differences in the effects of lipophilic and hydrophilic statins. Therefore, our aim is to compare the effectiveness of lipophilic atorvastatin and hydrophilic pravastatin in secondary prevention after AMI. Methods and results: This study is a prospective, randomized, open-label, multicenter study of 500 patients with AMI. Patients that have undergone successful percutaneous coronary intervention will be randomly allocated to receive either atorvastatin or pravastatin with the treatment goal of lowering their low-density lipoprotein-cholesterol level below 100 mg/dl for 2 years. The primary endpoint will be death due to any cause, nonfatal MI, nonfatal stroke, unstable angina, or congestive heart failure requiring hospital admission, or any type of coronary revascularization. Conclusion: This is the first multicenter trial to compare the effects and safety of lipophilic and hydrophilic statin therapy in Japanese patients with AMI. It addresses an important issue and could influence the use of statin treatment in the secondary prevention of coronary artery disease.

Iodine-123 metaiodobenzylguanidine (MIBG) imaging is useful for assessing prognosis of patients with acute myocardial infarction (AMI). The autonomic nervous system influences circadian rhythm of blood pressure. We sought to examine the additive value of ambulatory blood pressure monitoring (ABPM)