Successful recovery from cardiac arrest due to atlantoaxial subluxation in Down syndrome: a case report.

INTRODUCTION: Down syndrome is the most common chromosomal abnormality associated with intellectual impairments. Unexpected deaths are common with this disease. There are certain difficulties in clarifying the cause of death because the manifestations may be quite diverse and involve many organ systems. Atlantoaxial subluxation is a dangerous complication of Down syndrome, as it may lead to cervical cord-medullary compression. CASE PRESENTATION: Herein, we present a case of Down syndrome in a patient who completely recovered from cardiac arrest due to atlantoaxial subluxation. The neck was immobilized during post-cardiac arrest care, and the patient underwent surgery after 14 days. The patient could walk independently and was discharged 3 months later. At the last follow-up 5 years after surgery, the patient's general condition was good. DISCUSSION: Physicians should be aware that atlantoaxial instability can cause cardiac arrest in patients with genetic syndromes.

Transient Intussusception Mimicking Acute Coronary Syndrome.

Intussusception in adults is rare and usually associated with organic lesions. However, in the current era of computed tomography (CT), cases of idiopathic and transient intussusceptions are being increasingly diagnosed. Herein, we present a case of ileocecal intussusception with symptoms mimicking those of acute coronary syndrome. A male patient in his 80s with a history of myocardial infarction presented to the emergency department with acute onset of severe precordial and epigastric pain, cold sweating, and vomiting. Coronary angiography did not reveal any significant new lesion, while abdominal CT revealed ileocecal intussusception without bowel obstruction. The pain spontaneously subsided without any intervention, and the patient was discharged on the sixth hospital day. Cases of intussusception may go unnoticed in patients suspected of having chest pain with a normal coronary arteriogram, as idiopathic intussusception is relatively common and subsides spontaneously. Therefore, physicians should note that intussusception is one of the differential diagnoses of acute coronary syndrome.

Unexplained recurrent shock in peripheral T-cell lymphoma: A case report.

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.

Multisystem Inflammatory Syndrome in Children　- A New Syndrome Complicated With Acute Heart Failure Following Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection.

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.

A comprehensive protocol for ventilator weaning and extubation: a prospective observational study.

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.

T-wave alternans in a case with systemic lupus erythematosus-related myocarditis.

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. .

Impact of a negative D-dimer result on the initial assessment of acute aortic dissection.

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 ±â€¯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.

Cardiac hyaluronan may be associated with the persistence of atrial fibrillation.

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 < 0.01]. CS-HA levels were correlated with CS-dROM levels and peripheral BNP levels in PSAF patients (r = 0.417, P = 0.03 and r = 0.579, P < 0.001, respectively), but not in PAF patients (r = -0.115, P = 0.421 and r = 0.048, P = 0.740, respectively). CS-HA levels were elevated in both PAF and PSAF patients and were correlated with cardiac oxidative stress and BNP levels in PSAF patients. Cardiac HA may be associated with the persistence of AF.

Comparison of Inflammatory Biomarkers in Outpatients With Prior Myocardial Infarction.

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.

Characterization of cardiac oxidative stress levels in patients with atrial fibrillation.

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.

Rupture of gastrointestinal stromal tumor presenting with sudden onset chest and back pain and accompanied by gastric dilatation.

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.

Prognostic Significance of Neuroadrenergic Dysfunction for Cardiovascular Events in Patients With Acute Myocardial Infarction.

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 <1.96 (n=28) had a worse prognosis than those with either a dipper pattern (n=34) or an H/M ratio ≥1.96 (n=35; log-rank, P=0.013 and 0.010, respectively). Patients with both a non-dipper pattern and an H/M ratio <1.96 (n=12) had a significantly worse prognosis than did the other patients (P=0.0020). CONCLUSIONS: Dysregulation of BP variation and cardiac MIBG uptake were associated with cardiovascular events following AMI. Examining ABPM with MIBG imaging may potentially improve risk stratification in these patients.

Clinical Impact of Rapid Reduction of Low-Density Lipoprotein Cholesterol Level on Long-Term Outcome of Acute Myocardial Infarction in the Statin Era: Subanalysis of the ALPS-AMI Study.

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-naïve 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.

Impact of combination therapy with statin and ezetimibe on secondary prevention for post-acute myocardial infarction patients in the statin era.

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.

Assessment of lipophilic vs. hydrophilic statin therapy in acute myocardial infarction ­ ALPS-AMI study.

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 <100 mg/dl, and patients were followed for 2 years. The primary endpoint was the composite of death due to any cause, non-fatal myocardial infarction, non-fatal stroke, unstable angina or congestive heart failure requiring hospital admission, or any type of coronary revascularization. The primary endpoint occurred in 77 patients (30.4%) and in 80 patients (31.4%) in the pravastatin and atorvastatin groups, respectively (hazard ratio, 1.181; 95% confidence interval: 0.862-1.619; P=0.299), whereas greater reductions in serum total cholesterol and LDL-C were achieved in the atorvastatin group (P<0.001 for each). Changes in hemoglobin A1c, brain natriuretic peptide, and creatinine were not significant between the 2 regimens, and safety and treatment adherence were similar. CONCLUSIONS: On 2-year comparison of hydrophilic and lipophilic statins there was no significant difference in prevention of secondary cardiovascular outcome.

A 2-year follow-up of oxidative stress levels in patients with ST-segment elevation myocardial infarction: a subanalysis of the ALPS-AMI study.

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.

Impact of endovascular therapy on oxidative stress in patients with peripheral artery disease.

BACKGROUND: Atherosclerosis is believed to be caused by oxidative stress. Endovascular therapy (EVT) is effective for claudication of patients with peripheral artery disease (PAD). However, its effect on oxidative stress in PAD patients is unknown. Here, the impact of EVT on oxidative stress in PAD patients is investigated. METHODS AND RESULTS: Twenty-five PAD patients (Rutherford stage II or III) who underwent EVT were enrolled. The levels of diacron-reactive oxygen metabolite (d-ROM; an oxidative stress marker), ankle-brachial index (ABI), and maximum walking distance at baseline and at 3 months after EVT were measured. As compared with baseline values, the maximum walking distance and ABI improved significantly after EVT (109.9±104.2 vs. 313.7±271.8m, P<0.0001; 0.61±0.15 vs. 0.91±0.13m, P<0.0001, respectively). The improved exercise capacity and arterial flow induced a significant decrease in d-ROM levels (from 472.8±64.8 to 390.2±46.7U.CARR; P<0.0001). The decrease in d-ROM levels after EVT was more prominent in PAD patients with a high baseline d-ROM level. The increased ABI (r=0.524, P=0.0007) and maximum walking distance (r=-0.416, P=0.039) after EVT were significantly correlated with the decreased d-ROM levels. CONCLUSIONS: The improved exercise capacity and peripheral blood flow induced by EVT decreases oxidative stress in PAD patients.

Crucial role of hyaluronan in neointimal formation after vascular injury.

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.

Inflammasome activation of cardiac fibroblasts is essential for myocardial ischemia/reperfusion injury.

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-1ß 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.