Comparison of anti-inflammatory effects of rivaroxaban vs. dabigatran in patients with non-valvular atrial fibrillation (RIVAL-AF study): multicenter randomized study.

Some experimental studies have shown that direct oral anticoagulants (DOACs) have anti-inflammatory effects. However, the interval changes in inflammatory markers in patients with non-valvular atrial fibrillation (AF) who receive DOACs remain unknown. Between July 2013 and April 2014, a total of 187 AF patients randomly assigned to receive rivaroxaban (n = 91) or dabigatran (n = 96) were assessed for eligibility. The levels of the following inflammatory markers were serially evaluated: high-sensitivity C-reactive protein, pentraxin-3, interleukin (IL)-1ß, IL-6, IL-18, tumor necrosis factor-α, monocyte chemotactic protein-1, growth and differentiation factor-15, and soluble thrombomodulin (sTM). The aim in this study was to evaluate the anti-inflammatory effects of rivaroxaban and dabigatran in patients with AF, in addition to the impact of markers on bleeding events. Finally, 117 patients (rivaroxaban: n = 55, dabigatran: n = 62) were included in the analysis at 12 months. Although the interval changes in sTM levels tended to be greater in the dabigatran group [0.3 (0-0.7) vs. 0.5 (0-1.0) FU/ml, p = 0.061], there were no significant differences in the interval changes in any inflammatory marker between 2 groups. There were no significant differences in bleeding events between 2 groups. The interval changes in sTM levels were significantly greater in patients with bleeding compared with those without [0.8 (0.5-1.3) vs. 0.4 (- 0.1-0.8) FU/ml, p = 0.017]. There were no significant differences in the interval changes in any inflammatory marker between rivaroxaban and dabigatran treatments in patients with AF. The increased levels of sTM after DOACs treatment might be related to bleeding events.

Does Treatment of Impaired Glucose Tolerance Improve Cardiovascular Outcomes in Patients with Previous Myocardial Infarction?

PURPOSE: We evaluated the effects of an alpha-glucosidase inhibitor, voglibose, on cardiovascular events in patients with a previous myocardial infarction (MI) and impaired glucose tolerance (IGT). METHODS: This prospective, randomized, open, blinded-endpoint study was conducted in 112 hospitals and clinics in Japan in 3000 subjects with both previous MI and IGT receiving voglibose (0.6 mg/day, n = 424) or no drugs (n = 435) for 2 years. The Data and Safety Monitoring Board (DSMB) recommended discontinuation of the study in June 2012 after an interim analysis when the outcomes of 859 subjects were obtained. The primary endpoint was cardiovascular events including cardiovascular death, nonfatal MI, nonfatal unstable angina, nonfatal stroke, and percutaneous coronary intervention/coronary artery bypass graft. Secondary endpoints included individual components of the primary endpoint in addition to all-cause mortality and hospitalization due to heart failure. RESULTS: The age, ratio of males, and HbA1C were 65 vs. 65 years, 86 vs. 87%, and 5.6 vs. 5.5% in the groups with and without voglibose, respectively. Voglibose improved IGT; however, Kaplan-Meier analysis showed no significant between-group difference with respect to cardiovascular events [12.5% with voglibose vs. 10.1% without voglibose for the primary endpoint (95% confidence interval, 0.82-1.86)]; there were no significant differences in secondary endpoints. CONCLUSION: Although voglibose effectively treated IGT, no additional benefits for cardiovascular events in patients with previous MI and IGT were observed. Voglibose may not be a contributing therapy to the secondary prevention in patients with MI and IGT. TRIAL REGISTRATION: Clinicaltrials.gov number: NCT00212017.

Influence of omeprazole and famotidine on the antiplatelet effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes: a prospective, randomized, multicenter study.

BACKGROUND: It remains unclear whether concomitant use of omeprazole attenuates platelet function as compared with that of famotidine in patients with acute coronary syndromes (ACS) who receive clopidogrel. METHODS AND RESULTS: In this prospective study, 130 ACS patients treated with aspirin and clopidogrel who underwent stent implantation were randomly assigned to receive a Japanese standard dose of omeprazole 10mg daily or famotidine 20mg daily for at least 4 weeks. Between 14 and 28 days after enrollment, there was no significant difference in the platelet reactivity index (PRI) measured with vasodilator-stimulated phosphoprotein phosphorylation assay between the omeprazole group (n=65) and famotidine group (n=65) (55±17% vs. 51±19%; P=0.26). The cumulative rate of adverse cardiovascular events at 12 months was similar in the groups (13% vs. 17%; P=0.81). The PRI was similar (54.9±17.9% vs. 54.0±17.8%; P=0.83) in the omeprazole group (n=33) and the famotidine group (n=39) among patients with ST-elevation myocardial infarction (STEMI). However, there was a trend toward a higher PRI (55.2±15.9% vs. 46.4±19.4%; P=0.06) in the omeprazole group (n=32) as compared with the famotidine group (n=26) among patients without persistent ST-segment elevation ACS. CONCLUSIONS: As compared with famotidine, concomitant use of low-dose omeprazole does not significantly attenuate the antiplatelet effects of clopidogrel in patients with ACS, especially in those with STEMI.

Clinical usefulness of additional treatment with ezetimibe in patients with coronary artery disease on statin therapy. - From the viewpoint of cholesterol metabolism.-.

BACKGROUND: Ezetimibe-plus-statin therapy has been reported to provide greater reduction in low-density lipoprotein cholesterol (LDL-C) level than statin monotherapy. The aim of the present study was to evaluate the relationship between LDL-C lowering effect and baseline cholesterol absorption and synthesis markers in patients with coronary artery disease (CAD). METHODS AND RESULTS: A total of 171 patients with CAD whose LDL-C level was ≥ 100 mg/dl after treatment with atorvastatin (10mg/day) or rosuvastatin (2.5 mg/day) for 4 weeks were assigned to additionally receive ezetimibe (10mg/day) plus a statin or a double dose of statin for 12 weeks. The decreases in LDL-C (-30.0 ± 15.6 mg/dl vs. -19.2 ± 14.2 mg/dl) and the ratio of campesterol, an absorption marker, to total cholesterol levels (-1.35 ± 0.90 µg/mg vs. 0.33 ± 0.74 µg/mg) were greater in the ezetimibe-plus-statin group (P<0.05, respectively). The decrease in LDL-C level in the ezetimibe-plus-statin group was greatest in patients with baseline levels of higher absorption and lower synthesis markers and smallest in patients with baseline levels of lower absorption and higher synthesis markers (-34.3 ± 15.6 mg/dl vs. -21.5 ± 16.7 mg/dl, P<0.05). The decrease in LDL-C did not differ, irrespective of baseline levels of cholesterol absorption and synthesis markers, in the double-dose statin group, and was similar to that in patients with lower absorption and higher synthesis markers in the ezetimibe-plus-statin group. CONCLUSIONS: Ezetimibe-plus-statin therapy may be useful for lowering LDL-C level, irrespective of baseline levels of cholesterol absorption and synthesis markers.

Takotsubo Cardiomyopathy in a Patient with Previously Undiagnosed Hypertrophic Cardiomyopathy with Latent Obstruction.

A 62-year-old woman with takotsubo cardiomyopathy (TCM) accompanied by cardiogenic shock due to the obstruction of left ventricular outflow tract (LVOT) and massive mitral regurgitation (MR) was admitted to the emergency department. After successful treatment with intensive care, dobutamine stress-echocardiography was performed, which reproduced a dynamic LVOT gradient, severe MR and cardiogenic shock. A histological examination obtained from the right ventricular septum demonstrated hypertrophied and bizarre myocytes, with myocyte disarray. Besides TCM, a diagnosis of preexisting hypertrophic cardiomyopathy with latent obstruction was made. She was discharged with medical therapy including a beta-blocker, which would not be routinely employed in the treatment of a patient with TCM.

Cardiovascular Outcomes in Patients With Previous Myocardial Infarction and Mild Diabetes Mellitus Following Treatment With Pioglitazone: Reports of a Randomised Trial From The Japan Working Group for the Assessment Whether Pioglitazone Protects DM Patients Against Re-Infarction (PPAR Study).

BACKGROUND: Secondary prevention in patients with myocardial infarction (MI) is critically important to prevent ischaemic heart failure and reduce social burden. Pioglitazone improves vascular dysfunction and prevents coronary atherosclerosis, mainly via anti-inflammatory and antiatherogenic effects by enhancing adiponectin production in addition to antihyperglycemic effects, thus suggesting that pioglitazone attenuates cardiovascular events in patients with mild (HbA1c levels < 6·5%) diabetes mellitus (DM). Therefore, we evaluated the effects of pioglitazone on cardiovascular events in patients with both previous MI and mild DM. METHODS: In this multicentre, prospective, randomised, open, blinded-endpoint trial, we randomly assigned 630 patients with mild DM with a history of MI to undergo either DM therapy with (pioglitazone group) or without (control group) pioglitazone. DM was diagnosed using the 75-g oral glucose tolerance test, and mild DM was defined if HbA1c level was < 6·5%. The primary endpoint was the composite of cardiovascular death and hospitalisation caused by acute MI, unstable angina, coronary revascularisation (including percutaneous coronary intervention and cardiac bypass surgery), and stroke. FINDINGS: HbA1C levels were 5·9 and 5·8% (p = 0·71) at baseline and 6·0 and 5·8% (p < 0·01) at 2 years for the control and pioglitazone groups, respectively.The primary endpoint was observed in 14·2% and 14·1% patients in the control and pioglitazone groups during two years (95% confidential interval (CI):0.662-1·526, p = 0·98), respectively; the incidence of MI and cerebral infarction was 0·3% and 2·2% (95%CI: 0·786-32·415, p = 0·09) and 1·0% and 0·3% (95%CI: 0·051-3·662, p = 0·44), respectively. Post-hoc analyses of the 7-year observation period showed that these trends were comparable (21·9% and 19·2% in the control and pioglitazone groups, 95%CI: 0.618-1·237, p = 0·45). INTERPRETATION: Pioglitazone could not reduce the occurrence of cardiovascular events in patients with mild DM and previous MI.

Pulmonary Thromboembolism Caused by Prolonged Compression at the Femoral Access Site and a Venous Aneurysm of the Ipsilateral Popliteal Vein.

A 51-year-old female with dilated cardiomyopathy underwent a cardiac catheterization via right common femoral vein and artery. Prolonged compression with a bandage and extension of supine bed rest were needed. Immediately after standing up, she lost consciousness and developed electromechanical dissociation. The echocardiogram revealed a huge thrombus filling the main pulmonary trunk and massive enlargement of right ventricle, which suggested acute pulmonary thromboembolism (PTE). Images of computed tomography taken 2 months later detected a huge venous aneurysm of the right popliteal vein. Prolonged compression at the groin area might enhance blood stasis of the ipsilateral popliteal venous aneurysm, followed by life-threatening PTE.

B-type natriuretic peptide as a predictor of ischemia/reperfusion injury immediately after myocardial reperfusion in patients with ST-segment elevation acute myocardial infarction.

BACKGROUND: In animal models of acute myocardial infarction (AMI), B-type natriuretic peptide (BNP) administered before and during coronary occlusion limits infarct size. However, the relation between plasma BNP levels and ischemia/reperfusion injury remains unclear. METHODS: 302 patients with ST-segment elevation AMI (STEMI) received emergency percutaneous coronary intervention within six hours from the onset. The patients were divided into two groups according to the plasma BNP level before angiography: group L (n=151), BNP ≤ 32.2 pg/ml; group H (n=151), BNP >32.2 pg/ml. The Selvester QRS-scoring system was used to estimate infarct size. RESULTS: The rate of ischemia/reperfusion injury immediately after reperfusion, defined as reperfusion ventricular arrhythmias (26% vs. 11%, p=0.001) and ST-segment re-elevation (44% vs. 22%, p=0.008), was higher in group L than in group H. Group L had a greater increase in the QRS score during percutaneous coronary intervention (3.55 ± 0.17 vs. 2.09 ± 0.17, p<0.001) and a higher QRS score 1 h after percutaneous coronary intervention (5.77 ± 0.28 vs. 4.51 ± 0.28, p=0.002). On multivariate analysis, plasma BNP levels in the lower 50th percentile were an independent predictor of reperfusion injury (odds ratio, 2.620; p<0.001). The odds ratios of reperfusion injury according to decreasing quartiles of BNP level, as compared with the highest quartile, were 1.536, 3.692 and 4.964, respectively (p trend=0.002). CONCLUSIONS: Plasma BNP level before percutaneous coronary intervention may be a predictor of ischemia/reperfusion injury and the resultant extent of myocardial damage. Our findings suggest that high plasma BNP levels might have a clinically important protective effect on ischemic myocardium in patients with STEMI who receive percutaneous coronary intervention.

Impact of n-3 polyunsaturated fatty acids in predicting ischemia/reperfusion injury and progression of myocardial damage after reperfusion in patients with ST-segment elevation acute myocardial infarction.

BACKGROUND: In animal models of acute myocardial infarction, n-3 polyunsaturated fatty acids (PUFAs) administered before coronary occlusion have been suggested to prevent induction of ventricular arrhythmia and limit infarct size. However, the relation between the serum levels of n-3 PUFAs and ischemia/reperfusion (I/R) injury remains unclear. METHODS: 211 patients with ST-segment elevation acute myocardial infarction received emergency percutaneous coronary intervention (PCI) within 6h from the onset. The patients were divided into two groups according to the sum of serum eicosapentaenoic acid (EPA) levels and docosahexaenoic acid (DHA) levels before PCI: group L (n=106), EPA+DHA <155µg/ml and group H (n=105), EPA+DHA ≥155µg/ml. The Selvester QRS-scoring system was used to estimate the serial change in infarct size. RESULTS: Time to reperfusion was similar between the 2 groups. The QRS score before PCI was higher in group L than in group H (2.42±2.00 vs 1.85±2.01, p=0.015). The proportion of patients with I/R injury immediately after reperfusion, defined as reperfusion ventricular arrhythmias (25% vs 11%, p=0.006) and ST-segment re-elevation (44% vs 22%, p<0.001), was also higher in group L than in group H, followed by a greater increment in the QRS score during PCI (3.51±2.51 vs 2.54±1.91, p=0.006) and higher peak levels of creatinine phosphokinase (3552±241U/L vs 2660±242U/L, p<0.01). On multivariate analysis, serum level of EPA+DHA was an independent predictor of reperfusion injury (odds ratio 0.985, p=0.032). CONCLUSION: Serum level of n-3 PUFAs before PCI may be a predictor of I/R injury and the resultant extent of myocardial damage. These findings suggest a protective effect of serum n-3 PUFAs on ischemic myocardium.

Regional cerebral oxygen saturation monitoring for predicting interventional outcomes in patients following out-of-hospital cardiac arrest of presumed cardiac cause: A prospective, observational, multicentre study.

AIM: This study investigated the value of regional cerebral oxygen saturation (rSO2) monitoring upon arrival at the hospital for predicting post-cardiac arrest intervention outcomes. METHODS: We enrolled 1195 patients with out-of-hospital cardiac arrest of presumed cardiac cause from the Japan-Prediction of Neurological Outcomes in Patients Post-cardiac Arrest Registry. The primary endpoint was a good neurologic outcome (cerebral performance categories 1 or 2 [CPC1/2]) 90 days post-event. RESULTS: A total of 68 patients (6%) had good neurologic outcomes. We found a mean rSO2 of 21%±13%. A receiver operating characteristic curve analysis indicated an optimal rSO2 cut-off of ≥40% for good neurologic outcomes (area under the curve 0.92, sensitivity 0.81, specificity 0.96). Good neurologic outcomes were observed in 53% (55/103) and 1% (13/1092) of patients with high (≥40%) and low (<40%) rSO2, respectively. Even without return of spontaneous circulation (ROSC) upon arrival at the hospital, 30% (9/30) of patients with high rSO2 had good neurologic outcomes. Furthermore, 16 patients demonstrating ROSC upon arrival at the hospital and low rSO2 had poor neurologic outcomes. Multivariate analyses indicated that high rSO2 was independently associated with good neurologic outcomes (odds ratio=14.07, P<0.001). Patients with high rSO2 showed favourable neurologic prognoses if they had undergone therapeutic hypothermia or coronary angiography (CPC1/2, 69% [54/78]). However, 24% (25/103) of those with high rSO2 did not undergo these procedures and exhibited unfavourable neurologic prognoses (CPC1/2, 4% [1/25]). CONCLUSION: rSO2 is a good indicator of 90-day neurologic outcomes for post-cardiac arrest intervention patients.

Longitudinal stent deformation elongating to left main trunk.

A 67-year-old woman was admitted with an acute coronary syndrome. Angiographic examination revealed diffuse severe stenosis of the left circumflex artery. A Pressure Wire Certus (St. Jude Medical, St. Paul, MN, USA) was passed to the second post-lateral (PL) branch. To prevent side-branch occlusion, a SION wire (Asahi Intecc Co., Aichi, Japan) was left in the first PL branch, and a SION blue wire (Asahi Intecc) was placed in the second obtuse marginal branch. We implanted an everolimus-eluting stent (PROMUS Element 2.5 × 24 mm, Boston Scientific, Natick, MA, USA) in the culprit lesion. After retrieving the protection wire in first PL branch with resistance, we performed post-dilatation. However, the intravascular ultrasound images showed that the proximal portion of the implanted stent had elongated approximately 2 mm to the left main trunk (LMT), although the position of the distal edge of the stent was unchanged. We decided to additionally place a stent from the ostium of the LMT to the proximal left anterior descending coronary artery, and a biolimus-eluting stent (NOBORI 3.0 × 18 mm, Terumo Co., Tokyo, Japan) was implanted successfully. Longitudinal stent elongation might be caused by the small number of links between the hoops of a stent, originally intended to improve deliverability.

Constrictive pericarditis caused by immunoglobulin G4-related disease.

An 81-year-old man with congestive heart failure was admitted to our hospital. Computed tomography of the chest revealed pericardial thickening without calcification. Ultrasonic echocardiography and cardiac magnetic resonance imaging demonstrated diastolic dysfunction. Cardiac catheterization showed bilateral elevation of ventricular end-diastolic pressure with a square root sign. The preoperative serum immunoglobulin G4 (IgG4) level was abnormally high. Pericardiectomy and pericardiotomy were considered to be indicated and were performed. Histopathologic examination revealed tissue infiltration by IgG4-positive plasma cells, and constrictive pericarditis caused by IgG4-related disease was diagnosed. Postoperatively, the patient received additional corticosteroid therapy. The latest cardiac magnetic resonance image showed further improvement in diastolic function.

Refractory vasospasms of the coronary arteries due to multiple factors: an autopsy case.

A 41-year-old man was admitted with decompensated heart failure. Mechanical ventilation was maintained with a large dose of propofol. On day 4, significant ST elevation with complete atrioventricular block was noted, which subsequently induced cardiopulmonary arrest. Treatment with percutaneous cardiopulmonary support and therapeutic hypothermia was initiated. Emergent cardiac angiography showed simultaneous multivessel coronary spasms. Although nitroglycerin and nicorandil were ineffective, the intracoronary administration of fasudil, a Rho-kinase inhibitor, successfully resolved the vasospasms. However, during rewarming, the coronary vasospasms recurred, and the patient died of cardiogenic shock. In addition to hypertrophy, the autopsied heart demonstrated the accumulation of inflammatory cells in the pericardium and adventitia of the coronary arteries.

Platelet reactivity in the early and late phases of acute coronary syndromes according to cytochrome P450 2C19 phenotypes.

BACKGROUND: It remains unknown whether the time course of the antiplatelet effects of clopidogrel differs according to cytochrome P450 (CYP) 2C19 phenotype in Japanese patients with acute coronary syndromes (ACS). METHODS AND RESULTS: Platelet reactivity was serially assessed by VerifyNow-P2Y12 assay (Accumetrics, San Diego, CA, USA). Results were expressed as P2Y12-reaction-units (PRU) in 177 patients with ACS who underwent stent implantation and received aspirin plus a 300-mg loading dose of clopidogrel followed by 75 mg/day. High on-clopidogrel treatment platelet reactivity (HTPR) was defined as PRU>235. On the basis of the CYP2C19*2 and *3 alleles, 46 patients (26.0%) were classified as extensive metabolizers (EM), 103 (58.2%) as intermediate metabolizers (IM), and 28 (15.8%) as poor metabolizers (PM). At <7 days, the PRU level (232±102 vs. 279±70, 308±67, p<0.001) and the incidence of HTPR (49% vs. 74%, 86%, p=0.001) was lower in EM than in IM and PM. At 14-28 days the effects of CYP2C19 polymorphisms on PRU levels increased in a stepwise fashion (168±99 vs. 213±77 vs. 278±69, p<0.001), and EM and IM had lower percentages of HTPR than PM (28%, 37% vs. 73%, p<0.001). There was no significant difference in the cumulative frequency of 12-month adverse cardiovascular events among 3 phenotypes (16.5%, 14.1%, 9.2%; p=0.67). CONCLUSION: About three quarters of Japanese patients with ACS carried CYP2C19 variant alleles. The majority of IM and PM had increased platelet reactivity during the early phase of ACS. Although HTPR was frequently observed even 14-28 days after standard maintenance doses of clopidogrel in PM, the incidence of adverse outcomes did not differ, irrespective of CYP2C19 genotype.

Long-term effects of ezetimibe-plus-statin therapy on low-density lipoprotein cholesterol levels as compared with double-dose statin therapy in patients with coronary artery disease.

OBJECTIVE: To assess the mechanism of long-term LDL-C-lowering effect of ezetimibe-plus-statin. METHODS: Coronary artery disease patients whose LDL-C ≥ 70 mg/dL after treatment with atorvastatin 10 mg/day or rosuvastatin 2.5 mg/day were randomly assigned to receive ezetimibe 10 mg/day + statin (n = 78) or double-dose statin (n = 72) for 52 weeks. RESULTS: Greater LDL-C reduction was observed and maintained until 52 weeks in ezetimibe-plus-statin, while LDL-C levels re-increased after 12 weeks in double-dose statin. Although lathosterol/TC increased, campesterol/TC decreased more in ezetimibe-plus-statin. In contrast, lathosterol/TC unchanged and campesterol/TC increased, increasing campesterol/lathosterol ratio for 52 weeks in double-dose statin. Plasma PCSK9 levels were higher in double-dose statin than in ezetimibe-plus-statin at 12 weeks, but similar at 52 weeks. CONCLUSION: Although the difference in PCSK9 between 2 groups was transient, that in both campesterol and lathosterol persisted until 52 weeks. These results demonstrated simultaneous inhibition of cholesterol absorption and synthesis provides stable and greater decrease in LDL-C levels.

Current status of emergency care for ST-elevation myocardial infarction in an urban setting in Japan.

BACKGROUND: The door-to-balloon time (DTB) is an important predictor of the outcome for patients with ST-elevation myocardial infarction (STEMI). In Japan, percutaneous coronary intervention (PCI) can be performed at many hospitals, and the predominant strategy for reperfusion therapy is primary PCI. However, it remains unclear how rapidly reperfusion is achieved at these hospitals. METHODS AND RESULTS: The study group comprised 369 patients with STEMI who presented within 12 h of symptom onset to a tertiary emergency center (TEC) or at 11 community hospitals (CHs) in 2006 and underwent emergency coronary angiography. Median DTB was shorter in the TEC (63 vs 104 min, P<0.001), and the rate of DTB within 90 min was higher in the TEC (96% vs 39%, P<0.001). Lateral myocardial infarction, presentation during off-hours, and non-cardiologist as the first-contact physician were significantly associated with a prolonged DTB in CHs. There was a trend toward lower 30-day mortality from all causes in the TEC (2.0% vs 4.8%, P=0.08). Multiple logistic regression analysis demonstrated that prolonged DTB (>90 min) was an independent predictor of 30-day mortality (odds ratio 12.6; 95% confidence interval 1.85-86.2, P=0.01). CONCLUSIONS: Establishment of emergency cardiac care systems with the goal of DTB within 90 min is required in PCI-capable hospitals to improve clinical outcomes.

Serum lipoprotein(a) level and clinical coronary stenosis progression in patients with myocardial infarction: re-revascularization rate is high in patients with high-Lp(a).

BACKGROUND: High serum lipoprotein(a) (Lp(a)) levels are associated with coronary artery disease. METHODS AND RESULTS: The serum Lp(a) levels of 130 patients with acute myocardial infarction (AMI) who underwent direct percutaneous coronary intervention were investigated. On the basis of Lp(a) level at 1 month after the onset of AMI, the patients were classified into 2 groups (high-Lp(a) (> or =30 mg/dl) and low-Lp(a) (< 30 mg/dl)) for evaluation of the clinical coronary stenosis progression (CCSP) rate. CCSP is defined as either target lesion revascularization (TLR) or new lesion revascularization (NLR). The CCSP rate was significantly higher in the high-Lp(a) group than in the low-Lp(a) group (65.8% vs 29.3%, p<0.01). In patients who had coronary stents in the acute phase (n=79), the CCSP and NLR rates were significantly higher in the high-Lp(a) group than in the low-Lp(a) group (45.0% vs 20.3%, p<0.05; 35.0% vs 6.8%, p<0.01), but there was no significant difference in TLR rate between the 2 groups (10.0% vs 13.6%, p=0.858). CONCLUSIONS: High serum Lp(a) level is a significant risk factor for CCSP, but does not influence restenosis after stenting.

[Giant rheumatoid nodule causing simultaneous complete atrioventricular block and severe mitral regurgitation: a case report].

A 65-year-old female was first treated under a diagnosis of rheumatoid arthritis at the age of 62 years. Just after subcutaneous rheumatoid nodules appeared, she suddenly complained of shortness of breath and vomiting. The diagnosis was overt congestive heart failure with complete atrioventricular block and severe mitral regurgitation. She was treated with temporary pacing, and a permanent pacemaker was implanted 1 month later. She suffered recurrence of congestive heart failure and died 8 months later. Autopsy revealed a giant rheumatoid nodule located on the mitral valve and extending to the atrioventricular node. Presumedly this solitary giant nodule had induced complete atrioventricular block and severe mitral regurgitation.

Treatment of Churg-Strauss syndrome with high-dose intravenous immunoglobulin.

BACKGROUND: In some patients with Churg-Strauss syndrome (CSS), especially those with myocardial or neural involvement, conventional treatment with corticosteroids with or without cyclophosphamide is not effective. OBJECTIVE: To examine the effects of intravenous high-dose immunoglobulin (IVIG) in patients with CSS who showed poor responsiveness to conventional treatment. METHODS: We consecutively selected patients with CSS who showed any organ involvement despite corticosteroid treatment with or without cyclophosphamide. The diagnosis was based on the classification criteria of the American College of Rheumatology. IVIG therapy was performed with a dose of 400 mg/kg of immunoglobulin daily for 5 days. Neuropathy was evaluated with the manual muscle strength test and by the skin temperature of affected sites. Cardiac function was examined with ejection fraction by echocardiography and 2 imaging tests of myocardium (iodine 123 metaiodobenzylguanidine and thallium 201). RESULTS: The manual muscle strength test results were improved, and the skin temperature of both hands and legs was increased by IVIG therapy. In 5 patients with heart failure, the mean +/- SD ejection fraction of the left ventricle increased from 35.2% +/- 13.9% to 61.0% +/- 10.1% (P < .02). The uptake of iodine 123 metaiodobenzylguanidine of the myocardium increased, indicating that the myocardial viability was improved. The thallium 201 images revealed the presence of perfusion defects, which were improved by IVIG therapy. CONCLUSIONS: Patients with CSS who are resistant to corticosteroid treatment with or without cyclophosphamide may be treated effectively with IVIG therapy.