Rivaroxaban therapy resulting in the resolution of right atrial thrombosis resistant to ordinary control with warfarin in a patient with atrial fibrillation.

A 72-year-old man with non-valvular atrial fibrillation and metastatic liver and lung cancer after surgery for colon cancer developed thrombosis in the right atrium one month after decreasing the dose of warfarin due to the introduction of double anti-platelet therapy for coronary stent implantation. Restoring the warfarin dose with ordinary control for two months did not result in any changes in the size of the thrombus; however, the subsequent substitution of rivaroxaban (oral treatment with a direct Factor Xa inhibitor) for warfarin ultimately resolved the thrombosis.

Cyclophosphamide-induced cardiotoxicity with a prolonged clinical course diagnosed on an endomyocardial biopsy.

A 31-year-old woman with primary mediastinal large B-cell lymphoma refractory to conventional chemotherapy was treated with high-dose chemotherapy containing cyclophosphamide (CY). Subsequently, she was treated with auto peripheral blood stem cell transplantation. Although a complete remission was obtained, heart failure developed two months later. Echocardiography showed an impaired systolic function with pericardial effusion. A biopsy of the endomyocardial region from the left ventricle demonstrated spotty myocardial hemorrhage and myocardial fibrosis with disruption and aggregation of mitochondrial cristae. Based on these findings, CY-induced cardiotoxicity was diagnosed. The patient was treated with conventional therapy for heart failure, which required approximately one year to improve her condition.

Elevated levels of systemic pentraxin 3 are associated with thin-cap fibroatheroma in coronary culprit lesions: assessment by optical coherence tomography and intravascular ultrasound.

OBJECTIVES: This study sought to determine whether systemic levels of pentraxin 3 (PTX3), a novel inflammatory marker, are associated with thin-cap fibroatheroma (TCFA). BACKGROUND: Biomarkers predicting the presence of TCFA in vivo have not been established. METHODS: We evaluated 75 patients (stable angina pectoris, n = 47; acute coronary syndrome, n = 28) with de novo culprit lesions who were examined by optical coherence tomography and intravascular ultrasound. We defined TCFA as lipid-rich plaque with a fibrous cap <65 µm thick. Systemic levels of PTX3 were compared between patients with and without TCFA. RESULTS: Thirty-eight and 37 patients with and without TCFA, respectively, were identified. Levels of PTX3 were significantly higher in patients with than in those without TCFA (p < 0.001) and correlated inversely with fibrous cap thickness (r = -0.71, p = 0.001) and positively with the remodeling index (r = 0.25, p = 0.037). Multivariate logistic regression analysis showed that a higher PTX3 level was the most powerful predictor of TCFA (odds ratio: 3.26, 95% confidence interval: 1.75 to 6.05, p < 0.001). Receiver-operating characteristic curve analysis showed that >3.24 ng/ml of PTX3 could predict TCFA with 84% sensitivity and 86% specificity. CONCLUSIONS: Higher levels of systemic PTX3 are associated with TCFA. Systemic PTX3 levels comprise a useful inflammatory marker that reflects coronary plaque vulnerability.

Cardiogenic shock due to left ventricular outflow obstruction and complete atrioventricular block in a patient with hypertrophic cardiomyopathy with acute myocarditis.

A 67-year-old woman was referred to our hospital with a sudden syncopal attack. She suffered from cardiogenic shock due to left ventricular (LV) outflow stenosis with simultaneous complete atrioventricular (AV) block. An endomyocardial biopsy of the left ventricle demonstrated myocardial disarray and myocardial fibrous and edematous tissue with infiltration of mononuclear cells. Cardiac magnetic resonance imaging (cMRI) detected a damaged septal area that was likely associated with the conduction disturbance. The diagnosis was hypertrophic cardiomyopathy accompanied by acute myocarditis. Although the LV outflow stenosis was transient, the complete AV block was persistent, thus requiring permanent pacemaker implantation.

Very late stent thrombosis caused by rupture of lipid-laden neointima in a self-expanding coronary stent.

A 60-year-old man was admitted to our hospital due to acute ST-segment elevation myocardial infarction. He had a history of self-expanding stent implantation in the proximal left anterior descending artery due to stable angina pectoris 7 years earlier. Emergent coronary angiography on admission showed occlusion in the distal portion of the previously stented segment, in which observation by optical coherence tomography revealed the existence of a remarkable proliferation of lipid-laden neointimal tissues with rupture and thrombus. This suggests that very late stent thrombosis in a self-expanding stent may occur through the process of atheromatous formation.

Mass lesions surrounding coronary artery associated with immunoglobulin G4-related disease.

Immunoglobulin G4 (IgG4)-related diseases have been reported to be systemic diseases characterized by elevation of serum IgG4 concentration and infiltration of IgG4-positive plasma cells within the target organ. However, the involvement of coronary artery is very rare. Here, we report a 62-year-old man with mass lesions surrounding coronary artery and abdominal aorta associated with IgG4-related disease diagnosed by a needle biopsy of the mass lesion surrounding the coronary artery using echocardiography and computed tomography. After we started to treat the patient with prednisolone, his serum IgG4 level decreased, and the mass lesions of coronary and abdominal artery were markedly reduced in size after 4 months. In conclusion, IgG4-related disease should be considered in addition to tumors such as malignant lymphoma when mass lesions surrounding coronary artery are detected.

Culprit segments identified by optical coherence tomography in patients with acute myocardial infarction: two case reports.

The high resolution of optical coherence tomography (OCT) provides detailed information about coronary plaque morphology, which enables the mechanism of acute myocardial infarction to be evaluated. We describe two patients with acute myocardial infarction in whom culprit segments were identified by OCT, but not by either coronary angiography or intravascular ultrasound.

Low glomerular filtration rate is associated with high prevalence of vasospastic angina.

BACKGROUND: Although chronic kidney disease is associated with a high prevalence of cardiovascular disease, the relationship between coronary artery spasm and renal dysfunction has not been elucidated. METHODS AND RESULTS: We evaluated 139 patients with chest pain at rest who had no significant organic stenosis on coronary angiograms and who underwent coronary spasm provocation tests using acetylcholine or ergonovine. The results of the provocation tests revealed that 59 patients had vasospastic angina (VSA), and that 80 did not (non-VSA). We analyzed the association between VSA and renal dysfunction using the estimated glomerular filtration rate (eGFR). The eGFR was significantly lower in the VSA group than in the non-VSA group (P = 0.013). The patients were assigned to quartiles (Q) 1, 2, 3 and 4 based on eGFR (ml·min⁻¹·1.73 m²) < 64.1, 64.1-74.7, 74.8-85.0 and ≥ 85.1, respectively, in each of which the prevalence of VSA was 57%, 53%, 34% and 26%, respectively. The prevalence of VSA was significantly higher in Q1 than in Q4 (P = 0.008). Logistic regression analysis showed that the independent factors associated with the presence of VSA were a lower eGFR (P = 0.011) and male gender (P = 0.001). CONCLUSIONS: Lower levels of eGFR in our study population were significantly and independently associated with a high prevalence of VSA, suggesting that a lower eGFR could be a risk factor for VSA.

Impact of metabolic syndrome on the long-term survival of patients with acute myocardial infarction: potential association with C-reactive protein.

BACKGROUND: Population-based cohort studies demonstrate that metabolic syndrome (MeS) is associated with increased risk for cardiovascular diseases and related mortalities. The present study was designed to investigate the prognostic impact of MeS in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: The study group was 461 AMI patients without a history of previous myocardial infarction. On the basis of the National Cholesterol Education Program Adult Treatment Panel III criteria, MeS was defined having at least 3 of the following 5 conditions: dysglycemia (impaired fasting glucose, current use of insulin or oral hypoglycemic drugs), hypertriglyceridemia, low high-density lipoprotein-cholesterol level, hypertension and obesity. The prevalence of MeS was 37% (n=172). C-reactive protein (CRP) levels increased with the increase in the number of conditions of MeS. During follow-up at a median of 17.6 months, the incidence of major adverse cardiovascular events (MACE) was significantly different between patients with and without MeS. Furthermore, after adjustment of predictive factors (age, sex, Killip class, multivessel coronary artery disease, low ejection fraction and high CRP level), MeS was an independent risk factor for MACE. CONCLUSIONS: In patients with AMI, MeS is associated with systemic inflammation and is an important predictor for MACE, which suggests the need for early identification and medical intervention for secondary prevention of MeS.

Continuous milrinone infusion during preoperative anti-inflammatory therapy in inflammatory aortic aneurysm complicating severe congestive heart failure.

We report a 48-year-old man with inflammatory aortic aneurysm in the ascending aorta complicating severe heart failure due to massive aortic regurgitation. Continuous intravenous milrinone infusion was highly effective in reducing pulmonary arterial pressure and improving subjective symptoms during preoperative anti-inflammatory corticosteroid therapy over 7 weeks without any adverse effects or tolerance. Bentall's operation with a valved conduit was successfully performed after complete stabilization of inflammatory markers, and then milrinone was tapered off uneventfully. We consider that continuous milrinone infusion may be suitable for patients with surgically correctable inflammatory cardiovascular diseases complicating severe heart failure in whom maintenance of optimal hemodynamics is necessary for several weeks during preoperative anti-inflammatory corticosteroid therapy.