An extranodal Richter's syndrome presenting with cardiac diffuse large B-cell lymphoma: a case report.

BACKGROUND: Richter's syndrome (RS) defines the transformation of chronic lymphocytic leukemia into high-grade lymphoma, which usually involves lymph nodes and bone marrow. Extranodal involvement of the heart is an extremely rare condition. Patients with heart involvement tended to have a low response to chemotherapy and relative poor prognosis. The transformation process of RS is often insidious and nonspecific making it challenging to diagnose. CASE PRESENTATION: A 64-year-old woman wih a history of chronic lymphocytic leukemia (CLL) presented with intermittent chest pain and was diagnosed with non-ST-elevation myocardial infarction (NSTEMI). However, the contrast enhanced echocardiography revealed a large irregular mass, measuring about 75.4 mm × 37.5 mm, located on the lateral and posterior wall of the right ventricle. Biopsy of the cardiac mass and the results revealed diffuse large B-cell lymphoma. CONCLUSIONS: We present a case of a 64-year-old woman with aggressive diffuse large B-cell lymphoma involving the heart. This case could provide some insights in the diagnosis of cardiac lymphoma.

The microvesicle/CD36 complex triggers a prothrombotic phenotype in patients with non-valvular atrial fibrillation.

The mechanisms responsible for platelet activation, the prothrombotic state, in non-valvular atrial fibrillation (NVAF) are still obscure. Microvesicles (MVs) can transfer various messages to target cells and may be helpful for exploring the detailed mechanisms. We aimed to investigate the possible mechanisms by which proatherogenic factors of NVAF contribute to platelet activation. Two hundred and ten patients with NVAF were stratified as being at 'low to moderate risk' or 'high risk' for stroke according to the CHADS2 score. Levels of platelet-derived MVs (PMVs) and platelet activation were examined. CD36-positive or CD36-deficient human platelets were stimulated by MVs isolated from NVAF patients with or without various inhibitors in vitro. Levels of PMVs and platelet activation markers enhanced significantly in high-risk patients. The MVs isolated from plasma of NVAF patients bound to platelet CD36 and activated platelets by phosphorylating the mitogen-activated protein kinase 4/Jun N-terminal kinase 2 (MKK4/JNK2) pathways. However, CD36 deficiency protected against MV-induced activation of platelets. We reveal a possible mechanism of platelet activation in NVAF and suggest that the platelet CD36 might be an effective target in preventing the prothrombotic state in NVAF.

Plasma calprotectin was associated with platelet activation and no-reflow phenomenon in acute coronary syndrome.

BACKGROUND: No-reflow occurs in 3-4% of all percutaneous coronary interventions (PCIs) and has a strong negative impact on clinical outcomes of acute coronary syndrome (ACS). Therefore, the discovery of a biomarker that can early predict the occurrence of no-reflow has great clinical significance. Multiple factors including platelet activation are relevant to no-reflow. Calprotectin is found to be a biomarker of plaque instability and is identified to be a novel diagnostic and prognostic biomarker of cardiovascular diseases. The association of plasma calprotectin with platelet activation and no-reflow phenomenon in ACS is not clear. METHODS: In this prospective study performed at Yantai Yuhuangding Hospital from 2017 to 2018, a total of 176 Chinese patients with ACS who had undergone PCIs were recruited consecutively, aged from 30 to 88 years. Angiographic no-reflow was defined as thrombolysis in myocardial infarction grade less than 3. Blood samples were collected immediately at admission for the detection of plasma calprotectin and platelet-monocyte aggregates formation. Statistical analysis was performed for the variable's comparisons between groups and the prediction value of plasma calprotectin for no-reflow. RESULTS: The mean age of the 176 included ACS patients were 64(±11) years and acute ST-segment elevation myocardial infarction (STEMI) was present in 41.5% of patients. Twenty-two patients had no-reflow during the PCI procedures and the prevalence was 12.5%. Patients with higher plasma calprotectin had a higher level of platelet-monocyte aggregates (PMA) and a higher prevalence of no-reflow (p < 0.001). The multivariate regression showed that plasma calprotectin and admission hs-cTnI were independently associated with PMA, while plasma calprotectin and serum LDL-c were independent predictors of no-reflow (p < 0.001 and p = 0.017). AUC of calprotectin for predicting no-reflow were 0.898. The cut-off value of plasma calprotectin for no-reflow was 4748.77 ng/mL with a sensitivity of 0.95 and a specificity of 0.77. CONCLUSION: Plasma calprotectin was associated with platelet activation and may act as an early predictive biomarker of no-reflow in patients with acute coronary syndrome.

Platelet CD36 links overweight and a prothrombotic phenotype in patients with non-valvular atrial fibrillation.

Introduction: The pathophysiological mechanisms linking the overweight and prothrombotic state of non-valvular atrial fibrillation (NVAF) are incompletely understood. Our objective was to evaluate the effect of platelet CD36 on the risk of stroke associated with overweight in NVAF patients. Methods: A cross-sectional study enrolled 182 subjects with NVAF in two groups: normal weight (18.5 < body mass index(BMI) < 25.0 kg/m2) and overweight (BMI ≥ 25.0 kg/m2). Clinical data, medical history, vital signs, transthoracic echocardiography parameters, and medication were recorded. Biochemical characteristics including blood glucose and serum lipid were analyzed in the Laboratory. Results: The expression of platelet CD36 and integrin αIIbß3 was detected by flow cytometry. Among the 182 patients with NVAF, 68 (37.36%) were classified as normal weight, 114 (62.64%) as overweight. With an increase in BMI, waist-hip ratio, cholesterol, triglycerides, left atrium diameters, and the ratio of mitral inflow E velocity to myocardial e' velocity in the mitral annulus (E/e') increased significantly (P < 0.05). The mean fluorescent intensity of platelet CD36 increased significantly in overweight patients (P < 0.01), in line with platelet activation biomarkers (platelet integrin αIIbß3). Platelet CD36 was positively correlated with BMI and platelet integrin αIIbß3, respectively (P < 0.05). Additionally, platelet CD36 and BMI were independent risk factors for platelet activation in patients with NVAF. Conclusions: Platelet CD36 is speculated to mediate the complex crosstalk between overweight and platelet hyperactivity, leading to the prothrombotic state in overweight patients with NVAF. Platelet CD36 could be a potential target for preventing the prothrombotic state in overweight patients with NVAF.

Does types of atrial fibrillation matter in the impairment of global and regional left ventricular mechanics and intra-ventricular dyssynchrony?

Background: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, which is associated with cardiac dysfunction. This study aimed to compare the impairment severity of left ventricular strain and intra-ventricular dyssynchrony using echocardiography-derived velocity vector imaging in patients with different types of AF without heart failure. Methods: 168 non-valvular AF patients with normal left ventricular ejection fraction (98 paroxysmal AF patients and 70 persistent AF patients) and 86 healthy control subjects were included in this study. Regional and global left ventricular longitudinal and circumferential strain were measured. Time to regional peak longitudinal strain was measured and the standard deviation of all 12 segments (SDT-S) was used as a measure of intra-ventricular dyssynchrony. Results: Significantly lower GLS (-18.71 ± 3.00% in controls vs. -17.10 ± 3.01% in paroxysmal AF vs. -12.23 ± 3.25% in persistent AF, P < 0.05) and GCS (-28.75 ± 6.34% in controls vs. -24.43 ± 6.86% in paroxysmal AF vs. -18.46 ± 6.42% in persistent AF, P < 0.01) were observed in either persistent AF subjects or paroxysmal AF subjects compared with healthy control subjects (P < 0.05). The impairment was much worse in persistent AF subjects compared with paroxysmal AF subjects (P < 0.001). Intraventricular dyssynchrony was found in both persistent AF patients and paroxysmal AF patients, and it's worse in persistent AF patients (52 ± 18 ms in controls, 61 ± 17 ms in paroxysmal AF, and 70 ± 28 ms in persistent AF, P < 0.05). Multivariate regression analysis revealed AF types were independent risk factors of GLS, GCS, and intraventricular dyssynchrony. Conclusion: AF types were not only associated with impaired longitudinal and circumferential left ventricle mechanics but also intra-ventricular mechanical dyssynchrony. Worse systolic mechanics and intra-ventricular dyssynchrony were found in patients with persistent AF compared with these in patients with paroxysmal AF.

Calprotectin and Neutrophil Gelatinase-Associated Lipocalin As Biomarkers of Acute Kidney Injury in Acute Coronary Syndrome.

BACKGROUND: Acute kidney injury (AKI) is increasingly being seen in patients with acute coronary syndromes (ACS) and it is associated with higher short-term and long-term morbidity and mortality. Therefore, it is of paramount importance to identify those ACS patients at risk for the development of AKI. The objective of this study was to evaluate two different plasma biomarkers calprotectin and neutrophil gelatinase-associated lipocalin (NGAL) in early detecting the development of AKI in ACS patients. METHODS: 172 ACS patients admitted to the Coronary Care Unit in Yantai Yuhuangding Hospital were prospectively enrolled. Their blood samples were obtained on admission and subjected to enzyme-linked immunosorbent assay to determine the levels of novel biomarkers. The clinical data and biomarkers were recorded and analyzed. RESULTS: In this study, 23 (13.4%) patients had a diagnosis of AKI. Statistical analysis demonstrated that in ACS patients with AKI, the following two biomarkers were significantly higher than these without AKI: plasma calprotectin (5942.26 ± 1955.88 ng/mL vs. 3210.29 ± 1833.60 ng/mL, p < 0.001) and plasma NGAL (164.91 ± 43.63 ng/mL vs. 122.48 ± 27.33 ng/mL, p < 0.001). Plasma calprotectin and NGAL could discriminate the development of AKI respectively with an area under the ROC curve (AUC) of 0.864 and 0.850. A combination of the two plasma biomarkers calprotectin and NGAL could early discriminate AKI in ACS patients with an AUC of 0.898. CONCLUSIONS: This study demonstrated a promising panel of plasma calprotectin and NGAL as early diagnostic biomarkers for AKI in ACS patients.