Biventricular and right atrial thrombi in a middle-aged woman.
Ontology highlight
ABSTRACT:
SUBMITTER: Aikawa T
PROVIDER: S-EPMC8796801 | biostudies-literature | 2022 Jan
REPOSITORIES: biostudies-literature
Publications
Biventricular and right atrial thrombi in a middle-aged woman.
Aikawa Tadao T Ibe Tatsuro T Manabe Osamu O Oyama-Manabe Noriko N
European heart journal. Case reports 20211214 1
Similar Datasets
Project description: Not available
| S-EPMC10904301 | biostudies-literature
Project description: Not available
| S-EPMC10141454 | biostudies-literature
Project description:A rare case of biventricular thrombi complicating acute myocardial infarction detected during echocardiography is described.
| S-EPMC5067724 | biostudies-literature
Project description: Not available
| S-EPMC7303235 | biostudies-literature
Project description:Biventricular thrombi secondary to anterior myocardial infarction is very rare. We present a patient with giant biventricular thrombi subsequent to an old anterior wall myocardial infarction, and devastating consequences, including acute pulmonary artery and femoral artery embolism. We introduce a unique case report with demonstrative and illustrative images.
| S-EPMC5067763 | biostudies-literature
Project description:A 40-year-old woman with history of atopy and peripheral eosinophilia presented with clinical signs of heart failure. Echocardiography revealed a restrictive cardiomyopathy with biventricular thrombi. Hypereosinophilic syndrome resulting in eosinophilic myocarditis (Loeffler's syndrome) was diagnosed. This case highlights the workup, diagnosis, and management of hypereosinophilic syndrome with eosinophilic myocarditis. (Level of Difficulty: Advanced.).
| S-EPMC8299133 | biostudies-literature
Project description:Widely distributed osteosclerosis is an unusual radiographic finding with multiple causes. A 42-year-old premenopausal Spanish woman gradually acquired dense bone diffusely affecting her axial skeleton and focally affecting her proximal long bones. Systemic lupus erythematosus (SLE) diagnosed in adolescence had been well controlled. She had not fractured or received antiresorptive therapy, and she was hepatitis C virus antibody negative. Family members had low bone mass. Lumbar spine bone mineral density (BMD) measured by dual-photon absorptiometry (DPA) at age 17 years, while receiving glucocorticoids, was 79% the average value of age-matched controls. From ages 30 to 37 years, dual-energy X-ray absorptiometry (DXA) BMD Z-scores steadily increased in her lumbar spine from +3.8 to +7.9, and in her femoral neck from -1.4 to -0.7. Serum calcium and phosphorus levels were consistently normal, 25-hydroxyvitamin D (25OHD) <20 ng/mL, and parathyroid hormone (PTH) sometimes slightly increased. Her reduced estimated glomerular filtration rate (eGFR) was 38 to 55 mL/min. Hypocalciuria likely reflected positive mineral balance. During increasing BMD, turnover markers (serum bone-specific alkaline phosphatase [ALP], procollagen type 1 N propeptide [P1NP], osteocalcin [OCN], and carboxy-terminal cross-linking telopeptide of type 1 collagen [CTx], and urinary amino-terminal cross-linking telopeptide of type 1 collagen [NTx and CTx]) were 1.6- to 2.8-fold above the reference limits. Those of bone formation seemed increased more than those of resorption. FGF-23 was slightly elevated, perhaps from kidney disease. Serum osteoprotegerin (OPG) and TGFβ1 levels were normal, but sclerostin (SOST) and receptor activator of nuclear factor kappa-B ligand (RANKL) were elevated. Serum multiplex biomarker profiling confirmed a high level of SOST and RANKL, whereas Dickkopf-1 (DKK-1) seemed low. Matrix metalloproteinases-3 (MMP-3) and -7 (MMP-7) were elevated. Iliac crest biopsy revealed tetracycline labels, no distinction between thick trabeculae and cortical bone, absence of peritrabecular fibrosis, few osteoclasts, and no mastocytosis. Then, for the past 3 years, BMD Z-scores steadily decreased. Skeletal fluorosis, mastocytosis, myelofibrosis, hepatitis C-associated osteosclerosis, multiple myeloma, and aberrant phosphate homeostasis did not explain her osteosclerosis. Mutation analysis of the LRP5, LRP4, SOST, and osteopetrosis genes was negative. Microarray showed no notable copy number variation. Perhaps her osteosclerosis reflected an interval of autoimmune-mediated resistance to SOST and/or RANKL. © 2016 American Society for Bone and Mineral Research.
| S-EPMC5010446 | biostudies-literature
Project description:AimsRecommendations on cardiac resynchronization therapy (CRT) in patients with atrial fibrillation or flutter (AF) are based on less robust evidence than those in sinus rhythm (SR). We aimed to assess the efficacy of CRT upgrade in the BUDAPEST-CRT Upgrade trial population by their baseline rhythm.Methods and resultsHeart failure patients with reduced ejection fraction (HFrEF) and previously implanted pacemaker (PM) or implantable cardioverter defibrillator (ICD) and ≥20% right ventricular (RV) pacing burden were randomized to CRT with defibrillator (CRT-D) upgrade (n = 215) or ICD (n = 145). Primary [HF hospitalization (HFH), all-cause mortality, or <15% reduction of left ventricular end-systolic volume] and secondary outcomes were investigated. At enrolment, 131 (36%) patients had AF, who had an increased risk for HFH as compared with those with SR [adjusted hazard ratio (aHR) 2.99; 95% confidence interval (CI) 1.26-7.13; P = 0.013]. The effect of CRT-D upgrade was similar in patients with AF as in those with SR [AF adjusted odds ratio (aOR) 0.06; 95% CI 0.02-0.17; P < 0.001; SR aOR 0.13; 95% CI 0.07-0.27; P < 0.001; interaction P = 0.29] during the mean follow-up time of 12.4 months. Also, it decreased the risk of HFH or all-cause mortality (aHR 0.33; 95% CI 0.16-0.70; P = 0.003; interaction P = 0.17) and improved the echocardiographic response (left ventricular end-diastolic volume difference -49.21 mL; 95% CI -69.10 to -29.32; P < 0.001; interaction P = 0.21).ConclusionIn HFrEF patients with AF and PM/ICD with high RV pacing burden, CRT-D upgrade decreased the risk of HFH and improved reverse remodelling when compared with ICD, similar to that seen in patients in SR.
| S-EPMC11264293 | biostudies-literature
Project description:IntroductionCoronavirus 2019 (COVID-19) can cause cardiovascular manifestations including myocardial injury and thromboembolic events.Case presentationHere, we report a case of a 27-year-old female with dilated cardiomyopathy, right atrial and biventricular thrombi infected with COVID-19.DiscussionThere are several complex coagulation abnormalities in COVID-19 patients that have been suggested to create a hypercoagulable state. Evidence have shown that endothelial injury potentially leading to thromboembolic events is caused by direct invasion of endothelial cell by SARS-CoV-2 and complement activation contributed by the virus spike protein.ConclusionDCM can be complicated by atrial and biventricular thrombi due to coagulation abnormalities that are likely to persist after recovery from COVID-19. Thus, long-term careful monitoring of cardiac function is necessary after recovery of COVID-19.
| S-EPMC9259012 | biostudies-literature
Project description:A 59-year-old female with a history of stage IV lung adenocarcinoma presented with worsening shortness of breath and cough over several weeks. She was tachycardic, hypotensive, and tachypneic. Portable chest x-ray suggested bilateral pleural effusions and computed tomography angiography (CTA) revealed bilateral pulmonary emboli (PE) with suspected right heart strain. Upon admission to the medical intensive care unit for treatment of PE, bedside echocardiography was performed to direct management. Indicators of cor pulmonale and right heart strain were apparent including right ventricle dilation, reduced tricuspid systolic excursion, and a deformed left ventricle with "D sign". Most notably, a right atrial thrombus was detected, a finding not initially seen on CTA. Ultimately, prompt detection of the effects on the right ventricle by bedside echocardiography directed the next step in this patient's clinical course without delay.
| S-EPMC9618828 | biostudies-literature