warfarin and Cardiomegaly

Little is known about the effects of anticoagulation in patients with atrial fibrillation (AF) and left atrial enlargement (LAE).. Data of patients with AF were retrieved from Chang Gung Research Database during 2007-2016. We excluded patients who were not using oral anticoagulants, used anticoagulants for <30 days, used ≥2 agents concomitantly or switched anticoagulants, had left atrial diameter missing from their data, were aged <65, had received valve surgeries, had mitral stenosis, or had a history of cancer. The primary outcomes were ischemic stroke (IS)/systemic embolism (SE), major bleeding, and death from any cause.. We identified 40,777 patients who received a diagnosis of AF. After the exclusion criteria were applied, 6,445 patients remained, 4,922 with LAE, and they were followed up for 2.4 ±1.9 years. The mean age of the patients was 77.32 ± 0.18 in the NOAC group and 76.58 ± 6.91 in the warfarin group (p < 0.0001); 48.24% of patients in the NOAC group and 46.98% of patients in the warfarin group were men (p > 0.05). The mean CHA2DS2-VASc score was 3.26 ± 1.05 in the NOAC group and 3.07 ± 1.12 in the warfarin group (p < 0.0001). The mean HAS-BLED score was 3.87 ± 3.81 in the NOAC group and 3.86 ± 3.80 in the warfarin group (p > 0.05). Furthermore, the mean LA diameter was 4.75 ± 0.63 cm in the warfarin group and 4.79 ± 0.69 cm in the warfarin group (p > 0.05). Among patients with LAE, NOAC was associated with significantly reduced IS/SE events (CRR = 0.63, 95% CI = 0.52-0.77), no difference in major bleeding (CRR = 0.91, 95% CI = 0.78-1.05), and significantly reduced death from any cause (aHR = 0.65, 95% CI = 0.52-0.80) compared with warfarin.. In elderly patients with AF and LAE, NOAC was associated with reduced IS/SE and death from any cause compared with warfarin, whereas no difference in major bleeding was observed between these treatments.

Topics: Administration, Oral; Aged; Anticoagulants; Atrial Fibrillation; Cardiomegaly; Female; Follow-Up Studies; Heart Atria; Humans; Kaplan-Meier Estimate; Male; Treatment Outcome; Warfarin

Despite anticoagulation therapy, ischemic stroke risk in atrial fibrillation (AF) remains substantial. We hypothesize that left atrial enlargement (LAE) is more prevalent in AF patients admitted with ischemic stroke who are therapeutic, as opposed to nontherapeutic, on anticoagulation.. We included consecutive patients with AF admitted with ischemic stroke between April 1, 2015, and December 31, 2016. Patients were divided into two groups based on whether they were therapeutic (warfarin with an international normalized ratio ≥ 2.0 or non-vitamin K oral anticoagulant with uninterrupted use in the prior 2 weeks) versus nontherapeutic on anticoagulation. Univariable and multivariable models were used to estimate associations between therapeutic anticoagulation and clinical factors, including CHADS2 score and LAE (none/mild versus moderate/severe).. We identified 225 patients during the study period; 52 (23.1%) were therapeutic on anticoagulation. Patients therapeutic on anticoagulation were more likely to have a larger left atrial diameter in millimeters (45.6 ± 9.2 versus 42.3 ± 8.6, P = .032) and a higher CHADS2 score (2.9 ± 1.1 versus 2.4 ± 1.1, P = .03). After adjusting for the CHADS2 score, patients who had a stroke despite therapeutic anticoagulation were more likely to have moderate to severe LAE (odds ratio, 2.05; 95% confidence interval, 1.01-4.16).. LAE is associated with anticoagulation failure in AF patients admitted with an ischemic stroke. This provides indirect evidence that LAE may portend failure of anticoagulation therapy in patients with AF; further studies are needed to delineate the significance of this association and improve stroke prevention strategies.

Topics: Administration, Oral; Aged; Aged, 80 and over; Anticoagulants; Atrial Fibrillation; Brain Ischemia; Cardiomegaly; Cross-Sectional Studies; Drug Monitoring; Female; Humans; International Normalized Ratio; Logistic Models; Male; Multivariate Analysis; Odds Ratio; Retrospective Studies; Risk Factors; Stroke; Time Factors; Treatment Failure; United States; Warfarin

Lutembacher syndrome is characterized by a congenital ostium secundum atrial septal defect and an acquired mitral valve stenosis. We present a similar case in a 31-year old male who came in with orthopnoea, central cyanosis and pedal oedema. Examination revealed cardiac murmurs in tricuspid and apical regions. Chest x-ray showed signs of pulmonary congestion and ventricular enlargement. Electrocardiogaphy (ECG) revealed right axis deviation and right bundle branch block along with atrial fibrillation and Transthoracic Echocardiography (TTE) showed abnormal valves (mitral stenosis with calcification and tricuspid regurgitation) and dilated cardiac chambers. The patient was consequently treated with beta-blockers and diuretics and scheduled for valvular and septal repair via open heart surgery. The purpose of this case report is to assist cardiologists in diagnosing this syndrome accurately on the basis of symptoms and investigations.

Topics: Adrenergic beta-Antagonists; Adult; Amiloride; Anticoagulants; Atrial Fibrillation; Bundle-Branch Block; Calcinosis; Cardiac Surgical Procedures; Cardiomegaly; Cyanosis; Diuretics; Echocardiography; Edema; Electrocardiography; Foot; Furosemide; Heart Septal Defects, Atrial; Humans; Lutembacher Syndrome; Male; Mitral Valve Annuloplasty; Mitral Valve Stenosis; Tricuspid Valve Insufficiency; Warfarin

A 76 -year-old lady with a recent diagnosis of rheumatic heart disease (RHD), and a history of repeated lower respiratory tract infections, came with symptoms of gastritis unrelated to the primary disease but further diagnostic study in the hospital revealed poorly controlled atrial fibrillation, grossly dilated left atrium with two large left atrial thrombi and mitral valve area<1 cm(2). It was decided that the best approach in our patient would be mitral valve replacement with mechanical prosthesis. Despite the usual trend of using bioprosthesis in the elderly, our decision was influenced by the fact that the patient would need chronic anticoagulation for atrial fibrillation in any case. The purpose of our case presentation is to illustrate a late-presenting case of RHD with unusual associations and the challenges to choose the best possible management.

Topics: Aged; Anti-Arrhythmia Agents; Anticoagulants; Atrial Fibrillation; Cardiomegaly; Female; Gastritis; Heart Diseases; Heart Valve Prosthesis; Heart Valve Prosthesis Implantation; Humans; Mitral Valve Stenosis; Radiography; Rheumatic Fever; Thrombosis; Warfarin

Topics: Adrenergic beta-Antagonists; Cardiomegaly; Digoxin; Diuretics; Female; Heart Atria; Humans; Middle Aged; Mitral Valve Insufficiency; Mitral Valve Stenosis; Tomography, X-Ray Computed; Ultrasonography; Warfarin

Topics: Aspirin; Atrial Fibrillation; Cardiomegaly; Dyspnea; Echocardiography; Embolization, Therapeutic; Heart Failure; Heparin; Humans; Male; Middle Aged; Stroke Volume; Warfarin

In pulmonary arterial hypertension (PAH), thrombosis and thromboembolism occurs as a consequence of pulmonary microvasculopathy with a change of pulmonary vascular microenviroment toward a procoagulant, prothrombotic and antifibrinolytic pattern. Circulating antiphospholipid antibodies, increased plasma levels of platelet aggregating agents (serotonin, thromboxane), adhesion molecules (P selectin, von Willebrand factor), antifibrinolytic enzymes (plasminogen activator inhibitor 1) and prothrombotic cytokines have been identified in PAH patients so far. Thrombogenic pulmonary vasculopathy has been documented in many patients with PAH. Furthermore, most patients will not be diagnosed until right heart enlargement and impaired right ventricular function has developed. Thus, there is clear rationale for a treatment with anticoagulation. In four uncontrolled studies Warfarin improved the prognosis of patients with idiopathic and other forms of PAH. However, so far there are no prospective randomised studies evaluating the role of anticoagulants in the treatment of PAH. This review summarizes the current data and guidelines concerning anticoagulation in PAH.

Topics: Anticoagulants; Blood Platelets; Cardiomegaly; Cerebrovascular Disorders; Fibrinolysis; Humans; Hypertension, Pulmonary; Warfarin

Topics: Aged; Anticoagulants; Cardiomegaly; Coronary Thrombosis; Female; Heart Atria; Humans; Mitral Valve Insufficiency; Mitral Valve Stenosis; Thromboembolism; Ultrasonography; Warfarin

The thrombomodulin (TM) gene was ablated in mice in a cell type-restricted manner from vascular endothelium by Cre-recombinase-mediated excision controlled by the endothelial cell lineage-specific Tie2 promoter. Forty percent of mutant (TMLox-) mice display a distinct lethal embryonic phenotype not observed in completely TM-deficient embryos. The remaining 60% of TMLox mice survive beyond birth, but invariably succumb to a severe hypercoagulable state and massive thrombosis after 3 weeks, terminating in a lethal consumptive coagulopathy. The progression of thrombosis was age- and sex-dependent. Disruption of the TM/protein C pathway was not associated with a latent proinflammatory state. Disease onset and progression could be prevented by warfarin anticoagulation. These results show that in mice, loss of endothelial cell TM function causes spontaneous and fatal thrombosis in the arterial and venous circulation, resulting from unfettered activation of the coagulation system. The combination of complete disease penetrance, uniform disease onset at young age, large vessel thrombosis of the extremities and multiple organ systems, and consumptive coagulopathy as the disease end-point provides a unique mouse model of human thrombotic disease.

Topics: Age Factors; Animals; Anticoagulants; Blood Coagulation; Cardiomegaly; Disease Models, Animal; Disease Progression; Disseminated Intravascular Coagulation; Endothelium, Vascular; Female; Gene Expression Regulation; Gene Targeting; Genes, Lethal; Genes, Synthetic; Humans; Integrases; Male; Mice; Mice, Transgenic; Myocardium; Organ Specificity; Protein C; Receptor Protein-Tyrosine Kinases; Receptor, TIE-2; Recombinant Fusion Proteins; Recombination, Genetic; Sexual Maturation; Thrombomodulin; Thrombophilia; Thrombosis; Viral Proteins; Warfarin

Topics: Aged; Aorta, Abdominal; Aortic Aneurysm; Cardiomegaly; Coronary Disease; Heparin; Humans; Lung Diseases, Obstructive; Male; Pulmonary Embolism; Warfarin

We confirmed our previously reported findings that subcutaneous administration of heparin (200 U q 12 hr) in rats with experimental partial renal infarction prevents the development of progressive renal failure and hypertension, as well as the glomerular abnormalities which occur in the remaining viable renal tissue. In the present study, heparin, in the dosage used to prevent progressive renal failure, caused a marked and sustained prolongation of the activated partial thromboplastin time and prothrombin time, as well as a transient prolongation of the bleeding time. Administration of coumadin at doses which caused a significant prolongation of the prothrombin time and bleeding time also inhibited the development of progressive hypertension and uremia in rats with experimental partial renal infarction. These findings indicate that inhibition of blood coagulation effectively protects rats with experimentally decreased renal mass from the development of progressive renal failure and hypertension and support the concept that the glomerular thrombosis plays an important role in the pathogenesis of these complications.

Topics: Animals; Anticoagulants; Cardiomegaly; Female; Hemostasis; Heparin; Hypertension; Infarction; Kidney; Kidney Glomerulus; Rats; Rats, Inbred Strains; Uremia; Warfarin

A case of Bjork-Shiley mitral valve dysfunction is presented. The patient has not responded to anticoagulant therapy and had hypotension, dyspnea, chest pain, and a pulse deficit but normal sinus rhythm. Simultaneous echocardiogram, ECG, and arterial pulse tracing were used as noninvasive means of monitoring. Nonsurgical correction of a clinical emergency restored the patient to prior normal baseline cardiovascular function. This case illustrates the possibility of restoring normal prosthetic function by supporting the patient medically while undertaking diagnostic testing and arranging surgical intervention. To our knowledge, this is the first reported case of a malfunctioning Bjork-Shiley mitral valve corrected without surgery.

Topics: Aspirin; Cardiomegaly; Dipyridamole; Echocardiography; Female; Furosemide; Heart Murmurs; Heart Valve Prosthesis; Humans; Hypotension; Middle Aged; Mitral Valve Prolapse; Phenylephrine; Prothrombin Time; Warfarin

A low incidence rate of thromboembolism has been reported in mitral porcine valve recipients. In contrast, 5 of 22 single mitral porcine valve recipients (23 percent) followed up in our clinic for a mean of 16 months had thromboembolic events. All patients but one were receiving long-term anticoagulant therapy. One thromboembolic event resulted in death, three in permanent neurologic deficits and one in a peripheral arterial occlusion. All five patients with emboli had atrial fibrillation and left atrial enlargement. Three had thromboembolic events before porcine heart valve implantation. In addition, five mitral porcine valve recipients who were not receiving anticoagulant therapy were examined at autopsy. Thrombus was identified in the left atrium in three patients, at the tissue-valve interface (sewing ring) in two, on the porcine valve cusps in one and in the right atrium in one. Factors influencing thrombus formation such as left atrial enlargement, atrial fibrillation and a prosthetic device are present after mitral porcine valve implantation and are indications for long-term anticoagulation therapy.

Topics: Adult; Animals; California; Cardiomegaly; Female; Follow-Up Studies; Heart Atria; Heart Valve Prosthesis; Humans; Male; Middle Aged; Mitral Valve Insufficiency; Swine; Thromboembolism; Transplantation, Heterologous; Warfarin