Cardiac pathology may be a collection of diseases that involve the guts or blood vessels. The Cardiac Pathology Unit of the Department of Pathology and Cell Biology at Columbia University Medical Centre has extensive experience in cardiac and cardiac-transplant pathology. Each year, the unit reviews quite 2,000 cardiovascular specimens, including cardiomyopathy and post-transplant heart biopsies, heart and cardiac-valve explants, aneurysms, and biopsies of blood vessels. We even have extensive experience within the pathology of congenital heart condition.

In addition to diagnostic cardiac pathology, our faculty is actively involved in research projects. Among the main areas of interest are cardiac-transplant pathology, non-invasive monitoring of post-transplant status, evaluation of experimental drug and stem-cell therapies for cardiac allograft rejection, myocardial infarcts and arrhythmias in animal models, and therefore the biology of cardiovascular development and coronary failure.

Disorder includes arteria coronaria diseases (CAD) like myocardial infarct and angina. Other diseases like heart arrhythmia, valvular heart condition and congenital heart condition. It occurs in 40% of youngsters with SLE. The pericardium, myocardium, conduction system, valves, and coronary arteries are targets. Symptomatic pericarditis occurs in 25% of cases, either in isolation or as a part of a generalized serositis. Patients present with precordial pain, radiating to the left shoulder or back which will be related to fever, cough, or dyspnea. There could also be tachycardia, distant heart sounds, and a friction rub.

Cardiac Pathology is instrumental in diagnosing and planning treatment for the wide selection of heart diseases and disorders seen at the guts Institute. Electrocardiography reveals low voltages, mild ST-segment elevation, and T-wave inversion. Chest X-radiography shows an enlarged cardiac silhouette, and an echocardiogram is diagnostic. The pericardial fluid is exudative. Tamponade occurs in but 1% of patients. The pathogenesis of the cardiomyopathy is multifactorial: it's going to be an autoimmune phenomenon, or it's going to be secondary to atherosclerosis, hypertension, or antimalarial therapy. Presenting symptoms include dyspnea, orthopnea, cough, palpitations, and exercise intolerance. A physical examination reveals tachycardia, an S3 gallop, and rales. Chest X-radiography shows cardiac enlargement, with varying degrees of pulmonary edema. Echocardiography shows diminished ventricular systolic function. Adams-Stokes syndrome (1st, 2nd, and 3rd degree), fibrillation, and atrial or premature ventricular contractions may the results of an autoimmune phenomenon. Within the neonatal lupus syndrome, transplacental transfer of maternal autoantibodies (anti-SS-A, SS-B) may cause congenital complete Adams-Stokes syndrome. Valvular disease may be a common finding, but could also be asymptomatic and unrelated to overall lupus activity. In adults, valvular abnormalities were found in 61% and 53% of lupus patients on an initial and follow-up transesophageal echocardiography, respectively. The mitral and aortic valves are most ordinarily affected. Libmann–Sachs endocarditis may be a non-infectious inflammatory condition in SLE which will simulate bacterial disease. Dyslipidemia, premature atherosclerosis, and myocardial infarct are complications of juvenile SLE. The dyslipidemia could also be secondary to the underlying disease, corticosteroid use, or both. An increased carotid intima-media wall thickness can occur in young lupus patients with nephrotic-range proteinuria.

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Journal of Clinical and Experimental Pathology

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