Gene/Protein Disease Symptom Drug Enzyme Compound
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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protein C and protein S are vitamin K dependent anti-coagulant proteins required for the inhibition of activated protein V and VIII. In an inherited thrombophilia, hypercoagulability caused by the deficiency of protein C and protein S predisposes an individual to increased risk of thromboembolism (TE) that could herald as a venous thromboemboilsm (VTE) in the leg, pulmonary embolism (PE), stroke, or Budd-Chiari syndrome. However, very rarely does inherited thrombophilia cause coronary artery thrombosis leading to the development of myocardial infarction (MI). We report a case of a young male with combined protein C and protein S deficiency who presented with acute MI, worsened ventricular systolic function, and progressive declination of ejection fraction (EF) secondary to dilated cardiomyopathy (DCM).
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PMID:Acute Myocardial Infarction as an Initial Presentation of Protein C and Protein S Deficiency Followed by Dilated Cardiomyopathy in a Young Male. 3125 10

Increased troponin levels in HF are a frequent and significant finding, as it strongly correlates with the underlying pathogenic mechanisms, diagnosis and prognosis. The advent of hs-cTn testing, as opposed to conventional troponin testing, led to additional difficulties in result interpretation. Most frequently, though not exclusively, increased cTn levels in acute or chronic failure is correlated, with myocardial necrosis (AMI); the diagnosis of AMI is confirmed if other criteria are fulfilled, as described in the fourth Universal Definition of Myocardial Infarction. Increased cTn levels below the cut-off for AMI suggest acute or chronic injury, depending on the ascending and/or descending trend curve or stable levels of cTn on serial testing. In acute or chronic HF with reduced or preserved EF, increased cTn levels carry prognostic value for adverse outcomes. Acute and chronic HF, as well as other ischemic or non-ischemic conditions, may lead to a transient increase in cTn levels: hypertensive crises, tachyarrhythmias, valvular regurgitation, myocarditis, stroke, mandating differential diagnosis with ACS. There are multiple mechanisms that explain increased levels of cTn: myocardial necrosis or coronary thrombosis (type I MI), supply-demand mismatch with subendocardial ischemia/injury, cardiomyocyte apoptosis, inflammatory cytokines, neurohomonal changes. Screening for cTn levels in the population at high cardiovascular risk yields prognostic information on development of de novo HF or other cardiovascular adverse events.
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PMID:Troponins in Heart Failure - a Perpetual Challenge. 3215 68

BACKGROUND Heparin, often used as an anticoagulant, acts by binding to antithrombin III. Indeed, heparin binds to a variety of proteins other than antithrombin III. Among them, platelet factor 4 can bind and neutralize the anticoagulant activity of heparin. Upon binding with heparin, platelet factor 4 undergoes a conformational change and expresses immunogenic neo-epitopes that induce the generation of antibodies of the platelet factor 4 heparin complex. This immune reaction may lead to thrombocytopenia and venous, arterial, or microvascular thrombosis. However, the risk of such complications is quite variable, as it is affected not only by the source and dose of heparin and the clinical condition (e.g., cardiovascular surgery and orthopedic surgery) of the patient, but also the molecular size of the heparin formulation. Venous, arterial, and small-vessel thrombosis can lead to leg swelling, pulmonary embolism, stroke, skin necrosis, or gangrene requiring limb amputation or intestinal resection. Myocardial infarction due to coronary thrombosis also occurs, although it is less common and can be readily recognized. CASE REPORT Heparin-induced thrombocytopenia (HIT) is a potentially life-threatening complication of heparin therapy. We report the case of a 67-year-old woman who developed ST-segment elevation myocardial infarction and thrombocytopenia within 10 days of prophylactic enoxaparin therapy after undergoing bilateral total knee replacement surgery. She also had peripheral arterial and venous thrombosis. With thrombolysis and argatroban anticoagulation therapy, she recovered without residual sequelae. CONCLUSIONS Thrombocytopenia with coronary and other vascular thrombosis is a potentially serious complication of heparin therapy. A trend of decreased platelet count, decreased platelet count by 30% or more, and/or occurrence of any type of thrombosis should raise the suspicion of HIT. This case demonstrates that early recognition and prompt treatment of HIT can be life-saving.
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PMID:Myocardial Infarction with Limb Arterial and Venous Thrombosis in a Patient with Enoxaparin-Induced Thrombocytopenia. 3246 47

Corona virus 2 (SARS-CoV2/ Severe Acute Respiratory Syndrome Corona Virus 2) infection has emerged as a global health crisis. Incidence of thromboembolic disease is reported to be high in SARS-CoV2 disease and is seen in a multitude of organ systems ranging from cutaneous thrombosis to pulmonary embolism, stroke or coronary thrombosis sometimes with catastrophic outcomes. Evidence points towards a key role of thromboembolism, hypercoagulability and over production of proinflammatory cytokines mimicking a "cytokine storm" which leads to multiorgan failure. This brief narrative review highlights the pathophysiology and risk factors of thromboembolic disease and provides a framework for management of anticoagulation based on the current evidence.
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PMID:Thromboembolic disease in COVID-19 patients: A brief narrative review. 3293 66


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