Anticoagulants

Parenteral anticoagulation (unfractionated heparin, enoxaparin, fondaparinux, or bivalirudin) for all ACS at presentation: the antiplatelet stops new platelets from joining the clot; the anticoagulant halts propagation of the thrombus already there while the patient awaits — or undergoes — revascularization.

Thrombosis prophylaxis in immobility. "The annual incidence of coagulation abnormalities has been in the range of 3 and 11 percent"; prophylaxis "as per existing guidelines" has been advised.

Selective in DCM — only with atrial fibrillation, a prosthetic valve or known mural thrombus (the old practice of anticoagulating everyone is gone). In HCM with AF, lifelong regardless of stroke-risk score. In takotsubo, reserved for documented ventricular thrombus or embolism. In PPCM, often needed when EF falls below 30–35% or AF is present.

Before surgery, "If you take a medication that could cause bleeding during your surgery, your eye doctor may ask you to stop taking it for a little while." — only on the surgeon’s instruction.

VTE prevention in hospitalized patients (NIH guidelines, archived 2024): prophylactic-dose heparin unless contraindicated; therapeutic-dose heparin "for nonpregnant patients with D-dimer levels above the upper limit of normal who require conventional oxygen and who do not have an increased bleeding risk (CIIa)"; not therapeutic-dose anticoagulation for VTE prophylaxis in the ICU.

The heparin paradox: giving an anticoagulant to a patient who is bleeding from every line site is counter-intuitive, and the rationale is that the bleeding is driven by uncontrolled thrombin generation, so interrupting the clotting stops the consumption that causes the hemorrhage. The fetched evidence makes this strictly phenotype-dependent. Heparin is used when there is extensive clotting, in the non-symptomatic (pre-DIC) type, and as prophylaxis — "patients with DIC who are not actively bleeding should receive prophylactic anticoagulation with heparin or low molecular weight heparin." Heparin is not used in the bleeding or massive-bleeding types "due to the increased risk of bleeding." And in sepsis the evidence is actively unfavourable: a meta-analysis of nine trials found heparin "does not reduce organ injury or mortality, but was associated with an increase in the risk of bleeding." Where heparin is given for DIC, low molecular weight heparin is preferred over unfractionated. Two adjacent rules matter at the bedside: VTE prophylaxis is a separate question from treating DIC and has become standard of care, and antithrombin concentrate must be given without concomitant heparin, because heparin alters antithrombin’s protective effect.

Treats the deadliest part of afib and flutter — the clot, not the rhythm. The 2023 ACC/AHA/ACCP/HRS AF guideline anticoagulates once estimated annual stroke risk is ≥ 2%/year — conventionally CHA₂DS₂-VASc ≥ 2 in men / ≥ 3 in women; if afib has lasted > 48 h or onset is unknown, anticoagulate ≥ 3 weeks before and ≥ 4 weeks after cardioversion (or clear the atrium with a TEE first). Check coagulation parameters and teach stroke signs alongside every dose.

Not a treatment for GBS itself — a shield against the disorder’s most common preventable killer. The paralyzed patient is immobile and hypercatabolic, and pulmonary embolism is among the leading causes of GBS death. Every minimally ambulant or non-ambulant patient receives prophylactic unfractionated or low-molecular-weight heparin (ACCP guidance as reported by Harms 2011), layered with compression stockings or sequential compression devices; some centers hold the heparin on plasma-exchange days and rely on the mechanical devices. Prophylaxis continues into rehabilitation until the patient walks again — not until discharge.

AVOID unless "specifically recommended after careful risk-benefit assessment" (StatPearls, hemophilia B).

Stronger thromboprophylaxis for higher-risk patients on lenalidomide — "Thromboprophylaxis is recommended and the choice of regimen should be based on an assessment of the patient’s underlying risks."

Venous thromboembolism prophylaxis after hip or knee arthroplasty, attributed to the American Society of Hematology 2019 guideline as summarized in its published abstract. Two conditional recommendations apply after total hip or knee arthroplasty: aspirin or an anticoagulant — either is acceptable — and a direct oral anticoagulant over low-molecular-weight heparin. The orthopedic side agrees on aspirin: "many surgeons use aspirin, which has demonstrated suitable efficacy and outcomes equivalent to those of other agents for preventing symptomatic pulmonary embolism." That is the answer to a patient or a colleague asking why this person is "only on aspirin" — aspirin alone is prophylaxis, and the guideline says so. Two silences are deliberate. No duration in days or weeks is stated, because no permitted source here gives an orthopedic-specific duration. And no attribution to AAOS or ACCP appears, because neither text was obtainable and the AAOS venous-thromboembolism lineage dates to 2011 and 2012. Anticoagulant monitoring, reversal and bleeding management belong to the class page, and the DVT and PE page owns the disease itself.

Trousseau syndrome: "In patients with Trousseau syndrome, heparin is the preferred method of anticoagulation"; clots may keep recurring despite anticoagulation. Perioperative: deep vein thrombosis prophylaxis is part of the Whipple bundle.

After a clot. "In the setting of a first thrombotic event, an appropriate dose and length of anticoagulation are recommended." "There is currently no difference in treatment recommendations for patients with underlying PV." Anticoagulation adds bleeding risk.

The mainstay of PE treatment — but know what they actually do: anticoagulants stop the clot from extending and prevent new clot while the body’s own fibrinolysis clears the old one; they do not dissolve it. DOACs are preferred over warfarin for primary VTE treatment (ASH 2020); initial parenteral therapy favors LMWH or fondaparinux over unfractionated heparin (less major bleeding, less HIT), with UFH reserved for hemodynamic instability or renal impairment. Everyone gets at least 3 months — longer when the PE was unprovoked or risk factors persist. Pregnancy: LMWH (it does not cross the placenta); DOACs are contraindicated; cancer: LMWH or a DOAC such as apixaban or rivaroxaban, preferred over warfarin.

Lifelong in CTEPH once confirmed; generally not recommended in PAH, though it may be considered individually.

The cardioembolic answer: for atrial fibrillation, oral anticoagulation is the recommended prevention strategy — antiplatelets are not enough for a clot formed in the atria. After an ischemic stroke, anticoagulation starts 4–14 days after onset, not immediately. Absolutely avoided in hemorrhagic stroke — there, existing anticoagulation is reversed instead (vitamin K, prothrombin complex concentrates, FFP).

This class appears here as the cause, not the cure. Heparin in any form or amount can trigger HIT — including flushes, heparin-coated catheters and heparin in dialysate — and unfractionated heparin carries more risk than low-molecular-weight heparin because its longer saccharide chains bind plasma proteins and cells more readily. Fondaparinux "does not cause HIT, nor does it react with heparin-induced antibodies." When HIT is diagnosed, the response is not simply to stop: all heparin stops and a non-heparin anticoagulant starts immediately, because the prothrombotic state persists up to 30 days. Two further rules belong to this class. Warfarin must not be started until the platelet count has recovered — ideally to at least 150,000/µL or the patient’s baseline — and only after a non-heparin agent has overlapped for at least 5 days, or protein C and S depletion precipitates skin necrosis. And in ITP, anticoagulants are avoided altogether when the platelet count is below 20,000/μL.

Valve disease is a clot-forming disease at two sites: the enlarged fibrillating left atrium of mitral stenosis and the foreign surface of a mechanical prosthesis. Warfarin is the anticoagulant of choice for both — MS with AF, a prior embolus, or LA thrombus (INR about 2.5) and every mechanical valve for life: target 2.5 (2.0–3.0) for a mechanical aortic valve without risk factors, 3.0 (2.5–3.5) for a mechanical mitral valve or any mechanical valve with risk factors, plus low-dose aspirin 75–100 mg (per the 2020 ACC/AHA guideline as reported by Ryu & Tran 2022). DOACs are contraindicated with mechanical valves — the RE-ALIGN trial of dabigatran was stopped early for excess stroke and bleeding, because dabigatran blocks thrombin alone while warfarin blocks factors VII, IX, X, and II — and are not recommended in rheumatic MS. Bioprosthetic valves need warfarin only 3–6 months while the sewing ring endothelializes, then aspirin; after TAVR aspirin is the long-term default, and an AF patient may keep the original anticoagulant. Perioperatively, mechanical-valve patients are bridged with heparin, never simply stopped.

The definitive VTE therapy — venous clots are coagulation-driven fibrin clots, so treatment targets procoagulant factors, aiming to prevent PE, recurrence, and post-thrombotic syndrome. The concept exams love: anticoagulation does not dissolve the existing clot — it stops propagation while the body’s own fibrinolysis clears it. ASH 2020 suggests DOACs over warfarin (INR 2.0–3.0 where warfarin is used); LMWH is the preferred anticoagulant in pregnancy (StatPearls), and duration is set by provoked-vs-unprovoked status.

Slow heart rate & lower BP by blocking β-adrenergic receptors. Watch for bradycardia.

Lower BP by blocking angiotensin conversion. Classic dry cough & angioedema risk.

Lower LDL cholesterol via HMG-CoA reductase inhibition. Monitor for myopathy.

Injectable antibodies that protect the liver’s LDL receptors, cutting LDL cholesterol by about half and lowering cardiovascular events. Given subcutaneously every 2–4 weeks.

PPAR-α agonists that mainly lower triglycerides — used with diet for severe hypertriglyceridemia — with muscle, gallbladder, liver and kidney risks, highest for gemfibrozil combined with a statin.

Non-absorbed resins that trap bile acids in the gut, forcing the liver to use cholesterol and pull LDL from the blood. Constipation, drug binding and rising triglycerides are the issues to manage.