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Bivalirudin, a direct thrombin inhibitor, is an anticoagulant commonly used in invasive cardiology procedures. It has evolved from relative obscurity, as an anticoagulation option only utilized in rare instances of allergy or resistance to heparin products, to the now preferred antithrombotic anticoagulant in the cardiac catheterization laboratory. On the way to displacing unfractionated heparin as the preferred anticoagulant for percutaneous coronary intervention, multiple studies comparing bivalirudin with heparin have consistently shown equivalent ischemic efficacy endpoints (i.e. cardiovascular death, myocardial infarction, etc.), with significant reductions in bleeding. Bleeding has been directly linked to worse hospital outcomes in cardiac patient's undergoing invasive coronary artery revascularization procedures. More recent bivalirudin studies now demonstrate reductions in mortality, which has led to a paradigm shift to bivalirudin as the anticoagulant choice both in elective and emergent coronary procedures. We present the major studies that have brought bivalirudin to the forefront of coronary artery disease, specifically coronary interventional procedures.

63-year-old Hispanic woman with prior systemic hypertension was well until 39 days before death when she fainted in her kitchen and was hospitalized. An electrocardiogram and telemetry monitoring disclosed sinus bradycardia (50 beats per minute) with first-degree atrioventricular block, left bundle branch block, frequent atrial and ventricular premature complexes, and sinus pauses up to 8 seconds. An echocardiogram showed mitral regurgitation (2+/4+) and an ejection fraction of 60%. An angiogram disclosed normal coronary arteries. e left ventricular and aortic pressures were normal. During her 3 days in the hospital, she had recurrent sinus pauses with associated syncope, and a permanent atrioventricular sequential pacemaker was implanted. ereafter, she felt well and was active until 22 days before she died, when exertional dyspnea appeared and progressed, prompting rehospitalization 20 days before death. Her blood pressure was 120/75 mm Hg, her paced heart rate was 80 beats per minute, and her temperature was normal. A grade 2/6 apical systolic ejection murmur and a third heart sound were audible. She had diffuse pulmonary rales and decreased breath sounds at both lung bases. A chest radiograph showed pulmonary vascular congestion, cardiomegaly, and bilateral pulmonary effusions. An electrocardiogram disclosed atrioventricular sequentially paced rhythm with no ST-T changes. Her serum troponin I level was 6.6 ng/mL, and her creatine phosphokinase level was 189 U/L with an MB fraction of 39 ng/mL. Her brain natriuretic peptide level was 2570 ng/L, and her white blood cell count was 10.7 × 10 3 /mm 3. An echocardiogram showed severe global hypokinesis with an ejection fraction of 35%. Over the subsequent 19 days in the hospital, the patient's status progressively deteriorated, requiring intravenous inotropic support, mechanical ventilation, and continuous veno-venous hemodialysis. She also developed hemodynamically unstable