Subaortic stenosis secondary to pannus from a mechanical mitral valve.

A variety of conditions can lead to left ventricle outflow tract obstruction, but cases of subaortic stenosis decades following a mitral valve replacement are exceedingly rare. Any abnormal positioning of a prosthetic valve can result in continuous turbulence leading to permanent deposition of fibrous tissue. We present a case of a 56-year-old female that underwent mechanical mitral valve replacement, due to severe rheumatic mitral valve disease, with recurrent admissions for dyspnea.

Dueling Myxomas: A Rare Finding.

• Multiple cardiac myxomas are rare, most commonly seen in the left atrium. • Myxomas are most commonly attached on the left atrial side of the interatrial septum. • Echocardiography is key in acute CVA to identify cardioembolic sources.

Measurement of patients' bivalirudin plasma levels by a thrombelastograph ecarin clotting time assay: a comparison to a standard activated clotting time.

Standard activated clotting time (ACT) tests have a poor correlation to bivalirudin levels, leading to uncertainty regarding adequate anticoagulation in percutaneous coronary intervention patients. We tested a Thrombelastograph (TEG) ecarin clotting time (ECT) assay for sensitivity to bivalirudin using blood from 80 patients undergoing interventional cardiology procedures with bivalirudin anticoagulation. This was compared to a standard Hemochron ACT assay using diatomaceous earth.

A Thrombelastograph whole blood assay for clinical monitoring of NSAID-insensitive transcellular platelet activation by arachidonic acid.

Optical platelet aggregation (OPA) with platelet-rich plasma (PRP) was compared with a Thrombelastograph (TEG) whole blood assay for monitoring arachidonic acid (AA)-induced platelet activation. Assays were performed on 47 interventional cardiology and 24 general surgery patients receiving aspirin therapy for cardiovascular disease, as well as 48 volunteers asked to take nonsteroidal anti-inflammatory drugs (NSAIDs) or 12 volunteers on chronic NSAID therapy unrelated to diagnosed cardiovascular disease. Whole blood TEG monitoring of NSAID inhibition detected NSAID-insensitive AA activation of platelets in a significantly higher number of cardiology (23%) and surgery (25%) patients and normal volunteers on chronic NSAID (25%) therapy relative to normal subjects not on chronic NSAID therapy (0%).

A novel modification of the Thrombelastograph assay, isolating platelet function, correlates with optical platelet aggregation.

Flow cytometry, singlet platelet counting, and optical aggregation have been used to monitor clopidogrel and glycoprotein IIb/IIIa (GPIIb/IIIa) platelet antagonists. Optical aggregation is considered the gold standard, but neither it nor flow cytometry is convenient in larger-scale clinical studies or point-of-care systems. Singlet platelet counting, a point-of-care assay correlated with optical platelet aggregation, only provides a measurement of platelet function at a single point in time.

Frequency of nonresponse antiplatelet activity of clopidogrel during pretreatment for cardiac catheterization.

Platelet function was evaluated before and after clopidogrel therapy in 50 cardiology candidates scheduled for intervention; results were averaged from optical platelet aggregation with 2 significantly correlated point-of-care instruments, Thrombelastograph and Ichor PlateletWorks. Although this was a limited study with few complications, the failure of clopidogrel therapy (30% nonresponders with <10% average platelet inhibition) was not correlated with clinical pretreatment variables, including atorvastatin therapy, postintervention bleeding complications, or major adverse coronary events.