Use of non-warfarin oral anticoagulants instead of warfarin during left atrial appendage closure with the Watchman device.

Background: In the stroke prevention trials of left atrial appendage closure with the Watchman device (Boston Scientific), a postimplantation antithrombotic regimen of 6 weeks of warfarin was used.

Objective: Given the clinical complexity of warfarin use, the purpose of this study was to study the relative feasibility and safety of using non-warfarin oral anticoagulants (NOACs) instead of warfarin during the peri- and initial postimplantation periods after Watchman implantation.

Methods: This was a retrospective multicenter study of consecutive patients undergoing Watchman implantation and receiving peri- and postprocedural NOACs or warfarin.

Warfarin pharmacogenetics: a controlled dose-response study in healthy subjects.

The aim of this study was to determine how genetic variants contribute to warfarin dosing variability when non-genetic factors are controlled. Thirty healthy subjects were subjected to a warfarin dosing algorithm with daily international normalized ratio (INR) measurements to INR ≥ 2.0, then off warfarin to INR ≤ 1.

Copy number variation and warfarin dosing: evaluation of CYP2C9, VKORC1, CYP4F2, GGCX and CALU.

Aim: To determine if copy number variants contribute to warfarin dose requirements, we investigated CYP2C9, VKORC1, CYP4F2, GGCX and CALU for deletions and duplications in a multiethnic patient population treated with therapeutic doses of warfarin.

Patients & Methods: DNA samples from 178 patients were subjected to copy number analyses by multiplex ligation-dependent probe amplification or quantitative PCR assays. Additionally, the CYP2C9 exon 8 insertion/deletion polymorphism (rs71668942) was examined among the patient cohort and 1750 additional multiethnic healthy individuals.

Evolving anatomic, functional, and molecular imaging in the early detection and prognosis of hypertrophic cardiomyopathy.

Evolving imaging modalities in hypertrophic cardiomyopathy (HCM), such as tissue Doppler, speckle tracking, measures of myocardial blood flow, and cardiac magnetic resonance with gadolinium enhancement, have advanced our understanding of the pathogenesis of myocardial dysfunction in hypertrophic cardiomyopathy. These modalities have the potential to differentiate HCM from other causes of left ventricular hypertrophy when there is uncertainty about the diagnosis and to identify affected individuals in the pre-clinical phase of the disease process. Furthermore, preliminary data suggests that functional imaging techniques may add incremental value to conventional risk stratification tools to identify individuals at high risk for sudden death or progression to congestive heart failure.

Does medical therapy for thoracic aortic aneurysms really work? Are beta-blockers truly indicated? CON.

Thoracic aortic aneurysms (TAA) often represent the final manifestation of hereditary or degenerative disease processes. TAA are primarily caused by age-related degenerative changes. In this article, the authors highlight the most common pathophysiologic mechanisms responsible for TAA formation and review the paucity of evidence supporting the spectrum of medical therapies for TAA other than renin-angiotensin inhibition.

Anticoagulation for mechanical heart valves in patients with and without atrial fibrillation.

Surgical replacement of a native valve with a biological or mechanical prosthesis is the definitive treatment for many forms of advanced valvular heart disease. Mechanical heart valves are less prone to structural deterioration compared with bioprostheses, but require chronic oral anticoagulation to prevent thromboembolic events. Thromboembolic risk varies based on patient-related risk factors, including atrial fibrillation, advanced age, low ejection fraction, and hypercoagulability.

Cardiovascular risk factors in patients with chronic kidney disease.

Patients with chronic kidney disease have a higher burden of cardiovascular disease, which increases in a dose-dependent fashion with worsening kidney function. Traditional cardiovascular risk factors, including advanced age, diabetes mellitus, hypertension and dyslipidemia, have an important role in the progression of cardiovascular disease in patients who have a reduced glomerular filtration rate, especially in those with mild-to-moderate kidney disease. In patients with severe kidney disease, nontraditional or 'novel' risk factors, including inflammation, oxidative stress, vascular calcification, a prothrombotic milieu, and anemia, seem to confer additional risk.