The hottest research from various peer-reviewed journals. HALT, HAM Common After TAVR and SAVR? Hypo-attenuating leaflet thickening (HALT) with or without hypo-attenuation affecting motion (HAM) were identified as common findings after transcatheter and surgical aortic valve replacement (TAVR, SAVR) in a recent study published in the European Heart Journal. Researchers found HALT and HAM could develop or regress at variable and sometimes prolonged intervals following TAVR or SAVR. The study looked at 105 patients enrolled in the SAVORY registry who were treated by TAVR (n = 75) or SAVR (n = 30). Patients underwent two four-dimensional volume-rendered computed tomography (4DCT) scans at 3 months after valve implantation and received unchanged anti-thrombotic medication between scans. Researchers, led by Lars Sondergaard, MD, performed logistic regression analysis to assess HALT and HAM, while accounting for baseline variables like timing of the 4DCT scans, valve type and antithrombotic treatment. Overall results showed HALT in 32 patients (38.1 percent) and HAM in 17 (20.2 percent). Of these, progression was identified in 13 patients (15.5 percent) and regression in nine patients (10.7 percent). “The likelihood of observing progression was not influenced by the timing of the first CT scan,” noted Sondergaard, et al. “This suggests that the period during which the phenomenon may start to develop is not restricted to a brief window after valve implantation, but may develop over a prolonged period. However, our results do not exclude the early development and the earliest scan showing HALT was obtained 21 days after valve implantation.” Additional findings showed HALT progression was less likely among patients in both the TAVR and SAVR groups who were taking oral anticoagulation with vitamin-K antagonists (VKA) or non-VKA oral anticoagulants (odds ratio, 0.014; p = 0.036). Maintenance on chronic oral anticoagulation was found not to be a significant predictor of regression. “Results suggest a possible protective effect of oral anticoagulation, and do not exclude occasional regression without anticoagulation,” researchers said. “However, the findings here are only hypothesis generating and need confirmation.” They also suggest further research into the role of HALT and HAM in potential cardioembolic events. In a related editorial, Jeroen J. Bax, MD, PhD, FACC, and Victoria Delgado, MD, PhD, highlight that “the temporal development of bioprosthetic aortic valve thrombosis as detected on 4DCT” is a novelty of the study. “Is there progression, regression, or are there no changes at all?” they ask. “This information could have major implications for the type and duration of oral anticoagulation or antiplatelet therapy.” Sondergaard L, De Backer O, Kofoed KF, et al. Eur Heart J 2017; July 4:[Epub ahead of print]. Is CHIP Associated With Greater Risk of Coronary Artery Disease and Atherosclerosis? The presence of clonal hematopoiesis of indeterminate potential (CHIP) in peripheral-blood cells was associated with nearly a doubling in the risk of coronary artery disease (CAD) in humans in a study published June 21 in the New England Journal of Medicine. Accelerated atherosclerosis was also noted in mice. Researchers used whole-exome sequencing to detect the presence of CHIP in peripheral-blood cells. Its presence was associated with CAD using samples from four case-control studies with 4,726 participants with CAD and 3,529 controls. Additionally, researchers assessed atherosclerosis in mice by transplanting bone marrow from TET2 control mice or heterozygous or homozygous knockout mice into atherosclerosis-prone mice bred to have a knockout mutation for the gene encoding low-density lipoprotein receptor. Results from two prospective cohorts in a nested case-control analysis showed CHIP carriers had a 1.9-times greater risk of coronary heart diseases as noncarriers. In two retrospective case-control cohorts, participants with CHIP were at 4.0-times greater risk of myocardial infarction as noncarriers. Researchers also noted that CHIP carriers with DNMT31, TET2, ASXL1 and JAK2 mutations were at increased risk for coronary artery calcification, which may increase the risk of coronary events “owing to altered transcriptional output of macrophages.” Researchers note their results support several conclusions, including that “the relationship between CHIP and coronary heart disease appears to be a causal one.” They suggest that CHIP could be a modifiable risk factor, possibly through using cholesterollowering medications or targeting of specific inflammatory pathways. In a related editorial comment, John F. Keaney Jr., MD, FACC, writes that the study findings “should prompt a discourse about studying the use of anti-inflammatory agents in patients with CHIP to limit the most common cause of death in these patients – cardiovascular disease.” At the same time, he also writes that important questions also remain, including “whether CHIP or specific mutations in CHIP driver genes have an effect on other traditional risk factors for cardiovascular disease in a way that might also promote atherosclerosis.” Jaiswal S, Natarajan P, Silver AJ, et al. N Engl J Med 2017:377:111-21. Visit ACC.org/Latest-in-Cardiology for additional journal coverage, including Journal Scans and Trial Updates, handpicked weekly by the ACC.org Editorial Board led by Kim Eagle, MD, MACC.
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