Aloke Finn @AlokeFinn
Interventional Cardiologist, Physician-Scientist, Medical Director, CVPath Institute, Gaithersburg, MD Staff Cardiologist, University of Maryland, Baltimore, MD cvpath.org Maryland, USA Joined November 2017-
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Aloke Finn retweeted
#Lipoprotein(a) genetic risk variants were associated with a higher prevalence of coronary plaque rupture and greater Lp(a) accumulation in culprit thrombotic lesions among individuals with sudden coronary death of European ancestry. ja.ma/44D7PST
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Aloke Finn retweeted
More evidence in support of LDL-C as a causal factor in myocardial infarction. Among 954 from a sudden death autopsy registry, an LDL-C polygenic score was assoc w ↑ odds of plaque rupture, thrombosis, & obstruction. Not w erosion ahajournals.org/doi/10.1161/AT… @atvbahajournals
Aloke Finn retweeted
Congrats to @KelvinS_MD recipient of the 2024 Herman K. “Chip” Gold MGH Young Investigator Award for translational research in interventional cardiology! It’s wonderful to celebrate the legacy of Chip Gold every year, and quite honored to mentor this year’s recipient. Kelvin’s work takes a new approach to understanding coronary artery disease by intersecting cath lab phenotypes with genetics. He’ll be presenting some of his work with @tigerstatdoc at the upcoming #ESCCongress @escardio @MGHHeartHealth @mghcvrc @harvardmed
Aloke Finn retweeted
3/5 CD163+ Macrophages Induce Endothelial-to-Mesenchymal Transition in Atheroma by Mori et al bit.ly/3zvBHo0 @AlokeFinn @CVPath_Md
Aloke Finn retweeted
Mori & colleagues found in #atherosclerosis that #CD163+ #macrophages provoke #EndMT, which may promote plaque progression through fibrous cap thinning. Learn more at ahajrnls.org/3xUY7Pc @AlokeFinn
@JJheart_doc @MGHHeartHealth Jim, sorry to hear this. Not sure they make them like this anymore. His clinical acumen and PE were unparalleled as was his commitment to his patients. I remember seeing him rounding at 3 am in the ccu! Honor to have trained with him. He will be sorely missed in the halls of MGH.
Here we show CTO lesions demonstrate significantly greater medial thinning compared to non CTO lesions and suggest inflammation at the intimal medial border might contribute to this phenomenon.
Chronic total occlusion (CTO) PCI is an increasingly performed procedure. Although we tend to focus on characteristics of intimal plaque, the media is an important but poorly understood structure and target especially for techniques involving antegrade dissection and re-rentry.
This review in Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB) Centennial Issue comprehensively summarizes our understanding of atherosclerotic plaques as a cause of acute coronary syndromes and stable angina pectoris. @CVPath_Md ahajournals.org/doi/10.1161/AT…
Atherosclerotic vascular disease remains a major cause of death and disability. Because of the histological diversity of atherosclerotic lesions, it is essential to simplify plaques into unstable and stable plaques to accurately understand and provide better clinical context.
This promotes cap thinning. Great work by CVPath Institute, Inc. team including Masayuki Mori , Atsushi Sakamoto and Rika Kawakami together with collaborators including @clintomics and Jose Verdezoto Mosquera. ahajournals.org/doi/epdf/10.11…
Fibrous cap thinning is an indicator of plaque instability but what are the mechanisms by which it occurs? Here we show that intraplaque hemorrhage and CD163+ macrophages induce endothelial to mesenchymal transition in intraplaque endothelial cells and subsequent apoptosis.
Here we give our take on a recent reanalysis of the POEM using the Academic Research Consortium criteria to define HBR population in this trial and weigh in on the level of evidence provided for short-term DAPT in HBR on a stent-by-stent basis.
Tremendous effort and progress have been made in trying to minimize the duration of DAPT after PCI, especially in those at high bleeding risk (HBR). The POEM trial examined the use of short-term DAPT in subjects receiving the Synergy stent.
Although the trial missed its primary endpoint, is there a future for HDL enhancing therapies in the treatment of subjects at high risk for CAD-related events? Read my opinion here: sciencedirect.com/science/articl…
Here is my take on the recently published substudy from AEGIS II trial investigating the effect of infusions of Apolipoprotein A-1, the main component of HDL, on cardiac outcomes in patients with ACS.
Congratulations to our collaborators at Advanced Nanotherapies (Cleveland Clinic--Vinod Labhasetwar and Marwan Berrada-Sounni) on this excellent work. CVPath Institute, Inc. sciencedirect.com/science/articl…
But reintervention due to restenosis still occurs and distal embolization of drug or particulate matter remains a concern. Here we used nanoparticle delivery from a DCB using a combination of paclitaxel (low dose) and sirolimus and show excellent anti-proliferative effect.
Drug coated balloons are gaining momentum in interventional cardiology for the treatment of in stent restenosis and de novo coronary and peripheral arterial diseases. Currently, either paclitaxel or sirolimus are go to agents for drug delivery, both with proven track records.
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