Discover and read the best of Twitter Threads about #Atherosclerosis

Most recents (20)

#2 B-COMPLEX/MULTI VITAMIN. Buy a liposomal or other form that increases bio-availability. Take 1 capsule w/Breakfast and Lunch. If you have stomach upset, try sublingual (under tongue) EZ Melt B-Complex in AM & Multi w/iron for Dinner.…
#3 OMEGA 3s. Fish Oil, Krill Oil, Algae Oil are all good sources of Omega 3. Be careful the EPA/DHA ratio. EPA helps with inflammation/DHA helps with cognition. You need both! Opt for a 1:1 or 2:1 ratio of DHA to EPA (2:1 ratio eg. 800 DHA/400EPA)…
Read 93 tweets
9) Many risk factors modulate the propensity of LDL-C to traverse the endothelium and enter the arterial intima. See 🔓….
10) It now appears that the passage of #LDL into the #intima is not a merely passive process whereby the concentration in blood & the permeability of the endothelium determine LDL accumulation.
11) It’s #Transcytosis (an active process), through a vesicular pathway involving #caveolae, scavenger receptors (#SRB1) and activin like receptor kinase 1 (#ALK1). Hence for a given blood level of LDL-C the amount of atherosclerosis is variable.
Read 36 tweets
1) Welcome to an #accredited #tweetorial on the role of ⬆️ #LDL-C levels in the pathogenesis & pathophysiology of #ASCVD. I am Kausik Ray MD FRCP @profkausikray, Professor of Public Health & Cardiologist @imperialcollege London AND President of European Atherosclerosis Society
2) This #tweetorial, accredited for #CME/CE and intended for #physicians #physicianassociates #nurses #nursepractitioners #pharmacists is supported by an educational grant from Esperion Therapeutics. See faculty disclosures at
3) #Atherosclerosis starts in childhood, progresses in fits and spurts and presents in middle to late life in the form of major adverse cardiovascular events #MACE.
Read 4 tweets
1/ This is especially important timing.

As many of you know, we're conducting a study on #LMHRs (link later in thread) who not only have extremely high #LDL #Cholesterol, but many (likely most) have diets quite contrary to this advice by the @American_Heart.

Let's unpack...
2/ First, and most importantly, we do not know what the outcome of this prospective study is. So while I'll be outlining commonalities we observe with #LMHRs, this isn't an explicit endorsement of the diet nor any altered lipid levels as a result.

With that said...
3/ We have a lot of data between our standing survey, submissions to, and CC and LMHR Facebook groups (7.7k and 7.5k members, respectively).

Diets are often:
1) Low to no fruits & veg
2) Low to no grains
3) High animal protein
4) Low in plant oils
Read 6 tweets
Women are not smaller men! #Atherosclerosis genesis, progression & sequelae different in women. Plaque erosion causing ACS more common in women. Women have unique #SDOH, are undertreated with #cvPrev therapies & #GDMT, leads to worsening outcomes in women. @lesleejshaw #SCCT2021 ImageImageImage
Women’s CVD risk can be underestimated. Female specific risk enhancers help. #CAC if risk uncertain. Women have lower #CAC prevalence than men but prevalence increases after menopause. CAC when present confers greater risk of incident CVD in women than men. @lesleejshaw #SCCT2021 ImageImageImage
Prevalence of non-obstructive #CAD is higher in women but is prognostic of risk. @lesleejshaw #SCCT2021 ImageImageImage
Read 6 tweets
1/ This would be a good opportunity to clear the air on a few things...

Per @DrNadolsky's tweet, we don't know everything we want to know about #atherosclerosis. Almost everyone would agree it is multifactorial, and most of Med would ascribe the central risk driver to LDL/ApoB..
2/ If you see your LDL rise on a #keto/#lchf diet and you're uncomfortable with this, here's a thread I made for that 👇

3/ In the mean time, @DrNadolsky, @DrRagnar and I are literally in the final stages of IRB (knock on wood) to get clinical data via <obligatory plug>

Clinical data is almost always more valuable than anecdotal data (assuming good design, reputable team)..
Read 7 tweets
1/ Still one of my favorite studies in relation to the #LipidEnergyModel. One might wonder what happens to animals who become fat adapted due to fasting for a long period.

Obvious example: Hibernation

#LDL #Cholesterol goes up... does #Atherosclerosis?
2/ They were comparing bears in captivity and the wild. And in both, lipid levels during hibernation are "considerably higher than what is normally found in humans"
3/ In spite of the high lipid levels alongside other risk factors, they found no signs of atherosclerosis in brown bears.
Read 5 tweets
Happy 2021! @MBVanElzakker and I are excited to share our new article published in #Immunometabolism: “Pathogens Hijack Host Cell Metabolism: Intracellular Infection as a Driver of the Warburg Effect in Cancer and Other Chronic Inflammatory Conditions”:…
2/ In the paper, we detail molecular mechanisms by which #viral, #bacterial, and #parasite intracellular pathogens can induce, or contribute to, a Warburg-like #metabolism in infected host cells in order to meet their own replication and nutritional needs.
3/ We also discuss how host defense towards #infection may impact cellular metabolic changes (including how #mitochondria can participate in the innate immune response towards infection)
Read 9 tweets
1/ Thread -- Let's Get the Data

Many medical professionals (like my good friend and colleague, @DrNadolsky) feel strongly that #LowCarb-ers may be acting very recklessly by allowing their #LDL #Cholesterol to be much higher than the guidelines allow.…
2/ And this may well be the case.

Certainly if "diet induced" high LDL is the equivalent to genetically high LDL, such as those with #FamilialHypercholesterolemia (FH), then there should be likewise rapidly progressing #atherosclerosis.
3/ "The sine qua non of FH is severe elevation of total and LDL cholesterol levels."…

Often heterozygous FH is considered where LDL is 190 to 500 mg/dL, with homozygous being above 500.
Read 14 tweets
Time to catch up on some #Senescence papers, starting with beautiful work by @corina_amor_MD, Judith Freucht & @JosefLeibold. They used #CART #CellTherapy to clear #Senescent cells, and you'll never guess what happened next!…
Just kidding, you guessed it: disease model mice got better. Props to the authors for A) inducing #Senescence in 3 different ways, B) using 2 models of #NASH/liver #Fibrosis, and C) validating their senescence observations in human samples of #Cancer and #Atherosclerosis.
The linchpin of the paper was identifying a specific membrane marker on #Senescent cells, uPAR. They used bulk #Transcriptomics to identify candidates, then narrowed down with #Proteomic data. Go #Omics!
They didn't explore whether uPAR is causative for the #Senescent phenotype.
Read 8 tweets
For those of you who could not attend the #ENDO2020 sessions this am, due to scheduling or technical challenges, a summary thread #Diabetes #COVID19
We enter the #COVID19 era with an unprecedented set of pharmacological tools that can be used wisely to achieve personalized goals for #T2D
How should we think about the complex interactions between ACE2, DPP4, cardiometabolic inflammation, and the management of #T2D Normally, enhanced ACE2 and reduced DPP4 activity are favorable in PPL with #diabetes
Read 18 tweets
1/ Live Read Through Thread

1st... a setup:

A while ago I guested on @NutritionDanny's podcast #SigmaNutritionRadio. Alan Flanagan and I discussed #Lipids, #LDL #Cholesterol, #Atherosclerosis, etc. If you haven't already listened, I highly recommend it
2/ Today @NutritionDanny let me know they have an article out rebutting my points found here:

As always, I encourage you to read their article with an open mind. Then feel free to come back here for my first impressions.

Let's get started...
3/ Oh -- the beginning of the article includes a tweet from a #ListenThread I did when the podcast was dropped. That can be found here:
Read 28 tweets
1/ #ListenThread -

My guest appearance on #SigmaNutritionRadio just dropped where I have a very friendly #debate with @NutritionDanny and Alan Flanagan on #LDL #Cholesterol, #ApoB, #Atherosclerosis, #AllCauseMortality & much, much more!
2/ I did this podcast semi-sleep deprived and between interviews for #TheCCDoc. But I know my main hopes going in were to emphasize:

(1) Why I favor the "Lipid profile-centric" model over the "Lipoprotein-centric" model.
(2) How this is relevant to "the triad" ⬆️LDL⬆️HDL⬇️TG

(3) Why this triad is of particular interest to all of us as it relates to not just cardiovascular disease, but in particular -- all cause mortality (ACM)

I honestly couldn't remember how well I did in getting these core points across, thus relistening now...
Read 64 tweets
🚨 Watch out, time for another #cholesterol #tweetorial! 🚨This time we’re going to take a look at the very fundamental nature of cholesterol molecule. It has biochemical properties that make it 1) essential to life but 2) problematic in excess. So let’s get to it! (1/33)
First, as everyone can read in wikipedia or a high-school level biology book, cholesterol is used to make many things. It’s a good building block for certain hormones, cell membranes and bile acids. But why? (2/33)
The reason is this sturdy multi-ring structure that has many “corners” for attaching stuff. Depending on specific needs, different types of molecular side chains can be attached to this basic frame (3/33)
Read 33 tweets
⚡️ #YesCCT Coronary Plaque Assessment #Tweetorial ⚡️

By @CoronaryDoc + @AChoiHeart

✅ Why Plaque Assessment?
✅ High Risk Plaque Features
✅ Plaque Characterization/Quantification
✅ Supporting Clinical Data

#CardioTwitter #ACCImaging #SCCT2019 @heart_scct @journalCCT
As #SCD or #MI is 1st symptom of #atherosclerosis in 2/3 of pts, early ID of #CAD is of paramount importance

#YesCCT allows for
✅ ID of plaque
✅ Quant. of plaque
✅ Characterization of plaque
✅ Arterial remodeling

Lin, @LubbDup & @lesleejshaw:
Serial angiographic studies have demonstrated an accelerated & rapid plaque progression before most cases of ACS

Rapid plaque growth ➡️ plaque rupture ➡️ thrombus formation ➡️ MI

@LubbDup & @JonathonLeipsic et al:
Read 14 tweets
#Tweetorial time! 🚨 Looks like there’s another misconception about #cholesterol and #atherosclerosis making rounds again. This one has to do with the process of #LDL particles entering the arterial wall. So gather round friends and let me science the s*it out of this 🤓 (1/24)
For background, here’s a widely cited series of figures by Nakashima et al. (2007). They performed autopsies on 38 people aged 7-49, who died of non-#cardiovascular causes (2/24)
Nakashima et al. looked for atherosclerotic lesions at different stages, according to a previously published morphological classification scheme. They found them, took slices, stained them to find #lipids and #macrophages and organized them nicely (3/24)
Read 25 tweets
🚨 Thread time! 🚨 Fascinating research *letter* (lol, contains more data than many "regular" papers combined!) published in @nature. Looks at the molecular mechanism of how #LDL #cholesterol particles get into arterial walls and cause #atherosclerosis |…
The authors build upon previous knowledge that a particular scavenger receptor (SR-B1) has a key role. As the name implies, scavenger receptors pick up all sorts of stuff from their surroundings (2/14).
First, a transgenic mouse is made that has SR-B1 knocked out *specifically* from endothelial cells. This was done in combination with different athero-prone- and control mice and the data consistently shows that if there's no SR-B1, there's much less atherosclerosis (3/14)
Read 14 tweets
What’s Your “Shear Stress”?

Want to Know More?

Relax & Read ⤵️ #Tweetorial by @CoronaryDoc + @arnavkumar

⚡️Coronary Wall Shear Stress in 12 Tweets ⚡️

Main Readings:
#ACCImaging @ACCCardioEd
Wall shear stress (#WSS) is the frictional force of blood exerted tangential to endothelial surface of vessel wall & expressed in variety of units (1Pa=1N/m2=10 dynes/cm2)

It is derived from
• luminal geometry
• flow rate
• blood viscosity
• near wall velocity values
In vivo WSS calculations are derived from computational fluid dynamic (#CFD) simulations created from reconstructed 3D vessel geometries (from biplane angio/IVUS/OCT/CT/MR) combined with patient-specific pulsatile inlet/outlet velocity values (Doppler wire or other methods)
Read 12 tweets

Related hashtags

Did Thread Reader help you today?

Support us! We are indie developers!

This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3.00/month or $30.00/year) and get exclusive features!

Become Premium

Too expensive? Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal Become our Patreon

Thank you for your support!