The initial CAUGHT-CAD Trial results basically reinforced the “Got Plaque? Get a CAC!” approach to identifying coronary disease and intervening BEFORE the plaque becomes problematic.  People aged 40 to 70 with a family history of premature cardiovascular disease underwent testing with CAC and CCTA, but only one group was informed of the results.  The other group received the typical “Your cholesterol is a little high, but your 10-year risk score is ok, so just exercise once in a while and eat some broccoli and we’ll see you in a few years” advice. 

And over the 3-year trial, those who were aware that they had “experienced a break-in” as evidenced by positive CAC scores were more likely to be recommended an Extreme Makeover Home Edition in a safer Lipid Neighborhood…and comply with their change of address.  Put another way, when people CAN SEE THEY HAVE PLAQUE IN THEIR ARTERIES, they are much more likely to want that plaque to be stabilized (and possibly even regress the plaque burden) with available therapeutic options, which in this case was Atorvastatin 40 mg.  And the CAC-informed group did experience less progression in total plaque volume and assorted high-risk plaque features compared to the Do Nothing and Eat Broccoli group.  (There is certainly an argument that this “statin-only” approach lacked nuance given the evidence for Combination Therapy, but you can read Chapter 9 of THIS BOOK if you want more info on the various medication options that can help you move to a nice, safe Gated Community with fewer Lipid Criminals).

But that was an appetizer…we’re going to be EATing a main course of Epicardial Adipose Tissue (EAT), a vat of fat on the myocardial surface beneath the pericardium.  It sounds pretty gross at baseline, but even more disgusting is that EAT volume has been associated with increased major adverse cardiovascular events, such as in THIS STUDY!

We’re also going to chew the fat on PCAT, which stands for pericoronary adipose tissue.  This fat cloaks the coronary arteries and is thought to reflect local vascular inflammation.  Both PCAT and epicardial adipose seem to EAT your life away; it’s tough to tease out which adipose depot is the most felonious fat. But regardless, any mention of visceral fat around your organs should make you a little squeamish, and fatty heart should strike you as particularly malevolent. 

The short summary of this CAUGHT-CAD substudy was that changes in EAT attenuation were associated with vulnerable non-calcified plaque progression. Greater changes in attenuation are suggestive of Angry Adipose, and PCAT was thought to mediate the Inflammatory Angst in this study. Additionally, the associations between Fatty Heart and soft plaque progression were independent of LDL-C lowering, suggesting residual risk beyond Lipid Neighborhood management.

And what were the factors associated with high EAT levels?  Well, probably EATing too much, as those with the highest EAT tended to display signs of INSULIN RESISTANCE (elevated waist circumference and low HDL cholesterol).  Additionally, being a dude was also associated with high EAT levels…that Dad Bod is Bad, Dog.  It isn’t cute and cozy, no matter what the Influencers are saying these days. 

So if you’ve got a Fatty Heart, what can we do about it?  Well, a case is made for GLP-1s and SGLT2 inhibitors HERE.  Some might benefit from “Getting in the Zone” with pioglitazone.  And certain studies of lipid-lowering therapies show some beneficial effects on EAT and/or PCAT.  But ultimately, it doesn’t sound like a One Size Fits All approach…it sounds a lot like managing the individual components of the metabolic Home Security System while ensuring the safety of the Lipid Neighborhood.  Weird😊