My liver and muscle enzymes went up on 40 of lipitor. They're fine on pitavastatin. fwiw…..
Member not yet following any Groups.
Member not yet following any Pages.
2mg/d of pitavastatin (Livalo). I'd do an angio in a 'heartbeat' but I have a very bad reaction to contrast (delayed systemic hypersensitivity reaction – like systemic poison oak – lobster red skin and unmitigated itching for a month – totally disabling and unresponsive to everything). I must work and cannot be disabled or it'll be economically disastrous. Plus, as chief of my hospitalist service, I have to do all that this entails. Obviously, should I have a coronary event, I'll have to have an angio, and I'll pre-treat with high dose steroids, having to accept the risks inherent with that. Story of my life – lots of rocks and hard places….
Also, I had a high CAC score before I started statins. I know about the statin – calcification effect. So it goes.
OK, some results here. I had a stress treadmill and perfusion study, and they were fine. I did another CAC score and it is unchanged from a year ago at ~2600. I apparently wasted 3K on 20 chelation treatments. Oh well, I had to give it a try. I saw the article on minocycline possibly mitigating vascular calcium deposition. I assume most of you have come across it. I'll think about it. In the meantime, as I approach 73 years of age, I continue to take my statin and work out a lot. I'm otherwise going to do my best to not dwell on things I can't do anything about. None of us are gettin' out of here alive, so, carpe diem.
I thought I made it clear that I'm not pursuing chelation to lower MI risk. My goal is to reduce calcification of vessels that are otherwise turning to stone. I'm well aware that there is NO data to support (for or against) what I'm doing and I'm not recommending this for anyone else. It's totally an experiment on my part – an experiment that might end soon. It's not like there's a better approach to these astronomical CAC scores, other than the usual anti-atheroma approaches. But thanks for your input and concern, Kanaaz. jon
The ND from whom I'm getting chelation was one of the investigators in the TACT study. It was better than equivocal, but their target was a bit different that this. NO ONE KNOWS ABOUT THIS. If we're trying to decalcify our coronaries in the absence of significant atheroma load, then we're a different cohort than those in the TACT study. And even if we could achieve some degree of decalcification of our coronaries, how does that translate into survival? NO ONE KNOWS. In my case, I just feel driven to do something instead of nothing (to decalcify). When I drop dead, if I have a moment to reflect, I want to know that I gave it my best shot (given no real data – only reasoning from basic principles). Life – whaddya gonna do??
Hight dose K2 had no effect on my CAC score. I'm almost mid-way through a chelation protocol (eventually 40 infusions) and we'll see. Clearly, as I've said before, there does NOT seem to be any sort of linear relationship from low to VERY high CAC scores. Too many have these shockingly high scores with wide open vessels. I suspect this is calcification (without, or with minimal actual atheroma) from endothelial inflammatory disease – possibly stealth infection (ie Bartonella). But, who tf knows??