Me as well when last checked.
This is why I find this all so confusing because I have not found a cardiologist (out of only 5) that said they would do a preventative stent, no matter what they saw on a CCTA . @DrFraser says the good ones do and I believe him. I am hoping he answers when you do a CCTA vs a nuclear stress test or vice versa…
I have two nephews who have stents. They both got them to relieve symptoms. Their doctors never told them that they would prevent heart attacks.
“Stents may relieve chest pain (angina), shortness of breath, and fatigue caused by reduced blood flow to the heart.”
Stress test (idk where the ‘nuclear’ came from) is just jogging on a treadmill with some wires attached to you.
I’ve done both… nuclear is when they inject material in you and then they can see your heart etc… I can’t speak to the details.
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Sorry, I’m not a cardiologist so I really don’t know about the benefits of stenting vs not. Hopefully I never need to find out first hand!
Generally I’m familiar with what @desertshores is saying about symptom relief but no difference in MI/deaths, but that’s not a strongly held belief. That said, symptom relief is still a pretty worthy goal IMO. And, as you said, maybe the better stent technology would translate into reduced MIs, which does seem very plausible.
Also this, with reservation I haven’t looked at this carefully nor really know much about this:
The meta analysis compared coronary stents with PTCA (standard balloon angioplasty), not medical therapy alone which is what most people do when not doing stents.
So in that study, stents with balloon angioplasty didn’t detect a statistically significant difference compared with balloon angioplasty on its own, but it looks like there was a non-significant trend towards reduced death by 30% for the one including stenting:
Few patients died in either group (65 [1.2%] for the PTCA group; 39 [0.8%] for the stent group). The odds ratio for death was 0.69 (95% CrI, 0.43 to 1.05).
So in this study no difference between balloon angioplasty (PTCA) and that with stent, correct?
However if we look at a more recent study with drug eluting stents (as that didn’t have), and that compared to medical therapy alone.
We can see that stents in contemporary trials reduce heart attack rates by 11%, while non-stent trials hasn’t detected a reduction in heart attacks at all (this is the balloon angioplasty etc), where there even was a trend towards increase in heart attacks.
However, the estimates favored revascularization (RR, 0.89 [95% CI, 0.80–0.998]; P=0.05) in the more contemporary stent-era trials, whereas in the older non–stent-era trials, the estimates favored initial medical therapy (RR, 1.42 [95% CI, 0.97–2.07]; P=0.07)
So we can at least say that compared to medical therapy only, stents reduce heart attacks.
https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.120.048194
I didn’t read that trial carefully, but what I thought would be interesting is they used some specific methods to detect and find vulnerable plaque that was also non-flow limiting. That appears to me plaque that doesn’t cause heart pain?
I was thinking maybe this trial is worthwhile to investigate further and if good investigate if it matters for those who have a lot of plaque and relevant plaque, thus stenting (and replicating the method), for whatever benefits that might entail.
So the study basically found vulnerable plaque that might rupture, and stented it, and it seems found massive benefits?
Seem like obvious in hindsight if so, find vulnerable plaque that might rupture, and place a mesh on it, but I don’t know either…
Effect of ezetimibe on plasma adipokines: a systematic review and meta‐analysis
"Meta‐analysis of 23 controlled trials did not suggest any significant effect of adding ezetimibe on top of statin therapy on plasma concentrations of adiponectin (SMD 0.34, 95% CI –0.28, 0.96; P = 0.288), leptin (SMD –0.75, 95% CI: –2.35, 0.85; P = 0.360), plasminogen activator inhibitor 1 (SMD –1.06, 95% CI: –2.81, 0.69; P = 0.236) and interleukin 6 (SMD 0.30, 95% CI: –0.08, 0.67; P = 0.124). However, significantly greater reductions in plasma concentrations of tumour necrosis factor α (TNF‐α) (SMD –0.48, 95% CI –0.87, −0.08; P = 0.018) were achieved with ezetimibe/statin combination therapy."
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So the question came up in regard to nuclear stress and stress echocardiography.
A nuclear stress test does a decent job in telling whether you have inducible ischemia. That is essentially when your heart is put under stress that there are areas of your heart that are not getting adequate perfusion which indicates a hemodynamically significant lesion in your coronary arteries.
A stress echocardiogram will show if there are regional wall motion abnormalities consistent with ischemia when your heart is under physical stress.
The issue that I have with this approach is that it probably does a decent job on telling if you have a 90%+ stenosis of a coronary artery, but 70 per cent of myocardial infarctions are due to plaque rupture due to non hemodynamically significant lesions. Do you want to be reassured falsely by these tests as it will give a normal result in >70% of people who are going to have a heart attack in the near future?
It does somewhat get back to the question as to what might change in the recommended treatment if you know that you have scattered coronary artery disease based on a ctca. In general it increases how aggressive we will be on lipid management and oftentimes motivates patients to be more vigilant when they are aware of this.
Overall, information is useful when used appropriately, and there is a significant divergence between different cardiologists as to when they would recommend intervention and not. There are many that are very conservative and there are many that are overly aggressive and will stent almost everything. Probably some ground in the middle is the most reasonable, but I appreciate the two divergent approaches. I’ve seen some patients that literally have 10 or more stents which I think is probably not very sensible. I also see patients who have had significant disease and no inducible ischemia but then present with heart attack. It is not unusual to have patients with normal stress echoes and normal nuclear stress test present with an acute myocardial infarction.
Hopefully this answers the question. In general the CT Cardiac Calcium for someone at low risk genetically, lifestyle, lipids, metabolically, and is a non-smoker is a sensible screening test. Folks outside of these parameters, I like more information.
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Thanks for sharing this… I have previously tested with Rosuva 5mg + Ezetimibe 10mg + Bempedoic Acid 180mg… Now, swapping Rosuva 5mg for Pitavastatin 4mg… Will re-run my lipids after a few weeks and test my Apo(B)/LDLc
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FWIW, an update on my lipids after switching from 10mg/day atorvastatin to 4mg/day pitavastatin, on the pita for five months, results from Oct. 2024 for atorvastatin, and April 2025 for pita. No significant diet, exercise, lifestyle changes. Possible confounders: after going on pita, in time I also took empagliflozin 12.5mg/day, and rapamycin 6mg/1week.
TC 239 mg/dL on ator, 228 pita; LDL 146 (calc) ator to 123 pita; HDL 75 ator, 89 pita; TRIG 90 ator, 93 pita; ApoB 120 ator, 103 pita.
Pretty much as I expected. No big changes, but moving in the right direction. My next step is to add bempedoic acid 180mg/day - I expect another modest improvement. After that, I intend to add ezetimibe 10mg/day. My goal is to get LDL below 60mg/dL. The pita, BE, EZE combo may not get me there, at which point I’ll see about PCSK9i.
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Is there are reason for BA before EZE?
Oh yes, pitavastatin is quickly becoming my favorite statin aswell. Generics are starting to appear in several countries already too.
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No physiological reason really. Just curiosity. I want to see the isolated effects of stacking cholesterol production inhibition further upstream from adding BA. Then add EZE to see what reabsorption does, a completely different mechanism. Apparently there are different profiles of responses in people, some being hyperresponders to absorption, so I wonder where I fall along this spectrum. Additionally, in case I have side effects, it would be useful to isolate BA from EZE. Of course ideally I should do BA, then drop BA and add EZE to isolate EZE by itself (and if really going whole hog drop and add pita as well!), but the problem is time - I would need to give each intervention a few months to make sure there is the full effect, maybe even a washout period. And given that elevated LDL/ApoB over time is the problem, I don’t want to dilly dally too much before reaching my therapeutic goals. This is as far as I’m willing to go.
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I’m all for isolating. My question was intended to ask why b before e, vs. e before b. It’s possible, maybe not probable, that e alone could get to your goal. More probable than b, I think.
You are likely correct. If there is a spectacular success with the pita+BA+EZE combo, I may hazard dropping BA, as long as I’m below 60mg/dL on LDL, which is my goal. But there is the wrinkle, that for whatever reason, drugs often seem to lose effectiveness for me over time. When I first took atorvastatin 10mg/day at 60 years of age after a lifetime of very high LDL, it worked spectacularly - took LDL from 170mg/dL to 70 the first year. Every subsequent year it got worse, until Oct 2024, age 66, my LDL hit 146. Pita alone at 4mg/day after 5 months lowered it slightly to 123mg/dL. Who knows, the combo may work great initially, but not longer term. Lipids tend to get worse in older age (at least into the 70’s, though usually not beyond), hence medication might become less effective.
Starting May, it’s escalating empagliflozin to 25mg/day from the current 12.5, and adding 180mg/day BE. I guess I’ll keep stuffing myself full of drugs until something gives:sweat_smile:. It’s like a contest of wills, my body wanting to go along programmed senescence and general deterioration ending in ignominious death, and my iron will to impede that process as much as I can. With every drug escalation, I’m sending my body a message: "the beatings will continue until morale improves"
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But seriously, the time window for improvement of biomarkers is growing more narrow - I’ll be 67 very soon. I have to do something. And fast.
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