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The Fight for My Own Coronary Artery Scan: Why the System Fails Its Hardest Cases

By Nick HansonUpdated 12 min read

My cardiologist had every reason to say no.

I’d already been through the full workup. 12-lead ECG. Echocardiogram. Holter monitor. Nuclear stress test. All normal. All clean. A coronary CT angiography, or CCTA, a scan that produces detailed images of the arteries feeding your heart, just eight years earlier had come back pristine. Zero atherosclerosis. Not a speck. I was 44 with zero concerns for diabetes, no hypertension, no smoking history. My high-sensitivity C-reactive protein, the standard blood marker for systemic inflammation, was 0.45. That’s rock bottom. By every metric the medical system uses to stratify cardiac risk, I was fine.

The cardiologist was convinced this was musculoskeletal in nature, from spinal disc degeneration from my athlete and heavy weight lifting days, possibly amplified by the kind of hypervigilance that comes with knowing too much. He had a point. But something wasn’t right, and I knew it. My workouts didn’t have the same pep. I was getting tired sooner than normal. Small things that add up but don’t show up on an ECG.

I asked for the CCTA again. He was reluctant. I pushed. He agreed.

And as we know from previous posts I’ve shared, that scan found an 80% blockage of my right coronary artery.

I’ve told the story of what that blockage meant and why every standard test missed it. This post is about the question I couldn’t stop asking afterward: how did I go from zero disease to an 80% blockage in eight years with none of the usual explanations?

And the harder question underneath it: if the system almost missed someone like me, how many people is it actually missing?

Bottom Line: Rapid coronary artery disease progression without traditional risk factors is rare, but it happens. The standard screening pathway isn’t designed to catch it. The test that found my disease, CT coronary angiography (CCTA), is now recommended as first-line by every major cardiology guideline. But practice hasn’t caught up everywhere. If you’re symptomatic and your tests keep coming back normal, you have the right to ask about CCTA. And you should.

Standard cardiac tests check function. CCTA checks anatomy. Both can come back “normal” on the same patient with severe coronary disease.

I’m the Patient the Literature Says Doesn’t Exist

Let me be honest about something uncomfortable: the medical literature was mostly on my cardiologist’s side.

A 2022 JACC state-of-the-art review on managing cardiovascular risk in young adults focused on the risk factors that predict early-onset disease: family history of premature events, severe hypercholesterolemia, chronic inflammatory conditions, smoking, diabetes.1 I didn’t check any of those boxes. My LDL was mildly elevated, not severely. No family history. No diabetes. Clean prior imaging.

Young adults who present with heart attacks and have zero standard modifiable risk factors are so uncommon that when researchers analyzed the National Inpatient Sample database covering five years of U.S. hospital admissions, these “SMuRF-less” patients were a small fraction of all STEMI cases. And here’s what’s unsettling: they actually had worse in-hospital outcomes than patients who had the traditional risk factors.2 The system isn’t just failing to find these people. When it does find them, they’re sicker than expected.

My cardiologist looked at a 44-year-old with no red flags and a clean CCTA from 2016. In his position, most physicians would have made the same call. The guidelines supported it. The statistics supported it. The prior imaging supported it.

The problem is that “statistically unlikely” is cold comfort when you’re the outlier.

The Inflammation Problem Nobody Talks About

If you spend any time in the keto, carnivore, or low-carb world, you’ve heard the argument: mildly elevated LDL cholesterol doesn’t matter as long as your inflammation markers are low and you aren’t dealing with insulin resistance and are ‘metabolically healthy’. Their idea is that it’s not the cholesterol that causes the damage. It’s the inflammation. Keep your CRP low and stay metabolically healthy, and elevated LDL is harmless cargo floating through clean arteries.

I believed this for a long time. My hsCRP was 0.45 mg/L and my Levels glucose monitor showed phenomenal metabolic health. By any definition, I had no systemic inflammation. And I spent roughly a decade on a ketogenic diet without worrying much about my LDL creeping upward, because the influencers and podcasters I followed told me it was fine.

It wasn’t fine.

Here’s what the keto community gets wrong, and it’s not a small thing: hsCRP measures systemic inflammation. It tells you about the overall inflammatory state of your blood. What it does not tell you is what’s happening inside the walls of your arteries.

Researchers at Lund University in Sweden actually tested this directly. They measured hsCRP levels in patients undergoing carotid endarterectomy, a surgery where plaque is physically removed from the artery, and compared those blood levels to the actual inflammatory activity inside the extracted plaque tissue. The correlation was zero.3 Your blood test for inflammation can come back clean while the inside of your artery wall is on fire.

This matters because the inflammatory processes that drive atherosclerosis, things like interleukin-6 and other localized cytokines, operate at the tissue level. They’re doing their damage right where the plaque is forming, not circulating through your bloodstream at levels high enough to show up on a standard lab panel. So when someone tells you “my CRP is low, therefore my LDL is safe,” they’re measuring the wrong thing in the wrong place.

I’m not saying keto caused my blockage. I’m saying that the framework the keto community uses to dismiss LDL risk is built on a measurement that doesn’t measure what they think it measures. I broke down the study they rely on most in a previous post. And I’m saying this as someone who followed that framework for years and paid for it.

Why I Might Be an Outlier (And Why You Might Be One Too)

So if it wasn’t the standard risk factors, what was it?

I don’t have a definitive answer. Neither do some of the top interventional cardiologists at Mayo who have looked at my case and scratched their head. But there are emerging explanations worth paying attention to, and they’re the reason this blog exists.

Psoriasis. I have it. It’s been mostly in remission for years, just a few spots on my knees now and again, a very minor case by all accounts of what I’ve seen in others. Most people, including most physicians, think of psoriasis as a skin condition. It’s not. It’s a systemic inflammatory disease that shares molecular machinery with atherosclerosis. A 2022 study in Nature Communications used genetic data from over 70,000 cases to establish a causal link: psoriasis directly increases coronary artery disease risk through shared genetic pathways, in addition to every traditional risk factor.4 The same inflammatory molecules that drive psoriatic skin lesions, specifically IL-17 and TNF-alpha (proteins your immune system uses to signal inflammation), have been shown to drive vascular inflammation and damage to the inner lining of arteries in experimental models.5

What that means for someone like me: even though my psoriasis looked like a few dry patches on my knees, the same inflammatory machinery that causes those patches may have been quietly accelerating plaque buildup in my coronary arteries. Take that, add a decade of mildly elevated LDL from a ketogenic diet, and you might have a storm that no standard risk calculator would predict.

CHIP. Clonal Hematopoiesis of Indeterminate Potential. This is one of the most important emerging risk factors in cardiovascular medicine, and almost nobody outside of academic cardiology is talking about it. CHIP happens when mutations in your bone marrow stem cells cause one clone of white blood cells to expand and take over a disproportionate share of your blood cell production. Those mutant cells don’t just sit there. A 2024 study in Nature Medicine proved that the relationship is unidirectional: CHIP mutations cause new atherosclerosis to develop. Atherosclerosis does not cause CHIP to expand.6 It’s a one-way street, and it’s invisible to every standard cardiac workup and blood test.

I haven’t been tested for CHIP yet. I’m pushing for it. None of my Mayo cardiologists have mentioned it, which tells you how new this is.

I’ll write about both of these in detail in future posts. For now, the point is this: the list of things that can accelerate coronary artery disease is longer than what shows up on a standard lipid panel and a risk calculator. And if you’re one of the people carrying a risk factor that isn’t on the checklist, the system isn’t designed to find you.

The Test That Should Be First

The evidence for CCTA as the first-line test for suspected coronary disease isn’t ambiguous anymore.

The SCOT-HEART trial randomized 4,146 patients to standard care versus standard care plus CCTA. At five years, the CCTA group had a 41% relative reduction in coronary death or nonfatal heart attack: 2.3% versus 3.9%.7 The 10-year follow-up confirmed the benefit held: 6.6% versus 8.2% for coronary heart disease death or nonfatal myocardial infarction.8 The mechanism wasn’t that CCTA led to more procedures. It was that seeing plaque changed behavior. Think of it this way: telling someone their cholesterol numbers suggest they might develop heart disease someday is like telling them their house might flood. Showing them an actual image of plaque forming in their artery is like showing them water in the basement. One is a statistic. The other is a reason to act. Doctors started preventive therapy earlier. Patients took it more seriously.

A meta-analysis confirmed the behavioral shift: patients who received imaging showing plaque were nearly three times more likely to start a statin and more than two and a half times more likely to start aspirin.9 Seeing is believing. It shouldn’t be, but it is.

Every major guideline-writing body has caught up. The 2021 AHA/ACC guidelines made CCTA a Class I recommendation, the strongest possible, for evaluating chest pain in patients without known coronary disease.10 The UK moved even earlier, making CCTA first-line in 2016.11 The evidence has been there for years. The practice is what’s lagging.

What I’d Actually Do

If you’re experiencing symptoms, even vague ones like exercise intolerance or atypical chest tightness, and your standard workup comes back normal, ask about CCTA. Specifically.

Don’t say “I want a heart scan.” Say: “I’d like to discuss CT coronary angiography. The 2021 ACC/AHA guidelines recommend it as first-line for patients with chest pain and no known coronary disease. I want to understand why a stress test is being recommended instead, given my presentation.” That sentence tells your doctor you’ve done your homework, and it frames the conversation as a discussion rather than a demand.

If your doctor declines, ask them to document the request and the reason for declining in your medical record. This isn’t adversarial. It’s good medical practice. And physicians sometimes reconsider when the request and the refusal are going into the chart.

CCTA is not a cheap test. It requires IV contrast and can run two thousand dollars or more out of pocket. But consider the alternative: a cascade of stress tests, nuclear imaging, and follow-up visits that still might not find what a single CCTA would show on the first look. If your insurance requires pre-authorization, push the office to start that process. The 2021 ACC/AHA Class I recommendation is your leverage.

And if you have any of the emerging risk factors I mentioned, psoriasis, autoimmune conditions, a family history that doesn’t fit the standard calculators, or if you just know something is off and nobody can explain why, push harder. The system is built for the average patient. If you’re not average, you have to advocate for yourself.

I had every advantage. I’m an emergency department nurse at Mayo Clinic. I have a master’s in bioinformatics. I can cite the guideline and speak the language that makes a cardiologist pause. And it still took all of that to get the test ordered.

That scan is the reason I’m writing this instead of being a statistic. Not everyone has my advantages. But everyone deserves the same information.

The evidence has moved. Your doctor is smart enough to follow it. Sometimes they just need a patient who knows enough to ask.

The four-step script for the cardiology visit. The 2021 ACC/AHA Class I recommendation is your leverage.

Next in the series: I Was Doing Almost Everything Right. It Wasn’t Enough. — The biohacker resume, the cracks I didn’t see, and the question that started a year-long investigation.

Would you push for a CCTA if your cardiologist said you didn’t need one? Have you ever had a “normal” workup that didn’t match how you felt? I want to hear your story.

This is not medical advice. It’s one clinician’s experience and a review of the published data. Discuss screening decisions with your physician based on your individual risk profile.

References

  1. Stone NJ, Smith SC Jr, Orringer CE, et al. Managing Atherosclerotic Cardiovascular Risk in Young Adults: JACC State-of-the-Art Review. J Am Coll Cardiol. 2022;79(8):819-836. PMID: 35210038
  2. Shamaki GR, Markson F, Soji-Ayoade D, et al. Prevalence, predictors, and in-hospital outcomes of ST-elevation myocardial infarction among young adults without traditional cardiovascular risk factors in the United States. Am Heart J Plus. 2024. PMID: 38882592
  3. Grufman H, Schiopu A, Edsfeldt A, et al. Plasma levels of high-sensitive C-reactive protein do not correlate with inflammatory activity in carotid atherosclerotic plaques. J Intern Med. 2014;275(2):127-133. PMID: 24010553
  4. Patrick MT, Stuart PE, Zhang H, et al. Shared genetic risk factors and causal association between psoriasis and coronary artery disease. Nat Commun. 2022;13(1):6565. PMID: 36323703
  5. Karbach S, Croxford AL, Oelze M, et al. Interleukin 17 drives vascular inflammation, endothelial dysfunction, and arterial hypertension in psoriasis-like skin disease. Arterioscler Thromb Vasc Biol. 2014;34(12):2658-2668. PMID: 25341795
  6. Díez-Díez M, Ramos-Neble BL, de la Barrera J, et al. Unidirectional association of clonal hematopoiesis with atherosclerosis development. Nat Med. 2024;30(10):2857-2866. PMID: 39215150
  7. SCOT-HEART Investigators, Newby DE, Adamson PD, et al. Coronary CT Angiography and 5-Year Risk of Myocardial Infarction. N Engl J Med. 2018;379(10):924-933. PMID: 30145934
  8. Williams MC, Wereski R, Tuck C, et al. Coronary CT Angiography and 10-Year Outcomes of Patients with Suspected Angina Due to Coronary Heart Disease (SCOT-HEART). Lancet. 2025;405(10475):329-337. PMID: 39863372
  9. Gupta A, Lau E, Varshney R, et al. The Identification of Calcified Coronary Plaque Is Associated With Initiation and Continuation of Pharmacological and Lifestyle Preventive Therapies: A Systematic Review and Meta-Analysis. JACC Cardiovasc Imaging. 2017;10(8):833-842. PMID: 28797402
  10. Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain. Circulation. 2021;144(22):e368-e454. PMID: 34709879
  11. National Institute for Health and Care Excellence. Chest pain of recent onset: assessment and diagnosis. Clinical guideline CG95 (updated 2016); superseded by NG228 (2024). Available at: https://www.nice.org.uk/guidance/ng228