Today, the result of my coronary calcium scan: Zero. Again. Same as 7.5 yrs ago.
The scan comes with a disclaimer:
TECHNIQUE: Computerized axial tomography of the mediastinum was performed without contrast material. This study is performed without intravenous contrast and its sensitivity for pathology is reduced. This includes the detection of neoplasms, abscess, pulmonary embolism, and aortic dissection.
I asked Dr. Gary about a more detailed scan, but he said this was good enough, without me exhibiting any obvious pathology.
Researching on this test, I found:
"...guidelines make a large distinction between CAC = 0 and CAC >0. ... Once detected, CAC progresses... Because of the exponential nature of CAC, its relationship with risk is logarithmic, that is, each successive increase in CAC translates into a smaller increment in risk. Thus, quantifying high scores versus very high scores contributes only moderately to improved risk prediction. An important concept is that most of risk stratification occurs with the CAC score range between 0 and 100."
So, it seems that CAC = 0 is way better than CAC = 1, because once established, it progresses.
In terms of mortality, I read that:
Cancer was the leading cause of death for patients with baseline CAC = 0, whereas CVD overtook cancer above a threshold of CAC >300.
OK, so I'm probably more likely to die of cancer than heart disease.
My scan did show a hepatic cyst on my liver, so maybe that will be my death? These are somewhat common, usually benign, and in 18% of the population. Anyway, added a liver cancer test to my Ulta test package. I'm getting both lipid fractionation tests, standard lipid panel, alipoprotein profile (A&B), and the AFP liver cancer screening... all these tests for less than $170 with the Halloween discount. I'll probably do it in Dec sometime. Afterward, I'll be able to further assess my CVD risk and make a decision about statins.
Dr. Gary had some encouraging words:
"Zero means you have incredibly low cardiac risk. We usually don’t repeat this as we don’t have a handle on what progression means in terms of risk. Zero make less of a case for a statin drug. Hepatic cysts are very common. No need to pursue this further. Means nothing. Annual Skin cancer screening with a dermatologist and colonoscopies every 5-10 years are what I would recommend for cancer screening. Also, prostate cancer screening with annual PSA testing IS worthwhile despite historical commentary that it is not. And you do not need a stress echo or ECG. Given your cardiopulmonary fitness and CAC = 0, an ECG and/ or stress test will add nothing to determine your risk."
And... JP said it is immoral and impure to take drugs.
UPDATE:
I spoke with Allan T., orthopedic surgeon, fastest man in the world over age 60 (60m, 100m). He sent me this form that assesses the 10-year risk of the following ASCVD events: 1) CHD death, 2) Nonfatal MI, 3) Resuscitated cardiac arrest, 4) Coronary revascularization in patient with angina (bypass?).
According to this form, my risk of a 'cardiac event' in the next 10 yrs is not 'incredibly small' but is listed at 6.9%.
Allan has values similar to mine and worse, has a family history with his father having a heart attack at age 55. But he eschews statins.
Although not a cardiologist, he agrees with my theory that 'running the engine hot' or pushing HR to max a couple times a week may have anti-arteriosclerosic benefits.
Note that he said less of a case, not no case. In your enthusiasm for testing you are overlooking sensitivity specificity, false positives test maturity, etc.. For instance AFP has a high false positive rate. What are you going to do if it comes back positive?
ReplyDeleteI will try to have the cyst removed.
DeleteI have a liver cyst that hasn’t changed in 8 years of follow up
DeleteJust wait awhile and have it re imaged to see if it changed. 6 to 12 months.
DeleteThis is an example of why I don’t trust doctors explicitly. Or I trust and verify. An ECG is incredibly simple and takes literally 5 minutes. Catches issues other than arthroscopic disease. Catches athletic remodeling which sometimes can trigger cardiac events. I understand that most times the athletic remodeling doesn’t cause an issue and it takes extra effort and health care costs to confirm it, but for those that it does cause an issue it would really suck if it were missed when the detection is so simple.
ReplyDeleteAlso it provides a baseline for comparison in the future.
DeleteThe case for screening athletes with a ECG “A proportion of athletes do however manifest ECG patterns that overlap with cardiac pathology, including repolarisation and depolarisation abnormal- ities, ventricular ectopy and high-degree AVB. Given the potential consequences of failing to identify a serious cardiac condition, several systematic algorithms are available to investigate such athletes. In the absence of overt disease, annual surveillance is recommended whilst the athlete is competing. Assessment of first-degree relatives may provide invaluable clues about possible underlying pathology.”
ReplyDeleteAbnormal ECG Findings
in Athletes: Clinical Evaluation
and Considerations
https://link.springer.com/content/pdf/10.1007/s11936-019-0794-4.pdf
Now that is pretty scary. Just in time for the Day of the Dead.
DeleteExample of SCD - Dan McBride from SV, I think class of '79 or '80? He was 59. Immediately after a bike race.
DeleteWhich is why I say trust but verify Doctors. I think they get a little jaded by negative results. Just our sample size of two at least one has abnormal ECG at rest but no signal at max effort. How many athletes would he need to test to see abnormal rest ECG and evidence of heart issues with effort.? 10? 20? If I were one of the unlucky 20 I would like to know. Your case you are a outlier for HR. Is that real or electrical anomaly? Picking up arrhythmia? Probably not but brother had very rare stroke, arrhythmia increases risk of stroke. Tests to rule it out are simple resting ECG, zio monitor, any worrisome signals follow up with stress ECG/echo. But they just won't do it without ithe triggering diagnostic criteria, dizziness, patient reported irregular heart rate, chest pressure or discomfort. Yet ECG takes 5 minutes simple equipment and the software automatically reports out. Why it is not part of screening for the 50 plus crowd?
DeletePoint taken. It says "coronary artery disease is the predominant cause of death in older athletes". But... "Up to 80% of SCDs occur without any pre-warning signs.... abnormal ECG findings more commonly found in athletes who died of a cardiomyopathy (86%)" 36% of deaths are caused by hypertrophic cardiomyopathy. 17% of deaths are caused by an anomalous coronary artery, congenital. 4% of deaths are caused by the abnormality of electrical activity.
Delete. As I've detailed in the link above, "sprinting vs endurance running"... I personally know 4 people who've had heart issues related to life-long endurance training/running. I've read about it happening in various sports including running, however, never have heard of once single instance of this occurring in a track meet sprint race... but I'm sure there is. Jamaica Olympian distance runner Kemoy Campbell had a near death experience in a 3000m race at Millrose in '19, sudden cardiac arrest, and CPR was performed by bystanders. A defibrillator had to be used to revive him. He has retired.
Hypertrophic cardiomyopathy is a sprinter strength athlete thing. The hemodynamics differ greatly between sprint and endurance and the heart develops to meet the requirements. At the same or even a lower heart rate the stresses on the heart are significantly greater with sprints - significantly higher pressures more volume needed to deliver in a shorter period so thicker more muscular walls required. I get it about the difference between sprint and endurance for overall death and arrhythmia. It's also evident in all ECG and echo data. You can see it comparing me and you. I've serious sinus bradycardia and they want to put in a pacemaker. Ive got ecg t wave suppression and right bundle branch block. Typically that means blockage or a previous heart attack. In testing i have a estimated VO2 max of 60. My echo results look like a aerobic athlete. At max effort EKG shows no evidence of ischemia and echo measured heart wall motion is normal at max effort. All is good. Unlikely that you show these signals (if you were to be tested). But i think part of the data difference is volume - there are probably two orders of magnitude more practicing long endurance athletes than strength or sprint athletes. Have thousands of males do your 300 intervals multiple times weekly (example only) and I suspect problems would be more evident.
Deletehttps://www.imrpress.com/journal/RCM/23/12/10.31083/j.rcm2312405/htm?utm_source=TrendMD&utm_medium=cpc&utm_campaign=Reviews_in_Cardiovascular_Medicine_TrendMD_0
ReplyDeleteThe link above is another good one "How to Unmask Hidden Cardiovascular Diseases through Preparticipation Screening in Master Athletes?"
DeleteYour recent posts have been useful - as a result I'm going to ask to increase my baby lipitor dose from 10 to 20 mg to increase the probability of plaque stabilization.
ReplyDeleteCheck this one out https://www.ahajournals.org/doi/full/10.1161/CIRCIMAGING.120.011701
DeleteTrust but verify "However, the association of carotid plaque and
Deleteplaque score with long-term cardiovascular risk in individuals with baseline CAC score of 0, a group that
is at low risk, has not been studied to date. Here, we
show that presence and extent of carotid plaque are
independently associated with long-term CHD risk even
in the absence of CAC, which reaffirms that CAC of 0
defines a low risk group, not a no risk group". So I bet that 6 percent or so probability is more accurate than infinitesimal small. CaC misses non calcified or very low calcification those are the dangerous ones that lead to SCD.
I think this is a good paper and clever experiment. Each imaging modality has strengths and weaknesses US is sensitive to all plaques even those with low calcium content. The shallow depth of the carotid artery makes for easy US imaging with excellent resolution and the predictive value of carotid plaque is understood. There are so many layers and complexity to medicine.
DeleteAnother one "Prevalence of Noncalcified Coronary Plaque in Patients With Calcium Score of 0: The Silent Enemy" , "Noncalcified coronary artery plaques (NCAPs) are susceptible to rupture, resulting in coronary artery thrombosis. Using computer tomography coronary angiography (CTCA), we evaluated the prevalence and degree of stenosis caused by NCAP in patients without coronary artery calcification (CAC). Noncalcified coronary artery plaque was predominantly developed in the proximal segment of the left anterior descending artery. Noncalcified coronary artery plaque is present in up to 10% of patients with a CAC score of 0."
DeleteLink https://journals.sagepub.com/doi/abs/10.1177/0003319712440618
DeleteSki season starts soon need to pin those bad boys in place 8 inches at the snotel https://wcc.sc.egov.usda.gov/reportGenerator/view/customSingleStationReport/hourly/978:ID:SNTL%7Cid%3D%22%22%7Cname/-167%2C0/WTEQ%3A%3Avalue%2CSNWD%3A%3Avalue%2CPREC%3A%3Avalue%2CTOBS%3A%3Avalue?fitToScreen=false
ReplyDelete