AchillesHeal wrote:

At what age should one start to check calcium score? I have no significant family Hx of CAD. Just a couple parents with obesity and DM and HTN.

Timing of cardiac screening is an individual thing. I never send my patients for ischemic testing of any sort at age 35 or less. I have, on occasion, done CACS on some patients in their 30's to show their risk is truly low and that they have time *(as I expect it will be normal/0) to take better care of themselves.

I often say to patients that this is the only body you get, so take good care of it.

There are no guidelines for specifically what age to start screening of 'low risk' individuals but I did read an NIH paper saying 42 yo for M and 58 for F. I generally think ~45 yo for men an ~50-55 yo for women *(protected by hormones longer compared to M). You'd like it early enough to intervene meaningfully and not so early to cause anxiety for years.

It is still likely best for clinicians to use the ACC risk estimator and MESA calculators *(using CACS) to help assess risk.
https://tools.acc.org/.../calculate/estimate/

https://www.mesa-nhlbi.org/...Score/RiskScore.aspx

Here's the article on 'hardening of the arteries' in athletes by Dr. Aaron Baggish of MGH.

https://www.ahajournals.org/...LATIONAHA.117.028750

The MESA %ile calculator using the CACS
https://www.mesa-nhlbi.org/Calcium/input.aspx


It is my belief that there will be a shift towards CTA and ultimately CTA with AI *(from coronary artery calcium scoring) to evaluate for soft plaques in the coronary arteries eventually. We'll see. It's been talked about for a long time but much closer to reality now.




This is the downside of Rx with statins-issues with the muscles aka SAMS *(statin associated muscle symptoms)--- pain/achiness/muscle inflammation-myopathy/myalgia/concern about performance... It is real and varies in studies. Probably 5-25% of patients have some issue related to the muscles but it is still risk vs benefit and the discussion about an individual's personal risk and best plan to optimally treat needs to be shared decision making with the patient and the provider. The actual % of patients that have very significant issues may be as low as 1%, but that is not 0. There has never been any paper saying statins truly reduce muscle function but if they hurt, you will not be training appropriately. Some of the statins seem to affect the muscles more than others and there have been papers also suggesting that CoQ offsets this and that is why it is suggested-even though there is no hard clinical data to prove a benefit. Many of these studies are small so hopefully over time there will be better information to make informed choices. *edited to add: the meta analysis of all co Q 10 studies was only about 6 or 8 studies of ~240 participants. That muscle biopsy study you cited only had 48 patients...

It is suggested that diagnosis should be based on the triad of (i) temporal relationship of symptoms and/or CK elevation to initiation of statin therapy; (ii) disappearance of symptoms on withdrawal; and (iii) re-appearance on re-challenge with statin therapy
SAMS can be further classified based on muscle symptoms, the presence and degree of CK elevation. Muscle symptoms with no elevation in CK, often referred to as myalgia, is regarded as the mildest form. The term myositis is sometimes used to describe symptoms associated with significant CK elevation (>10 times upper limit of normal range). Rhabdomyolysis is the most severe form, and may result in myoglobinuria and renal impairment. CK levels in rhabdomyolysis may rise to >40 times upper limit of normal range.
The pathophysiology of and mechanisms leading to SAMS is yet to be fully understood.

Going 'low and slow' and finding a statin that is tolerated can be a challenge and take some time and effort. Multiple with-drawl trials are usually needed and re-challenging to find out if symptoms are truly related and to assess severity. It is still best to do whatever is necessary to optimally treat patients despite how difficult the effort.

It always starts with assessing risk...

While scrolling around, I did see a nice summary from the ACC about Primary Prevention and Reclassification of Risk using CACS so I copied those below.
Top 10 Take-Home Messages for the Primary Prevention of Cardiovascular Disease

1. 
   The most important way to prevent atherosclerotic vascular disease, heart failure, and atrial fibrillation is to promote a healthy lifestyle throughout life.
   
2. 
   A team-based care approach is an effective strategy for the prevention of cardiovascular disease. Clinicians should evaluate the social determinants of health that affect individuals to inform treatment decisions.
   
3. 
   Adults who are 40 to 75 years of age and are being evaluated for cardiovascular disease prevention should undergo 10-year atherosclerotic cardiovascular disease (ASCVD) risk estimation and have a clinician–patient risk discussion before starting on pharmacological therapy, such as antihypertensive therapy, a statin, or aspirin. The presence or absence of additional risk-enhancing factors can help guide decisions about preventive interventions in select individuals, as can coronary artery calcium scanning.
   
4. 
   All adults should consume a healthy diet that emphasizes the intake of vegetables, fruits, nuts, whole grains, lean vegetable or animal protein, and fish and minimizes the intake of trans fats, red meat and processed red meats, refined carbohydrates, and sweetened beverages. For adults with overweight and obesity, counseling and caloric restriction are recommended for achieving and maintaining weight loss.
   
5. 
   Adults should engage in at least 150 minutes per week of accumulated moderate-intensity physical activity or 75 minutes per week of vigorous-intensity physical activity.
   
6. 
   For adults with type 2 diabetes mellitus, lifestyle changes, such as improving dietary habits and achieving exercise recommendations are crucial. If medication is indicated, metformin is first-line therapy, followed by consideration of a sodium-glucose cotransporter 2 inhibitor or a glucagon-like peptide-1 receptor agonist.
   
7. 
   All adults should be assessed at every healthcare visit for tobacco use, and those who use tobacco should be assisted and strongly advised to quit.
   
8. 
   Aspirin should be used infrequently in the routine primary prevention of ASCVD because of lack of net benefit.
   
9. 
   Statin therapy is first-line treatment for primary prevention of ASCVD in patients with elevated low-density lipoprotein cholesterol levels (≥190 mg/dL), those with diabetes mellitus, who are 40 to 75 years of age, and those determined to be at sufficient ASCVD risk after a clinician–patient risk discussion.
   
10. 
    Nonpharmacological interventions are recommended for all adults with elevated blood pressure or hypertension. For those requiring pharmacological therapy, the target blood pressure should generally be <130/80 mm Hg.

Utility of CAC in Reclassifying ASCVD Risk
For individuals with intermediate predicted risk (≥7.5% to <20%) or for select adults with borderline (5% to <7.5%) predicted risk, CAC measurement can be a useful tool in refining risk assessment for preventive interventions (e.g., statin therapy). In these groups, CAC measurement can reclassify risk upward (particularly if CAC score is ≥100 Agatston units or ≥75th age/sex/race percentile) or downward (if CAC is zero) in a significant proportion of individuals.
In adults at intermediate risk, CAC measurement can be effective for meaningfully reclassifying risk in a large proportion of individuals. In such intermediate-risk adults, those with CAC ≥100 Agatston units or CAC ≥75th percentile have ASCVD event rates for which initiation of statin therapy is reasonable. Those with CAC scores of zero appear to have 10-year event rates in a lower range for which statin therapy may be of limited value. Therefore, for patients with CAC scores of 1-99, it is reasonable to repeat the risk discussion. If these patients remain untreated, repeat CAC measurement in 5 years may have some value, but data are limited. It is important to note that the absence of CAC does not rule out noncalcified plaque, and clinical judgment about risk should prevail. Clinicians should not down-classify risk in patients who have CAC scores of zero but who are persistent cigarette smokers, have diabetes, have a family history of ASCVD, or, possibly, have chronic inflammatory conditions. In the presence of these conditions, a CAC score of zero may not rule out risk from noncalcified plaque or increased risk of thrombosis.
CAC might also be considered in refining risk for selected low-risk adults (<5%), such as those with a strong family history of premature coronary heart disease. CAC measurement is not intended as a screening test for all but rather may be used as a decision aid in select adults to facilitate the clinician-patient risk discussion. The following candidates for CAC measurement may benefit from knowing that their CAC score is zero:

• Patients reluctant to initiate statin who wish to understand their risk and potential for benefit more precisely
• Patients concerned about the need to reinstitute statin therapy after discontinuation for statin-associated symptoms
• Older patients (men 55-80 years of age; women 60-80 years of age) with low burden of risk factors who question whether they would benefit from statin therapy
• Middle-aged adults (40-55 years of age) with pooled cohort equations-calculated 10-year risk of ASCVD 5% to <7.5% with factors that increase their ASCVD risk.

I hope this helps...