From someone just recently diagnosed, I wanted to say thanks to all for sharing information here. I also have a question: does anyone have a cardiologist in California that they are happy with? The first cardiologist I saw does not have any knowledge of athletes, and seemed somewhat surprised that I am struggling with statins and training and muscle soreness. (She told me there were no known issues with that.)
Background: 54yo, completely asymptomatic (FTP 350w with no issues at all at high intensity), recently returned CAC score of 467. When I asked for the CAC referral my dr said insurance probably wouldnāt pay for it because I had no risk factors, but now I am obviously very glad I did the test. I am just now trying to catch up and learn what all this means, and all the links and videos are very helpful. Thanks especially to dtoce for generously sharing his knowledge.
so glad you had that done and now know that you can modify risk going forward-
Jae had great advice for people for primary prevention in terms of going low and slow. Iāve quoted it below from the āstatins: experience training and racing on themā thread
This is where we move away from evidence-base medicine. As you are aware, the CV outcomes trials for statins were evaluated with on-label regimens, which were daily administration. However, the totality of evidence strongly supports the LDL hypothesis, and intermittent regimens, so long as LDL is efficaciously reduced, should translate into reduced CV events.
There are so many permutations of intermittent statin regimens, and are in balance with what you can tolerate versus your LDL-C goals. This is why partnering with an experienced lipidologist who specializes in statin intolerance can help. Your case is even more special because your regimen needs to fit an endurance athleteĆ¢ā¬ā¢s lifestyle (I refuse to believe your tibia fracture can permanently set you back! We will cheer you from the sidelines to start running again once recovered!!!). Again, with the usual caveats to take anything a stranger online will say with a grain of salt and to partner with your doc:
- Since your presentation is primary prevention and not secondary prevention due to ACS, it means you can probably afford to go Ć¢ā¬Ålow and slowĆ¢ā¬Ā.
- Depending upon your level of intolerance: if very intolerant, might start with 2.5 mg or 5 mg rosuvastatin once weekly. If you can tolerate, can start or titrate to twice weekly (eg. Mon/Thurs) or 3 times weekly (eg. Mon/Wed/Fri) 2.5 to 5 mg rosuvastatin. Switching to fluvastatin or pravastain is also on the table if the above does not work. Also, you can further titrate rosuvastatin dose to achieve your goals or add ezetimibe help achieve LDL-C goals if needed. PCSK9 inhibitors are also available, but is much more expensive and not sure if it is cost-effective for you.
- The elimination half-life of rosuvastatin is ~19 hours. It will take about 3-5 doses on whichever regimen to achieve Ć¢ā¬Åsteady-stateĆ¢ā¬Ā, to see where you land before making further changes or titrations. Suffice to say, intermittent regimens will result in higher Ć¢ā¬Åpeak trough fluctuationsĆ¢ā¬Ā in plasma concentration. You can leverage this peak trough fluctuation to your benefit in terms of timing your exercise sessions!
- I would take the statin at night (ie, before bedtime). While long duration statins like rosuvastatin tend to allow time of administration at any time of day, you are trying to get the most Ć¢ā¬Åbang for your buckĆ¢ā¬ĀĆ¢ā¬āmost cholesterol synthesis occurs at night, which means at least on those days you take the statin, the highest concentrations of the nightly-administered statin occurs at the time when it is most needed. Taking the statin at night also gives you a practical way to manage exercise⦠next bullet
- Taking the statin at night on an intermittent regimen means the daytimes on the days you take the statin are Ć¢ā¬ÅtroughĆ¢ā¬Ā or nadir levels of statin in your body and may be the ideal days for your higher intensity exercise sessions. For example, if you are due to take your statin Monday night, Monday morning could be you higher intensity or longer training session day.
- PrefaceĆ¢ā¬āthis is REALLY anecdotal and NOT evidence-based: but for really big exercise days, eg a triathlon race, you might consider pausing your statin for 3 or more days before (which is >3 elimination half-lives). Big races result in CK releases (or muscle injury pattern) in even healthy people without medical conditions, and people on statins are shown to have even higher CK releases. SInce you are in the primary prevention category, you might consider this since races are few and far in between and should not unduly affect your overall Ć¢ā¬Åtime under the curveĆ¢ā¬Ā on LDL-C reduction.
Take care and good luck!
My response in the that thread quotes the studies proving importance of statin Rx.
In answer to the question,** most active patients tolerate needed statin medicine just fine**. I have quite a lot of patients who have known CAD/with or without revascularization, or risk equivalents like abnormal coronary calcium scores who are on drug therapy and continue to train and race without any issues at all. This list includes: people who do every aerobic sport, including lots of triathletes.
Depending on why you are taking a statin, the path to achieving the desired LDL level can be fast or slow. My patients with ACS (acute coronary syndromes) or AMI (acute MI) have no choice but to begin high intensity statin immediately and we deal with side effects and taper the med as able, when able. Most people placed on a statin take it for primary prevention-not secondary prevention: ie to prevent the first cardiac event. There is often less urgency and additional non-drug Rx can help lower the need for medication. Eating better, exercising regularly (*less of an issue with most, but not all, triathletes) and losing weight helps lower lipid numbers. I usually start low and titrate up to the needed dose to achieve an LDL goal of 40-70 for patients with known CAD or risk equivalents *(this includes any abnormal coronary calcium score or having a CT scan with vascular/coronary calcification). There is no evidence that CoQ10 works via studies, but I do encourage those with myalgia to try it.
Also, since this always comes up and people want to know what the real risk is about competing in triathlon once diagnosed with heart diseaseā¦so to be complete, Iāll throw in this one
āSudden death in triathlonā
https://forum.slowtwitch.com/...riathlon_P6427784-2/
I do wish you the best!
Please discuss options and any concerns with your MD, and be honest about side effects. Sometimes there is a perceived association with a med that may or may not be valid. Cardiac health is almost always most important for all, although the better we get at treating heart disease, the longer the patients are living and now getting CAā¦
edited this thread to add these LDL-C studies:
Bigger, broader and better āEvidence Based Medicineā clearly shows that lowering LDL-C is associated with risk reduction and statins are a very useful mechanism for achieving this.
The Cholesterol Treatment Trialists Collaboration-CTT (dec LDL-C 22% less CV events --90,056 pts)
Heart Protection Study-HPS (same benefit in each tertile of baseline LDLā20,536 pts)
PROVE IT, TNT, FOURNIER (more intensive treatment=lower LDL, even fewer events)

above from PROVE IT
MIRACL (Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering), PROVE-IT (PRavastatin Or atorVastatin Evaluation and Infection Therapy) and IDEAL-ACS (Acute Coronary Syndromes) studies outline the benefits of high-dosage atorvastatin therapy started within 24-96 hours, 10 days or 2 months, respectively, of an acute coronary syndrome. Relative to placebo, pravastatin and simvastatin, atorvastatin reduced the risk of death or major cardiovascular events by 16-18%
ASCOT-LLA (Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm), revealed that atorvastatin reduced the relative risk of primary coronary heart disease (CHD) events by 36% (p = 0.0005) compared with placebo in patients with hypertension.
followed by NCEP (National Cholesterol Education Program) committee update-new goal for high risk pts=LDL<70
followed by ACC/AHA Guidelines change in 2013 (tried to be fully evidence based)
ALLIANCE (Aggressive Lipid-Lowering Initiation Abates New Cardiac Events) and GREACE (GREek Atorvastatin and Coronary-heart-disease Evaluation) trials highlight the benefits of atorvastatin in the āreal worldā setting in patients with stable CHD. Compared with āusualā care, atorvastatin reduced the risk of nonfatal MI by 47-59%
IMPROVE IT Among 18,144 patients, there were 9,545 total PEP events (56% were first events and 44% subsequent events). Total PEP events were significantly reduced by 9% with ezetimibe/simvastatin vs placebo/simvastatin
IDEAL- TNT (Incremental Decrease in End Points Through Aggressive Lipid Lowering) and TNT (Treating to New Targets) trials demonstrate the preventive efficacy of atorvastatin in patients with stable CHD. Relative to simvastatin (in the IDEAL trial) and low-dosage atorvastatin (in the TNT trial), intensive atorvastatin therapy (80 mg/day) reduced the risk of nonfatal myocardial infarction (MI) by 17-22% (p < or = 0.02).
more statin decreasing stroke data
SPARCL (16% reduction in CVA in group without carotid stenosis and in the group with carotid artery stenosis, treatment with atorvastatin was associated with a 33% reduction in the risk of any stroke)
2018 ACC/AHA Guidelines states āThis confirms the general principle that ālower is betterā for LDL-Cā.
2019 European Sociaty of Cardiology Guidelines states āThroughout the range of LDL-C levels, lower is betterā.


Table 1
Randomized cardiovascular outcomes study with high intensity LDL-lowering therapy in patients with coronary artery disease.
TrialMean Reduction in LDL Cholesterol; mmol/L (mg/dL)OutcomeRR (95% CI) (per mmol/L)CTT meta-analysis (high-intensity vs. standard statin; subgroup < 2.0 mmol/L) 17]1.71 (66) vs. 1.32 (50)MI, CHD death, stroke, coronary revascularisation0.71 (0.56Ć¢ā¬ā0.91)IMPROVE-IT (ezetimibe plus simvastain vs. simvastatin) 12]1.55 (70) vs. 1.40 (54)CV death, MI, stroke, UA, coronary revascularisation0.94 (0.89Ć¢ā¬ā0.99)FOURIER (evolocumab plus high-dose statin Ʊ ezetimibe vs. high-dose statin Ʊ ezetimibe) 19]2.37 (92) vs. 0.78 (30)CV death, MI, stroke, UA, coronary revascularisation0.85 (0.79Ć¢ā¬ā0.92)ODYSSEY OUTCOMES (alirocumab plus high-dose statin Ʊ ezetimibe vs. high-dose statin Ʊ ezetimibe) 20]2.37 (92) vs. 1.37 (53)MI, CHD death, stroke, UA0.85 (0.78Ć¢ā¬ā0.93)
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CHD, coronary heart disease; CV, cardiovascular; MI, myocardial infarction; UA, unstable angina.

**Last edited by: **dtoce: Sep 20, 23 9:56
I have PMād you for your latest question-
Dale