So, usually I have to jump in late in a thread and dispel 'misinformation'. For this, I'll highlight comments that I've made in other threads through the years. Cardiology continues to evolve and I personally always attempt to practice 'evidence based medicine' that is in line with best practices. As always, you should discuss this with your own doctor, doctor.
We have had:
'Statins and training' https://forum.slowtwitch.com/...st=last-6643505#last
'Worried about my heart' https://forum.slowtwitch.com/...tring=dtoce#p6619853
'Heart health screening thread' https://forum.slowtwitch.com/...st=last-7150717#last
That said, these threads all have had some good info and some breakdowns. Anecdotal information is not optimal for best medical practice but can give some insight. The problem is that is can become biased by the few instances rather than rely on information from the masses, or better from the studies which are evidence based and drive changes in practice. There is always variability in the ways medicine is practiced and PCP's are often very different from Cardiologists. The driving force should be trying to do what is best for the individual patient. My daily life involves 'risk vs benefit'. There is a place for drug Rx and a bigger place for communication about what we know and why recommendations are made. In reality, it seems there is never enough time to go over all of the questions that come up....
It never surprises me that even those in the medical field want reassurance from 'triathlete patients' that they can continue their active lifestyle despite the need for drug therapy. There are so many medical threads here on ST in the tri forum...I have personally had to wrap my head around the possibility of needing to take statin for the rest of my life, but was fortunate enough to get 0's on my coronary calcium score last year. *(Can't change my age or family history of premature heart disease...)
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 disease...so to be complete, I'll throw in this one
'Sudden death in triathlon' 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 CA...
(I am hopeful that the thread does not devolve)
edited this thread to add these LDL-C studies:
Bigger, broader and better 'Evidence Based Medicine' 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 LDL--20,536 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 'real world' setting in patients with stable CHD. Compared with 'usual' 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 "This confirms the general principle that 'lower is better' for LDL-C".
2019 European Sociaty of Cardiology Guidelines states "Throughout the range of LDL-C levels, lower is better".
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 (0.56â€“0.91)IMPROVE-IT (ezetimibe plus simvastain vs. simvastatin) [12
]1.55 (70) vs. 1.40 (54)CV death, MI, stroke, UA, coronary revascularisation0.94 (0.89â€“0.99)FOURIER (evolocumab plus high-dose statin Â± ezetimibe vs. high-dose statin Â± ezetimibe) [19
]2.37 (92) vs. 0.78 (30)CV death, MI, stroke, UA, coronary revascularisation0.85 (0.79â€“0.92)ODYSSEY OUTCOMES (alirocumab plus high-dose statin Â± ezetimibe vs. high-dose statin Â± ezetimibe) [20
]2.37 (92) vs. 1.37 (53)MI, CHD death, stroke, UA0.85 (0.78â€“0.93) Open in a separate window
CHD, coronary heart disease; CV, cardiovascular; MI, myocardial infarction; UA, unstable angina.