1. Can you give the optimal screening frequency in primary prevention if the initial screening does not reveal a need for a statin? Is it different for those at risk for ASCVD, but whose calculation suggests no need for a statin?
Every 5 years. If new risk factors develop, then risk assessment should be performed again.
2. If a statin is indicated as in the guidelines for primary prevention or for a statin-indicated condition, how soon after starting the stain should the non HDL/LDL/Apo B be repeated to ensure that targets have been met?
3. So many elderly patients fit the definition for Chronic kidney disease (a statin-indicated condition).
a) If a 75 year old patient (or older) has CKD by definition and is not on a statin, should a statin be started?
Yes, unless they have < 2 year life-expectancy
b) Up until what age would you start a statin for CKD?
Any age unless < 2 year life-expectancy or major comorbidities that affect quality of life.
c) At what age does the benefit of starting a statin for CKD start to decline?
No data for this specific subgroup but the data for statin benefits in patients > 75 years in general is quite favorable.
4. I see many patients with incidental findings of atheromatous plaque on the aorta and arterial calcification (outside the coronary arteries) on imaging. (I realize coronary artery calcification is a separate issue). Should all these patients be started on a statin, or just the patients with atheromatous plaque on aorta? Does it depend on the age of the patient? If the decision to start a statin is made for atheromatous plaque on the aorta, should a low dose ASA be started as well?
This is increasingly reported as an incidental finding and the evidence is not well-established. My first approach is to evaluate whether the patient should be on a statin based on primary prevention criteria. In many cases, these patients with incidental findings of atherosclerosis have indications for statins based on primary prevention criteria. If no, I decide based on the extent of atherosclerosis reported. When extensive plaque (more than just intimal thickening) is described in the aorta than I will often recommend statins. I don’t consider ASA for these patients, unless there is evidence for extensive atherosclerosis (and patient has a low risk of bleeding)
5. Does the degree of Lp(a) elevation parallel the patient's risk? (eg do I treat a patient with Lp(a) >1000mg/L similar to a patient with Lp(a) 375mg/L, assuming all other Risk Factors are equal?)
First, I only consider Lp(a) to be clinically significant if it reaches > 500 mg/L (or 100 nmol/L). We don’t have a lot of data to answer whether different levels of Lp(a) should be handled differently. The general principle is to optimize all risk factors (diet, exercise, no smoking, blood pressure, diabetes, and lipoproteins). My goal is to get apoB < 0.8 g/L (or LDL-C < 2.0 mmol/L) for all patients with high Lp(a) in primary prevention. In select patients who have extreme elevations of Lp(a) (i.e. >1500 mg/L), it may be reasonable to be more aggressive (apoB < 0.7 g/L or LDL-C < 1.8 mmol/L).
6. Is there ever any benefit/indication to switching statins for either optimization of treatment, or, minimizing side effects?
The evidence is minimal that switching statins has any major effect for efficacy or tolerability. However, in my practice, for patients who have difficulty tolerating statins, I will often try several different statins to find one that is tolerable. Pravastatin seems to lead to less muscle side-effects. The other consideration for side-effects is trying lower doses or alternate day dosing regimens.
7. In terms of lifestyle modifications, what are the main 'soundbites' you share with the patient that are easy to convey and doable?
30 mins of moderate intensity exercise 5 times per week
Eat a well-balanced diet (Mediterranean type)
1 serving of fruits and/or vegetables at each meal
At least 1 serving of oily fish per week (salmon, cod etc)
8. Given that Framingham is only assessing for short term risk, is there value in Reynold's score, or other calculator to look at lifetime/longer term risk?
Most scores are based on a 10-yr time frame (including Reynold’s). However, there is a Framingham 30-yr risk score that can be used and can be very valuable for younger patients. The alternative is to use calculated vascular age as described in the CCS guidelines.
9. Why do some labs take up to 2 months to report Lp(a) values while others send the results shortly after test is done?
This is a recent problem due to the larger volume of Lp(a) requests seen at the laboratory. This should return back to normal turn-around times (1-2 weeks) in the next few months. Lp(a) measurement is not particularly complicated and doesn’t require more time than other proteins.