Statin Treatment for Atherosclerosis in the Elderly


I have a lipid problem that I would be grateful for your

consultant's opinion on. I saw her originally in 1984 with Graves' hyperthyroidism and treated her with 10.6 mCi of I131, after which, she became hypothyroid and has since then been on an appropriate dose of Thyroxine. She is completely asymptomatic at the present time, and there are no abnormal findings on physical examination. She is a nonsmoker, and on March 28, 2008, her blood pressure was 120/70 mm Hg.

Her mother died at age 91 of a stroke. She has ten siblings, >> neither of whom has ischemic heart disease.

On February 1, 2008, she had a total cholesterol of 4.61 mmol/L (4 - 5.2 mmol/L), triglycerides 1.55 mmol/L (0.40 - 1.9 mmol/L), HDL cholesterol 1.52 mmol/L (0.9 - 2.0 mmol/L), LDL Cholesterol 2.39 mmol/L (1.68 - 3.4 mmol/L), and cholesterol/HDL ratio 3.03 (0 - 4). Her Apo-B is low at 0.68 g/L. Her fasting blood glucose is 4.5 mmol/L and other routine blood work is normal.

Sonographic evaluation of the abdominal aorta shows no evidence of aneurysm. There is mild atheromatous change with early calcification in the distal abdominal aorta.

On chest X-ray, there is evidence of calcification in the aortic arch.

Echocardiogram shows mild aortic valve sclerosis with minimal stenosis and mild aortic insufficiency.

Bilateral cerebrovascular duplex scan of the carotid arteries shows a small amount of heterogeneous plaque in the bulb and bifurcation. There is no evidence of flow restriction or

turbulent flow. There is no evidence of stenosis.

Two of our cardiologists, on the basis of these findings of early plaque formation in the carotid arteries, have advised her to have statin therapy and daily Aspirin therapy. They have referred me to the Canadian Cardiovascular Society Position Statement for the Diagnosis and Treatment of Dyslipidemia and Prevention of Cardiovascular Disease published in September 2006 in the Canadian Journal of Cardiology, Volume 22, Number 11, Page 913.

On page 920 the statement is made, "Although intimal medial thickness quantification is not yet a standard measure, evidence of early carotid atherosclerosis by routine carotid ultrasonography is an indication for statin therapy."

I would be grateful if your consultant could express an opinion as to the validity of these recommendations. Yours sincerely, D. W. Ingram, MB, FRCPC, FACP


The question raised by Dr Ingram is very interesting and of course there is no straight answer to it. In summary, his patient is a healthy 71 year old woman with no family history of cardiovascular disease and with no cardiovascular risk factors who was found to have aortic arch calcifications and carotid plaques. The question is whether statin therapy should be initiated or not. To make matters more complicated, her LDL cholesterol is below the NCEP target level for all dyslipidemia patients with the exception of those at "very high risk" (documented coronary artery disease AND diabetes or uncontrolled risk factors).

No clinical endpoint cholesterol lowering study has ever enrolled a patient with these characteristics, therefore an evidence based answer can not be directly provided. Most family physicians faced with such findings on a routine physical examination would probably not recommend statin therapy. Cardiologists who are usually consulted because of patient concern will respond to it by recommending statin therapy on the grounds that the risk of such therapy is low and statins have been shown to decrease cardiovascular risk in most situations. A third solution which I would favor is to make recommendations for additional testing which might enable an evidence based answer.

1. The mere presence of aortic calcifications is a qualitative rather than a quantitative result. The quantitative approach to this finding is electron bean computer tomography (EBCT). This test is relatively affordable and considered an acceptable method of evaluation of the atherosclerosis burden. It determines the amount of calcium deposited on the coronary arteries and it is graded according to age adjusted standards. There is evidence that its results provide information concerning cardiovascular risk prediction which is additive to Framingham risk factors. The finding of a high coronary calcium score in this patient would justify a therapeutic approach equivalent to that reserved to a patient with higher levels of traditional risk factors. To note is that five different studies have showed that statins do not prevent the progression of calcifications and consequently the method could be used for the evaluation of risk but not for the evaluation of the results of therapy.

2. The mere presence of carotid plaques is a qualitative rather than a quantitative result. Carotid plaques are found at autopsy in North American children and adolescents. The guidelines quoted by Dr Ingram are probably referring to a quantitative test, the determination by ultrasound of carotid intima-media thickness (CIMT). CIMT is frequently used as a surrogate outcome for interventions aimed at reducing cardiovascular risk. . There is evidence that its results provide information concerning cardiovascular risk prediction which is additive to Framingham risk factors. An estimate of CIMT in this patient could also refine the evaluation of cardiovascular risk and justify the intervention.

3. Finally, the estimate of C reactive protein (CRP) is very inexpensive and could be ordered. CRP level correlates with carotid plaques and with EBCT. Should it found to be high it could directly justify the intervention based on the recently completed (but not published) JUPITER trial. This trial which was stopped because of overwhelming success enrolled patients with elevated CRP of which a quarter had LDL cholesterol lower than Dr Ingram 's patient.

I hope this answer will satisfy Dr Ingram. I would be delighted to add additional information or provide references. DAN STREJA, M.D., FRCPC, FACP.