Cardiovascular Disease - Primary Prevention

Effective Date: April 15, 2014
Revised Date: December 15, 2014

Recommendations and Topics



Key Recommendations

Assessment of Risk

Management of Risk




This guideline provides recommendations on the primary prevention of cardiovascular disease (CVD) in adults aged ≥ 19 years without clinical CVD. It does not apply to patients with a known history of CVD or who currently have signs or symptoms of CVD, as this would require treatment and secondary prevention. The recommendations include how to assess a patient’s risk of CVD and how to manage their CVD risk factors.


Key Recommendations

  • Assess asymptomatic men (aged ≥ 40) and asymptomatic women (aged ≥ 50) for cardiovascular disease (CVD)risk.
  • Consider lifestyle management (e.g., smoking cessation, healthy diet) as the first-line intervention for all risk groups in CVD primary prevention.
  • Manage other clinical conditions (e.g., diabetes (DM), hypertension (HTN), chronic kidney disease (CKD)) in all risk groups. DM is a major risk factor for CVD, but do not automatically consider a patient with DM high risk for CVD.1
  • Initiate statin therapy as a second-line intervention only after evaluating the risks and benefits objectively, by having an individualized discussion with the patient.
  • Treatment with a statin is expected to result in a significant reduction (> 30%) in the elevated baseline lipid levels. Treating to a specific lipid target is not recommended.2

Assessment of Risk

Who to assess
Consider assessing CVD risk in:

  • all asymptomatic men at age ≥ 40 and asymptomatic women at age ≥ 50 to establish a baseline;
  • all patients with pre-existing risk-related conditions (e.g., hypertension (HTN), diabetes (DM), chronic kidney disease (CKD)); and
  • all patients with a known family history of premature CVD (defined as men aged < 55 years and women aged < 65 years in first degree relatives*).

All symptomatic patients should be assessed for CVD risk, but treatment of symptoms is out of the scope of this guideline.

A patient may be reassessed in 1 to 5 years depending on their initial risk assessment or if their risk factors change significantly. For further details, refer to Appendix A: Primary Prevention of Cardiovascular Disease Algorithm (PDF, 129KB).

* First degree relatives have a blood relationship to the patient: parents, brothers, sisters and children.

Risk Assessment Investigations

  1. Risk assessment tool - The Framingham Risk Score (FRS) is recommended.

    The FRS, or any CVD risk assessment tool, is a risk estimation only of a patient's CVD risk. Since these scores are plus or minus several percentage points, it is important to consider modifying the risk estimation based on other known risk factors (e.g., family history, ethnicity) and a practitioner’s clinical judgement. For example, the Canadian Cardiovascular Society (CCS) suggests that among individuals 30 - 59 years of age without DM, the presence of a positive history of premature CVD in first degree relatives increases a patient’s FRS by approximately 2-fold.3

    For risk assessment tools, refer to Associated Document: Cardiovascular Disease - Primary Prevention: Resource Guide for Physicians (PDF, 358KB). Paper-based scores use groups of measurements for the risk factors to assign points; and online calculators use the exact measurements for the risk factors. A risk score from an online calculator allows for a more individualized estimate of risk.

  2. Medical history - ask about risk factors (modifiable and non-modifiable) in Table 1. The major risk factors for CVD are age, gender, smoking, elevated blood pressure and elevated lipids.

    Table 1. Modifiable and non-modifiable risk factors for CVD

    Modifiable Risk Factors Non-modifiable Risk Factors
    • smoking4 - 6
    • low physical activity levels / sedentary lifestyle4, 7, 8
    • poor diet4, 9
    • excessive body weight / body mass index (BMI) / waist circumference4, 10, 11
    • elevated blood pressure/hypertension4
    • diabetes4, 12, 13
    • elevated lipid levels4
    • socioeconomic factors14 (e.g., income, level of education, employment)
    • psychosocial factors4, 15, 16(e.g., stress levels, depression, anxiety)
    • age - chronological and biological age (frailty)17
    • gender - men
    • family history of CVD18 or familial hyperlipidemia
    • ethnicity19 - 21 - First Nations, South Asians (defined as Indian, Pakistani, Bangladeshi or Sri Lankan origin)
    • chronic kidney disease22
    • certain autoimmune inflammatory diseases23 (e.g., rheumatoid arthritis, psoriatic arthritis, systemic lupus erythematosus, vasculitis (polyarteritis nodosa))
  3. Physical examination - conduct a focused cardiovascular physical examination, including assessing for any physical signs of dyslipidemias.
  4. Test for lipids - order full fasting lipid profile including: total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), non-high-density lipoprotein cholesterol§ (non-HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG).
  5. Test for type 2 diabetes - order fasting plasma glucose (FPG) OR hemoglobin A1c level.

No other investigations are usually indicated in the risk assessment for asymptomatic patients unless stratification of intermediate risk patients is warranted (as outlined below). Though it may have a role in intermediate risk patients, routinely testing most patient’s high-sensitivity C-reactive protein (hsCRP) is not indicated.

† Though the FRS is recommended, there are other risk assessment tools. Refer to Associated Document: Cardiovascular Disease - Primary Prevention: Resource Guide for Physicians (PDF, 358KB).

‡ For paper-based FRS, refer to Appendix B: Framingham 10-year Risk Estimation (PDF, 124KB).

§ As of October 2013, a non-HDL-C measurement has been included in the full lipid profile or as a separate test on the Standard Outpatient Laboratory Requisition. For more information, refer to Appendix C: Lipid Testing in Primary Prevention of Cardiovascular Disease (PDF, 141KB).

Assessment Stratification
The patient can be classified as low, intermediate, or high risk for CVD based on the risk assessment. Any patient that is considered very high risk or is symptomatic should be treated accordingly, and this would be considered as secondary prevention (out of the scope of this guideline). The FRS defines low risk as < 10%, intermediate risk as 10 - 19% and high risk as ≥ 20%. These groupings are an arbitrary convenience, not a scientifically validated stratification.

A patient in the intermediate risk group may warrant a secondary assessment to raise or lower their risk stratification. However, further investigations may not be appropriate if the results would not influence the decision of how to manage the risk or treat the patient.

Secondary assessment may include exercise stress test, carotid ultrasound, hsCRP, or coronary artery calcium (CAC) scoring. In BC, CAC scoring is a patient pay test for primary prevention (i.e., those patients without signs or symptoms of CVD).¶

¶ According to the Medical Services Commission (MSC) Payment Schedule (April 2013), cardiac CT/CT coronary angiography may be covered by Medical Services Plan (MSP), but not for the purpose of CAC scoring.


Management of Risk

1. Lifestyle Management

Lifestyle management needs to be strongly advocated as the first-line intervention for all risk groups. Adequate explanations and support should be provided to patients so they clearly understand the nature and significance of CVD, and that they have the primary responsibility for adopting the healthy lifestyle changes required for reducing their risk.

Promote smoking cessation and avoidance of second-hand smoke.5, 6 When talking to a patient about quitting: 1) ask the patient about their degree of tobacco use, 2) advise them to quit, 3) assess for willingness to quit, 4) assist in a quit attempt, 5) arrange for a follow-up.

  • For assistance to quit, refer patients to QuitNow at HealthLinkBC by telephone at 8-1-1 or website:
  • For more information on effective pharmacological aids for smoking cessation, refer to BC Smoking Cessation program at website: Electronic cigarettes, also known as e-cigarettes (available with or without nicotine) may play role as an aid in smoking cessation. At present time, their risk and benefits have not been clearly established24 and are not included as a pharmacological aid.

Physical Activity
Encourage 30 minutes or more of moderate to vigorous intensity physical activity on most days of the week (weekly total ≥ 150 minutes).25, 26 Write the patient a prescription for physical activity. Prescriptions for those at high risk, with other conditions, or who are starting from a sedentary lifestyle, may need to be adapted. Consider an exercise stress test for previously sedentary people with additional risk factors for CVD who wish to undertake exercise more vigorous than brisk walking.

  • For assistance, refer patients to the Physical Activity Line (PAL) by telephone at 1-877-725-1149 (Toll Free) or 604-241-2266 or website:

Recommend a well-balanced diet.9 This may include the Mediterranean diet27, 28 (which emphasizes fruits, vegetables, legumes, whole grains and olive oil, with moderate consumption of fish, dairy products, poultry and minimizing meats and sweets) or the Dietary Approaches to Stop Hypertension (DASH) diet.29 Consumption of fish or fish oil supplements, high in omega-3 fatty acids may reduce CVD risk.30

  • For assistance with personalized diet advice, refer patient to a dietitian at HealthLinkBC by telephone 8-1-1 or website:

Body Composition
Recommend maintaining a healthy body weight and composition. Emphasize healthy diet and physical activity prescription in patients with a BMI ≥ 30.

  • For more information, refer to BCGuidelines.caOverweight and Obese Adults: Diagnosis and Management.

Follow-up to Lifestyle Management
Men and women with elevated lipids from their initial risk assessment may be followed up with a non-HDL-C or an apolipoprotein B (apoB) in 4 - 6 months to assess the impact of lifestyle management. If elevated lipids are still a concern consider pharmaceutical management.

Table 2. Lipids levels that may be considered elevated relative to a patient’s risk level

Risk Level LDL-C3 (mmol/L) Non-HDL-C (mmol/L) ApoB* (g/L)
High > 2.0 > 2.6 > 0.8
Intermediate > 3.5 > 4.3 > 1.05
Low > 5.0 - > 1.25

*An apoB test is not part of the initial risk assessment, but may be used as follow-up test.

Both non-HDL-C and apoB appear to be stronger predictors than LDL-C for major future cardiovascular events.31 - 35Non-HDL-C may also be a better indicator of residual risk after statin therapy than LDL-C.36 Another advantage of these tests is that fasting is not required. Non-HDL-C has the slight advantage over apoB because it is the cheaper test ($12.20 vs $16.10).

2. Pharmaceutical Management

Statin Therapy
The decision for initiating statin therapy should not be based on lipid levels alone. A patient-specific discussion regarding the potential risks and benefits of statin use should be undertaken.

Two tools to assist in individualizing this discussion include:

If statin therapy is decided upon, consider using a low dose of one of the newer statins.37 For dosages and adverse effects, refer to Appendix D: Pharmaceutical Table – Statins (PDF, 134KB). For women, currently, there is a lack of strong evidence to support the use of statins for primary prevention. It appears that high risk women or those with persistently elevated lipids may benefit. Similarly, there is a lack of strong evidence as to the efficacy of initiating statin therapy for primary prevention in older men (e.g., aged > 65 years old) who are intermediate risk because of age alone. Older men with additional risk factors might benefit from statin therapy for primary prevention.

Prior to the initiation of statin therapy:

  1. Inform the patient of adverse effects and advise they be reported - adverse effects may include muscle pain/myopathy,38 rhabdomyolysis,38 cataracts,39 elevated blood glucose and diabetes,37, 40, 41 acute renal failure,42 and liver injury.43
  2. Educate the patient about any possible drug interactions with other prescribed medication, over-the-counter remedies and non-pharmaceuticals - consult a pharmacist or product monograph for a complete list.
  3. Emphasize the importance of long-term compliance - it is estimated that 75% of primary prevention patients aged > 65 years old started on statins stop their therapy within 2 years.44

Follow-up to Statin Therapy
Within 4 - 6 months of the initiation of statin therapy, follow-up with the patient. This may include:

  1. Measure lipids with a non-HDL-C or an apoB - to assess patient adherence to statin therapy and any response to statin therapy (see Controversies in Care). A full lipid profile is not indicated. If both lifestyle management and a statin intervention have not been successful and lipids are still elevated in the follow-up investigation, consider any other causes of elevated lipids (e.g., hypothyroidism).
  2. Inquire about any adverse effects. If muscle symptoms are reported, measure creatine kinase (CK).
  3. Measure liver transaminase enzyme (aspartate aminotransferase (ALT)), if recommended by product monograph. If a patient has elevated liver transaminase enzymes consider secondary causes.

Further follow-ups as clinically needed. After the initial follow-up, routine monitoring of CK and ALT is not indicated for asymptomatic patients. More frequent routine monitoring with a full lipid profile, non-HDL-C or an apoB is considered not necessary for the sole purpose of treat-to-target.2

Controversies in Care: Statin Therapy in Primary Prevention
Despite the lack of strong evidence to support the use of statins for primary prevention, both the CCS3 and the American College of Cardiology and American Heart Association (ACC/AHA)2 have recommended a more aggressive approach for statin use (see Table 3).

Table 3. Comparison of statin therapy recommendations between the CCS and ACC/AHA

Criteria CCS Recommendations3 ACC/AHA Recommendations2
Risk assessment tool FRS - low risk, intermediate risk, high risk. Pooled Cohort Equations - elevated risk (≥ 7.5%), not elevated risk (≤ 7.5%).

The 7.5% approximately equates to a FRS score of 15% +/- 3% (depending on the risk factors).
Intermediate risk Treat with statins based on FRS (10 -19%) if LDL-C ≥ 3.5 mmol/L. Treat with statins based on Pooled Cohort Equations ≥ 7.5%.
High risk Treat with statins based on FRS (≥ 20%). Treat with statins based on Pooled Cohort Equations ≥ 7.5%.
LDL-C ≥ 5 mmol/L Treat with statins. Treat with statins.
DM Treat with statins if patient aged ≥ 40 years OR if aged ≥ 30 years with a diagnose of DM for > 15 years. Treat with statins if patient aged 40 to 75 years and LDL-C *gt; 1.8 mmol/L.
CKD or high risk HTN Treat with statins. No specific recommendation.


Controversies in Care: Treat-to-Target Approach
Both the CCS3 and the ACC/AHA2 acknowledge target lipid levels to be arbitrary, as they are based on extrapolation from studies that were not designed to test specific lipid targets. The ACC/AHA does not support the continued use of treat-to-target approach due to the lack of evidence,2 though they do recommend a therapeutic response of 30% to 50% reduction in LDL-C. The CCS does recommend treating high risk and intermediate risk patients to a specific LDL-C target of ≤ 2.0 mmol/L or a ≥ 50% reduction from baseline. Alternate targets include an apoB target of ≤ 0.8 g/L and a non-HDL-C target of ≤ 2.6 mmol/L. Low risk patients are recommended to be treated to 50% of their baseline LDL-C.

This guideline is more aligned with the ACC/AHA2 recommendations in that treatment with statins is expected to result in a significant reduction (> 30%) in the elevated baseline lipid levels.

Due to the lack of evidence, this guideline recommends no specific LDL-C, non-HDL-C and/or apoB treatment targets for primary prevention. Treat-to-target approach is not supported and may even lead to increased anxiety and adverse effects.

Acetylsalicylic Acid (ASA) Therapy
Routine ASA therapy may have a role in primary prevention in men and women who are assessed as high CVD risk and low bleed risk.44

Controversies in Care: ASA Therapy in Primary Prevention
Recent studies have questioned the value of routine ASA in primary prevention (see Table 4 and 5). ASA use in primary prevention may reduce the risk of myocardial infarction (MI) in men and may reduce the risk of ischemic stroke among women, with no significant effect on stroke in men and MI in women.46 The risk of bleeding may outweigh the low absolute net benefit in the prevention of serious vascular events.

Table 4. Absolute risk reduction (ARR) and numbers needed to treat (NNT) in ASA primary prevention trials45, 47

Event ARR for one year NNT for one year
Any serious vascular event * 0.07% 1,428
Major coronary event (primarily driven by a reduction in non-fatal MI) ^ 0.06% 1,667
Ischemic stroke 0.02% 5,000
Mortality No benefit

*defined as MI, stroke, or death from a vascular cause; ^ defined as MI, coronary death, or sudden death

Table 5. Absolute risk increase (ARI) and numbers needed to harm (NNH) in ASA primary prevention trials45, 47

Event ARI for one year NNH for one year
Major extracranial bleed 0.03% 3,333
Hemorrhagic stroke 0.01% 10,000


3. Management of Other Clinical Conditions**

A number of clinical conditions contribute significantly to the risk of developing CVD.

Blood Pressure Control
Instigate lifestyle management, followed by the use of antihypertensive medications when appropriate, with consideration for the presence of other CVD risk factors.

Diabetes Care
Instigate lifestyle management, followed by the use of medications when appropriate to control blood glucose. DM is a major risk factor for CVD, but a patient with DM does not need to be automatically considered high risk for CVD.1 CCS3defines a patient with DM high risk for CVD if they are aged ≥ 40 OR they are aged ≥ 30 with a diagnose of DM for > 15 years. While the current FRS now includes diabetic status, to individualize a type 2 DM patient's risk, use the United Kingdom Prospective Diabetes (UKPDS) risk calculator or table, website:

CKD Management

In patients with CKD, the combination of simvastatin plus ezetimibe has shown some benefit in reducing major atherosclerotic events when compared to placebo; however, no benefit on all-cause mortality has been demonstrated.48

**BC Guidelines for these clinical conditions with effective dates before this one may not reflect the updates in this guideline (e.g., the addition of non-HDL-C as a measurement).




  1. Bulugahapitiya U, Siyambalapitiya S, Sithole J, et al. Is diabetes a coronary risk equivalent? Systematic review and meta-analysis. Diabet Med. 2009;26(2):142-8.
  2. Stone NJ, Robinson J, Lichtenstein AH. 2013 ACC/AHA Guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology /American Heart Association task force on practice guidelines. Circulation. 2013.pii:S0735-1097(13)06028-2.
  3. Anderson TJ, Grégoire J, Hegele RA, et al. 2012 update of the Canadian Cardiovascular Society guidelines for the diagnosis and treatment of dyslipidemia for the prevention of cardiovascular disease in the adult. Can J Cardiol. 2013;29(2):151-67.
  4. Yusuf S, Hawken S, Ounpuu S, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004;364(9438):937-52.
  5. Shields M, Wilkins K. Smoking, smoking cessation and heart disease risk: A 16-year follow-up study. Health Reports. 2013:24(2):12-22.
  6. Centers for Disease Control and Prevention (US); National Center for Chronic Disease Prevention and Health Promotion (US); Office on Smoking and Health (US). How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General. Atlanta (GA): Centers for Disease Control and Prevention (US); 2010.
  7. Warburton DE, Nicol CW, Bredin SS. Health benefits of physical activity: The evidence. CMAJ. 2006;174(6):801-9.
  8. Wilmot EG, Edwardson CL, Achana FA, et al. Sedentary time in adults and the association with diabetes, cardiovascular disease and death: Systematic review and meta-analysis. Diabetologia. 2012;55:2895-2905.
  9. Mente A, de Koning L, Shannon HS, et al. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med. 2009;169(7):659-69.
  10. Berrington de Gonzalez A, Hartge P, et al. Body-mass index and mortality among 1.46 million white adults. N Engl J Med. 2010;363(23):2211-9. . Accessed January 30, 2008.
  11. Prospective Studies Collaboration. Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies. Lancet. 2009;373(9669):1083-96.
  12. Emerging Risk Factors Collaboration. Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: A collaborative meta-analysis of 102 prospective studies. Lancet. 2010;375(9733):2215-22.
  13. Boussageon R, Bejan-Angoulvant T, Saadatian-Elahi M, et al. Effect of intensive glucose lowering treatment on all cause mortality, cardiovascular death, and microvascular events in type 2 diabetes: Meta-analysis of randomised controlled trials. BMJ. 2011;343:d4169.
  14. Albert MA, Glynn RJ, Buring J, et al. Impact of traditional and novel risk factors on the relationship between socioeconomic status and incident cardiovascular events. Circulation. 2006;114(24):2619-26.
  15. Roest AM, Martens EJ, de Jonge P, et al. Anxiety and risk of incident coronary heart disease: A meta-analysis. J Am Coll Cardiol. 2010;56(1):38-46.
  16. Low CA, Thurston RC, Matthews KA. Psychosocial factors in the development of heart disease in women: Current research and future directions. Psychosom Med. 2010;72(9):842-54.
  17. Afilalo J, Karunananthan S, Eisenberg MJ, et al. Role of frailty in patients with cardiovascular disease. Am J Cardiol. 2009;103(11):1616-1621.
  18. Myers RH, Kiely DK, Cupples LA, et al. Parental history is an independent risk factor for coronary artery disease: The Framingham study. Am Heart J. 1990;120(4):963-9.
  19. Chiu M, Austin PC, Manuel DG, et al. Comparison of cardiovascular risk profiles among ethnic groups using population health surveys between 1996 and 2007. CMAJ. 2010;182(8): E301-E310.
  20. Anand SS, Yusuf S, Vuksan V, et al. Differences in risk factors, atherosclerosis, and cardiovascular disease between ethnic groups in Canada: The study of health assessment and risk in ethnic groups (SHARE). Lancet. 2000;356:279-284.
  21. Anand SS, Yusuf S, Jacobs R, et al. Differences in risk factors, atherosclerosis, and cardiovascular disease among aboriginal people in Canada: The study of health assessment and risk in aboriginal people (SHARE-AP). Lancet. 2001;358:1147-1153.
  22. Go AS, Chertow GM, Fan D, et al. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med. 2004; 351(13):1296-1305.
  23. Roifman I, Beck PL, Anderson TJ, et al. Chronic inflammatory diseases and cardiovascular risk: A systematic review. Can J of Cardiol. 2011;27:174-182.
  24. Bullen C, Howe C, Laugesen M, et al. Electronic cigarettes for smoking cessation: A randomised controlled trial. Lancet. 2013;382(9905):1629-37.
  25. Tremblay MS, Warburton D, Janssen I, et al. New Canadian physical activity guidelines. Appl Physiol Nutr Metab. 2011;36:36-46.
  26. Warburton D, Charlesworth S, Ivey A, et al. A systematic review of the evidence for Canada's physical activity guidelines for adults. Int J Behav Nutr Phys Act. 2010;7:39.
  27. Estruch R, Ros E, Salas-Salvado J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2013; 368(14):1279-90.
  28. Rees K, Hartley L, Flowers N, et al. 'Mediterranean' dietary pattern for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2013;8:CD009825.
  29. Salehi-Abargouei A, Maghsoudi Z, Shirani F, et al. Effects of Dietary Approaches to Stop Hypertension (DASH)-style diet on fatal or nonfatal cardiovascular diseases incidence: A systematic review and meta-analysis on observational prospective studies. Nutrition. 2013 Apr;29(4):611-8.
  30. Superko HR, Superko SM, Nasire K, et al. Omega-3 fatty acid blood levels: Clinical significance and controversy. Circulation. 2013;128(19):2154-2161.
  31. Liu J, Sempos CT, Donahue RP, et al. Non-high-density lipoprotein and very-low-density lipoprotein cholesterol and their risk predictive values in coronary heart disease. Am J Cardiol. 2006;98:1363-8.
  32. Pischon T, Girman CJ, Sacks FM, et al. Non-high-density lipoprotein cholesterol and apolipoprotein B in the prediction of coronary heart disease in men. Circulation. 2005;112:3375-83.
  33. Ridker PM, Rifai N, Cook NR, et al. Non-HDL cholesterol, apolipoproteins A-I and B100, standard lipid measures, lipid ratios, and CRP as risk factors for cardiovascular disease in women. JAMA. 2005;294:326-33.
  34. Emerging Risk Factors Collaboration, Di Angelantonio E, Sarwar N, et al. Major lipids, apolipoproteins, and risk of vascular disease. JAMA. 2009;302:1993-2000.
  35. Sniderman AD, Williams K, Contois JH, et al. A meta-analysis of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B as markers of cardiovascular risk. Circ Cardiovasc Qual Outcomes. 2011;4:337-45.
  36. Boekholdt SM, Arsenault BJ, Mora S, et al. Association of LDL cholesterol, non-HDL cholesterol and apolipoprotein B levels with risk of cardiovascular events among patients treated with statins: A meta-analysis. JAMA. 2012;307(12):1302-1309.
  37. BC Provincial Academic Detailing Service. Statins and coronary heart disease. 2012.
  38. Law M, Rudnicka AR. Statin safety: A systematic review. Am J Cardiol. 2006;97:52C-60C.
  39. Leuschen J, Mortensen EM, Frei CR, et al. Association of statin use with cataracts: A propensity score-matched analysis. JAMA Ophthalmol. 2013;131(11):1427-34.
  40. Preiss D, Seshasai SR, Welsh P, et al. Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy: A meta-analysis. JAMA. 2011;305:2556-64.
  41. Health Canada. New statins labeling update: Risk of increased blood sugar levels and diabetes. [updated 2013 Jan 24;cited 2013 Mar 22].
  42. Dormuth CR, Hemmelgarn BR, Paterson JM, et al. Use of high potency statins and rates of admission for acute kidney injury: Multicenter, retrospective observational analysis of administrative databases. BMJ. 2013;346:f880.
  43. Cohen DE, Anania FA, Chalasni N, National Lipid Association Statin Safety Task Force Liver Expert Panel. An assessment of statin safety by hepatologists. Am J Cardiol. 2006;97:77C-81C.
  44. Jackevicius CA, Mamdani M, Tu JV. Adherence with statin therapy in elderly patients with and without acute coronary syndromes. JAMA. 2002;288:462-7.
  45. Bell AD, Roussin A, Cartier R, et al. The use of antiplatelet therapy in the outpatient setting: Canadian Cardiovascular Society guidelines. Can J Cardiol. 2011;27:S1-S59.
  46. Berger JS, Roncaglioni MC, Avanzini F, et al. Aspirin for the primary prevention of cardiovascular events in women and men: A sex-specific meta-analysis of randomized controlled trials. JAMA. 2006;295:306-13.
  47. Antithrombotic Trialists’ Collaboration. Aspirin in the primary and secondary prevention of vascular disease: Collaborative meta-analysis of individual participant data from randomised trials. Lancet. 2009;373:1849-60.
  48. Baigent C, Landray MJ, Reith C, et al. The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease (Study of Heart and Renal Protection): A randomised placebo-controlled trial. Lancet. 2011;377(9784):2181-92.



Associated Documents
The following document accompanies this guideline:

This guideline is based on scientific evidence current as of the effective date.

This guideline was developed by the Guidelines and Protocols Advisory Committee, approved by the British Columbia Medical Association and adopted by the Medical Services Commission.


The principles of the Guidelines and Protocols Advisory Committee are to:

  • encourage appropriate
    responses to common
    medical situations
  • recommend actions
    that are sufficient
    and efficient, neither
    excessive nor deficient
  • permit exceptions
    when justified by
    clinical circumstances.

Contact Information
Guidelines and Protocols
Advisory Committee
PO Box 9642
Victoria BC V8W 9P1
Web site:


Disclaimer The Clinical Practice Guidelines (the "Guidelines") have been developed by the Guidelines and Protocols Advisory Committee on behalf of the Medical Services Commission. The Guidelines are intended to give an understanding of a clinical problem and outline one or more preferred approaches to the investigation and management of the problem. The Guidelines are not intended as a substitute for the advice or professional judgment of a health care professional, nor are they intended to be the only approach to the management of clinical problems.  We cannot respond to patients or patient advocates requesting advice on issues related to medical conditions. If you need medical advice, please contact a health care professional.