Findings from studies designed to measure the effects of treatment on clinical outcomes clearly support the use of statin therapy in the primary and secondary prevention of CHD. Intensive dosing more effectively lowers lowdensity lipoprotein cholesterol (LDL-C) and reduces CHD risk, compared with standard dosing levels, (5-7) but these trial results have not yet been widely translated into clinical practice. Family physicians are critical arbiters of CHD risk assessment and management. A survey of members of the American Academy of Family Physicians found that more than 90% of respondents conducted CHD risk evaluation (history and lipid profile) for their patients without a diagnosis of CHD. (8) However, data suggest that family physicians may not fully optimize statin therapy to reach LDL-C goals. Underdosing of statins in relation to the doses used in studies with clinical outcome end points appears to be the norm. (9) Goal attainment can be influenced by many factors, including patient noncompliance, costs associated with lipid-lowering therapy, access to care, limitations imposed by managed care plans, and inadequate awareness and application of guideline-specified goals, as well as concern over the potential for statin-induced toxicity and side effects.
The consequences of not treating to LDL-C goals are significant. In a series of 173 post-MI patients, a second coronary event occurred within 30 months for 43% of those who received suboptimal statin therapy (LDL-C [greater than or equal to] 115 mg/dL), compared with only ll% of those who received optimal statin therapy (LDL-C <ll5 mg/dL). (10) Failure to reach the LDL-C goal doubled the risks for coronary death and a second MI in these patients. (10) As family physicians, we should not hesitate to optimize statin therapy by increasing the dose to reach aggressive LDL-C goals or by switching from one statin to another if dosage increases are not effective.
For various reasons, many patients stop taking statin therapy within the first year, (11) and approximately 1 of every 4 patients stops taking statins in the first 6 months? Conventional wisdom would suggest that patients with serious CHD would be adherent to treatment prescribed by their physician; it is an unfortunate fact that this is not the case. A survey of more than 48,000 patients who survived an acute MI revealed that only 27% of patients seen in a primary care setting filled a prescription for statin therapy within the first 6 months after MI, and 46% filled a statin prescription between 6 months and 1 year after MI. (9) Nonadherence to statin therapy was estimated to occur in 71% of these patients within the first month of treatment following an acute MI. (9) Compliance/adherence with statin therapy needs to be improved significantly, particularly in patients at high risk for recurrent events.
Concern about treatment-emergent adverse effects can have a profound negative influence on medication adherence and on our ability to help patients reach LDL-C goals. As a class, the statins have a favorable safety profile. Statins are associated with rare dose-related increases in hepatic transaminases. Myopathy also is relatively rare (< 1 in 1000 patients). (12, 13) Further, elevated hepatic transaminases and myopathy do not appear to be associated with aggressive lowering of LDL-C. (14) Rates of statin-induced myopathy were not significantly different in the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Trial-Thrombolysis in Myocardial Infarction 22), Aggrastat-to-Zocor (A to Z), and TNT (Treating to New Targets) trials for patients who achieved aggressive LDL-C goals (<70 mg/dL), compared with patients who did not. (5-7) For patients who present with muscle pain, a thorough evaluation in the office with a careful history is needed before the statin dose is reduced or treatment is discontinued altogether. Frequently, patients who report myalgia actually are experiencing arthralgia, muscle strain, injury not stemming from statin therapy, or, on occasion, an anginal equivalent when complaining of chest, shoulder, or neck soreness/discomfort. (13)
Management of CHD begins with risk assessment, and family physicians must take the lead in determining which of our patients are at risk and the degree to which therapeutic interventions are necessary. As Dr Michael Davidson writes in this supplement, numerous CHD risk assessment tools are available for use in clinical settings, The types of instruments vary widely--from pen-and-paper risk charts (Framingham Risk Score) to electronic versions, such as computer programs for handheld personal digital assistants, spreadsheets for use on personal computers, and risk calculators found on the Internet. (15) Despite their differences, all incorporate 2 important commonalities: (1) CHD risk factors cluster; and (2) multiple risk factors increase CHD risk. Any patient with [greater than or equal to] of the following should be examined more closely for the presence of other risk factors: dyslipidemia (elevated LDL-C or triglyceride or low serum levels of high-density lipoprotein cholesterol), hypertension, cigarette smoking, diabetes or impaired fasting glucose levels, overweight, abdominal obesity, and physical inactivity. (16) Last, as Dr Sandra Lewis points out in this supplement, achieving treatment goals is paramount in appropriate management of CHD.
As family physicians, we need to find a method for determining risk, reaching treatment goals, and ensuring maximum adherence that works with our individual practices, and we must use this method consistently for all our patients so as to optimally
* Integrate CHD risk assessment into routine office visits in all patients, beginning in early adulthood
* Simplify medication regimens with a minimal number of drugs and once-daily dosing if possible
* Strive to reach aggressive LDL-C goals and use optimally effective doses of statins to reach these goals
* Provide clear, easy-to-comprehend instructions and verify that patients and their families understand what is expected of them
* Address medication adherence at every visit
* Thoroughly evaluate patient complaints suggestive of statin-related adverse effects and provide reassurance as appropriate to increase long-term adherence
* Focus efforts on patients who have not reached treatment goals
* Follow up with a phone call to patients who miss appointments
* Encourage patients to become active participants in their health management and provide positive reinforcement as risk factor burden is reduced and optimized
* Help patients educate themselves through the use of informational brochures and scientifically accurate health care websites from trusted sources (eg, professional associations, schools of medicine, peer-reviewed sites).
The author thanks Sally Laden, MS, freelance medical writer, and Jinling Wu, PhD, and Judy Fallon, PharmD, from Scientific Connexions, Newtown, Pennsylvania, for medical writing support, and Maria D'Alessandro and Dolores Matthews from Scientific Connexions for editorial assistance, all funded by AstraZeneca LP, Wilmington, Delaware.
Dr Toth has disclosed that he has sewed as a consultant to Abbott, AstraZeneca, Merck, Merck-Schering-Plough, and Kowa Pharmaceuticals. He has served on the speakers bureaus of Abbott, AstraZeneca, Merck, Merck-Schering-Plough, GSK, and Takeda.
(1.) American Heart Association. Heart Disease & Stroke Statistics--2009 Update. Dallas, TX: American Heart Association; 2009.
(2.) Kuller L, Borhani N, Furberg C, et al. Prevalence of subclinical atherosclerosis and cardiovascular disease and association with risk factors in the Cardiovascular Health Study. Am J Epidemiol. 1994;139:1164-1179.
(3.) Ingelsson E, Sullivan LM, Murabito JM, et al. Prevalence and prognostic impact of subclinical cardiovascular disease in individuals with the metabolic syndrome and diabetes. Diabetes. 2007;56:17181726.
(4.) Lewis SJ, Fox KM, Grandy S, for the SHIELD Study Group. Self-reported diagnosis of heart disease: results from the SHIELD study. Int J Clin Pract. 2009;63:726-734.
(5.) Cannon CP, Braunwald E, McCabe CH, et al, for the Pravastatin or Atorvastatin Evaluation and Infection Therapy--Thrombolysis in Myocardial Infarction 22 Investigators. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004;350:1495-1504.
(6.) de Lemos JA, Blazing MA, Wiviott SD, et al, for the A to Z Investigators. Early intensive vs a delayed con servative simvastatin strategy in patients with acute coronary syndromes. Phase Z of the A to Z trial. JAMA. 2004;292:1307-1316.
(7.) LaRosa JC, Grundy SM, Kastalein JJP, et al, on behalf of the Treating to New Targets (TNT) Steering Committee and Investigators. Safety and efficacy of atorvastatin-induced very low-density lipoprotein cholesterol levels in patients with coronary heart disease (a post hoc analysis of the Treating to New Targets [TNT] study). Am J Cardiol. 2007;100:747752.
(8.) Eaton CB, Galliher JM, McBride PE, et al. Family physician's knowledge, beliefs, and self-reported practice patterns regarding hyperlipidemia: a national research network (NRN) survey, J Am Board Pam Med. 2006;19:46-63.
(9.) Gislason GH, Rasmussen JN, Ablidstrom SZ, et al. Long-term compliance with beta-blockers, angiotensin-converting enzyme inhibitors, and statins after acute myocardial infarction. Eur Heart J. 2006;27:1153-1158.
(10.) Baessler A, Fischer M, HufV, et al. Failure to achieve recommended LDL cholesterol levels by suboptimal statin therapy relates to elevated cardiac event rates, Int J Cardiol. 2005;101:293-298.
(11.) Chapman RH, Banner JS, Petrilla AA, et al. Predictors of adherence with antihypertensive and lipid-lowering therapy. Arch Intern Med. 2006; 165:1147-1152.
(12.) Jacobson TA. Statin safety: lessons from hew drug applications for marketed statins. Am J Cardiol. 2006;97(suppl):44C-51C.
(13.) Toth PP, Harper C, Jacobson T. Clinical characterization and molecular mechanisms in stalin myopathy. Expert Rev Cardiovasc 3bar. 2008;6:955-969.
(14.) Alsheikh-Ali AA, Maddukuri PV, Han H, et al. Effect of the magnitude of lipid lowering on risk of elevated liver enzymes, rhabdomyolysis, and cancer. J Am Coil Cardiol. 2007;50:409-416.
(15.) Sheridan S, Pignone M, Mulrow C. Framinghambased tools to calculate the global risk of coronary heart disease: a systematic review of tools for clinicians, J Gen Intern Med. 2003;18:1039-1062.
(16.) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of the third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;266:2486-2497.
Peter P. Toth, MD, PhD, FAAFP, FICA,
FNLA, FCCP, FAHA, FACC
Director of Preventive Cardiology
Sterling Rock Falls Clinic, Ltd.
Sterling, IL 61081
Peter P. Toth, MD, PhD, FAAFP, FICA, FNLA, FCCP, FAHA, FACC Clinical Associate Professor Department of Family and Community Medicine University of Illinois School of Medicine Peoria, Illinois Director of Preventive Cardiology Sterling Rock Falls Clinic Sterling, Illinois
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|Title Annotation:||coronary heart disease|
|Author:||Toth, Peter P.|
|Publication:||Journal of Family Practice|
|Date:||Nov 1, 2009|
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