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ACC Prevention Ineffective Therapies

ACC Prevention Ineffective Therapies

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  • This slide represents a summary of major observational and randomized trials involving vitamin E, vitamin C, and beta-carotene prior to 2007. The significant benefit noted in early observational studies was not demonstrated in subsequent randomized trials. <br />
  • In the second Physician’s Health Study, 14,641 men >50 years of age were randomized in a 2 x 2 x 2 x2 factorial design to vitamin E (400 IU every other day), vitamin C (500 mg daily), a multivitamin, or beta-carotene (50 mg every other day) for a mean of 8.8 years. Treatment with Vitamin C or E resulted in no cardiovascular benefit and in fact, treatment with Vitamin E was associated with an increased risk of hemorrhagic stroke (HR, 1.74 [95% CI, 1.04-2.91]; p=0.04). <br />
  • In the Women’s Antioxidant Cardiovascular Study (WACS), 8,171 women with known CV disease or with >3 CV risk factors were randomized in a 2 x 2 x 2 factorial design to treatment with Vitamin C (500 mg/day), Vitamin E (600 IU every other day), or beta carotene (50 mg every other day) for a mean of 9.4 years. Compared to placebo, treatment with vitamin E, Vitamin C, and beta carotene resulted in no CV benefit. <br />
  • Folic acid, vitamin B12, and vitamin B6 are co-factors involved in the metabolism of homocysteine. Elevated levels of homocysteine have been associated with increased CV risk. <br />
  • Although elevated homocysteine levels have been associated with increased CV risk, this meta-analysis failed to demonstrate any CV benefit from lowering of homocysteine levels through the use of B vitamins or folic acid. <br />
  • In the Women’s Antioxidant and Folic Acid Cardiovascular Study (WAFACS), 5,442 high risk women with known CV disease or ≥3 CV risk factors were randomized to folic acid (2.5 mg daily), vitamin B6 (50 mg daily), and vitamin B12 (1 mg daily) vs. placebo for 7.3 years. Compared with placebo, treatment with B vitamins and folic acid significantly reduced homocysteine levels (p=0.001). Despite this, there was no difference in CV events in the B vitamin and folic acid group (p=0.65). <br />
  • The HOPE-2 trial randomized 5,522 patients (>55 years of age) with diabetes or vascular disease to daily treatment either with placebo or with the combination of folic acid (2.5 mg), vitamin B6 (50 mg), and vitamin B12 (1 mg) for a mean of five years. The primary outcome was a composite of myocardial infarction, stroke, and cardiovascular mortality. <br /> The mean plasma homocysteine levels increased by 0.8 µmol/L in the placebo group and decreased by 2.4 µmol/L in the active-treatment group. Although treatment with B-vitamins did not reduce the risk of the primary endpoint (RR, 0.95; 95% CI, 0.84 to 1.07; P=0.41), there was a decrease in the risk of stroke (relative risk, 0.75; 95 percent confidence interval, 0.59 to 0.97). <br />
  • The Norwegian Vitamin (NORVIT) trial sought to evaluate the effects of B vitamin and folic acid supplementation in patients with a recent myocardial infarction. A total of 3,749 patients were randomized to one of four treatment arms: (a) vitamin B6 (40 mg), vitamin B12 (0.4 mg), and folic acid (0.8 mg), (b) vitamin B12 (0.4 mg) and folic acid (0.8 mg), (c) vitamin B6 (40 mg), or (d) placebo. The primary endpoint was a composite of myocardial infarction, stroke, and sudden death attributed to coronary heart disease. <br /> Homocysteine levels decreased by an average of 27 percent in patients given folic acid plus vitamin B12 as compared to placebo. This, however, did not translate into a reduction in the primary end point (RR 1.14; 95% CI 0.98 to 1.32; P=0.09). There was a trend towards increased risk in the group given folic acid, vitamin B12, and vitamin B6 (RR, 1.22; 95% CI 1.00 to 1.50; P=0.05). <br />
  • In this study, 238 diabetic patients were randomized to supplementation with B vitamins and folic acid vs. placebo for 31.9 months. Patients randomized to B vitamins and folic acid had more CV events (composite of MI, stroke, revascularization, and all-cause mortality) when compared with placebo (HR 2.0; p=0.04). <br />
  • In the Women’s Health Initiative, 16,608 postmenopausal women aged 50-79 years were randomized to conjugated equine estrogen (0.625 mg) plus medroxyprogesterole acetate (2.5 mg) or placebo for 5.2 years. The data and safety monitoring board recommended prematurely terminating the estrogen + progestin trial because the overall risk exceeded the benefit (the planned follow up period was 8.5 years). Combined hormone therapy was associated with a hazard ratio for coronary heart disease of 1.24 (nominal 95 percent confidence interval, 1.00 to 1.54; 95 percent confidence interval after adjustment for sequential monitoring, 0.97 to 1.60). The elevation in risk was most apparent at one year (hazard ratio, 1.81 [95 percent confidence interval, 1.09 to 3.01]). <br />
  • The Heart and Estrogen/progestin Replacement Study (HERS) sought to evaluate the effect of hormone replacement therapy on vascular events in women with known coronary artery disease. A total of 2,763 postmenopausal women were randomized to conjugated equine estrogen (0.625 mg) and medroxyprogesterone (2.5 mg) vs. placebo for 4.1 years. <br /> When event rates were reviewed by year of follow-up, there was a statistically significant time trend demonstrating (a) an increase in CHD events during the first 8 months of treatment with HRT, (b) no difference in CHD events during years 1 through 3 of treatment, (c) a 35% reduction in CHD events with HRT by year 4 of treatment, and (d) a favorable effect of HRT on lipid parameters. Although HRT was not shown to be effective overall, its favorable effect after several years of therapy could warrant continued treatment for women already on HRT. <br />
  • In this meta-analysis of 31 randomized trials (44,113 subjects), HRT was associated with an increase in the rate of stroke (odds ratio, OR, 1.32, 95% confidence intervals, CI, 1.14-1.53) and VTE (OR 2.05, 95% CI 1.44-2.92), with no increase in the rate of CHD events (OR 1.02, 95% CI 0.90-1.11). Although most trials included older subjects, age did not significantly affect risk. The addition of progesterone to estrogen doubled the risk of VTE. <br />
  • This study included 121 randomized trials of at least four week’s duration that compared a selective COX 2 inhibitor to placebo or a selective COX 2 inhibitor to a traditional NSAID. In this study, use of a COX-2 inhibitor significantly increased the risk of myocardial infarction (HR 1.86, p=0.0003). <br />
  • This meta-analysis included cohort or case-control studies that reported CV events (predominantly myocardial infarction) in association with exposure to a COX-2 inhibitor, NSAID, or both. A total of 17 case-control and 6 cohort studies were included in the analysis. <br /> Among nonselective NSAIDs, diclofenac had the highest CV risk (HR 1.40, 95% CI 1.16-1.70). Other nonselective NSAIDs had a neutral effect: naproxen (HR 0.97, 95% CI 0.87-1.07), piroxicam (HR 1.06, 95% CI 0.70-1.59), and ibuprofen (HR 1.07, 95% CI 0.97-1.18). <br />
  • This meta-analysis included cohort or case-control studies that reported CV events (predominantly myocardial infarction) in association with exposure to a COX-2 inhibitor, NSAID, or both. A total of 17 case-control and 6 cohort studies were included in the analysis. <br /> Among nonselective NSAIDs, diclofenac had the highest CV risk (HR 1.40, 95% CI 1.16-1.70). Other nonselective NSAIDs had a neutral effect: naproxen (HR 0.97, 95% CI 0.87-1.07), piroxicam (HR 1.06, 95% CI 0.70-1.59), and ibuprofen (HR 1.07, 95% CI 0.97-1.18). <br />
  • In this meta-analysis of 6 trials, 7,950 patients with conditions other than arthritis were treated with celecoxib at varying doses. Cardiovascular risk increased in a dose-dependent fashion (linear trend from placebo to 400 mg once daily to twice-daily doses of 200 mg and 400 mg, p&lt;0.001), most notably among patients with high baseline CV risk (high vs moderate vs low baseline CV risk, P=0.034 for the interaction). <br />
  • This nationwide Danish administrative registry evaluated prescription claims for NSAIDs after discharge among all patients with a first MI between 1995 and 2002. Among a total of 58,432 patients discharged alive, 9,773 experienced rehospitalization for MI and 16,573 died. <br /> A total of 5.2% of patients received rofecoxib, 4.3% celecoxib, 17.5% ibuprofen, 10.6% diclofenac, and 12.7% other NSAIDs. For any use of rofecoxib, celecoxib, ibuprofen, diclofenac, and other NSAIDs, the hazard ratios and 95% confidence intervals for death were 2.80 (2.41 to 3.25; for rofecoxib), 2.57 (2.15 to 3.08; for celecoxib), 1.50 (1.36 to 1.67; for ibuprofen), 2.40 (2.09 to 2.80; for diclofenac), and 1.29 (1.16 to 1.43; for other NSAIDS), with dose-related increases for all drugs. There was a trend of increased rehospitalization for MI with the use of both selective COX-2 inhibitors and the nonselective NSAIDs. <br />
  • While increased COX-2 selectivity is associated with increased CV risk, increased COX-1 selectivity is associated with increased GI risk. The size of the circles approximates variation in sample sizes among the trials. <br />
  • This represents a stepwise pharmacologic approach in the treatment of musculoskeletal symptoms among patients with known CV disease or risk factors. It is recommended that acetaminophen, aspirin, tramadol, or short term narcotic agents being used first line in order to minimize exposure to COX-2 selective NSAIDs. <br />

8 acc prevention ineffective therapies 8 acc prevention ineffective therapies Presentation Transcript

  • The Evidence for Current Cardiovascular Disease Prevention Guidelines: Ineffective Therapies in American College of Cardiology Cardiovascular Disease Best Practice Quality Initiative Subcommittee and Prevention Committee
  • Classification of Recommendations and Levels of Evidence *Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may be a very clear clinical consensus that a particular test or therapy is useful or effective. †In 2003, the ACC/AHA Task Force on Practice Guidelines developed a list of suggested phrases to use when writing recommendations. All guideline recommendations have been written in full sentences that express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document (including headings above sets of recommendations), would still convey the full intent of the recommendation. It is hoped that this will increase readers’ comprehension of the guidelines and will allow queries at the individual recommendation level.
  • Icons Representing the Classification and Evidence Levels for Recommendations I IIa IIb III I IIa IIb III I IIa IIb III I IIa IIb III I IIa IIb III I IIa IIb III I IIa IIb III I IIa IIb III I IIa IIb III I IIa IIb III I IIa IIb III I IIa IIb III
  • Evidence for Current Cardiovascular Disease Prevention Guidelines Antioxidant Vitamins Evidence and Guidelines
  • Pre-2007 Data on Antioxidant Vitamins in Cardiovascular Prevention Largest Observational Studies Study Vitamin E Vitamin C Beta-Carotene Nurses Health Study 34% in CHD1 28% in CHD2 -- Health Professionals Follow-Up Study 41% in CHD3** 25% in CHD3** 29% in CHD3** 42% in CVD4* -- NHANES 1 -- * Applies to men in this study. Women in this study had a 25% relative risk reduction in CVD. ** These finding apply to men only. CHD=Coronary heart disease, CVD=Cardiovascular disease, NHANES=National Health and Nutrition Examination Survey Sources: Stampfer MJ et al. NEJM 1993;328:1444-1449 2 Osganian SK et al. JACC 2003;42:246-252 3 Rimm EB et al. NEJM 1993;328:1450-1456 4 Enstrom JE et al. Epidemiology 1992;3:194-202 1
  • Pre-2007 Data on Antioxidant Vitamins in Cardiovascular Prevention Largest Randomized Studies Study Vitamin E Vitamin C Beta-Carotene ATBC 10% in CHD1 -- 1% in CHD1 Cambridge Heart Antioxidant Study (CHAOS) 47% in CVD2 -- -- GISSI 5% in CVD3 -- -- HOPE NS4 -- -- Beta-Carotene and Retinol Efficacy Trial (CARET) -- -- 26% in CVD5 Physican’s Health Study (PHS) -- -- 0% in CVD6 NS7 NS7 NS7 Primary Prevention Project (PPP) 6% in CVD8 -- -- Women’s Health Study 7% in CVD9 -- 17% in CVD10 Heart Protection Study (HPS) ATBC=Alpha-Tocopherol Beta-Carotene Cancer Prevention study, CHD=Coronary heart disease, CVD=Cardiovascular disease, GISSI=Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico, HOPE=Heart Outcomes Prevention Evaluation study, NS=Non-significant Virtamo J et al. Arch Intern Med 1998;158:668-675 2 Stephens NG et al. Lancet 1996;347:781-786 3 GISSI Investigators. Lancet 1999;354:447-555 4 Yusuf S et al. NEJM 2000;342:154-160 5 Omenn GS et al. NEJM 1996;334:1150-1155 6 Hennekens CH et al. NEJM 1996’334:1145-1149 7 HPS Collaborative Group Lancet 2002;360:23-33 8 PPP Study Group. Lancet 2001;357:89-95 9 Lee IM et al. JAMA 2005;294:56-65 10 Lee IM et al. J Natl Cancer Inst 1999;92:2102-106 1
  • Vitamin C and E: Primary Prevention Physicans’ Health Study II (PHS II) Number of cardiovascular events**/1000 personyears 14,641 men (>50 years) randomized (2 x 2 x 2 x 2) to Vitamin C (500 mg/day), Vitamin E (400 IU every other day), a multivitamin, or betacarotene (50 mg every other day)* for a mean of 8 years HR=0.99 P=0.91 12 10.8 10.9 HR=1.01 P=0.86 10.8 10.9 8 4 0 Vitamin C Placebo Vitamin E Placebo Antioxidants provide no benefit to men without cardiovascular disease *Beta-carotene intervention was stopped by the data and safety monitoring board prior to study completion **Includes nonfatal myocardial infarction, nonfatal stroke, and cardiovascular death Sesso HD et al. JAMA 2008;300:2123-2133
  • Vitamin C, E, and Beta Carotene: Secondary Prevention Women’s Antioxidant Cardiovascular Study (WACS) Number of major cardiovascular events* 8,171 women with known CV disease or with >3 CV risk factors randomized (2 x 2 x 2) to Vitamin C (500 mg/day), Vitamin E (600 IU every other day), or beta carotene (50 mg every other day) for a mean of 9.4 years 800 750 HR=1.02 P=0.71 731 719 700 0 Vitamin C Placebo HR=0.94 P=0.23 742 708 Vitamin E Placebo HR=1.02 P=0.71 731 719 BetaPlacebo Carotene Antioxidants provide no benefit to women with CV disease *Includes myocardial infarction, stroke, coronary reveascularization, or cardiovascular disease death CV=Cardiovascular Cook NR et al. Arch Intern Med 2007;167:1610-8
  • Antioxidant Vitamin Guidelines Secondary Prevention I IIa IIb III Antioxidant vitamin supplements (e.g., vitamins E, C, or beta carotene) should not be used for secondary prevention in NSTE-ACS. NSTE-ACS=Non-ST-segment elevation acute coronary syndrome Anderson JL et al. JACC 2007;50:652-726
  • Evidence for Current Cardiovascular Disease Prevention Guidelines B Vitamins and Folic Acid Evidence and Guidelines
  • B Vitamins, Folic Acid, and Homocysteine: Mechanism of Action Cofactors of Homocysteine Metabolism • Vitamin B6 • Vitamin B12 • Folic acid Welch G et al. NEJM 1998;338:1042-1050
  • Pre-2006 Data on B Vitamins and Folic Acid in CV Prevention Randomized Trials of Lowering Homocysteine Levels CV=Cardiovascular Wald DS et al. BMJ 2006;333:1114-1117
  • B Vitamins and Folic Acid: Primary and Secondary Prevention Women’s Antioxidant and Folic Acid Cardiovascular Study (WAFACS) 14 P=0.001 P=0.99 12.5 12.1 12 11.8 9.8 10 0 B-vitamins/ Folic acid Placebo Number of cardiovascular events*/10000 personyears Median homocysteine level (micromoles/L) 5,442 women with known cardiovascular disease or >3 cardiovascular risk factors randomized to folic acid (2.5 mg), vitamin B6 (50 mg), and vitamin B12 (1 mg) or placebo for 7.3 years 300 HR=1.03 P=0.65 227 200 220 100 0 B-vitamins/ Placebo Folic acid B-vitamins and folic acid provide no benefit in 1o/2o Prevention *Includes myocardial infarction, stroke, coronary revascularization, or cardiovascular disease mortality Albert CM et al. JAMA 2008;299:2027-2036
  • B Vitamins and Folic Acid: Secondary Prevention Heart Outcomes Prevention Evaluation (HOPE)-2 Study Mean homocysteine level (micromoles/L) 5,522 patients with vascular disease or DM randomized to folic acid (2.5 mg), vitamin B6 (50 mg), and vitamin B12 (1 mg) or placebo for 5 years 14 12.9 12.2 12.2 12 9.7 10 0 B-vitamins/ Folic acid Placebo B-vitamins and folic acid provide no benefit in 2o Prevention DM=Diabetes mellitus HOPE 2 Investigators. NEJM 2006;354:1567-1577
  • B Vitamins and Folic Acid: Secondary Prevention Norwegian Vitamin (NORVIT) Trial 3,749 patients with a recent myocardial infarction randomized in a 2 x 2 factorial design to B-vitamins + folic acid or placebo for 40 months Treatment Arms * • Vitamin B6 (40 mg), Vitamin B12 (0.4 mg), and Folic acid (0.8 mg)† • Vitamin B12 (0.4 mg) and Folic acid (0.8 mg)‡ • Vitamin B6 (40 mg)^ • Placebo Homocysteine Level Vit B6/12 Folic acid Vit B12 Folic acid Vit B6 Placebo Baseline 13.1 12.9 13.3 13.2 Study End 9.5 9.8 13.3 13.6 B-vitamins and folic acid provide no benefit in 2o Prevention *Includes recurrent myocardial infarction, stroke, and sudden death attributed to coronary artery disease † HR=1.22, P=0.05 compared to placebo, ‡HR=1.08, P=0.31 compared to placebo, ^HR=1.14, P=0.09 compared to placebo Bonna KH et al. NEJM 2006;354:1578-1588
  • B Vitamins and Folic Acid: Primary and Secondary Prevention Mean homocysteine level (micromoles/L) 238 diabetic patients randomized to folic acid (2.5 mg), vitamin B 6 (25 mg), and vitamin B12 (1 mg) or placebo for 31.9 months 20 18.1 15.5 15 13.3 * 15.5 10 0 P<0.001 B-vitamins/ Folic acid Placebo B-vitamins and folic acid provide no benefit in diabetics *Secondary end point which includes composite of MI, stroke, revascularization, and all-cause mortality House AA et al. JAMA 2010;303:1603-1609
  • B Vitamins and Folic Acid Guidelines I IIa IIb III Secondary Prevention Folic acid, with or without B6 and B12, should not be used for secondary prevention in NSTE-ACS NSTE-ACS=Non-ST-segment elevation acute coronary syndrome Anderson JL et al. JACC 2007;50:652-726
  • Evidence for Current Cardiovascular Disease Prevention Guidelines Hormone Replacement Therapy Evidence and Guidelines
  • Hormone Replacement Therapy: Primary Prevention Women’s Health Initiative (WHI) Nonfatal MI or CHD death (%) 16,608 postmenopausal women aged 50-79 years randomized to conjugated equine estrogen (0.625 mg) plus medroxyprogesterole acetate (2.5 mg) or placebo for 5.2 years HR=1.24, 95% CI 0.97-1.60 Years of follow up HRT provides no cardiovascular benefit CHD=Coronary heart disease, HRT=Hormone replacement therapy, MI=Myocardial infarction Manson JE et al. NEJM 2003;349:523-534
  • Hormone Replacement Therapy: Secondary Prevention Heart and Estrogen/progestin Replacement Study (HERS) Number of CV Events* 2,763 postmenopausal women with known CAD randomized to conjugated equine estrogen (0.625 mg) and medroxyprogesterone acetate (2.5 mg) or placebo for 4.1 years 60 Placebo HRT 50 40 Year RR 1 2 3 4+5 1.52 1.00 0.87 0.67 ** 0 Year 1 Year 2 Year 3 Year 4 + 5 HRT provides no CV benefit in women with known CAD *Includes coronary revascularization, unstable angina, congestive heart failure, resuscitated cardiac arrest, transient ischemic attack or stroke, peripheral arterial disease, and all-cause mortality **P=0.009 for trend-time analysis CAD=Coronary artery disease, CV=Cardiovascular, HRT=Hormone replacement therapy Hulley S et al. JAMA 1998;280:605-613
  • Hormone Replacement Therapy: Primary and Secondary Prevention Meta-analysis of 35 randomized clinical trials evaluating the effect of hormone replacement therapy on cardiovascular outcomes HRT provides no cardiovascular benefit in primary and secondary prevention Sare GM et al. Eur Heart J 2008;29:2031-2041
  • Hormone Replacement Therapy Guidelines Secondary Prevention I IIa IIb III I IIa IIb III HRT with estrogen plus progestin, or estrogen alone, should not be given de novo to postmenopausal women after NSTE-ACS for secondary prevention of coronary events. Postmenopausal women who are already taking estrogen plus progestin, or estrogen alone, at the time of NSTE-ACS in general should not continue HRT. Women who are more than 1-2 years past the initiation of HRT who wish to continue therapy for another compelling indication should weigh the risks and benefits, recognizing the greater risk of CV events and breast cancer (combination therapy) or stroke (estrogen). CV=Cardiovascular, HRT=Hormone replacement therapy, NSTEACS=Non-ST-segment elevation acute coronary syndrome Anderson JL et al. JACC 2007;50:652-726
  • Evidence for Current Cardiovascular Disease Prevention Guidelines Nonsteroidal Anti-inflammatory Drugs Evidence and Guidelines
  • Nonsteroidal Anti-inflammatory Drugs: Primary Prevention Meta-analysis of 121 randomized trials evaluating the CV effects of COX-2 inhibitors COX-2 NSAIDs increase the risk of adverse CV events CV=Cardiovascular, COX-2=Cyclooxygenase 2, NSAIDs=Nonsteroidal anti-inflammatory drugs Kearney PM et al. BMJ 2006;332:1302-1306
  • Nonsteroidal Anti-inflammatory Drugs: Primary and Secondary Prevention Meta-analysis of 23 studies evaluating the CV effects* of NSAIDs COX-2 NSAIDs increase the risk of adverse CV events *Predominantly includes myocardial infarction and sudden cardiac death CV=Cardiovascular, COX-2=Cyclooxygenase 2, NSAIDs=Nonsteroidal anti-inflammatory drugs McGettigan P et al. JAMA 2006;296:1633-1644
  • Nonsteroidal Anti-inflammatory Drugs: Primary and Secondary Prevention Meta-analysis of 23 studies evaluating the CV effects* of NSAIDs COX-2 NSAIDs increase the risk of adverse CV events *Predominantly includes myocardial infarction and sudden cardiac death CV=Cardiovascular, COX-2=Cyclooxygenase 2, NSAIDs=Nonsteroidal anti-inflammatory drugs McGettigan P et al. JAMA 2006;296:1633-1644
  • Nonsteroidal Anti-inflammatory Drugs: Primary and Secondary Prevention Celecoxib regimen Meta-analysis of 6 randomized trials evaluating the CV effects of celecoxib There is a dose dependent increase in CV risk with celecoxib CV=Cardiovascular Solomon SD et al. Circulation 2008;117:2104-2013
  • Nonsteroidal Anti-inflammatory Drugs: Secondary Prevention Case-crossover analysis of the death rate relative to NSAIDs in 58,432 patients discharged following an acute MI NSAIDs in patients with previous MI increase the risk of adverse CV events CV=Cardiovascular, NSAIDs=Nonsteroidal antiinflammatory drugs, MI=Myocardial infarction Gislason GH et al. Circulation 2006;113:2906-2913
  • Nonsteroidal Anti-inflammatory Drugs: Balance of CV and GI Risks CV=Cardiovascular, COX-1=Cyclooxygenase 1, COX-2=Cyclooxygenase 2, GI=Gastrointestinal Grosser T et al. JCI 2006;116:4-15
  • Stepwise Approach to Pharmacologic Therapy for Musculoskeletal Disease ASA=Aspirin, CV=Cardiovascular, COX-2=Cyclooxygenase 2, NSAIDs=Nonsteroidal anti-inflammatory drugs Antman EM et al. Circulation 2007;115:1634-1642
  • Nonsteroidal Anti-inflammatory Drug Guidelines Secondary Prevention I IIa IIb III I IIa IIb III At hospital discharge, the patient’s need for treatment of chronic musculoskeletal discomfort should be assessed, and a stepped-care approach to treatment should be used, starting with acetaminophen, small doses of narcotics, or nonacetylated salicylates. It is reasonable to use nonselective NSAIDs, such as naproxen, if initial therapy with acetaminophen, small doses of narcotics, or nonacetylated salicylates is insufficient. NSAIDs=Nonsteroidal anti-inflammatory drugs Anderson JL et al. JACC 2007;50:652-726
  • Nonsteroidal Anti-inflammatory Drug Guidelines (Continued) Secondary Prevention I IIa IIb III It is reasonable to use nonselective NSAIDs, NSAIDs with increasing degrees of relative COX-2 selectivity may be considered for pain relief only for situations in which intolerable discomfort persists despite attempts at steppedcare therapy with acetaminophen, small doses of narcotics, nonacetylated salicylates, or nonselective NSAIDs. In all cases, the lowest effective doses should be used for the shortest possible time COX-2-Cyclooxygenase 2, NSAIDs=Nonsteroidal anti-inflammatory drugs Anderson JL et al. JACC 2007;50:652-726
  • Nonsteroidal Anti-inflammatory Drug Guidelines (Continued) Secondary Prevention I IIa IIb III I IIa IIb III NSAIDs with increasing degrees of relative COX-2 selectivity may be considered for pain relief only for situations in which intolerable discomfort persists despite attempts at stepped-care therapy with acetaminophen, small doses of narcotics, nonacetylated salicylates, or nonselective NSAIDs. In all cases, the lowest effective doses should be used for the shortest possible time. NSAIDs with increasing degrees of relative COX-2 selectivity should not be administered to NSTE-ACS patients with chronic musculoskeletal discomfort when therapy with acetaminophen, small doses of narcotics, nonacetylated salicylates, or nonselective NSAIDs provides acceptable levels of pain relief. COX-2-Cyclooxygenase 2, NSAIDs=Nonsteroidal anti-inflammatory drugs, NSTE-ACS=Non-ST-segment elevation acute coronary syndrome Anderson JL et al. JACC 2007;50:652-726
  • Evidence for Current Cardiovascular Disease Prevention Guidelines Other Therapy Evidence and Guidelines
  • Ginkgo Biloba: Primary and Secondary Prevention Cardiovascular Health Study (CHS) Substudy Rate of cardiovascular events per 1000 person-years (%) 3,069 patients (>75 years) randomized to Ginkgo biloba (120 mg/day) or placebo for a mean of 6.1 years Placebo Ginko biloba 30 HR=1.16 P=0.30 20 10 0 10.5 12.1 HR=1.04 P=0.70 HR=1.06 P=0.78 5.0 Myocardial infarction 22.2 23.0 5.3 CHD Death Total Death Ginkgo biloba has no effect on the rate of MI or death CHD=Coronary heart disease, MI=Myocardial infarction Kuller LH et al. Circ Cardiovasc Qual Outcomes 2010;3:41-47
  • Multivitamin: Primary and Secondary Prevention Physicians’ Health Study II 14641 men randomized to a daily multivitamin or placebo for a median of 11.2 years Placebo Multivitamin A multivitamin had no effect on the rate of adverse CV events CV=Cardiovascular Sesso HD et al. JAMA 2012;308:1751-1760