7-Point Prevention Rx for Patients at Risk for CVD and Hyperlipidemia


The goal when evaluating patients for CVD risk is to know what signs to look for and to devise an evidence-based, individualized treatment plan.

During his presentation, “Hyperlipidemia: Applying the Evidence to Prevent Vascular Disease,” Wednesday at the 2010 AAFP Scientific Assembly, Brian Reamy, MD, FAAFP, discussed the primary and secondary prevention of cardiovascular disease (CVD); the impact of cholesterol, hyperlipidemia, and other factors on patients’ CV risk, and key treatment considerations. He began by reminding the audience that heart disease and stroke are still the number one and number three causes of death in the US, with one of every 2.8 deaths in US due to cardiovascular disease. The goal for clinicians when evaluating patients for risk of CVD is to know what to look for and how to devise a treatment plan based on the patient’s clinical presentation. Reamy said that the four key CV risk factors to consider are smoking, family history, hypertension, and dyslipidemia. The most commonly used tool to calculate is the Framingham Risk Calculator. Reamy said that this tool does have its drawbacks, chief of which are that it does not take into account the patient’s family history of CV events. Reamy also noted that when calculating CV risk, physicians rarely make mistakes when assigning patients to low- and high-risk groups, because the guidelines and data are rather precise in these cases. However, the intermediate risk classification is imprecise, often leading physicians to attribute a lower level of risk than that patient actually has.

According to the NCEP/ATP III guidelines, the “first step in selection of LDL-lowering therapy is to assess a person’s risk status,” which requires “measurement of LDL cholesterol as part of lipoprotein analysis and identification of accompanying risk determinants.” Thus, when evaluating a patient, the first step is to obtain a complete and fasting lipid profile. The ATP III guidelines classify lipid levels as follows:

LDL Cholesterol

<100 Optimal

100-129 Near optimal/above optimal

130-159 Borderline high

160-189 High

>190 Very high

Total Cholesterol

<200 Desirable

200-239 Borderline high

>240 High

HDL Cholesterol

<40 Low

>60 High

When treating patients at risk for CVD who have had a prior CVD event, clinicians should “try to get LDL to 100 mg/dl in order to arrest further damage,” said Reamy. The data also says that if a patient’s LDL is above goal, he or she should increase the intake of soluble fiber in his or her diet; Reamy said that beans, pears, and oat bran are particularly high in soluble fiber. Patients in this range should also replace butter and margarine with plant sterol/stanol spreads. Other goals for treatment include reducing BMI to below 25 through diet and increased physical activity — at least 30 minutes three times/week. “Every little bit helps,” said Reamy.

When selecting a pharmacologic component of a CVD and cholesterol-lowering regmin, physicians and patients have a wide range of options. The resins (colesevelam, etc) have been shown to lower LDL when given as an adjunct to statins, but they are also associated with GI side effects. If considering prescribing a fibrate (fenofibrate, gemfibrozil,etc), clinicians are advised not to combine gemfibrozil with a statin. Combination therapy with simvastatin/ezetimibe) lowers LDL well but may not actually improve CVD outcomes. Fish oil is also beneficial but can potentially interfere with clotting times in patients on warfarin. Statins are effective but are not safe in pregnancy. Reamy said that the anti-inflammatory effect is basically equal in all statins, and these drugs are more potent by 10-15% with evening dosing. Atorvastatin is “great for LDL lowering,” said Reamy. Pravastatin has the fewest drug interactions. Rosuvastatin is a potent agent, but pitavastatin may be even more potent, but is so new that more data needed.

Next, Reamy presented three cases that highlighted current dilemmas faced by practicing physicians who are treating patients at risk for CVD. When evaluating these patients, physicians should develop a “seven-point CVD prevention prescription” that that takes into consideration exercise, dietary interventions, steps to lower BMI, smoking cessation, aspirin use, blood pressure optimization, and lipid optimization.

The first hypothetical case Reamy outlined involved a 49-year-old male who had suffered a “small heart attack” (two vessel angioplasty, left wall MI). The patient was also a social drinker and smoker, and was currently taking aspirin and a beta-blocker. Family history revealed that no men in the patient’s family had reached age 55 without a heart attack or other CV event. His LDL was 110 mg/dl, HDL was 25, total cholesterol (TC) 175, triglycerides (TG) 200, BMI 28.5, and blood pressure (BP) was 128/80. Based on this information, the patient’s 10-year Framingham risk for MI is 12%, which is much higher than would appear at first glance from his vital signs. A treatment regimen for this patient would optimize weight and diet (Reamy recommended a nutritional consultation), prescribe low-dose baby aspirin and beta-blocker qd, maintain BP control, take measures to help the patient to stop smoking, and prescribe a statin to lower LDL to less than 70 mg/dl. However, Reamy noted that even if a treatment plan accomplished all of these goals, the patient’s CVD risk would still be at about 5%. A key and overlooked issue in patients such as this one is HDL, “the forgotten lipid,” said Reamy. A treatment plan that raised this patient’s HDL to more than 50 mg/dl would “reduce his CV risk to age-related only. Always remember that HDL levels are powerful inverse predictors of CV events,” said Reamy. Although “we don’t have great tools for this at this time” for raising HDL, there are several measures that have been proven to be effective, said Reamy. These include aerobic exercise (increases HDL 5%), tobacco cessation (increases HDL 10%), weight loss if BMI is greater than 25, reducing alcohol consumption to 1-2 drinks per day in men and 0-1 in women (increases HDL 12%), statin use (increases HDL 5-10%), and niacin (raises HDL 15-20%).

Reamy’s second case study involved a 55 year-old male who had been diagnosed with type 2 diabetes and hypertension for five years. He had refused treatment for high cholesterol previously, but is now concerned for his health because his younger brother recently had a heart attack. He also has had GERD and other comorbid conditions. His father and paternal grandfather had MI at age 58 and 61, respectively. He has normal thyroid function, TC is 235, HDL 28, TG 185, LDL 170, and BP 136/82. The patient’s BMI is elevated, exacerbated by a sedentary lifestyle. Clearly, said Reamy, this patient has cardiometabolic syndrome and is at high risk for CVD. The treatment plan for this patient should include: exercise five days per week, optimized diet and nutrition counseling, and simvastatin 20 mg po qd. The patient’s LFT should be checked at 12 weeks, and the treating physician should consider changing the patient to combination therapy with statin/niacin or statin/fibrate; “don’t ignore the low HDL and high TG in patients like this,” said Reamy.

What about aspirin for this patient? Reamy said that the growing body of evidence on the benefits and harms of aspirin prophylaxis for the prevention of CVD should lead to an update to the USPSTF guidelines. He advised that aspirin should not be used in men under 45 and women under 55 for CVD prevention. He also said that the evidence is insufficient for use of aspirin in patients older than 80. Women age 55-79 should use aspirin when the benefit of reduced stroke risk exceeds that of GI bleed risk; men age 45-79 should use aspirin if heart attack risk exceeds GI bleed risk.

The third case presented a 45-year-old woman whose routine lipid screen showed TC 203, HDL 48, TG 155, and LDL 124. Her past medical history was negative. She smokes and takes a daily vitamin. Family history revealed that her father had a heart attack at age 60 (technically not a risk factor for this patient), mother had MI at age 64. Patient’s BP is 118/68, pulse 72, BMI is normal. Her Framingham risk is 5%, which is considered intermediate (but doesn’t take into account her family history, smoking, etc.) Reamy recommended a hs-CRP test for this patient, which he said should only be done for patients at intermediate risk. A score of less than 1 mg/l is low risk; 1-3 mg/l is intermediate; higher than 3 mg/l is high risk. A score higher than 10 mg/l should prompt for screen for other non-CVD risk (lupus, cancer, etc). “Hs_CRP is a risk marker, not a risk factor for ASCVD. If hs-CRP is elevated, consider use of a statin,” Reamy said. This patient’s hs-CRP came back at 3.2 mg/l (ie, high risk). Her treatment plan should optimize weight and diet, promote smoking cessation and exercise. It should not include daily low-dose aspirin (she’s under age 55).

Recent Videos
Carl C. Awh, MD: | Image Credit:
Raj K. Maturi, MD: 4D-150 for nAMD in PRISM Population Extension Cohort | Image Credit: Retina Partners Midwest
Charles C. Wykoff, MD, PhD: Interim Analysis on Ixo-Vec Gene Therapy for nAMD | Image Credit: Retina Consultants of Texas
Edward H. Wood, MD: Pharmacodynamics of Subretinal RGX-314 for Wet AMD | Image Credit: Austin Retina Associates
Dilsher Dhoot, MD: OTX-TKI for NPDR in Interim Phase 1 HELIOS Results  | Image Credit: LinkedIn
Katherine Talcott, MD: Baseline EZ Integrity Features Predict GA Progression | Image Credit: LinkedIn
Veeral Sheth, MD: Assessment of EYP-1901 Supplemental Injection Use in Wet AMD | Image Credit: University Retina
Brendon Neuen, MBBS, PhD | Credit: X.com
HCPLive Five at ADA 2024 | Image Credit: HCPLive
Ralph DeFronzo, MD | Credit: UT San Antonio
© 2024 MJH Life Sciences

All rights reserved.