Coronary heart disease primary prevention

Coronary heart disease Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Differentiating Coronary heart disease from other Diseases
Epidemiology and Demographics
Risk Factors
Screening and Risk Stratification
Natural History, Complications and Prognosis
Diagnosis
Pretest Probability
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Coronary heart disease primary prevention On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Coronary heart disease primary prevention All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Coronary heart disease primary prevention
CDC on Coronary heart disease primary prevention
Coronary heart disease primary prevention in the news
Blogs on Coronary heart disease primary prevention
Directions to Hospitals Treating Type page name here
Risk calculators and risk factors for Coronary heart disease primary prevention

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The LDL target in primary prevention depends upon the patient's risk factors. If the patient has CHD or its equivalent, then the LDL goal is under 100 mg/dl. If the patient has 2 risk factors, the LDL goal is 130 mg/dl. If the patient has < 2 risk factors, the LDL goal is < 160 mg/dl.

Risk Equivalents in Primary Prevention

If CHD or a risk equivalent is present, the LDL goal is < 100 mg/dl. You are essentially considered to have the equivalent of coronary heart disease if you have any of the following "risk equivalents":

• Aortic aneurysm
• Diabetes
• Framingham Risk Score (FRS) of > 20% (A 20% risk of death or MI over 10 years)
• Peripheral vascular disease (PVD) (defined as claudication, an Ankle Brachial Index (ABI) of < 0.9)
• Symptomatic carotid artery disease (defined as prior stroke or TIA)

CV Risk Factors in the Setting of Primary Prevention

If you have two or more of the following risk factors, the LDL goal is < 130 mg/dl:

• Cigarette smoking
• Family history of premature coronary artery disease (CAD)
• High LDL (defined as LDL > 130 mg /dl)
• Hypertension ( defined as a BP ≥140/90 mm Hg or if the patient is on antihypertensive drugs)
• Low HDL (defined as HDL < 40 mg/dL males, < 50 mg/dL in females)
• Older Age (men ≥45 years old; women ≥55 years old)

If you have < two risk factors, the goal is an LDL < 160 mg/dl.

Primary Prevention: LDL Goals for Various Categories of Risk

Risk Category	LDL-C Goal	Consider Drug Therapy
CHD or CHD risk equivalent	<100 mg/dl	>130 mg/dl*
> 2 Risk Factors
10 yr risk 10-20%	<130 mg/dl	>130 mg/dl
10 yr risk < 10%	<130 mg/dl	> 160 mg/dl
< 2 Risk Factors	<160 mg/dl	>190 mg/dl

• After lifestyle modification, if LDL is 100-129, consider a statin, niacin, or fibrate therapy.

Avoid Drug Interactions with the LDL-Lowering Agents Simvastatin, Atorvastatin or Lovastatin

While LDL-lowering agents are widely prescribed in primary prevention, care should be taken to select the appropriate statin based upon concommittant medications. As a result of the metabolism via the CYP 3A4 pathway, simvastatin, atorvastatin and lovastatin interact with the following agents and should be avoided. The patient should be switched to pravastatin.

• HIV protease inhibitors
• Itraconazole (Sporanox)
• Ketoconazole (Nizoral)
• Posaconazole (Noxafil)
• Erythromycin
• Clarithromycin
• Telithromycin (Ketek)
• Grapefruit juice
• Nefazodone
• Gemfibrozil
• Cyclosporine
• Danazol

Reduce Simvastatin Dosing in the Following Scenarios

Simvastatin drug interactions include the following:

• Simvastatin 10 mg should be the maximum dose when prescribed with:

• Amiodarone
• Verapamil
• Diltiazem

• Simvastatin 20 mg should be the maximum dose when prescribed with:

• Amlodipine (Norvasc)
• Ranolazine (Ranexa)

Treat Underlying Causes of Hyperlipidemia

• Hypothyroidism can increase LDL and triglycerides.
• Obstructive liver disease can increase LDL and increase HDL.
• Uncontrolled diabetes may increase triglycerides and reduce HDL.
• Nephrotic syndrome markedly increases LDL.
• Renal failure increases LDL, increases triglycerides and decreases HDL.

Treatment of Triglycerides

• Triglyceride lowering is a secondary target of primary prevention.
• The independent and causal relationship of elevated triglycerides to CHD outcomes is not clear, although hypertriglyceridemia is a stronger risk factor for women than men.
• Triglyceride levels > 500 mg/dl are associated with acute pancreatitis.
• Hypertriglyceridemia is associated with the following conditions:

• Alcohol abuse
• Chronic renal failure
• Diabetes mellitus
• Metabolic syndrome
• Nephrotic syndrome

Class IB

• If the triglycerides are 200-499 mg/dL, then the non-HDL-C should be < 130 mg/dL

Class IIa

Further reduction of non-HDL to < 100 mg/dL is reasonable

Class IC

If TG are > 500 mg/dL, treat to prevent, pancreatitis before LDL-lowering therapy.

Avoid Drugs that Cause Dyslipidemia

• Androgenic steroids (↑LDL ↓HDL)
• Progestogens/estrogens (↑HDL/TG)
• Retinoic acid (Accutane) (↑TG)
• Corticosteroids (↑LDL/TG)
• Protease inhibitors (↑TG ↓HDL ↑LDL)
• Thiazide diuretics (↑LDL/TG)
• Beta-blockers (↑LDL/TG)

Lifestyle Modification Goals

• Reduce obesity
• Treat hypertension
• Encourage smoking cessation
• Encourage exercise

Aspirin in Primary Prevention

Aspirin, in doses of less than 75 to 81 mg/d, can reduce the incidence of cardiovascular events, but may increase the risk of intracranial hemorrhage in men. The U.S. Preventive Services Task Force 'strongly recommends that clinicians discuss aspirin chemoprevention with adults who are at increased risk for coronary heart disease'. The Task Force defines increased risk as 'Men older than 40 years of age, postmenopausal women, and younger persons with risk factors for coronary heart disease (for example, hypertension, diabetes, or smoking) are at increased risk for heart disease and may wish to consider aspirin therapy'. More specifically, high-risk persons are 'those with a 5-year risk ≥ 3%'. A risk calculator is available.

Regarding healthy women, the more recent Women's Health Study randomized controlled trial found insignficant benefit from aspirin in the reduction of cardiac events; however there was a signficant reduction in stroke. Subgroup analysis showed that all benefit was confined to women over 65 years old. In spite of the insignficant benefit for women < 65 years old, recent practice guidelines by the American Heart Association recommend to 'consider' aspirin in 'healthy women' <65 years of age 'when benefit for ischemic stroke prevention is likely to outweigh adverse effects of therapy'.

Modification of Risk Factors that do not have a Robust Evidence Base

Just because something has been identified as a risk factor, that does not mean that lowering the risk factor improves outcomes. This is because the risk factor may not lie in the causal pathway for CHD. Risk factors that when modified may not improve outcomes include the following:

• There is little evidence that aggressive blood sugar control actually improves cardiac risk.
• Lowering uric acid and homocysteine levels
• Omega-3 fatty acids. The benefit of fish oil is controversial with conflicting conclusions reached by a negative meta-analysis of randomized controlled trials by the international Cochrane Collaboration and a partially positive systematic review by the Agency for Healthcare Research and Quality. Since these two reviews, a randomized controlled trial reported a reduction on coronary events in Japanese hypercholesterolemic patients. Omega-3 fatty acids are also found in some plant sources including flax seed oil, hemp seed oil, and walnuts. Plant sources may be safer as fish products have been shown to contain heavy metals and other fat soluble pollutants.
• Vitamin C
• The World Health Organization (WHO) recommends "low to moderate alcohol intake" to reduce risk of coronary heart disease.
• Avoidance of fats that are readily oxidized (e.g., saturated fats and trans-fats). The consumption of trans fat (commonly found in hydrogenated products such as margarine) has been shown to cause the development of endothelial dysfunction, a precursor to atherosclerosis.
• Limit carbohydrates and processed sugars to reduce production of Low density lipoproteins while increasing High density lipoproteins.
• It has been suggested that coronary heart disease is partially reversible using an intense dietary regimen coupled with regular cardio exercise.

2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non -ST-Elevation Myocardial Infarction (DO NOT EDIT)

Identification of Patients at Risk (DO NOT EDIT)

Class I

"1. Primary care providers should evaluate the presence and status of control of major risk factors for CHD for all patients at regular intervals (approximately every 3 to 5 years). (Level of Evidence: C)"

"2. Ten-year risk (National Cholesterol Education Program [NCEP] global risk) of developing symptomatic CHD should be calculated for all patients who have 2 or more major risk factors to assess the need for primary prevention strategies. (Level of Evidence: B)"

"3. Patients with established CHD should be identified for secondary prevention efforts, and patients with a CHD risk equivalent (e.g., atherosclerosis in other vascular beds, diabetes mellitus, chronic kidney disease, or 10-year risk greater than 20% as calculated by Framingham equations) should receive equally intensive risk factor intervention as those with clinically apparent CHD. (Level of Evidence: A)"