Executive Summary of the 3Rd Report of the Ncep Expert Panal on Detection, Evaluation

CHEST PAIN

EXECUTIVE SUMMARY OF THE 3RD REPORT OF THE NCEP EXPERT PANAL ON DETECTION, EVALUATION, AND TX OF HIGH BLOOD CHOLESTEROL IN ADULTS (ADULT TX PANAL III)

-ATP I- primary prevention of CHD in persons with high LDL > 160 mg/dL or those with borderline high LDL (130-160) and 2+ risk factors.

-ATP II- added intensive management of LDL in people with established CHD; new goal of < 100.

-ATP III- adds LDL lowering therapy in certain groups of people with multiple risk factors.

-LDL is the major cause of CHD and is the primary target of therapy.

-1st step in risk management is risk assessment.

-People older than 20 should have a fasting lipid panal checked every five years.

-If non-fasting lipids, then can only look at total chol. And HDL.

-CHD risk equivalents with risk of coronary events equal to CHD (> 20% per 10 years) are other atherosclerotic disease, diabetes, multiple risk factors that confer a 10 year risk of CHD >20%.

-DM has a higher death rate post-MI.

-For CHD or CHD risk equivalent the goal LDL is < 100mg/dL.

-Multiple 2+ risk factors with 10 year risk of CHD 20%, goal LDL <130.

-0-1 risk factors, goal LDL < 160 mg/dL.

-Risk factors are smoking, HTN > 140/90, HDL < 40, Family hx of early CHD (male < 55 y.o./female < 65 y.o.), age (men 45 y.o./ women 55 y.o.)

-Estimating 10 yr. CHD risk- First, count the # of risk factors. Second, for people with more than 2 risk factors, assessment is carried out with the Framingham scoring to identify people with short term risk (10 year) which need intensive tx. When 0-1 risk factors, no Framingham scoring. Framingham scoring includes age, total chol., HDL, BP, and smoking. It divides people with 2+ risk factors into risk > 20%, 10-20%, and <10% of CHD in the next 10 years,

-Other secondary risk factors which don’t alter LDL goals but can increase risk and are good to modify include obesity, physical inactivity, and artherogenic diet

-Metabolic syndrome- 3 or more of the following risk determinants- Abdominal obesity (> 40 inches in men, > 35 inches in women), TGs 150, HDL (<40 in men, < 50 in women), BP 130/85, fasting glucose 110 mg/dL. This is the s3econdary target of therapy after LDL reduction.

-Lifestyle changes are the most cost effective way to reduce risk for CHD, but meds. Are needed for those who are high risk.

-Reduce intake of saturated fat and chol., increase physical activity, and weight control.

-The higher the absolute risk of a person for CHD, the lowere the LDL goal.

-Should rule out secondary dyslipidemia- DM, hypothyroidism, obstructive liver disease, chroninc renal failure, and medications before treating.

-CHD or CHD risk equiv. (10 yr. risk > 20%)- LDL goal < 100. If 100, initiate lifestyle changes. If 130 than drug therapy.

-2+ risk factors (10 yr. risk 20%) - LDL goal < 130. If 130, initiate lifestyle changes. If 130 and 10 year risk 10-20% or if 160 and 10 yr. risk < 10% than drug therapy.

-0-1 risk factor- LDL goal < 160. If 160 than lifestyle changes. If 190 than drug therapy.

-Lifestyle changes- Diet with saturated fat < 7% of total calories and < 200 mg of chol./day.

-After 6 weeks of lifestyle change, recheck LDL. If goal not achieved considering adding plant stanols/sterols 2g/day and increase viscous fiber to 10-25g/day. Re-eval. in 6 weeks and if goal not met, consider drug therapy.

-LDL chol. declines in first few hours after MI and may be low for several weeks and may, therefore appear lowere than usual for the pt.

-Start pt. On LDL lowering agent at time of discharge from the hospital if LDL 130 and maybe if 100-130.

-Start drug therapy at third visit of dietary therapy and cont. lifestyle changes.

-Usually a statin is used and should be prescribed at a moderate dose.

-Assess response to drug at 6 weeks and if goal not met than increase current med or add a bile acid sequestrant or nicotinic acid.

-If goal still not achieved in 6 weeks, refer to lipid specialist.

-Once LDL goal is met, tx metabolic syndrome with weight reduction and physical activity.

-Also tx HTN, use aspirin in pts. With CHD, and tx increased TGs and low HDL.

-Elevated TGS are an independent risk factor for CHD. Normal TGs < 150; Borderline 150-199; High 200-499; Very high >500.

-Goal of non-HDL chol. In persons with high TGs is 30 mg/dL higher than that for the LDL chol. On the premise that VLDL is 30 mg/dL.

-With borderline high or high TGs, the primary aim of therapy is LDL.

-TGs of 150-199, weight reduction and exercise.

-TGs of 200-499, non-HDL chol. Becomes the secondary target and drug therapy can be considered.

-TGs > 500, the initial aim is TG lowering to prevent acute pancreatitis. Use diet, exercise, and fibrates or nicotinic acid.

-Once TGs < 500 then LDL should be addressed.

-HDL < 40 is also an independent risk factor for CHD, but there is no specific goal for therapy.

-Diabetic dyslipidemia= atherogenic dyslipidemia in persons with type 2 diabetes. Primary target of therapy is LDL. Goal LDL < 100; Use drug therapy if LDL 130. When TGs 200 than non-HDl becomes a secondary target.

-Middle aged men (35-65 y.o.) have a high prevalence of major risk factor and are predisposed to abdominal obesity and the metabolic syndrome.

-Women (45-75 y.o.) have onset of CHD delayed by 10-15 years compared with men and most CHD occurs over the age of 65.

-There is some doubt on the use of HRT to reduce CHD in post-menopausal women.

-Women should be treated similarly to men for secondary prevention.

-Older persons (men 65 and women 75) experience most CHD events. High LDL and low HDL are still predictive, and the elderly showed significant reduction with statin therapy.

-Young adults (men 20-35 and women 20-45) with elevated serum chol. Have a higher rate of premature CHD in middle age.

-African-Americans have the highest overall CHD mortality rate and the highest out of hospital coronary death rates of any other ethnic group in the U.S., particularly at a younger age. CHD risk factors are also more prevalent in this population.

Atypical Chest Pain

-3 questions: 1) Is the discomfort substernal? 2) Is it precipitated by exertion? 3) Is prompt relief provided by rest or nitroglycerin?

If YES to all 3: Typical angina

If YES to 2 out of 3: Atypical angina

If YES to 1 out of 3: Nonanginal chest pain

*Typical angina has the highest probabiltiy of CAD.

Sources of atypical chest pain:

Pericarditis- mimics MI because can show ST-segment elevation w/ acute episode; use of thrombolytic therapy can cause hemorrhagic tamponade.

-pain is stabbing, exacerbated in recumbent position, and alleviated with sitting and leaning forward; pain aggravated with inspiration and may radiate to left shoulder.

-Friction rib.

-Pressler’s syndrome= autoimmune inflammatory process that occurs several weeks past-MI with manifestations similar to pericarditis- Tx w/ aspirin

Pulmonary Disease

-Pulmonary embolism causes chest pain 72% of the time.

-pain is sharp, pleuritic, located in lateral chest and accompanied with dyspnea, atrial arrythmia, tachycordia, cyanosis, fever, or CHF.

-Hemoptysis is uncommon

-Pulmonary HTN can cause chest pain similar to angina.

Aortic Dissection

-Pain is midline chest & radiates to interscapular areas, abdomen, or lower back.

-Tearing w/ ripping sensation

-Confirmed by chest films, TEE, or CT of chest.

GI Disorders

-Points with CAD have GERD in up to 70% of episodes of chest pain.

-Chest pain also caused by peptic esophagitis, esophageal spasm or rupture, hiatal hernia, ulcers, cholecystitis, and pancreatitis.

-Esophageal spasm has pain radiation similar to MI and is relieved by nitroglycerin.

Atypical Chest Pain

-Esophageal spasm- responds to Calcium blockers & nitrates, but not really antaeids.

Chest Wall Pain

-Pain from ribs, intercostal muscles with nerves, pleural surfaces, costochondral junctions (Tiezte’s syndrome), xiphoid process, or cervical & thoracic pain.

-Early herpes zoster can cause severe pain on light touch; lesions appear in 2-3 days.

Mitral Valve Prolapse

-Healthy women- prevalence of 6%.

-Apical location, sharp pains of 1-2 seconds, dull aching, emotional disturbance, palpatations, and arrythmias, fatigue, dizzy spells, dyspnea, and depression.

-Tx with B-blockers.

Psychogenic Factors

-Neurocirculatory asthenia (DaCosta’s syndrome) is an anxiety state that has been linked w/ emotional strain and fatigue. Common in soliders.

-Lacinating pain for 1-2 seconds in infamammary area, palps, hyperventilation, numbness and tingling in extremities, sighing, dyspnea, and point tenderness in chest wall.

Atypical versus Typical Chest Pain

Location- Typical: center of chest, retrosternal, down left arm; aching, numbness, tingling into ulnar distribution of the arm and into the last 2 digits of the hand; sometimes only radiation to other body parts is found= angina equivalent.

Atypical: often felt in left submammory area or in left hemithorax.

Quality-Typical: tightness, squeezing, or heaviness; point may exhibit Levine’s clenched fist sign-tightened fist held over anterior portion of chest.

Atypical: not such profound symptoms and not substernal unless an esophageal disorder

Duration- Typical: about 10-12 min; resolves with rest of sublingual nitroglycerin pain for more than 1 hour may be an MI or nonischemic source, pain that is constant is not likely ischemic.

Intensity- An increase in frequency of episodes or nocturnal pain may herald an impending infarction. Esophageal disorders also cause nocturnal pain. Must test to Dx.

-Fived-lesion or fixed threshold angina-caused by obstructive lesion, not due to spasm.

Setting- Typical: occurs w/ exertion, emotional disturbance or excitement. Can occur while sitting or TV watching.

-Chest pain more common in early morning because of diurnal variations in platelet adhesiveness, cortisol levels, and catecholamine levels.

Atypical: from GI source related to meals, but postprandial chest discomfort may be a sign of severe CAD.

-Chest wll pain has pain w/ body movement.

-If sublingual nitroglycerin is given and the drug is active, angina is relieved within 3 minutes in most cases.

-Pain not relieved by 3 nitroglycerin tablets taken in 5 min. intervals is either severe ischemia or a nonischemic source.

-Atypical chest pain also may be relieved by sublingual nitroglycerin.

Systematic Manifestation

-Angina pecturis may be accompanied by weakness, SOB, dizziness, palps, nausea (with or without vomiting), paroxysmal nocturnal dyspnea, and diaphoresis.

-Atypical pain usually doesn’t have such severe symptoms.

MI

-Intense pain which radiates, symptoms of indigestion, nausea & vomiting.

-May be more difficult to Dx in the elderly because presentation may be subtle.

-Initial EKG may be normal in 20% of cases, and may be abnormal in about 50% of patients with chronic angina.