Practice Guidelines - January 15, 2000 - American Academy of Family Physicians

Practice Guidelines

American Thoracic Society Issues Consensus Statement on Sarcoidosis
SHARON SCOTT MOREY

The American Thoracic Society (ATS), in collaboration with the European Respiratory Society and the World Association of Sarcoidosis and Other Granulomatous Disorders, has issued a consensus statement on sarcoidosis. Appearing in the August 1999 issue of the American Journal of Respiratory and Critical Care Medicine, the statement provides information on the epidemiology, pathogenesis, diagnosis and treatment of sarcoidosis. It was written by a 14-member panel of authorities on sarcoidosis who primarily developed the recommendations on the basis of expert opinion and consensus.

The panel members summarized the known aspects of sarcoidosis as follows: the incidence and prevalence, the clinical features and syndromes of the disease, how to make a diagnosis, the effectiveness of corticosteroids for short-term therapy, some genetic factors that alter expression of the disease and the immunologic characteristics of the initial onset of the disease. In addition, the panel members identified questions about the disease they would like to have answered: Is there a test to predict disease progression? Do corticosteroids alter the natural history of the disease? What is the optimal length of therapy? Are there less toxic therapies than corticosteroids or cytotoxic agents? What genetic factors alter the expression of the disease? What are the mechanisms of lung injury and fibrosis? What mechanisms are associated with persistent disease? What is the cause of sarcoidosis?

The following highlights the discussion on epidemiology, pathogenesis, diagnosis and treatment of sarcoidosis.

Epidemiology

According to the ATS consensus statement, sarcoidosis occurs primarily in adults younger than 40 years of age. The peak incidence occurs in the third decade of life. One population-based study revealed that the rates of disease in men and women are 5.9 cases and 6.3 cases, respectively, per 100,000 person-years. In the United States, the lifetime risk of sarcoidosis is estimated to be 2.4 percent for blacks and 0.85 percent for whites.

The clinical presentation and severity of the disease differ among ethnic and racial groups. For example, studies suggest that the disease is more severe in blacks, while whites are more likely to present with asymptomatic disease. Extrathoracic manifestations are more common in some groups, such as uveitis in blacks, lupus pernio in Puerto Ricans and erythema nodosum in Europeans.

Clusters of the disease have been reported, leading to speculation about person-to-person transmission or a shared exposure to an environmental agent. There have been case reports of familial clustering of sarcoidosis as well as husbandwife disease. A case-control study of residents of the Isle of Man found that 40 percent of the persons with sarcoidosis had been in contact with a person known to have the disease, compared with 1 to 2 percent of the control subjects. Studies have also revealed seasonal clustering of cases in the winter and early spring. Occupational risk factors, such as exposure to beryllium and other metal dusts, fumes and organic antigens, also have been studied. One study reported three cases of sarcoidosis among 57 firefighters who apprenticed together. In the Isle of Man study, 18.8 percent of the cases of sarcoidosis occurred in health care workers (mainly nurses), compared with an incidence of 4.2 percent in the control group. Whether environmental or occupational exposure plays a role in sarcoidosis requires further investigation.

Pathogenesis

Although the cause of sarcoidosis remains unknown, the panel members note that the hypothesis that sarcoidosis results from exposure of genetically susceptible persons to specific environmental agents is supported by three lines of evidence: (1) epidemiologic studies that show clusters of cases; (2) the inflammatory response in the lungs is most consistent with an immune response triggered by an antigen; and (3) studies of T-cell receptors in patients with sarcoidosis suggest a specific antigen that triggers the development of sarcoidosis.

Clinical Presentation and Organ Involvement

According to the consensus statement, nonspecific symptoms such as fever, fatigue, malaise and weight loss occur in approximately one third of patients with sarcoidosis. The lungs are affected in more than 90 percent of patients with the disease. Pulmonary manifestations include dyspnea, dry cough and chest pain. Roentgenographic stages in pulmonary disease range from no radiographic abnormalities (Stage 0), to bilateral hilar lymphadenopathy (Stage I), to bilateral hilar adenopathy and parenchymal infiltration (Stage II), to parenchymal infiltration without hilar adenopathy (Stage III) and, finally, to advanced fibrosis with evidence of honey-combing, hilar retraction, bullae, cysts and emphysema (Stage IV).

Peripheral lymph nodes, most frequently cervical, axillary, epitrochlear and inguinal, are palpable in about one third of patients. Myocardial involvement, found in approximately 5 percent of patients, ranges from benign arrhythmias or high-degree heart block to sudden death. The electrocardiogram may be negative. Studies suggest that as many as 50 to 80 percent of patients are found to have hepatic granulomas on biopsy, but the liver is palpable in less than 20 percent of patients. Abnormalities on liver function tests are common in patients with sarcoidosis.

Erythema nodosum and lupus pernio are two cutaneous lesions associated with sarcoidosis. Erythema nodusum, the hallmark of acute sarcoidosis, is common in European, Puerto Rican and Mexican patients. Lupus pernio is characterized by indurated plaques in association with discoloration of the nose, cheeks, lips and ears. It is more common in black women.

Uveitis is the most common ocular manifestation. Other ocular lesions include conjunctival follicles, lacrimal gland enlargement, keratoconjunctivitis sicca, dacryocystitis and retinal vasculitis.

Neurosarcoidosis occurs in less than 10 percent of patients. Common nervous system manifestations include facial palsies, and hypothalamic and pituitary lesions.

The joints most commonly affected by sarcoidosis include the knees, ankles, elbows, wrists and small joints of the hands and feet. Joint pain has been reported in 25 to 39 percent of patients, but deforming arthritis is rare. Symptomatic muscle involvement is rare.

The gastrointestinal tract is affected in less than 1 percent of patients. The stomach is the most commonly involved part.

Hematologic abnormalities in sarcoidosis are frequent but nonspecific. Anemia may occur in 4 to 20 percent of patients, and leukopenia may be found in as many as 40 percent. Other abnormalities in patients with sarcoidosis include parotitis, hypercalcemia, hypercalciuria, asymptomatic granulomas of the female reproductive tract, interstitial nephritis and renal failure related to hypercalcemia and nephrocalcinosis.

Diagnosis

According to the ATS statement, the diagnosis of sarcoidosis requires the blend of a compatible clinical picture, the demonstration of noncaseating granulomas and exclusion of other disorders capable of producing a similar clinical or histologic picture. Four goals of the diagnostic work-up are cited: to provide histologic confirmation, to determine the extent and severity of disease, to assess whether the disease is stable or is likely to progress and to determine if therapy will be beneficial.

Transbronchial lung biopsy is recommended in most cases. However, lung biopsy may not be required in some patients, such as those who present with fever, erythema nodosum, arthralgias and bilateral hilar lymphadenopathy and who subsequently have rapid, spontaneous remission of the disease.

After the diagnosis of sarcoidosis has been established, recommended studies include urinalysis, electrocardiography, ophthalmologic examination, tuberculin skin test, peripheral blood count, serum chemistries (calcium, liver enzymes, creatinine, blood urea nitrogen) and pulmonary function testing.

Treatment

Topical steroid therapy may be all that is required in patients with mild manifestations such as skin lesions, anterior uveitis or cough. Oral corticosteroids are often used to treat systemic symptomatic disease. According to the ATS statement, systemic therapy is clearly indicated for cardiac disease, neurologic disease, eye disease unresponsive to topical therapy and hypercalcemia. Oral corticosteroids often result in improvement of pulmonary symptoms, but recurrence is common after discontinuation of therapy. The panel of experts notes that no randomized prospective trials have been conducted to determine the optimal dosage and duration of corticosteroid therapy.

Other agents used in the treatment of sarcoidosis include cytotoxic agents, antimalarial agents and nonsteroidal anti-inflammatory drugs. Methotrexate and azathioprine are the preferred cytotoxic agents for most patients with refractory disease. In a study of 50 patients with sarcoidosis, methotrexate alone produced a response in 33 patients, and nine additional patients responded to low-dose prednisone combined with methotrexate. The efficacy of azathioprine appears to be similar to that of methotrexate. There have been no studies to determine when cytotoxic drugs are indicated in the treatment of sarcoidosis. Chloroquine and hydroxychloroquine are also used in the treatment of sarcoidosis. Nonsteroidal anti-inflammatory drugs are effective, particularly for musculoskeletal symptoms and erythema nodosum. Pulmonary rehabilitation may be beneficial in patients with systemic symptoms, such as myalgias and fatigue, and in patients with significant respiratory insufficiency.

ACOG Practice Bulletin on Management of Herpes in Pregnancy
MONICA PREBOTH

The Committee on Practice Bulletins of the American College of Obstetricians and Gynecologists (ACOG) has developed a practice bulletin on the management of herpes in pregnancy. The guidelines were designed to help physicians make decisions about appropriate obstetric and gynecologic care. The complete practice bulletin appears in the October 1999 issue of Obstetrics and Gynecology.

The guidelines cover the following aspects of the management of herpes simplex virus (HSV) infection in pregnancy: etiology and incidence; presentation of infection, including primary infection, nonprimary first episode, recurrent infection and neonatal herpes infection; various paths of transmission, including sexual and direct contact, transmission from mother to fetus and transmission during pregnancy; and clinical considerations and recommendations.

The ACOG committee makes the following recommendations based on limited or inconsistent scientific evidence:

Women with primary HSV infection during pregnancy should be treated with antiviral therapy.

Cesarean delivery should be performed in women with first-episode HSV infection who have active genital lesions at the time of delivery.

For women at or beyond 36 weeks of gestation with a first episode of HSV infection occurring during the current pregnancy, antiviral therapy should be considered.

The ACOG committee also makes the following recommendations based mainly on consensus and expert opinion:

Cesarean delivery should be performed on women with recurrent HSV infection who have active genital lesions or prodromal symptoms at delivery.

Expectant management of patients with preterm labor or preterm premature rupture of membranes and active HSV infection may be warranted.

For women at or beyond 36 weeks of gestation who are at risk for recurrent HSV infection, antiviral therapy also may be considered, although such therapy may not reduce the likelihood of cesarean delivery.

In women with no active lesions or prodromal symptoms during labor, cesarean delivery should not be performed on the basis of a history of recurrent disease.

Antiviral Treatment for Herpes Simplex Virus

Indication
Valacyclovir
Acyclovir
Famciclovir

First clinical episode 1,000 mg twice a day for 7 to 14 days 200 mg five times a day or 400 mg three times a day for 7 to 14 days 250 mg three times a day for 7 to 14 days

Recurrent episodes 500 mg twice a day for 5 days 200 mg five times a day or 400 mg three times a day for 5 days 125 mg twice a day for 5 days

Daily suppressive therapy 500 mg once a day (¾ 9 recurrences per year) or 1,000 mg once a day or 250 mg twice a day (> 9 recurrences per year) 400 mg twice a day 250 mg twice a day

Reprinted with permission from Baker DA. Antiviral therapy for genital herpes in nonpregnant and pregnant women. Int J Fertil Womens Med 1998;43:243-8.

Clinical Considerations and Recommendations

Medical Management of Pregnant Women with Primary HSV Infection. Antiviral therapy is recommended for women with primary HSV infection during pregnancy to reduce viral shedding and help in the healing of lesions. Primary HSV infection cannot be distinguished from nonprimary first-episode disease without serology. Primary infection poses a higher risk of vertical transmission than does recurrent infection.

Medical Management of Pregnant Women with Recurrent HSV Infection. A randomized trial of acyclovir given after 36 weeks of gestation in women with recurrent genital herpes infection showed a significant decrease in clinical recurrences. There was also a reduction in the number of cesarean deliveries performed for active infection, although this finding was not statistically significant.

Drug Treatment of HSV Infection During Pregnancy. Many antiviral compounds are available for the treatment of HSV infection (see Table); however, none has received approval from the U.S. Food and Drug Administration (FDA) for use in pregnancy. Oral acyclovir reduces viral shedding, reduces pain and heals lesions faster when compared with placebo. The drug is safe and has minimal side effects, but only 20 percent of each oral dose is absorbed.

Valacyclovir and famciclovir have been approved by the FDA for the treatment of primary genital herpes, recurrent disease and suppression of recurrent outbreaks.

Role of Universal Screening for HSV During Pregnancy or Delivery. Universal screening for HSV is not recommended for pregnant women with current or past HSV infection because viral cultures are expensive and imprecise.

Role of Cesarean Delivery in Women with HSV Infection. Women with active genital lesions or symptoms of vulvar pain or burning should deliver by cesarean. While the incidence of infection in infants whose mothers have recurrent infections is low, cesarean delivery is recommended because of the potentially serious nature of the disease. Cesarean delivery is not necessary in women with a history of HSV but no active genital disease during labor.

Cesarean delivery is not recommended in women who have recurrent HSV infection and nongenital lesions because the risk of transmission is notably low. Nongenital lesions should be covered with an occlusive dressing before vaginal delivery.

The ACOG guidelines also discuss the following: how the diagnosis of HSV infection can be confirmed; when vaginal delivery is appropriate in patients with active HSV infection and ruptured membranes; how to manage women with active HSV infection and preterm rupture of membranes; which invasive procedures are contraindicated in women with HSV infection; and whether women with active HSV infection should breastfeed.

AHA Examines Cardiovascular Problems in Diabetes
SHARON SCOTT MOREY

The American Heart Association (AHA) has issued recommendations for interventions to reduce the risk of cardiovascular complications in patients with diabetes mellitus. Developed by the AHA Science Advisory and Coordinating Committee, the AHA scientific statement appears in the September 7, 1999 issue of Circulation. It is also available on the Circulation Web site (http://www.circulationaha.org). In addition, single reprints may be obtained by calling 800-242-8721 or writing the American Heart Association, Public Information, 7272 Greenville Ave., Dallas, TX 75231-4596. The following summarizes the recommendations for reducing the risk of cardiovascular disease and its complications in patients who have diabetes.

Predisposing Risk Factors for Cardiovascular Disease

The AHA scientific statement begins with the assertion that "from the point of view of cardiovascular medicine, it may be appropriate to say 'diabetes is a cardiovascular disease.'" The report notes that the combination of insulin resistance, dyslipidemia, hypertension and prothrombotic factors often precedes the development of type 2 diabetes (formerly known as noninsulin-dependent diabetes) by many years. This constellation is referred to in the report as the metabolic syndrome.

According to the AHA report, myocardial ischemia from coronary atherosclerosis frequently is asymptomatic in patients with diabetes. As a result, atherosclerosis has often progressed to involve multiple vessels before ischemic symptoms occur and before treatment is initiated. In addition, the poor prognosis in patients with diabetes and ischemic heart disease seems to relate to an enhanced myocardial dysfunction that leads to accelerated heart failure. Factors that probably underlie diabetic cardiomyopathy include severe coronary atherosclerosis, prolonged hypertension, chronic hyperglycemia, microvascular disease, glycosylation of myocardial proteins and autonomic neuropathy. Diabetic cardiomyopathy may be prevented or forestalled by good glycemic control, better control of hypertension and the use of cholesterol-lowering agents to prevent atherosclerosis. In addition, prevention or treatment of obesity and promotion of physical activity are advocated as important measures for preventing cardiovascular disease and diabetes.

Insulin Resistance and the Metabolic Syndrome

According to the report, studies suggest that insulin resistance is a multisystem disorder that induces multiple metabolic alterations. Metabolic risk factors that commonly occur in patients with insulin resistance are atherogenic dyslipidemia, hypertension, glucose intolerance and a prothrombotic state. The dyslipidemia is characterized by an elevated very-low-density lipoprotein level, small low-density lipoprotein (LDL) particles and a low high-density lipoprotein (HDL) level. Coagulation alterations that predispose the patient to arterial thrombosis include an increased fibrinogen level, increased plasminogen activator inhibitor-1 and various platelet abnormalities.

Risk Assessment and Clinical Evaluation

The report states that the first step in reducing the risk of cardiovascular disease in patients with diabetes is identification of risk factors such as cigarette smoking, hypertension, abnormal serum lipid levels, excess body weight and abdominal obesity, physical inactivity and a family history of cardiovascular disease.

Early detection of cardiovascular disease may reduce morbidity and mortality in patients with diabetes. Detection of subclinical disease requires a careful assessment for evidence of claudication, angina, dyspnea on exertion and cerebrovascular disease. Carotid and femoral arteries should be assessed for bruits and peripheral pulses should be evaluated. The ratio of ankle-to-brachial artery systolic blood pressure may serve as a marker for peripheral vascular disease. The urine should be checked for microalbuminuria. Electrocardiographic evidence of left ventricular hypertrophy is a strong predictor of morbidity and mortality from coronary heart disease.

Special considerations for exercise stress testing include the blunted blood pressure and heart rate responses that are often present in patients with diabetes. In addition, painless ST-segment depression is common in these patients, and the diagnostic specificity of ST-segment depression is often reduced in patients with diabetes because of a previous silent myocardial infarction, conduction abnormalities and increased left ventricular mass. An alternative to exercise testing is perfusion scintigraphy. Although not recommended routinely, ambulatory electrocardiographic monitoring may be useful for detecting silent ischemia.

The report notes that autonomic dysfunction is associated with a 50 percent mortality rate at five years. Periodic evaluation should include an assessment for evidence of autonomic dysfunction. Autonomic dysfunction increases the risk of general anesthesia and complications following elective surgery. Autonomic dysfunction may be present if two or more of the following abnormalities are found on examination: a resting heart rate (supine) of 100 beats per minute, an excessive diastolic blood pressure response to hand-grip exercise, an abnormal expiratory/inspiratory RR-interval ratio and postural hypotension.

Table 1 outlines important points for evaluating and monitoring the patient's renal status. Aggressive management of hypertension, to blood pressure levels of less than 130/85 mm Hg, is recommended as a measure to prevent the development of end-stage renal disease.

TABLE 1
Important Considerations for Evaluation of Renal Status in Patients with Diabetes

Urine albumin and protein

Yearly screening for microalbuminuria seven years after the onset of type 1 diabetes (formerly called insulin-dependent diabetes) and type 2 diabetes (formerly called noninsulin-dependent diabetes) and in all hypertensive patients with diabetes; thereafter, test urine for albumin yearly.
Microalbuminuria: urine albumin of 30 to 300 mg per day or 30 to 300 mg per g of creatinine in the first morning urine specimen.*
Rule out other kidney diseases that cause proteinuria.
Detect increased urine albumin and protein.
   Macroalbuminuria: urine protein >300 mg per day (or >300 mg per g of creatinine) in the first morning urine specimen.*
   Nephrotic syndrome: urine protein >3 g per day.
   If either is present, further renal evaluation is necessary.
Patients with microalbuminuria or proteinuria and those with high serum creatinine or nephrotic syndrome should be evaluated by a nephrologist to detect other causes of kidney disease and to develop a treatment strategy.

Urinalysis

The presence of hematuria, pyuria and a large number of casts (e.g., red blood cell casts, white blood cell casts or >2 granular casts per high-power field) is often an indication that a nondiabetic disease is also affecting the kidney. Such patients should be evaluated by a nephrologist to develop a treatment strategy if needed.

Blood pressure evaluation

If hypertension is present, exclude secondary causes, including advancing renal insufficiency.
Treatment with an ACE inhibitor may be preferred unless there is hyperkalemia or other complications.

BUN, serum creatinine and GFR

BUN is affected by the degree of renal insufficiency and dietary protein; therefore, it is not a satisfactory estimate of renal function.
The serum creatinine becomes high only after >50% of kidney function is lost; therefore, it is not useful for detecting early renal insufficiency. A rising serum creatinine indicates progressive renal failure, and a plot of the reciprocal of serum creatinine versus time is useful for tracking the progressive decline in renal function.
The GFR is the most accurate estimate of the degree of renal dysfunction, but it generally requires administration of a radioisotope and at least four hours of the patient's time. The loss of GFR also provides the most accurate estimate of the rate of loss of kidney function.

ACE = angiotensin converting enzyme; BUN = blood urea nitrogen; GFR = glomerular filtration rate.
*--Urine collections must be done when there is no complicating condition that can elevate protein excretion; this includes fever, heavy exercise, poor glucose control, heart failure and urinary tract infection. Also, certain drugs can depress albumin excretion; these include nonsteroidal anti-inflammatory drugs and ACE inhibitors.
Adapted with permission from Grundy SM, Benjamin IJ, Burke GL, Chait A, Eckel RH, Howard BV, et al. Diabetes and cardiovascular disease: a statement for healthcare professionals from the American Heart Association. Circulation 1999;100:1134-46.

Primary Prevention

The AHA statement notes that type 2 diabetes can be viewed as the end product of years of metabolic stress accompanying insulin resistance. As the report states, "the clock starts ticking for acceleration of atherogenesis long before the onset of hyperglycemia." Early detection of risk factors associated with the metabolic syndrome is needed to institute primary prevention measures in patients at risk of diabetes. Evidence of insulin resistance includes the presence of abdominal obesity or borderline abdominal obesity, high-normal blood pressure or mild hypertension, high-normal triglycerides (150 to 250 mg per dL [1.70 to 2.82 mmol per L]), reduced HDL cholesterol (less than 40 mg per dL [1.05 mmol per L] in men and less than 50 mg per dL [1.30 mmol per L] in women) and borderline high-risk LDL cholesterol (130 to 159 mg per dL [3.35 to 4.10 mmol per L]). In some patients, impaired fasting glucose (110 to 126 mg per dL [6.10 to 7.00 mmol per L]) may be present. Impaired fasting glucose usually signifies longstanding insulin resistance and is a strong risk factor for type 2 diabetes. The report states that early implementation of primary measures for prevention of cardiovascular disease will probably delay the onset of type 2 diabetes as well as reduce the risk of cardiovascular disease.

Interventions for Risk Reduction in Cardiovascular Disease

According to the AHA statement, clinical trials show that comprehensive medical intervention in patients with diabetes and atherosclerotic cardiovascular disease can have a considerable impact. It can extend the overall rate of survival, improve quality of life, decrease the need for intervention procedures such as angioplasty and coronary artery bypass surgery, and reduce the incidence of subsequent myocardial infarction. Table 2 on page 567 summarizes the recommendations for interventions to reduce the risk in patients with diabetes and evidence of cardiovascular disease.

TABLE 2
Guide to Risk Reduction in Patients with Diabetes and Cardiovascular Disease

Risk intervention
Recommendation

Smoking cessation Strongly encourage patient and family to stop smoking.
Provide counseling, nicotine replacement and formal cessation programs as appropriate.

Blood pressure control, with goal of ¾135/85 mm Hg Initiate lifestyle modification (e.g., weight control, physical activity and moderate sodium restriction) in all patients with blood pressure of >135 mm Hg systolic or >85 mm Hg diastolic.
Add antihypertensive agent, individualized to other patient requirements and characteristics (i.e., age, race, need for drugs with specific benefits) if blood pressure is not <140 mm Hg systolic or <90 mm Hg diastolic in three months or if initial blood pressure is >160 mm Hg systolic or >100 mm Hg diastolic.

Lipid levels, with primary goal of LDL ¾ 100 mg per dL (2.60 mmol per L) and secondary goal of HDL >35 mg per dL (0.90 mmol per L) and TG <200 mg per dL (2.26 mmol per L)

Start low-fat diet in all patients: ¾30 percent fat, <7 percent saturated fat and <200 mg per day of cholesterol.
Assess fasting lipid profile.
Immediately start cholesterol-lowering drugs if baseline LDL level is >130 mg per dL (3.35 mmol per L).

For LDL level <100 mg per dL (2.60 mmol per L), no drug therapy is recommended; for LDL level of 100 to 129 mg per dL (2.60 to 3.35 mmol per L), consider adding drug therapy to diet; for LDL level of >=130 mg per dL (3.35 mmol per L), add drug therapy to diet. Suggested drug therapy: if TG level is <200 mg per dL (2.26 mmol per L), use statin or resin; if TG level is 200 to 400 mg per dL (2.26 to 4.50 mmol per L), use statin or fibrate; if TG level is >400 mg per dL (4.50 mmol per L), consider combined drug therapy (statin plus fibrate).

If HDL level is <35 mg per dL (0.90 mmol per L), emphasize weight management and physical activity. Advise smoking cessation.

Glucose control, with goal of near-normal fasting glucose and hemoglobin A_1c of >=1 percent above normal First-step therapy: weight reduction and exercise
Second-step therapy: oral hypoglycemic agents (sulfonylureas and/or metformin; ancillary: acarbose, glitazone)
Third-step therapy: insulin therapy

Physical activity, with a minimum of 30 minutes of exercise three to four times per week Assess risk, preferably with exercise test, to guide prescription.
Encourage minimum of 30 to 60 minutes of moderate-intensity activity (walking, jogging, cycling or other aerobic activity) three to four times per week, supplemented by increase in daily lifestyle activities (e.g., walking breaks at work, using stairs, gardening, household work).
Maximum benefit: five to six hours per week
Advise medically supervised programs for moderate-risk and high-risk patients.

Weight management Start intensive dietary therapy and appropriate physical activity in patients whose BMI is >=25 kg per m².
Particularly emphasize need for weight loss in patients with hypertension, elevated TG or elevated
glucose levels.

Antiplatelet agents, anticoagulants Start aspirin, 80 to 325 mg per day if it is not contraindicated.
Manage warfarin to INR of 2.0 to 3.5 in post-MI patients unable to take aspirin.

ACE inhibitors in post-MI patients Start early after infarction in high-risk patients (anterior MI, previous MI, Killip class II [S₃ gallop, rales, radiographic congestive heart failure]).
Continue indefinitely in all patients with left ventricular dysfunction (ejection fraction ¾ 40 percent) or symptoms of failure.
Use as needed to manage blood pressure or symptoms in other patients.

Beta blockers Start in high-risk post-MI patients (arrhythmia, left ventricular dysfunction, inducible ischemia) at five to 28 days. Continue six months minimum. Observe usual contraindications. Appropriate use of beta blockers not contraindicated in patients with diabetes.
Use as needed to manage angina, rhythm or blood pressure in all other patients.

Estrogen Observational studies (but not clinical trials) suggest benefit. Limited data in women with diabetes.
Individualize recommendation consistent with other health risks.

LDL = low-density lipoprotein; HDL = high-density lipoprotein; TG = triglycerides; BMI = body mass index; INR = international normalized ratio; MI = myocardial infarction; ACE = angiotensin converting enzyme.
Adapted with permission from Grundy SM, Benjamin IJ, Burke GL, Chait A, Eckel RH, Howard BV, et al. Diabetes and cardiovascular disease: a statement for healthcare professionals from the American Heart Association. Circulation 1999;100:1134-46.

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