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HOME FEATURE ARTICLES PREVENTION OF CORONARY HEART DISEASE IN MIDDLE AGED MEN
  Prevention of Coronary Heart Disease in Middle Aged Men
Sep-02
Jul-03
Oct-03
 





By Simeon Margolis, MD, PhD, Professor of Medicine and Biological Chemistry

Prevention of Coronary heart Disease in Middle Aged Men

Coronary heart disease (CHD) is caused by narrowing or blockage of the coronary arteries that supply oxygen and nutrients to the heart.� When one of these arteries is narrowed by about 75% or more, the limitation of oxygen delivery to the heart results in angina pectoris, or angina for short.� Angina is defined by a characteristic type of chest pain that usually occurs with physical activity, or sometimes with anxiety or stress, and is quickly relieved by rest or a nitroglycerin pill.� Angina affects about 6 million Americans, mostly men.� Complete occlusion of a coronary artery leads to a heart attack (myocardial infarction) that is associated with death of heart muscle (myocardial) tissue.� Heart attacks are most often associated with severe, persistent chest pain, but about a quarter of� heart attack victims do not complain of chest pain when seen in an emergency room with a proven heart attack.� And, nearly one in three people with a heart attack dies suddenly, before they are able to receive any medical attention.� About one million Americans suffer a heart attack each year. Heart attacks are far more common among middle-aged men than women although, after the menopause, women have heart attacks as frequently as men.

Based on these dismal consequences of CHD, it is obvious that prevention is the only sensible approach, and much can be done to diminish the risk.

CHD is due to atherosclerosis, sometimes referred to as "hardening of the arteries". Atherosclerosis involves arteries throughout the body and is also responsible for most strokes and peripheral artery disease which can cause pain in the legs during exercise.�� Atherosclerosis begins with the accumulation of cholesterol within the artery walls.� The deposition of cholesterol and an accompanying inflammation leads to the formation of atherosclerotic plaques.� In addition to cholesterol, these plaques contain white blood cells, smooth muscle cells, fibrous material, and calcium.� A heart attack (or stroke) occurs when a rupture or breakdown of one of these plaques leads to the formation of� a blood clot that completely occludes an artery.� Measures to prevent coronary artery disease and heart attacks are aimed at preventing the development of plaques and the formation of blood clots.

Risk factors

During the past 40 years many studies have clearly defined the major factors, called risk factors, that predispose to the development of CHD.� These factors can be divided into those that can not be altered and those that can be modified by lifestyle measures or medications.� The greater the number of risk factors, the greater the risk of CHD.� Although they can not be changed, even the unalterable risk factors must be considered because of their contribution to risk and their use in making decisions on dealing with those factors that can be modified.

Table 1: Major Unmodifiable Risk Factors

Male gender

Age

Family history of a premature heart attack

before the age of 50 in men

before the age of 60 in women

in a first degree relative (parent, sibling, child)

As mentioned earlier, during their middle ages men are at greater risk for CHD than women.� As men, and women, grow older, there is a progressive increase in their risk for CHD. ���Also at greater risk for CHD are men with a family history of premature manifestations of CHD in first degree relatives (parents, siblings, or children).� This higher risk is due to Inherited traits, like a tendency to develop hypertension, and other unidentified factors.

Table 2: Major Modifiable Risk Factors

Cigarette smoking

Abnormal serum lipids and lipoproteins

Elevated LDL cholesterol

Low HDL cholesterol

Elevated triglycerides

High blood pressure (Hypertension)

Metabolic syndrome and diabetes mellitus

Cigarette smoking

Cigarette smoking is the most dangerous and preventable factor leading to CHD.� The risk is greatest in men who have smoked the most cigarettes for the longest time.� The good news is that the risk gradually wanes and disappears about five years after smoking cessation. Smoking cigars, but not a pipe, increases the risk for CHD, though less than cigarette smoking.

Abnormal serum lipids and lipoproteins

Because they do not dissolve in water, the two major lipids (fats) in the blood, cholesterol and triglycerides, are combined with proteins to form lipoproteins so they can be transported in the bloodstream.� (Think of how the oil layer of an oil and vinegar salad dressing rapidly separates to the top of the bottle after shaking.)�� These fats are transported on three lipoproteins that are always present in the blood.�(Table 3).�

Table 3: Serum lipoproteins

Lipoprotein

Major component

Coronary disease risk

Very low density lipoprotein (VLDL)

Triglycerides

Moderate

Low density lipoprotein (LDL)

Cholesterol

High

High density lipoprotein (HDL)

Protein

Protective

The most dangerous lipoprotein is low density lipoprotein (LDL), the major cholesterol-carrying lipoprotein, which deposits its cholesterol into certain cells (macrophages and smooth muscle cells) within the walls of arteries to initiate the formation of atherosclerotic plaques.�� LDL must be modified by oxidation before it can enter these cells.� As a result, there has been widespread use of antioxidants in an effort to prevent the development or progression of atherosclerotic plaques.� High density lipoprotein (HDL) protects against atherosclerosis by removing cholesterol from arterial walls and returning it to the liver for disposal.� Very low density lipoprotein (VLDL) transports triglycerides from the liver to the rest of the body.� Although VLDL itself is not atherogenic (promoting the development of atherosclerosis), it is converted to atherogenic breakdown products; and elevated levels of VLDL convert LDL to a form that accumulates more readily in the walls of arteries.�

Lipid and lipoprotein levels are obtained with a lipid profile test that measures cholesterol, triglycerides, and HDL cholesterol.� These results are used to calculate the LDL cholesterol.� Total and HDL cholesterol measurements can be done at any time, but triglycerides must be determined after a 12 hour fast.� VLDL is not measured directly; rather elevated triglyceride levels indicate increased levels of VLDL.�

High levels of total and LDL cholesterol and low levels of HDL cholesterol are risk factors for CHD.� Five large, long term clinical trials have shown that lowering total and LDL cholesterol can markedly reduce the incidence of CHD complications (events), including death from a heart attack, as well as the need to undergo either angioplasty (opening of coronary arteries by expanding a balloon in the artery) or coronary artery bypass surgery.� In addition, lowering LDL cholesterol substantially reduces the risk of strokes. Other studies have found that lowering total and LDL cholesterol slow the progression of coronary artery narrowing and even cause regression (reduction in the size of the narrowings).� Long term studies strongly suggest, but have not proven, that raising HDL cholesterol levels reduces the incidence of coronary events.��

High blood pressure (hypertension)

About one in five middle-aged men suffer from high blood pressure.� High blood pressure has traditionally been defined as pressures greater than 140/90 (the upper number is the systolic pressure, the lower number is the diastolic pressure).� In fact, no specific value of blood pressure separates "normal" from "high" blood pressure.� Rather, the lower the blood pressure the better.Table 4details the so-called optimal, normal, and other categories of blood pressure.�� While it was once thought that a high diastolic pressure was the important determinant of risk, it is now apparent that an elevated systolic pressure is more significant.� A high systolic pressure along with a normal diastolic pressure,� referred to as isolated systolic hypertension, is clearly recognized as a risk factor for CHD and stroke.� Systolic pressures commonly rise with age, while diastolic pressures often fall.� The resulting greater difference between the systolic and diastolic pressures (pulse pressure = systolic pressure - diastolic pressure) is also associated with an increased risk of CHD.

Table 4: Categories of Blood Pressure

Category

Systolic (mm Hg)

Diastolic (mm Hg)

Optimal

<= 120

<= 80

Normal

< 130

< 85

High normal

130-139

85-89

Hypertension

>= 140

>= 90

Isolated systolic hypertension

>= 140

> 90

Metabolic syndrome and diabetes mellitus

There is an alarming epidemic of obesity and overweight(Table 5), the metabolic syndrome, and type 2 diabetes in this country.� More than half of Americans are either overweight or obese, 16 million Americans have type 2 diabetes (and half of them don’t even know it, and the frequency of the metabolic syndrome has risen by leaps and bounds, especially in older people.

Table 5: Definitions of Overweight and Obesity

Category

BMI*

Overweight

25 to 29.9

Obesity

>= 30

* BMI (Body Mass Index) is calculated as follows:
Height (inches) divided by the square of weight (lbs)
multiplied by 705. 705 x Ht (in)/ Weight (lbs)2

Overweight and obesity, especially when accompanied by excessive accumulation of fat in the abdomen (the so-called male pattern of obesity defined by an abdominal circumference of 40 inches or greater) and aging are frequently associated with resistance to the action of insulin.� The pancreas puts larger amounts of insulin into the blood (hyperinsulinemia) in order to overcome this insulin resistance and maintain normal blood sugar (glucose) levels.� Hyperinsulinemia leads to the metabolic syndrome (Table 6): higher blood glucose levels, hypertension, elevated triglyceride levels, a low HDL cholesterol, and a greatly increased risk of diabetes mellitus, CHD and the other manifestations of atherosclerosis.�

Table 6: One Definition of the Metabolic Syndrome

Presence of three or more of the following risk factors

Risk factor

Defining level

Abdominal obesity

 

Waist circumference

 

In men

> 40 in

In women

> 35 in

Triglycerides

>150 mg/dl

HDL cholesterol

Men

<40 mg/dL

Women

<50 mg/dL

Blood pressure

>135/85 mm Hg

Fasting glucose

>110 mg/dL

Abnormalities in blood glucose are usually defined by measuring fasting blood glucose levels: glucose values between 110 and 126 are termed impaired fasting glucose or pre-diabetes; glucose values of 126 or higher on at least two separate occasions indicate the presence of diabetes.� Either impaired fasting glucose or the presence of the metabolic syndrome is associated with a greater likelihood for CHD.� Diabetes is such a great risk that, for treatment purposes, it is considered equivalent to already having CHD.� This conclusion is based on the extremely high incidence of CHD in diabetic men; in fact, they are at the same risk for a first heart attack as are men who have already had a previous heart attack.��

Emerging risk factors

During the past decade the lay press has brought wide attention to several additional factors that are associated with an increased risk of CHD (Table 7).��

Table 7: Emerging Risk Factors

Markers of inflammation (C-reactive protein)

Homocysteine

Coronary calcium score by fast CT

Inflammation within the arterial wall is an important component of atherosclerosis; and increased blood levels of several substances that are related to arterial wall inflammation, such as C-reactive protein, are associated with a greater subsequent incidence of a coronary event.� Population studies have shown that men with higher blood levels of the amino acid homocysteine are also at higher risk for coronary events and strokes.� In addition, coronary events are more common when large amounts of calcium are detected within the coronary arteries using a procedure known as a fast CT scan.� Several problems cloud the interpretation of these measurements of coronary calcium: some atherosclerotic plaques do not contain calcium, and the presence of calcium does not predict whether that plaque is likely to rupture and lead to a blood clot and completely blocks an artery. None of these measurements or procedures is recommended for routine screening of healthy men who have no other risk factors.� They may be valuable, however, in making decisions on whether aggressive preventive measures should be initiated in men who are positive for one or more of the major risk factors.

Preventive measures������

Cigarette smoking

No preventive measure for CHD is more important than to stop smoking cigarettes!� Easier said than done.�

Unfortunately, men find it extremely difficult to break their long-standing addiction to cigarette smoking even when they recognize its great impact on CHD, as well as on lung cancer, chronic lung disease, and other life-threatening disorders.� The only hope for success is to reach a firm resolution to stop smoking.� Traditional recommendations are to establish a firm date for smoking cessation, throw away all cigarettes, matches, and ash trays, and seek support from family and friends.� Studies have shown that only about one in twelve men succeed in stopping smoking without some additional assistance.� Individual or group counseling sessions can enhance the chances of success.� Men who are addicted to smoking face withdrawal symptoms, such as� irritability, anxiety, and restlessness, when they stop smoking.�� By helping to overcome these symptoms,� nicotine gum, skin patches, nasal spray, or inhaler can double the chance of quitting.�� Some people may be assisted in their efforts with the prescription medication bupropion (Zyban) which reduces withdrawal symptoms and craving even though it contains no nicotine.� The increased appetite that often accompanies nicotine withdrawal can lead to weight gain, but this imparts far less risk than the smoking itself.

Abnormal lipids and lipoproteins

The first step is to be sure to obtain a lipid profile if one has not been done before or within the past 5 years.�

Total and LDL cholesterol

The LDL cholesterol level is combined with the number of risk factors (Table 8) to determine when measures should be taken to lower total and LDL cholesterol. (Table 9).� Although a sensible diet is advisable for all men regardless of their LDL cholesterol or risk� status, a cholesterol-lowering diet is specifically recommended for men whose LDL cholesterol is 190 mg/dL or greater, for those with two or more risk factors and an LDL cholesterol of 160 mg/dL or greater, and for all men who have CHD, other manifestations of atherosclerosis, or diabetes and an LDL cholesterol greater than 100 g/dL.�� Medications are often needed to achieve the targets of an LDL cholesterol less than 100 mg/dL for men with known CHD, peripheral artery disease, or diabetes and less than 130 mg/dL for men with two or more risk factors.

Table 8: CHD Risk Factors (Other Than LDL Cholesterol)

Positive risk factors

Age (years)

Men >=45

Women >=55 or postmenopausal

Family history of premature CHD

Current cigarette smoking

Hypertension

HDL cholesterol <40 mg/dL

Impaired fasting glucose or metabolic syndrome

 

Negative risk factor

HDL cholesterol >=60 mg/dL

 

Table 9: Decisions for Drug Treatment Based on LDL-cholesterol

 

Initiation level

Minimal Goal

Low risk

> 190 mg/dl

< 160 mg/dl

Two or more risks

> 160 mg/dl

< 130 mg/dl

Very high risk

> 100 mg/dl

< 100 mg/dl

 

Table 10: Dietary Measures to Reduce Total and LDL Cholesterol

Limit total fat to < 30% of calories

Limit saturated fat to < 7% of calories

Replace saturated fats with monounsaturated fats

Restrict dietary cholesterol to 200 mg/day

Control weight

Increase intake of water-soluble fiber

Although restriction of dietary cholesterol would seem the most logical way to lower blood cholesterol levels, most important is a reduction in the intake of total fat to less than 30% of calories and saturated fats to less than 7% of total calories.� A relative increase in carbohydrate intake can reduce the amount of total fat in the diet, and polyunsaturated, or preferably monounsaturated fats, can replace saturated fats.� Red meats and dairy products are major sources of saturated fats.� Chicken and fish can substitute for red meats.� Use of a tub margarine instead of butter and replacing whole milk with skim milk also decrease saturated fat intake.� Mono- and polyunsaturated fats are abundant in plant foods and oils.� Margarines are manufactured by chemically modifying unsaturated oils to harden the liquid oils and to preserve shelf life. This chemical treatment, however, results in the formation of trans fatty acids which raise LDL cholesterol and lower HDL cholesterol.� Trans fatty acids are less abundant in soft tub margarines than in solid ones.�

A further reduction in LDL cholesterol can be achieved by limiting dietary cholesterol to less than 200 mg a day.� In addition to red meat and dairy products, eggs and crustaceans (crabs, shrimp, and lobster) are rich in cholesterol.� One egg, for example, contains about 225 mg of cholesterol.� Most people can not afford to purchase enough shrimp or lobster to raise their cholesterol levels.�� Table 11 shows the effects of dietary cholesterol and the different types of fat on LDL and HDL.

Table 11: Effects of Different Fats and Cholesterol on LDL and HDL

Type of fat

LDL

HDL

Saturated

Monounsaturated

-

Polyunsaturated

Trans

increase, decrease, - no change

 

Table 12: Lipid-lowering Drugs and Their Mechanism of Action

Statins

Inhibit cholesterol synthesis

Bile acid sequestrants

Inhibit bile acid absorption

Niacin

Inhibit VLDL synthesis

Fibrates

Speed conversion of VLDL to LDL

Ezetimibe*

Inhibits absorption of cholesterol

*Ezetimibe not yet approved by the FDA.

Medications are considered when a person does not follow the diet or the dietary measures do not lower cholesterol enough to reach the targets.

The HMG CoA reductase inhibitors, commonly referred to as statins, lower blood cholesterol levels by blocking the rate-limiting step in the synthesis of cholesterol in the liver.� Depending on the choice of drug and dose, statins can lower the total and LDL cholesterol by as much as 50%.� The most potent statin is atorvastatin (Lipitor), followed by simvastatin (Zocor), then pravastatin (Pravachol) and lovastatin (Mevacor), and finally fluvastatin (Lescol), which is the least potent, but also the least expensive of the statins. They are safe and well tolerated. Though liver damage is an uncommon side effect, tests of liver enzymes are required periodically. The most common side effect is muscle aches that are eliminated when the drug is stopped.� A rare, serious adverse effect is severe muscle inflammation (myositis) that can release into the blood muscle proteins that can seriously damage the kidneys.� Myositis, detected by a large increase in blood levels of creatine kinase (CK), requires immediate cessation of the medication.� Although it can occur with the use of statins alone, myositis is far more common when people are taking other drugs, such as the fibrates used to lower triglyceride levels.

The bile acid sequestrants, cholestyramine (Questran), colestripol (colestid), and colesevelam (WelChol), are members of another class of medications effective in lowering total and LDL cholesterol levels.� They work by binding bile acids in the intestine and removing them in the stools.� As a result, the liver converts more cholesterol to bile acids to replace those lost in the stools.� Large doses of the sequestrants can lower LDL cholesterol by about 25%.� They are quite safe since they act only in the intestine and never enter the blood stream, but compliance with the sequestrants is poor because they often cause bloating and constipation.�� Low doses of these drugs are now used mainly to supplement the effects of the statins.��

Large doses (500 mg to 3 gm) of the vitamin niacin can lower total and LDL cholesterol by about 25%.� Since niacin blocks the production of triglyceride-rich VLDL, it can also reduce triglyceride levels by approximately 25%.� Niacin is the most effective drug to raise HDL cholesterol levels.� A problem with niacin is its side effects which include liver damage, gout, abdominal pain and nausea.� Niacin should not be taken by people with liver disease, gout, or a history of peptic ulcers.� Because it can raise blood glucose levels in some individuals, niacin should be used with caution in people with diabetes.� The best available preparation of niacin is Niaspan which can be taken as a single dose at bedtime.� Regular niacin tablets should be taken with meals to lessen their gastrointestinal side effects.� Niacin can be purchased without a prescription in health food stores, but it is unwise to take it except under the supervision of a physician who can monitor for potentially dangerous adverse effects.

The most recently developed medication to lower cholesterol is ezetimebe which interferes with the absorption of cholesterol from the intestine.� The medication is presently being tested in combination with the statin simvastatin.� The combination lowers total and LDL cholesterol by about 10% more than simvastatin alone. It is anticipated that the combination product will soon be approved by the FDA.

Triglycerides

Normal triglyceride levels are less than 150 mg/dL.� Elevated triglycerides are not only a risk factor for coronary disease but also can lead to attacks of acute pancreatitis when levels are extremely high (> 1000 mg/dL).� High triglyceride levels are often associated with low levels of HDL cholesterol, and these levels may increase when triglycerides are lowered.�� Both dietary measures and medications are often needed to lower triglycerides.

Table 13: Dietary Measures to Lower Plasma Triglycerides

Same measures as to lower cholesterol. In addition,

WEIGHT REDUCTION

Limit alcohol intake

Replace simple sugars with complex carbohydrates

The dietary measures for elevated triglyceride levels include the same restrictions on saturated fats and cholesterol as for a cholesterol-lowering diet.� By far the most effective way to lower triglycerides, however, is by weight loss through� a combination of caloric restriction and increased physical activity.� Alcohol intake must be restricted because it can raise triglyceride levels considerably.� Simple sugars should be replaced as much as possible with starches and� high fiber foods.

Medications

Medications are used to lower triglycerides when the lifestyle measures described above fail to lower triglycerides to an acceptable level.

The most effective triglyceride-lowering drugs are the fibrates, gemfibrozil (Lopid) and fenofibrate (Tricor).� These medications are safe and well tolerated.� Occasionally they may produce some reversible liver damage, and they do increase the risk of severe myositis when taken in combination with a statin.� As already mentioned, niacin can lower triglycerides by about 25%; statins lower triglycerides by 10 to 25%, depending on the level of triglycerides and the choice of statins.� Their relative efficacy in lowering triglycerides is similar to their efficacy in lowering cholesterol levels.

The most recent guidelines recommend that a statin should be used first in an attempt to lower LDL levels when triglycerides are between 200 and 500 mg/dL.� If triglycerides remain above 200 mg/dL, one of the fibrates is added.� Because of the risk of pancreatitis, a fibrate is started whenever the triglycerides remain above 500 mg/dL despite dietary efforts.

HDL cholesterol

HDL cholesterol levels are largely under genetic control and it is difficult to raise them.� Lifestyle measures that may raise HDL cholesterol modestly include exercise, weight reduction, and smoking cessation.� Alcohol can increase HDL cholesterol considerably, but it is unwise for a teetotaler to start drinking in order to raise his HDL cholesterol.�

Niacin is the most effective medication; it can raise HDL cholesterol levels by as much as 25%.� The statins and fibrates both increase HDL cholesterol by an average of 8%.� Table 14 summarizes the effects of each of the lipid-lowering medications on LDL and HDL cholesterol

Table 14: Effects of Lipid-lowering Drugs on Serum Lipids and Lipoproteins

Drug

Cholesterol

Triglycerides

HDLCh

Sequstrants

+++

+

+

Niacin

++

++

++++

Statins

++++

++

++

Fibrates

+

++++

++

Hypertension

Lifestyle measures

Unless blood pressure is extremely high, treatment is usually started with lifestyle changes to determine if they achieve adequate control during a period of six months or so. The most effective lifestyle measures to lower blood pressure are weight loss, increased physical activity, and salt (sodium) restriction.� Increased exercise not only helps with weight reduction but also lowers blood pressure through an independent effect.� Though probably unnecessary in people with a normal blood pressure, salt restriction can lower blood pressure significantly in men with hypertension and may prevent the development of hypertension in men whose pressure is in the high normal range.� Salt restriction requires more than limiting salt use at the table and in cooking because so many prepared and canned foods are high in salt.

Other measures to lower blood pressure include moderation in alcohol intake, increased dietary intake of potassium, and possibly reduced caffeine consumption.� Men need to be aware that some dietary supplements for weight loss contain ephedra, which can raise blood pressure.

Medications

Table 15:Classes of Blood Pressure-lowering Medications

Diuretics

Beta-blockers

ACE inhibitors

Angiotensin II receptor blockers

Calcium channel blockers

Alpha-blockers

Central alpha antagonists

Peripheral-acting adrenergic antagonists

Direct vasodilators

Medications, along with lifestyle measures, are started immediately in men with extremely high blood pressures, and they are added when lifestyle measures fail to lower blood pressure adequately after an appropriate trial.� As indicated in Table 15, a large number of different types of medications are available for the treatment of� hypertension.� Most commonly used, however, are diuretics, beta-blockers, ACE inhibitors, angiotensin II receptor blockers, and calcium channel blockers.� In addition, a large number of individual drugs are marketed within each of these drug classes.� Drug treatment for mild to moderate hypertension is usually started with a low dose of one of these medications.� The dose is gradually raised when blood pressure control is inadequate.� If a man does not respond to a full dose of that agent, he is switched to another drug in the same class or to a drug from a different class, or a second or third different type of drug may be needed when blood pressure responds poorly.

There are several advantages to the availability of a variety of drugs to treat hypertension.� Although each of these classes of drugs is about equally effective in lowering blood pressure, some are more suitable in particular situations.� For example, diuretics (often referred to as water pills) work by increasing salt and water excretion in the urine and therefore are particularly useful in men with edema (swelling of the legs due to fluid retention).� The ACE inhibitors have proven especially effective in slowing the progression of kidney disease in diabetics.� Angiotensin II receptor blockers are often substituted for ACE inhibitors when they cause a persistent dry cough.� And recent trials have shown that these receptor blockers are as effective as the ACE inhibitors themselves in slowing the progression of kidney disease.�� In addition to their blood pressure lowering effects, beta-blockers and calcium channel blockers can improve angina; beta-blockers reduce the likelihood of a second heart attack; and ACE inhibitors have been shown to prevent type 2 diabetes and to reduce mortality in men who have congestive heart failure or have suffered a heart attack.

Another advantage of the large number of medications is the opportunity to combine drugs from two or even three different drug classes to treat the many hypertensive men whose blood pressure can not be controlled with one agent. Finally, each class of drugs has a different set of side effects, so that it is usually possible to overcome such adverse effects by switching from one class of drugs to another.

Metabolic syndrome and diabetes

Weight loss, through diet and exercise, have long been thought to overcome the insulin resistance of the metabolic syndrome and to prevent or delay the development of diabetes.� A recent study conclusively proved for the first time that weight loss does prevent diabetes in high risk men.� Such preventive measures are especially important in men with a family history of type 2 diabetes.

While it is obviously extremely important for men with diabetes to control their blood glucose levels with diet, oral medications or insulin, studies have failed to show that diabetic control alone is effective in lowering the risk of CHD.� Rather, trials have shown that lowering blood pressure substantially reduces the incidence of coronary events in diabetic men.� For that reason the blood pressure goal for men with diabetes is less than 130/85.� A number of long-term statin trials have conclusively shown that lowering total and LDL cholesterol is at least as effective, and possibly more effective, in preventing coronary events in diabetic men as in non-diabetic men.� Statin treatment is often needed to achieve the recommended LDL cholesterol goal of less than 100 mg/dL for men with diabetes.� Elevated triglycerides and low HDL cholesterol, the most common lipid and lipoprotein abnormalities in diabetic men, often requires treatment with one of the fibrates.

Prevention of blood clots

Regular use of low doses of� aspirin is the most effective way to prevent the blood clots that lead to a heart attack or stroke.�� Because this benefit of aspirin can be counterbalanced by its potential serious side effects of bleeding in the gastrointestinal tract or into the brain, men should not start regular aspirin use without input from their doctor.� Efforts have been made to determine when these risks are outweighed by the cardioprotective effects of aspirin.� All men with known CHD should take aspirin unless they are allergic to it or have had troublesome side effects. The U.S. Preventive Service Task Force has concluded that the heart benefits of aspirin outweigh its risks when a man who is 40 years of age or older has a 3% or greater chance of developing a heart attack over the next 5 years.� Healthy middle-aged men with no risk factors for coronary disease should not take aspirin.� Men with several risk factors for coronary heart disease would probably benefit from daily aspirin and should discuss this with their doctor.� The American Diabetes Association has recommended that all diabetic men over the age of 30 should take aspirin.

The most effective and safest dose of aspirin is not entirely clear.� Generally recommended is a daily baby aspirin or a regular aspirin (325 mg) every other day.

Antioxidants

Antioxidants, primarily beta-carotene, vitamin E and vitamin C, have been frequently� prescribed by physicians and widely promoted by others as a way to prevent CHD by blocking the oxidation of LDL.� As of now, there is no evidence to support the use of antioxidants for this purpose.� In three studi


 
 
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