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Nutritional Treatment of Cardiovascular Disease

 

Rationale for the Nutritional Treatment of Cardiovascular Disease

In a nutshell, the epidemiology supports the use of nutrition in treating this rather rampant series of diseases. Over 50 million Americans have Hypertension, 12.4 million have Coronary Heart Disease, and 4.5 million have had a stroke. Cardiovascular Disease is the number one killer in the US (a little less than a million deaths per year). Studies have shown dietary management to be a cornerstone in the management of these diseases.

 

Some Risk factors for Coronary Artery Disease

  • Hypertension, diabetes, hyperlipidemia, family history, cigarette smoking (promotes Cardiovascular Disease and kidney disease), obesity, metabolic syndrome, sedentary life style, high fat diet, diabetes, etc. (more listed on the slide).
  • Nutrition can modify the first three (bolded) as well as help obesity, etc.
  • It is important to note that each risk factor you have adds an additional level of risk to one’s overall Coronary Heart Disease risk. This is illustrated in the data from the Framingham study- which shows that every risk factor added increased the Coronary Heart Disease risk for all cholesterol levels (used as a baseline). This relation is easy to see… the lines showing risk just keep going up and up as you pile on the factors…

 

Dietary Fat

From here the discussion shifted to talk about various aspects of diet. We begin with fats. There are two types of dietary fat: saturated and unsaturated. 

Saturated fats are fatty acids with no double bonds. It is well established that they adversely affect serum cholesterol level. For every 1% increase in calories from saturated fats, serum LDL increases by 2%. LDL, as we all know, is the BAD cholesterol. And considering that the typical American diet contains 11% total calories from saturated fats, we would do well to limit such input. Overall point? Tell your patients to reduce saturated fat intake– it will lower their LDL. 

So now on to unsaturated fats… These guys contain double bonds, and when substituted into the diet reduce cholesterol levels. They are typically found in fish and plant foods.

  • Monounsaturated fats (one type of unsaturated fat) are found in the widely acclaimed Mediterranean diet. This diet has been associated with a lower incidence of Coronary Heart Disease because it may lower LDL while preserving HDL and triglyceride levels. A representative Coronary Artery DiseaseA is oleic acid, and Coronary Artery DiseaseA sources include olive oil, canola oil, nuts, and avocado.
  • Polyunsaturated fatty acids (the other type) consist of two major categories:
    • Omega 6 Fatty acids include linoleic acid, which is found in vegetable oils such as corn, sunflower and safflower oil.
    • Omega 3 Fatty acids are found in canola and flax seed oils as well as fish oils. The ones in fish oil (EPA and DHA) are apparently effective in lowering triglycerides when administered at high dosages. The American Heart Association recommends consumption of fish at least twice a week. (going to Red Lobster does not count!)

 Trans-fatty acids– these are the crazy hybrids of the fat world. When an unsaturated fatty acid is hydrogenated (has hydrogen atoms added to it), the double bond can shift from a cis configuration to a trans configuration. The effect? It tastes better and lasts longer, but raises our total cholesterol and LDL levels. Urge your patients to look out for and avoid this double agent.
 

 

Phytosterols and Stanols

These chemicals are naturally occurring plant sterols that have been shown to reduce serum cholesterol. They are found in tress, soybeans, corn, squash, vegetable oils and grains. Over 20 published studies have supported these and stanol ester (modified sterols) effects. Cholesterol absorption is nearly halved, total cholesterol is reduced 10% and LDL is reduced by up to 14%. Not bad at all. 

As an aside, check out the AHA dietary guidelines as well as the Mediterranean diet.

 

Homocystinemia

This condition involves high levels of homocysteine. It is considered a risk factor for heart disease and should be look at in lab studies (fasting Hcy level). A 10% increase in plasma Hcy results in a 10% increase in Coronary Heart Disease risk. Pretty crazy.

If you notice an increased fasting Hcy, check for a folate deficiency. Folate is involved in the conversion of homocysteine to methionine, and intake of folate, B6 and B12 can lower homocysteine levels. This is especially important in dialysis patients because folate is removed during dialysis.

 

Vitamin and antioxidant supplementation

Folic acid may improve endothelial dysfunction independent of homocysteine levels.

Although controversial, daily vitamin E administration (400IU) may reduce LDL oxidation, and thus protect the heart from recurrent MI. Other antioxidants, such as vitamin C, beta-carotene, Coenzyme Q10 and selenium have been show to offer cardioprotection in some studies.

Dr. Reddi recommends the vitamin Reenax to his dialysis pts because it contains all the above listed vitamins and elements.    

The NCEP ATP III study recommends this complex looking diet (see slide) for patients with Coronary Heart Disease. The most important aspect is that saturated fats should be <7% of total calorie intake, unsaturated fats should be around 30%, and cholesterol should be <200 mg/day. Balance energy intake and expenditure to maintain a steady weight. For clinicians, the study suggests that we ought to try lifestyle modifications for hyperlipidemia management first. After assessing patient compliance and efficacy of the modifications, pharmacological intervention can be added into the regimen. Ideally, we would like to keep LDL as low as possible (<100 mg/dL, or even 60!) to reduce Coronary Heart Disease risk. Although this is out of place here—alcohol (moderate, ~2 drinks/day) can increase HDL—which is a good thing. 

So now a shift to the treatment of CHF (Coronary Heart Failure).

 
Medical nutrition therapy for Congestive Heart Failure

In general, dietary modification of CHF treatment involves limiting dietary Na (<100 meq/L) as well as limiting fluid intake, calorie intake, and maintaining a positive nitrogen balance (appropriate amount of protein intake).

Sodium intake is restricted because the proximal tubule reabsorbs 50-60% of filtered Na, and along with it a whole lot of water. Since CHF pts already have pulmonary congestion, you don’t want to increase the intravascular volume any more than it already is. By the same token, restricting fluid intake to urine output + 500mL (covers insensitive loss) keeps the intravascular volume constant…and telling the patient to drink less would result in fluid loss.
 

Hypertension

New classifications: preHypertension (120-139/80-89), Stage 1 Hypertension (140-159/90-99), Stage 2 (greater than that…) 
 

Lifestyle Modifications for prevention and management of Hypertension

1. Weight reduction, if overweight

2. Aerobic exercise, if indicated

3. Diet - avoid excess calories

4. Restrict Na+ intake (70-90 mEq/day), and increase K+ intake, if possible

(Sodium and BP are definitely related; studies show that increased Na will increase BP)

5. Complex carbohydrates (50-60% of total calories)

6. Increase dietary fiber content, if possible (note: too much fiber can cause gas. It might be a good idea to advise your patients.)

7. Restrict saturated fat to <10 g/day and cholesterol to <300 mg/day

8. Maintain adequate intake of Ca2+ and Mg2+ to continue general health

9. Limit alcohol use to 2 oz 100-proof whiskey, 24 oz beer or 10 oz wine

10. Stop or avoid excess smoking

 

Urinalysis can help to determine whether patients are following your dietary recommendations.

 It would behoove us to remember the DASH diet in some fashion (see picture attached at end of notes). 

Studies have shown that even modified versions of this diet (DASH) can reduce systolic and diastolic BP, especially one focusing on fruits and vegetables (as shown in the slide). Another study also showed that if the DASH diet was combined with a low sodium diet, the overall effect on BP was equivalent to pharmacological treatment! And the great thing is that unlike some drugs, DASH works on everyone, including African Americans (they’re at a higher risk for end organ damage).  

At this point, I’d like to address the two cases that Dr. Reddi spoke about in class. I’ve reproduced both of them in their entirety here:


Case 1

A 64 y/o nonobese Indian male was referred for control of Hypertension. PMH includes type 2 diabetes, recent stroke, CRF, proteinuria and benign prostatic hypertrophy. BP 160/70 with pulse rate of 64.

Labs:

Na=136; K=4.4; Cl=100; HC03=23; BUN=27; creatnine 2.2. Chol=463;

TG=556; HDL=43;  LDL=200; HgA1c=13.1(n=<6.5%).24-h urine protein= 8.1g

 

Based on the history and lab data, identify the risk factors for coronary  heart disease?

A= Hypertension; B=type 2 diabetes with possible insulin resistance; C=hyperlipidemia; D=renal insufficiency; E=proteinuria (metabolic syndrome)

 

How does the pt benefit from nutritional therapy?

According to the nutritional analysis, this pt’s fat intake was 36% of his total caloric intake. He needs reduction of his fat intake. Also, he needs glucose and Hypertension control, which will improve hyperlipidemia. Lowering proteinuria by low protein diet with addition of essential amino acids and ketoanalogues may improve not only proteinuria but also hyperlipidemia. In addition to nutritional therapy, he needs pharmacologic therapy.  Addition of losartan (an ARB to control BP), Avandia (a glitazone to lower glucose) and Lipitor (a statin to reduce lipids) improved all of his metabolic abnormalities.

 

Case 2

 This 52 y/o African American female was referred for further management of Hypertension. Her BP was 170/90 mm Hg. She was on enalapril 60 mg/day. Phys exam was normal. Her serum chemistry and lipid levels were normal.

 1.       How would you manage her Hypertension?

 Since the pt is on a good dose of ACE-I, (enalapril), the failure to respond may partially be related to high Na intake. A low dose diuretic was added. A 24-h urinary Na excretion prior to the addition of diuretic showed 160 mEq. A diet in low Na intake (<100 mEq/day) was recommended by the dietician. Her BP improved to

150/85 mm Hg. The pt subsequently followed even lower Na intake on her own with the result of further improvement in BP. Eventually she was off all medications for at least 5 years.


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