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Cardiovascular Disease

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					Cardiovascular Disease

   D. Bellis McCafferty
        NFSC 370
Cardiovascular Disease – general term
 that means diseases of the heart and
 blood vessels
  – Coronary Heart Disease (CHD) – AKA
    Coronary Artery Disease and Ischemic
    Heart Disease – lack of blood flow to the
    network of blood vessels surrounding (and
    serving) the heart. The major cause is
    atherosclerosis.
  – Ischemia – insufficient blood flow in a
    tissue due to functional constriction or
    actual obstruction of a blood vessel.
– Atherosclerosis – thickening and hardening of
  the walls of the blood vessels caused by
  deposits of fatty material. Arteries most often
  affected are the abdominal aorta, coronary and
  carotid arteries.
– Myocardial Infarction (MI) – Ischemia in the
  coronary arteries resulting in necrosis, tissue
  damage and sometimes sudden death.
– Cerebrovascular Accident (CVA) – event in
  which the blood flow to a part of the brain is
  cut off.
– Transient Ischemic attack (TIA) – temporary
  reduction in cerebral blood flow that causes
  temporary symptoms that mimic those of a
  CVA.
Atherosclerosis
Pathogenesis: “Response to Injury” theory
1. Formation of fatty streaks along arterial
  walls
2. Proliferation of smooth muscle cells,
  WBC and calcium  plaques.
  – Plaques cause the arteries to lose elasticity
  – Narrowing of arterial lumen
  – (Most people have well-developed plaques
    by age 30)
Consequences
1. Loss of elasticity  injury to arterial wall
2. Platelet aggregation and blood clotting
  (response to injury)
  – Thrombosis: blood clot obstructs blood flow,
    causing tissue death
  – Embolism: clot breaks off and travels to
    smaller vessel and obstructs blood flow,
    causing tissue death.
  – Angina: pain, pressure, and tightness in
    chest, back, neck, and arms, caused by lack
    of O2 to heart muscle


3. Hypertension (more pressure required
  to deliver blood to tissues if arteries are
  narrowed)
  – Further damage to blood vessels  more
    clots, etc.
Dietary Treatment of High Blood
      Cholesterol in Adults
NCEP’s updated clinical guidelines for cholesterol
 testing and management: ATP III
 (Adult Treatment Panel III)

http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3
   xsum.pdf

“These guidelines are intended to inform, not
  replace, the physician’s clinical judgment, which
  must ultimately determine the appropriate
  treatment for each individual.”
   Focus: Lowering LDL cholesterol (major cause
  of CHD, and LDL-lowering therapy reduces risk
  for CHD)

Major new feature: focus on primary prevention in
 persons with multiple risk factors.

   New recommendation: All adults aged 20 yrs or
  older should obtain a fasting LP profile every 5
  years (TC, HDL, LDL, TG).
                    Blood Lipid Levels
• Total cholesterol (adults)
   – desirable               < 200 mg/dl
   – borderline high         200-239 mg/dl
   – high risk               240 mg/dl

• LDL cholesterol
   – optimal                <100 mg/dl       (goal if CVD, DM or
                                               multiple RF’s*)
   – Above optimal          100-129 mg/dl
   – borderline high        130-159 mg/dl (<130 goal if 2+ RF’s**)
   – high risk              >160 mg/dl    (<160 goal if 0-1 RF)

• HDL cholesterol           40 mg/dl     (60: neg. risk factor)
• Triglycerides (TG)         150 mg/dl   (requires tx beyond LDL
                                          lowering if >200)
To convert mmol/l of HDL or LDL cholesterol to mg/dl,
  multiply by 39.
To convert mg/dl of HDL or LDL cholesterol to mmol/l,
  divide by 39.
To convert mmol/l of triglycerides to mg/dl, multiply by
  89.
To convert mg/dl of triglycerides to mmol/l, divide by 89.
Risk Factors
RF’s that modify LDL Goals: blue
• Category I risk factors:
  – Intervention has been proven to decrease CVD
    risk
• Category II risk factors:
  – Intervention is likely to decrease CVD risk
• Category III risk factors:
  – Intervention may decrease risk
• Category IV risk factors:
  – Intervention does not decrease risk
Category I Risk Factors
1. Cigarette smoking
   – Doubles CVD risk
   – Synergistic w/other risk factors
   –  HDL, VLDL and BG levels
2. LDL Cholesterol
   –  sat’d fat intake
   –  cholesterol intake in some people
   –  trans FA intake
   – obesity
3. Hypertension
  –  Risk for stroke, CHD, and CHF
  – 140/90 mm Hg
  – Risk : AA, age, obesity
Category II Risk Factors
1. Diabetes
  – LDL chol goal for people w/DM is 100 mg/dl
2. Physical Inactivity
  – Sedentary people (60% of US) have double the
    risk of developing CVD as active people.
  – Modifies other risk factors
3. HDL cholesterol <40 mg/dl
  – Greater effect than LDL?
  – Reverse cholesterol transport
  – Increased with: EXERCISE, estrogen
    replacement, loss of body fat, moderate
    consumption of alcohol
4. Obesity
  – BMI ranges
  – Affects glu tolerance, blood lipids, BP, etc.
  – Body fat distribution
Category III Risk Factors
1. Psychosocial Factors
  – Correlated w/risk, but intervention is not
    strongly correlated with decreased risk.
  – Type “A” personality, stress, depression
  – Low education level
2. Triglycerides
  – Inversely correlated w/HDL
  – Increased with: high CHO, low fat, vegetarian
    diet, obesity, uncontrolled DM, excessive EtOH
    (and factors that decrease HDLs)
3. Lp(a): Early studies indicated strong correlation
  w/CHD risk
  – Conflicting evidence
4. Homocysteine
  – Strong + correlation w/premature ds.
  – with inadequate folate, B6 and B12
  – Also smoking, inactivity, coffee (>1c/day)
5. Oxidative stress*
  – LDL damage
  – Inhibited* by vits C, E, b-carotene, mufa’s
  –  w/Iron, copper, zinc, and sat’d fat
  *no conclusive evidence (randomized trials) that
    supplemental antioxidants reduce disease risk - food
    vs. supplements
6. Alcohol consumption - moderate

Category IV Risk Factors
1. Age
   Male gender and over 45 y/o
   Female gender and over 55 y/o
2. Family history
   MI <age 55 in a male first degree relative
   MI <age 65 in a female first degree relative
    (familial dyslipidemias)
  Therapeutic Lifestyle Changes (TLC)

• Reduced intakes of saturated fats (<7% of total
  calories) and
• Cholesterol (<200 mg per day)
• Therapeutic options for enhancing LDL lowering
  such as plant stanols/sterols (2 g/day) and
  increased viscous (soluble) fiber (10-25 g/day)
• Weight reduction
• Increased physical activity
    Nutrient Composition of the TLC Diet

Nutrient              Recommended Intake
Saturated fat*        Less than 7% of total calories
Polyunsaturated fat   Up to 10% of total calories
Monounsaturated fat Up to 20% of total calories
Total fat             25-35% of total calories
Carbohydrate†         50-60% of total calories
Fiber                 20-30 g/day
Protein               Approximately 15% of total calories
Cholesterol           Less than 200 mg/day
Total calories        Balance energy intake and expenditure
(energy)‡             to maintain desirable body
                      weight/prevent weight gain
Drugs Affecting Lipoprotein Metabolism
• HMG CoA reductase inhibitors (statins)
   – HDL (5-15%)  LDL (18-55%)  TG (7-30%)
   – Lovastatin, atorvastatin (Lipitor), simvstatin, etc.
• Bile acid sequestrants
   –  hepatic synthesis of cholesterol
   – HDL (3-5%)  LDL (15-30%)
   – Cholestyrmaine
• Nicotinic acid
   –  hepatic VLDL synthesis and thus LDL formation
   –  LDL (5-25%)  TG (20-50%)
• Fibric Acids
   – Several mechanisms of action
   – HDL (10-20%)  LDL (5-20%)  TG (20-50%)
   – Gemfibrozil
                Metabolic Syndrome
• Cluster of risk factors that enhance risk for CHD at any
  given LDL cholesterol level.
• Diagnosis: 3 or more of the following risk determinants:
    Risk Factor          Defining Level
    Abdominal Obesity*   Waist Circumference†
           Men                  >102 cm (>40 in)
           Women                >88 cm (>35 in)
    Triglycerides        ³150 mg/dL
    HDL cholesterol
           Men                  <40 mg/dL
           Women                <50 mg/dL
    Blood pressure       ³130/³85 mmHg
    Fasting glucose      ³110 mg/dL
• Treatment of Metabolic Syndrome:
  – Treat/reduce underlying causes
  – TLC Diet: a higher intake of total fat
    (mostly unsaturated) can help  TG and
    HDL cholesterol in persons
    w/Metabolic Syndrome
  – Weight control
  – Physical activity
  – Plant stanols/sterols
  – Viscous (soluble) fiber
Other Strategies
•  folate, B6, B12 ( Homocysteine)
•  w-3 FAs ( TG and VLDL,  platelet
  aggregation/clotting,  BP)
•  soluble fiber intake
•  intake of soy products
   – approved health claim, must have over 6 gram
     per serving to make claim
   – 25 g/day will lower LDL-cholesterol levels by
     about 5-12%
• Plant Sterols/Stanols
  – Naturally present in vegetable oils, nuts,
    cereals, beans
  – “Benecol” margarine produced by Finnish
    company/”Take Control”
  – Sterols/stanols interfere with dietary and biliary
    cholesterol absorption
     •  TC,  LDL
  – May complement statin therapy
• Alcohol
• CABG: Coronary Artery Bypass Graft: vein from
  leg or artery from chest is used to alter blood flow
  around a diseased vessel. New vessels are still
  subject to atherosclerosis.

• Carotid endarterectomy: surgical removal of
  plaque in carotid artery to prevent stroke.

• Coronary Angioplasty: balloon catheter is
  inserted through an artery in the groin and is
  guided into the narrowed coronary artery. The
  balloon is inflated and compresses plaque back
  onto the arterial wall to allow better blood flow.
  Restenosis of artery is common.
• Holistic treatment:
  – Dean Ornish’s program shown to reverse
    atherosclerotic plaque. Radical: includes
    extremely lowfat/low chol. diet (10-15%
    fat, 5mg cholesterol, vegetarian) in
    conjunction with conventional treatment,
    exercise, stress management, smoking
    cessation. His studies showed pts had less
    plaque after 1 year (via angiogram) and
    had lower BP and lipid levels.
     Congestive Heart Failure
• Congestive Heart Failure (CHF)
  – heart loses ability to provide adequate blood flow
    to the rest of the body
  – tries to compensate by increasing in size,
    increasing force of contraction, increasing HR
  – reduced blood flow to kidneys stimulates kidneys
    to conserve Na and H2O
  – As heart fails, blood begins to pool in the
    pulmonary veins and capillaries  pulmonary
    edema (ergo “congestion”)
• Cardiac Cachexia: Chronic PEM
  2heart disease
  –  nutrient needs 2   work of heart and
    lungs
  – Poor delivery of nutrients/oxygen to
    tissues
  – Repeated respiratory infections
  – Anorexia, nausea, altered taste, physical
    exhaustion
  – Edema may mask weight loss until severe
  – PEM  weakening of heart/lungs; 
    infections
• Nutrition Therapy: Don’t overfeed!
  – Increases cardiac workload
  – Safe rate of weight loss if indicated (not if
    PEM, of course)
  – Sodium restriction proportionate to fluid
    retention
  – Fiber: avoid constipation; straining
    increases cardiac work
              Hypertension
       New Blood Pressure Cutoffs (2003)



Normal: <120/<80 mm Hg

Prehypertension: 120-139/80-89 mm Hg

Stage 1 hypertension: 140-159/90-99 mm Hg

Stage 2 hypertension: >160/>100 mm Hg
• Essential or Primary Hypertension:
  – No identifiable cause
• Secondary Hypertension:
  – Due to underlying disease such as kidney
    disease
• White-coat Hypertension:
  – Caused by anxiety in a hospital setting.
    Spanish study reports as many as 2 in 5
    diagnoses!
               Consequences
•   CHF
•   Kidney disease
•   Peripheral vascular disease
•   Stroke
•   Impaired vision/blindness
    Risk Factors for Hypertension
           Uncontrollable
1. Age

2. Heredity
   African Americans: 4x death rate vs.
   whites
3. Family history
             Risk Factors
        Controllable/Modifiable
1. Overweight/Obesity
2. Smoking
3. Excessive EtOH
4. Sodium intake
   2400mg = 6g (1tsp) table salt
5. Other minerals:
   Adequate K+ does lower blood pressure.
   Inadequate data that Ca and Mg supplementsI
   prevent HTN.
   K+: fruits, vegetables, dairy foods, and fish.
       Prevention/Treatment of
            Hypertension
1. Follow a healthy eating pattern
  DASH diet
  Dietary
  Approaches to
  Stop
  Hypertension
• DASH: Dietary Approaches to Stop Hypertension
   – Diet high in fruits, vegetables, and nonfat dairy
   – Low in fat, saturated fat, and cholesterol
• Sodium
• Potassium
• (Calcium and Magnesium)
• Alcohol
• Exercise
• Obesity/Weight Management
               1st DASH study
• 133 subjects with mild hypertension
• 326 subjects with normal blood pressure
• 8 week study
  1) control diet: average levels of fat/cholesterol; below
  average levels of K, Ca, Mg
  2) fruit and vegetable diet: same as control diet but
  had 8-10 servings of fruit/veges (hi in K, Mg and fiber)
  3) combination diet: Cut fat and cholesterol, high
  fruit/vege, high in low-fat dairy (Ca-rich)
                Results
• Lowest blood pressure on DASH diet
      2nd DASH sodium Trial
• 412 subjects (120-159/80-95)
• 2 weeks of typical American high-Na diet
  then 30 day intervention
• Then typical diet or DASH diet with
  1) 3300 mg Na
  2) 2400 mg Na
  3) 1500 mg Na
               Findings
• Lower sodium correlated with lower blood
  pressure
• Best results: DASH diet with 1500 mg Na+
2. Exercise
• Several studies show exercise lowers blood
  pressure (by about 10 mmHg)
• How?
How? Not clear but may
-  peripheral resistance
-  serum catecholamine ( SNS
  response)
-  renin activity (renin activates
 angiotensin/aldosterone -  Na
 retention)
-  central fat (?)/  insulin levels
      Guidelines for Exercise
Stage 1 Hypertension:
• 50-85% of VO2 max for 20-60 minutes
  3-5 days per week
Stage 2 Hypertension:
• 40-70% of VO2 max for 20-60 minutes
  3-5 days per week
Resistance Exercise:
• Mild to moderate is OK (30-60% of
  maximal effort)
Drugs
• Diuretics
• beta-blockers
  – (atenolol, metoprolol, propranolol) act as
    competitive antagonists at the adrenergic beta
    receptors