dr. Luh Eka Purwani, M.

Kes, SpGK
Cardiovascular disease
Cardiovascular disease (CVD) is a group of interrelated
diseases that include :
coronary heart disease (CHD),
atherosclerosis,
hypertension,
ischemic heart disease,
Peripheral vascular disease,
heart failure (HF)
Cardiovascular Disease Risk Factors
Cardiovascular Disease Risk Factors
Dyslipidemia
Dyslipidemia is a condition in whichLDL levels are elevated
and high-density lipoprotein (HDL) levels are low.
A variety of other dyslipidemic conditions can also exist,such
as the combination of normal LDL and high triglyceride
levels.

Etiology :
primary hyperlipoproteinemia
Secondary hyperlipoproteinemia
(Obesitas, diabetes, hipotiroid, ESRD, liver disease,
cushings syndrome)
Lipoprotein
Because lipid is not water soluble, it is carried in the
blood bound to protein.

These complex particles, called lipoproteins, vary in

composition, size, and density.

Lipoproteins measured in clinical practice-

chylomicrons, verylow-density lipoprotein (VLDL) ,
low-density lipoproteins (LDL), and high-density
lipoproteins (HDL)-consist of varying amounts of
triglyceride, cholesterol, phospholipid, and protein
Chylomicrons
Chylomicrons, transport dietary fat and cholesterol from
the small intestine to the liver and periphery.
Once in the bloodstream, the triglycerides within the
chylomicrons are hydrolyzed by lipoprotein lipase (LPL),
located on the endothelial cell surface in muscle and
adipose tissue
When approximately 90% of the triglyceride is hydrolyzed,
the particle is released back into the blood as a remnant.
The liver metabolizes these chylomicron remnants, but
some deliver cholesterol to the arterial wall and thus are
considered atherogenic.
Consumption of high-fat meals produces more
chylomicrons and remnants.
VLDL
Synthesized in the liver to transport endogenous
triglyceride and cholesterol.
Triglyceride accounts for 60% of the VLDL particle.
The large, buoyant VLDL particle nonatherogenic.
Smaller VLDL particles (i.e., remnants) are formed
from triglyceride hydrolysis by LPL.
Normally these remnants, called intermediate-density
lipoproteins (IDLs), are atherogenic
IDL and are taken up by receptors on the liver or
converted to LDLs.
LDL
Some of the smaller LDL in blood are oxidized, and are
then taken into the arterial wall
LDL is the primary cholesterol carrier in blood, formed by
the breakdown of VLDL.
After LDL formation, 60% is taken up by LDL receptors on
the liver, adrenals, and other tissues.
The remainder is metabolized via nonreceptor pathways.
Both the number and activity of these LDL receptors are
major determinants of LDL cholesterol levels in the blood.
High LDL cholesterol is specifically associated with
atherosclerosis.
HDL
HDL particles contain more protein than any of the
other lipoproteins, which accounts for their metabolic
role as a reservoir of the apolipoproteins that direct
lipid metabolism.

Apo A-I, the main apolipoprotein in HDL, is an

antiinflammatory, antioxidant protein that also helps
to remove cholesterol from the arterial wall to the liver
Lipoprotein
The triglyceride-rich lipoproteins include
chylomicrons, VLDLs, and any remnants or
intermediary products formed in metabolism.

Of these triglyceride-rich lipoproteins, chylomicrons

and VLDL remnants, and LDL are known to be
atherogenic because they activate platelets, the
coagulation cascade, and clot formation
Dyslipidemia
The following values have been classified as abnormal
and are associated with increased CHD risk:
1. Total cholesterol higher than 240 mg/dL
2. Triglycerides higher than 150 mg/dL
3. NonHDL-C (total cholesterol HDL-C) higher than
190 mg/dL
4. LDL-C higher than 160 mg/dL
5. HDL-C lower than 40 mg/dL in men and lower than
50 mg/dL in women
Lipid transport
Reverse cholesterol transport
Diagnosis
Management
Non Pharmacology
Nutrition management
Weight loss and exercise

Pharmacology
Statin
Bile acid sequestrant
Fibric acid derivate
Management
Nutrition management
Nutrition management
Hypertension
Hypertension refers to a chronic elevation in BP.
There are two types of hypertension.
Primary or essential hypertension is idiopathic, which
means there is no known cause, 90%of all cases.
Secondary hypertension occurs as a result of another
primary problem, such as renal disease,other
cardiovascular disease,endocrine disorders, or
neurogenic disorders
Hypertension
Though its cause is unknown, primary hypertension
may be a result of a variety of factors.
Lifestyle factors such as diet (including excessive
sodium intake, low potassium intake, excessive alcohol
intake),
lack of exercise, smoking, stress
Resistance is dependent upon the radius of all
arterioles, length of the vessel, and the blood viscosity.
Regulation of blood pressure
Patophysiology of hypertension
Assesment
Anamnesis :
Diagnoses/date of diagnosis Comorbidities
Medications
Previous medical conditions or surgeries
Socioeconomic status/food security
Support systems
Education levelprimary language
Assesment
Nutrition history :
Meals/snackspatterns, frequency
Portion sizes
Saturated andtransfat from dairy products and fatty meats
commercial snack foods and pastries, fried foods, and
added fats and oils
Refined carbohydrates from baked products,
desserts,cookies,and other sweets
Sweetened beverages (juice drinks, soda) and alcohol
Major sources of sodium from processed foods, eatingout,
and added salt
Frequency of restaurant meals, fast food, take-out food
Assesment
Physical examination :
Blood pressure
Antropometric Measurement :
Height/length
Current weight
Weight history if adult: highest adult weight; usual
bodyweight
Bodymass index
Waist circumference
Assesment
Laboratorium Examination :
Erythrocyte
Glucose,BUN, Cr
Electrolytes
Triglyceride, total cholesterol, HDL, LDL
Albumin
Prealbumin
Diagnosis
Management
Medical management
Diuretics
ACE Inhibitors
Beta-1-Blocker
Alpha Adrenergic Blockers
Calcium Channel Blockers
Aldosterone Antagonists
Angiotensin II Receptor Blockers
Nitrate
Digitalis
Nutrition Management
DASH diet
FOOD GROUP DAILY SIGNIFICANCE
SERVINGS
grains and grain product 7-8 Major sources energy and fiber
vegetables 4-5 Rich sources potassium, Mg,
and fiber
fruits 4-5 Rich sources potassium, Mg,
and fiber

low fat or fat free dairy 2-3 Ca, protein

food
meats, poultry, fish 2 OR LESS Protein, Mg
nuts, seeds and dry 4-5/WK Energy, prot, Mg, K, fiber
beans
fats and oil 2-3 Lows fat
sweets 5/WK Low fat
Tips reducing sodium intake
Avoid fast-food restaurants, because these food choices are
prepared with large amounts of salt.
Ask how foods are prepared. Request that they be
prepared without added salt, monosodium glutamate
(MSG), or salt containingingredients.
Know the terms that indicate high sodium content:
pickled, soysauce
Do not use any added salt in food preparation or at the
table.
Limit condiments, such as mustard, pickles, and sauces
with salt-containing ingredients.
Choose fruits or vegetables instead of salty snack foods.
ATHEROSCLEROSIS AND
CORONARY HEART DISEASE
Atherogenesis is the process leading to development of
atherosclerosis.
It is a chronic, local, inflammatory response to risk
factors, such as high levels of low-density lipoprotein
(LDL) cholesterol, that are injurious to the arterial wall
Pathophysiology
Pathophysiology
Pathophysiology
Pathophysiology
Proposed Events in the Process of
Atherogenesis
Native low-density lipoprotein (LDL) penetrates the arterial intima.
In the intima the polyunsaturated fatty acid esterified to the cholester in LDL is
oxidized.
Oxidized LDL attracts macrophages.
The macrophages become lipid-engorged foam cells.
The oxidized LDL is cytotoxic to the endothelial cell creating an injury that
attracts platelets.
Platelets release platelet-derived growth factor that stimulates the proliferation
of the smooth muscles cells of the intima.
The smooth muscle cells take up oxidized LDL by endocytosis and become
foam cells.
The macrophages, activated by the phagocytosis of oxidized LDL, release
macrophage chemotaxins, which attracts additional macrophages, which
perpetuate the process.
Eventually, the proliferation of foam cells and smooth muscle cells form a
plaque, which enlarges enough to narrow the lumen of the artery, restricting
blood flow.
Pathophysiology
Clinical manifestation
Clinical Finding
Elevated serum total cholesterol
Elevated LDL cholesterol
Elevated serum triglycerides
Elevated C-reactive protein
Low HDL-cholesterol
Nutrition Assessment
BMI evaluation
Waist circumference; waist to hip ratio (WH R)
Dietary assessment for: SFA, trans-fatty acids, omega 3
fatty acids, fiber,
sodium, alcohol, and refined carbohydrates
Medical management
Bile acid sequestrants
H MG CoA reductase inhibitors (statns)
Triglyceride-lowering medication
Blood pressure-lowering medication
Medication for glucose management
Percutaneous coronary intervention (PCI)
Balloon
Stent
Coronary artery bypass graft (CABG)
Antiplatelet Therapy
Nutrition management
TLC dietary pattern -7% kcal from SFA
AHA dietary pattern-7% kcal from SFA
DASH dietary pattern
Weight reduction if needed
Increase dietary fiber to 25-30 g/day or more
Add stanols and sterols (2-3 g/day) in multiple doses
Add omega-3
Add fruits and vegetables for antioxidants
Reduce dietary cholesterol-<200 mg/day
Nutrition management
Heart failure
Patient with moderate to severe heart failure, 35% to
53% have malnutrition : cardiac cachexia.
Increase when the balance between catabolism and
anabolims is impaired
Increased catabolic cathecolamine ( epinephrine,
cortisol)
Increased TNF
Physiologic Contributors
to Malnutrition and Cachexia in Heart Failure
Intestinal ischemia
Decreased splanchnic circulation from increased
sympathetic nervous system activity:
1. impaired epithelial function and increased mucosal
permeability;
2. exposure to endotoxin and infl ammatory
cytokine release
Physiologic Contributors
to Malnutrition and Cachexia in Heart Failure
Hypercatabolism
Increased levels of stress hormones and
neurohormones:
1. epinephrine;
2. norepinephrine;
3. cortisol
Decreased levels of anabolic hormones:
1. dehydroepiandrosterone sulfate;
2. insulin-like growth factor-1
Increased circulating levels of cytokines
Physiologic Contributors
to Malnutrition and Cachexia in Heart Failure
Malabsorption
Reduced gut circulation
Gut edema:
1. decreased fat absorption;
2. protein loss
Anorexia
Nausea and early satiety from gut/hepatic edema
Multiple medication use
Clinical depression
Medical nutrition therapy fo CHF
Energy
- Obese : 1000-2000kcal/day
- Undernourished : increased by 30-50 % above basal
level (35 kcal/kg BB/day)
Sodium restricted diet
- 3 g (131 mEq) of sodium per day/no added salt diet:
high sodium diet limited an intake no more than tsp
of table salt is allowed daily
Medical nutrition therapy fo CHF
- 2 g (87 mEq) of sodium per day/no added salt diet:
high sodium diet limited, moderate sodium food
limited an intake no more than 1/4 tsp of table salt is
allowed daily
- 1 g (43 mEq) of sodium per day/no added salt diet:
high sodium diet limited, moderate sodium food
limited an intake no table salt is allowed.
- 500 mg (22mEq) high sodium diet limited, moderate
sodium food limited an intake no table salt is allowed.
1 tsp of salt = 2400mg atau 104 mEq Na
Medical nutrition therapy fo CHF
Some diuretics increase potassium excretion
Potassium depletion : anorexia, nausea, vomiting,
abdominal discomfort, hallucinations, depressions,
drowsiness, and cardiac arrythmias.
Potassium supplement
Medical nutrition therapy fo CHF
During hospitalization, fluids commoly restricted 500-
2000 mL daily
Half of patient with severe heart failure have
osteopenia or osteoporosis
Diuretics increase excretion of magnesium
Loop Diuretics increase excretion of thiamin
Medical nutrition therapy fo CHF
Feeding strategy : small, frequent feeding, soft food
Supplement : all guidelines currently avoid
recomendations of supplement
High sodium food
Smoked, processed meat and fish (ham, corned beef,
sausage, tuna, sardines)
Salted snack
Prepackaged frozen food
Canned soup
Cheeses
High sodium food
Salt used at the table
Salt or sodium added during preparation or processing
food
Inherent sodium in food ( milk, cheese, egg, poultry,
and fish)
Chemically softened water
Nonnutrient sources of sodium (spices, herb, and
seasoning)
Nondietary sources of added sodium ( toothpaste,
barbiturat, stomach alkalizer, laxative, mouthwash)