How are lipids carried
on lipoproteins in the blood because they are insoluble in water
Proteins found on lipoproteins
apolipoproteins
Density
... [Show More] of lipoprotein with less lipid and greater protein
more dense
Density of lipoprotein with more lipids and less protein
less dense
Major bloodstream lipoproteins
chylomicrons, vLDL, LDL, HDL
Chylomicrons
least dense of the lipoproteins and are triglyceride-rich particles that are formed in the intestine
Function of Chylomicrons and where they can be found
Transport dietary fat and can be found in the bloodstream at highest concentration soon after a meal
Least to most dense lipoprotein particles
Chlyomicron, vLDL, LDL, HDL
lipoprotein that is the most atherogenic of all lipoproteins
LDL
LDL carries
60-70% of the cholesterol in the blood
HDL carries
20-30% of the cholesterol in the blood
Equation for total LDL-C in bloodstream
LDL= TC-(HDL-C-(TG/5))
When does calculating LDL-C become inaccurate
when TG exceeds 400mg/dL
Desirable total cholesterol level
<200
Borderline high total cholesterol level
200-240
High total cholesterol level
>240
Optimal TG level
<150
Borderline high TG level
150-199
High TG level
200-499
Very high TG levels
>500
Optimal in men HDL levels
>40
Optimal in women HDL levels
>50
Optimal LDL-C levels
<100
Near optimal LDL-C levels
100-129
Borderline high LDL-C levels
130-159
High LDL-C levels
160-189
Very high LDL-C levels
>190
Hypertriglycerdemia is associated with high levels of
VLDL-C
Non-HDL-Cholesterol calculation
HDL-C - Total cholesterol
Atherogenic dyslipidemia
Elevated levels of TG, low HDL-C and only modest elevations of LDL-C
Metabolic syndrome
requires the presence of any 3 of the following conditions: abdominal obesity, elevated TG, low HDL, elevated BP and hyperglycemia
Criteria for metabolic syndrome: Abdominal obesity
WC >102 cm (40 in) for men
WC >88cm (35 in) for women
Criteria for metabolic syndrome: Hypertriglyceremia
≥150 or drug treatment
Criteria for metabolic syndrome: Low HDL
<40 for men
<50 for women
Criteria for metabolic syndrome: Elevated BP
SBP ≥130
DBP ≥85
or drug treatment
Criteria for metabolic syndrome: Hyperglycemia
Fasting glucose ≥100
or drug treatment
AACVPR understanding of atherosclerosis
Traditional risk factors are a source of inflammatory changes in the blood vessel wall --> which attract lipid laden macrophages and other inflammatory cells to enter the blood vessel wall --> where they proliferate and develop atherosclerotic plaques --> which are the source of the clinical manifestations of CHD
Fatty streaks
lipid deposition (daily lipid laden macrophages) in the arterial wall
Lumen
opening inside of the blood vessel
fibrous plaque
Larger and more obstructive lesoions consisting of an outer fibrous
Why do plaque ruptures occurs prior to the development of cardiovascular symptoms in many cases
Atherosclerotic plaques that are prone to rupture tend to be younger, more immature plaques that usually do not produce the degree of luminal narrowing required to develop exertion symptoms
What occurs after a plaque rupture
Clot formation within the lumen of the coronary artery, potential resulting in an acute coronary syndrome from the sudden development of severe obstruction to coronary blood flow
Examples of foods high in dietary cholesterol
Animal products ( meat, poultry, fish, eggs, butter, cheese, whole and 2% milk)
Examples of foods high in saturated fatty acids
high fat meats (beef, lamb, pork, poultry with skin, beef fat, lard), dairy products, tropical oils ( palm oil, palm kernel oil, coconut oil)
Examples of foods high in trans fatty acids
fried foods, baked goods, stick margarines, shortenings
Examples of foods high in monounsaturated fatty acids
vegetable oils (olive oil, canola oil, peanut oil, sunflower oil, sesame oil) , avocados, peanutbutter, nuts and seeds
Examples of foods high in polyunsaturated fatty acids
vegetable oils (soybean oil, safflower oil), fatty fish ( salmon, mackerel, herring, trout) nuts (walnuts), seeds (sunflower seeds)
ACC/AHA Lifestyle Management Guidelines Dietary recommendations for lowering LDL-C
1) consume a dietary pattern that emphasizes; vegetables, whole grains and fruits; low fat dairy products, fish, legumes, non-tropical oils and nuts; limit sweets, sugared beverages and red meats
2) Aim for a diet of 5-6% of calories from saturated fats
3) Reduce percent calories from saturated fats
4) Reduce percent of calories from trans fats
What are unrefined carbohydrates referred as
whole grains
Strongest evidence for dietary patterns
DASH diet
(dietary approach to stop hypertension)
Function of statins
reduce cholesterol production in the liver by inhibiting the enzyme HMG CoA reductase
When to investigate into possible secondary causes of hyperlipidemia
LDL-C >190 mg/dL and triglycerides >600mg/dL
LDL-C reduction on low intensity statin
<30%
LDL-C reduction on moderate intensity statin
30-<50%
LDL-C reduction on high intensity statin
>50%
Secondary causes of elevated LDL
diets high in saturated fat/trans fat, weight gain, anorexia, diuretics, cyclosporine, glucocorticoids, amiodarone, binary obstruction, nephrotic syndrome, hypothyroidism, obesity, pregnancy
Secondary causes of elevated triglycerides
Diets high in refined carbs, weight gain, very low fat diets, excessive alcohol intake, estrogens, glucocorticoids, bile acid sequestrates, protease inhibitors, retinoid acid, anabolic steroids, sirolimus, ralozifene, tamoxifen, beta blockers, thiazide diuretics, chronic renal failure, nephrotic syndrome, lipodystrophies, diabetes, hypothyroidism, obesity, pregnancy
Rosuvastatin 5, 10mg intensity
moderate
Rosuvastatin 20, 40 mg intensity
high
Atorvastatin 10, 20 mg intensity
moderate
Atorvastatin 40, 80mg intensity
high
Simvastatin 10mg intensity
low
Simvastatin 20, 40 mg intensity
moderate
Pravastatin 10, 20 mg intensity
low
Pravastatin 40, 80mg intensity
moderate
Lovastatin 20mg intensity
low
Lovastatin 40mg intensity
moderate
Fluvastatin XL 80mg intensity
moderate
Fluvastatin 20, 40mg intensity
low
Fluvastatin 40 mg BID intensity
moderate
Pitavastatin 1mg intensity
low
Pitavastatin 2, 4mg intensity
moderate
Moderate - High intensity Statins
Rosuvastatin, Atorvastatin
Low-Moderate intensity Statin
Simvastatin
Pravastatin
Lovastatin
Fluvastatin
Pitavastatin
What is the decision based on about whether to initiate statin therapy and what dose
based on an individuals global CVD risk rather than LDL level
Reassessment recommendations of lipid profile repeating
repeat in 4-12 weeks after initiation of statin therapy and 3-12 months periodically thereafter to access for the expected response to therapy
Four clinical groups that benefit from statin therapy
-Clinical ASCVD
-LDL-C ≥190
-Diabetes, aged 40-75, LDL 70-189 and no clinical ASCVD
-Aged 45-70, LDL 70-189, no diabetes or clinical ASCVD and 10 year risk for ASCVD ≥7.5%
Intensity of statin recommended for groups with Clinical ASCVD
High intensity for those ≤75
Moderate intensity for those >75
Intensity of statin recommended for groups with LDL ≥190
High intensity
Intensity of statin recommended for groups with Diabetes, aged 40-75, LDL 70-189 and no clinical ASCVD
Moderate intensity
*If 10 year risk ≥7.5%, option use of high intensity
Intensity of statin recommended for groups with Ages 45-70, LDL 70-189, no DM, or clinical ASCVD and 10 year risk for ASCVD ≥7.5%
Moderate to high intensity
Clinical ASCVD
- acute coronary syndrome
- history of MI
- stable or unstable angina
- coronary or other arterial revascularization
- stroke/TIA
- peripheral artery disease
Two most common reasons the result in non-adherance to statin therapy
Muscle side effects and transaminitis
Lipid effects of Niacin
flushing, transaminitis, hyperglycemia, hyperuricemia
Lipid effects of bile acid sequestrates
hypertriglycermia
Lipid effects of cholesterol absorption inhibitors
transaminitis
Lipid effects of vibrates
myopathy, renal dysfunction
Lipid effects of omega 3 ftty acids
DI disturbances, skin changes, bleeding
Transaminitis
having high levels of certain liver enzymes called transaminases.
Myalgias
muscle pain
Rhabdomyolysis
-condition in which damaged skeletal muscle breaks down rapidly (caused by trauma, extreme exertion, or drug toxicity; in severe cases renal failure can result)
-death of muscle fibers and release of their contents into the bloodstream.
What type of contraindication: Recent changes in ECG
absolute
What type of contraindication: unstable angina
absolute
What type of contraindication: uncontrolled cardiac arrhythmias
absolute
What type of contraindication: symptomatic severe aortic stenosis or other valvular disease
absolute
What type of contraindication: decompensated symptomatic heart failure
absolute
What type of contraindication: acute PE or pulmonary infarction
absolute
What type of contraindication: acute non cardiac disorder that may affect exercise performance or may be aggravated by exercise (infection,thyrotoxisosis)
absolute
What type of contraindication: acute myocarditis or pericarditis
absolute
What type of contraindication: acute thrombophlebitis
absolute
What type of contraindication: physical disability that would preclude safe and adequate exercise performance
absolute
What type of contraindication: electrolyte abnormalities
relative
What type of contraindication: tachyarrhythmias or bradyarrhythmias
relative
What type of contraindication: high degree atrioventricular block
relative
What type of contraindication: atrial fibrillation with uncontrolled rate
relative
What type of contraindication: hypertrophic obstructive cardiomyopathy with peak resting left ventricular outflow gradient of >25mmHg
relative
What type of contraindication: known aortic dissection
relative
What type of contraindication: severe resting arterial HTN (SBP >200 and DBP >100)
relative
What type of contraindication: mental impairments leading to inability to cooperate with testing
relative
Adverse réponse to inpatient exercise leading to exercise discontinuation
-DBP ≥110 mmHg
-Decreased SP >10mg
-Significant ventricular or atrial dysrhythmias
-second or third degree heart block
-s/s of exercise intolerance including angina, dyspnea, EKG changes suggestive of ischemia
P wave normal response to exercise
minor and insignificant changes in morphology
P and T wave of successive beats normal response to exercise
superimposition
Septal Q wave amplitudes normal response to exercise
increases
R wave amplitudes normal response to exercise
slightly decreases
T wave amplitude normal response to exercise
increases
QRS duration normal response to exercise
minimal shortening
J point normal response to exercise
depression
QT interval normal response to exercise
rate related shortening
ST segments may be affected by
resting ECG configuration (BBB, LVH) and pharmacological agents
Depression of J point that leads to marked ST segment up sloping is due to
competition between normal depolarization and delayed terminal depolarization faces rather than to ischemia
Exercise induced myocardial ischemia may be manifested by three different types of ST segment changes in ECG
-ST segment elevation
-ST segment depression
-ST segment normalization or absence of change
ST segment elevation represents (electric conductivity)
early depolarization
If ST segment is seen in normal ECG, increase HR may cause
elevated ST segment to return to isoelectric baseline
Exercise induced ST-segment elevation in leads displaying a previous Q wave infarction may be indicative of
wall motion abnormalities or ventricular aneurysm
Exercise induced ST segment elevation on a normal EKG (except aVR or V1-V2) indicates
significant myocardial ischemia and localizes the ischemia to a specific area of the myocardium
ST segment elevation indicates myocardial injury when followed by
the evolution of significant Q-waves
St segment depression criteria
depression of the j point and the slope at 80 sec past the J point
St segment depression is the most common manifestation of
exercise-induced myocardial ischemia
Horizontal or downsloping St segment depression is more indicative of
myocardial ischemia than is up-sloping depression
The standard criteria of a positive stress test is (St segment depression)
≥1mm of horizontal or down sloping ST segment 80msec after the J point
slowly up-sloping St segment depression should be considered
a borderline response
St segment depression does not localize
ischemia to a specific area of myocardium
The more leads with apparent ischemic ST segment shifts,
the more sever the disease
St segment depression occurring only in recovery likely represents
a true positive response and should be considered an important diagnostic finding
In the presence of baseline ST abnormalities on the resting EKG, additional ST segment depression during exercise is
less specific for myocardial ischemia
ST segment abnormalities for those with LBBB developed during exercise are
uninterpretable with respect to evidence of ischemia
In RBBB exercise induced ST segment depression in the anterior precordial leads (V1, V2 and V3)
are not used at diagnose ischemia
In RBBB exercise induced ST segment depression in the lateral leads (V4, V5 and V6)
may be indicative of ischemia even in the pretense of RBBB
ST/HR index
ratio of the maximal ST-segment change to the maximal change in HR from rest to peak exercise
ST/HR index of ≥1.6
abnormal
ST/HR slope evaluates
the maximal slope relating the amount of ST segment depression to HR during exercise
ST/HR slope of >2.4mV/beat/min
abnormal
ECG abnormalities at rest (T wave inversions/ST segment depression) may return to normal during
anginal symptoms and during exercise for some patients
Major mechanism of dysrhythmias
increased sympathetic drive and changes in extracellular and intercellular electrolytes, PH and oxygen tension contribute to disturbances in myocardial and conducting tissue automaticity and reentry
Atrial flutter or atrial fibrillation may occur in
organic heart disease or may reflect endocrine, metabolic, or drug effects
Criteria of frequent ectopy
>7 beats per minute
Criteria for terminating exercise based on ventricular ectopy includes
sustained ventricular tachycardia, multifocal PVCs, and triplets of PVCs also influenced by simultaneous evidence of ischemia and/or s/s
Muscular strength
ability of a muscle to exert a maximal force through a given range of motion or at a single given point
Muscular endurance
the capacity of a muscle to exert a sub maximal force through a given range of motion or at a single point over a given time
cardiovascular endurance
ability to continue training the cardiovascular system for a period longer than twenty minutes
flexibility
ability of a joint to move through a full range of motion
body composition
the ratio of lean body mass to fat body mass
CAD patients are more likely to have a maximal MET capacity of
5-10 METs
Oxygen uptake
the amount of oxygen consumed by the body's tissues
oxygen uptake through Fick equation
VO2=cardiac output x artery-venous oxygen content difference
What can limit VO2 peak
central and/or peripheral impairments
peak oxygen uptake levels of very low functional capacity [Show Less]