CVD

• Cardiovascular diseases (CVD) include:

- coronary heart disease (CHD),
- atherosclerosis,
- hypertension,
- ischemic heart disease,
- Peripheral vascular disease
- heart failure (HF).
• Of all causes of death, CHD, cancer, and stroke
are the leaders
• Atherosclerotic cardiovascular disease (ASCVD)
• Involves the narrowing of small blood vessels that
oxygenate the heart muscle by the build-up of
plaque (the lesion in the blood vessels).
• The plaque, known as atherosclerosis, can
rupture, causing a blood clot to form that blocks
the artery or travels somewhere else in the body,
causing blockage at that site
• The result can be a myocardial infarction (MI),
which is also called a heart attack or stroke
• Until the age of 65 years, black men have the
highest rates of ASCVD deaths; thereafter,
white men have the highest rates.
• Black women have higher rates than white
women at all ages
 I- ATHEROSCLEROSIS AND
CORONARY HEART DISEASE
• Blood vessels are composed of three layers.
• The outer layer is mainly connective tissue
that gives structure to the vessels.
• The middle layer is smooth muscle that
contracts and dilates to control blood flow and
blood pressure.
• The inner lining is a thin layer of endothelial
cells (the endothelium) that in a healthy state
is smooth and responsive
• Endothelial cells sense changes in blood flow and
respond with the release of bioactive substances
that maintain vascular homeostasis.
• One such substance is nitric oxide (NO)
(derivative from arginine).
• Decreased NO is a factor in the endothelial cell
dysfunction that disrupts vascular balance and
can result in vasoconstriction, platelet activation,
leukocyte adherence, and vascular inflammation.
• Pathophysiology
• ASCVD involves the accumulation of plaque within
the walls of the arteries.
• It starts with injury to the endothelial cells with an
associated inflammatory response involving
phagocytes and monocytes.
• Once in the tissue, monocytes evolve into
macrophages that ingest oxidized cholesterol and
become foam cells and then fatty streaks in these
vessels
• Intracellular microcalcification occurs, forming deposits
within the vascular smooth muscle cells of the surrounding
muscular layer
• Fig 33.1
• A protective fibrin layer (atheroma) forms between the
fatty deposits and the artery lining. Atheromas produce
enzymes that cause the artery to enlarge over time, thus
compensating for the narrowing caused by the plaque.
• Atheromas can rupture or break off, forming a thrombus
(blood clot), where they attract blood platelets and activate
the clotting system in the body.
• This response can result in a blockage and restricted blood
flow.
• Only high-risk or vulnerable plaque forms thrombi.
• Vulnerable plaque are lesions with a thin fibrous cap, few
smooth muscle cells, many macrophages (inflammatory
cells), and a large lipid core
• The clinical outcome of impaired arterial function arising
from atherosclerosis depends on the location of the
impairment.
• In the coronary arteries atherosclerosis can cause angina
(chest pain), MI, and sudden death; in the cerebral arteries
it causes strokes and transient ischemic attacks; and in the
peripheral circulation it causes intermittent claudication,
limb ischemia (inadequate blood supply), and gangrene
(see Figure 33-4).
• Thus atherosclerosis is the underlying cause of many forms
of CVD.
• Dyslipidemia refers to a blood lipid profile that
increases the risk of developing
atherosclerosis.
• Typically it is a condition in which LDL levels
are elevated and HDL levels are low.
• Three important biochemical measurements
in CVD include lipoproteins, total cholesterol,
and triglycerides.
 I-2: Lipoprotein
• Lipoproteins measured in clinical practice-
chylomicrons, very low- density lipoprotein (VLDL) ,
low-density lipoproteins (LDL), and high-density
lipoproteins (HDL)-consist of varying amounts of
triglyceride, cholesterol, phospholipid, and protein.
• The physiologic role of lipoprotein:
- transporting lipid to cells for energy, storage, or use as
substrate for synthesis of other compounds such as
prostaglandins, thromboxanes (cause blood clotting),
and leukotrienes (inflammatory mediators)
• a) CM
• The largest particles, 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 → 90% hydrolyzed→ remnant of CM
• Apolipoproteins carry lipids in the blood and also
control the metabolism of the lipoprotein molecule.
Apo C-II, one of the apolipoproteins, is a cofactor for
LPL.
• The liver metabolizes these chylomicrons
remnants, but some deliver cholesterol to the
arterial wall and thus are considered
atherogenic.
• Consumption of high-fat meals produces more
chylomicrons and remnants.
• When fasting plasma studies are done,
chylomicrons are normally absent
• b) Very-low-density lipoprotein (VLDL)
• They are synthesized in the liver to transport
endogenous triglyceride and cholesterol.
• Triglyceride accounts for 60% of the VLDL particle. The
large VLDL particle is believed to be nonatherogenic.
• Vegetarian and low-fat diets increase the formation of
large VLDL particles.
• Smaller VLDL particles (i.e., remnants) are formed from
triglyceride hydrolysis by LPL. Normally these
remnants, called intermediate-density lipoproteins
(IDLs), are atherogenic and are taken up by receptors
on the liver or converted to LDLs.
• Clinically, a total triglyceride level is a
measurement of the triglycerides carried on
both the VLDL and the IDL remnants.
• c) Low density lipoprotein (LDL)
• 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.
• Apo B-I00 (apo B) constitutes 95% of the
apolipoproteins in LDL.
• Persons with a high triglyceride level usually have
high apo B levels, giving these particles a longer
time to deposit lipid in the arterial wall
• High LDL cholesterol is specifically associated with
atherosclerosis.
• d) HDL: High density lipoprotein
• 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
• Numerous groups promote evaluation of apo A-I or the
ratio of apo B to apo A-I to determine risk and
treatment
• The lower the ratio, the lower the CHD risk.
• Both apo C and apo E on HDL are transferred to
chylomicrons.
• Apo E helps receptors metabolize chylomicrons
remnants and also inhibits appetite. Therefore high HDL
levels are associated with low levels of chylomicrons;
VLDL remnants; and small, dense LDLs.
• Subsequently, high HDL implies lower atherosclerotic
risk, except in patients with familial
hypercholesterolemia (FH) who can have a
triglyceride-enriched HDL3 fraction that is
proatherogenic
• e) Total cholesterol
• A total cholesterol measurement captures
cholesterol contained in all lipoprotein
fractions: 60% to 70% is carried on LDL, 20%
to 30% on HDL, and 10% to 15% on VLDL.
• Studies have consistently shown that a high
serum cholesterol level (specifically high LDL
cholesterol) is one of the key causes of CHD,
stroke, and mortality.
• f) Triglycerides
• Of these triglyceride-rich lipoproteins,
chylomicrons and VLDL remnants are known to
be atherogenic because they activate platelets,
the coagulation cascade, and clot formation
• All contain the apo B lipoprotein.
• Fasting triglyceride levels are classified as normal
(<150 mg/dl.), borderline high (150 to 199
mg/dL), high (200 to 499 mg/dL), and very high
>500 mg/dL)
• Triglycerides in the very high range place the
patient at risk for pancreatitis.
• These patients usually have
hyperchylomicromenia and require diets very low
in fat (i.e., 10% to 15% of calories derived from
fat) and medications.
• Triglyceride measurements are now considered
along with glucose intolerance, hypertension, low
HDL cholesterol, and high LDL cholesterol as part
of the metabolic syndrome.
 Medical Diagnosis

• Noninvasive tests such as electrocardiograms, treadmill

stress tests, thallium scans, and echocardiography are used
initially to establish a cardiovascular diagnosis.
• A more definitive, invasive test is angiography (cardiac
catheterization), in which a dye is injected into the arteries
and radiographic images of the heart are obtained.
• Magnetic resonance imaging scans show the smaller
lesions and can be used to follow atherosclerosis
progression or regression following treatments.
• To predict MI or stroke, measuring the intimal thickness of
the carotid artery may be used
• Finally, the calcium in atherosclerotic lesions can be
assessed
• Approximately two thirds of cases of acute
coronary syndromes (unstable angina and
acute MI) happen in arteries that are
minimally or mildly obstructed.
 I-3 Prevention and Management of
Risk Factors
• The primary prevention of these disorders
involves the assessment and management of
the risk factors in the asymptomatic person.
• Persons with multiple risk factors are the
target population, especially those with
modifiable factors
• Many coronary events could be prevented
with adoption of a healthy lifestyle (eating a
heart-healthy diet, exercising regularly,
managing weight, and not using tobacco) and
adherence to lipid and hypertension drug
therapy
• In the medical model, primary prevention of
ASCVD and stroke involves altering similar risk
factors toward a healthy patient profile.
• For ischemic stroke, atherosclerosis is the
underlying disease.
• Therefore optimal lipid levels, as determined
by the National Cholesterol Education
Program (NCEP) for hypercholesterolemia, are
also the target levels to prevent stroke.
• AHA suggests that primary prevention of CVD should begin in
children older than age 2
• Dietary recommendations for children are a bit more liberal
than those for adults.
• Activity is emphasized in maintaining ideal body weight.
• Early screening for dyslipidemia is recommended for children
with a family history of hypercholesterolemia or ASCVD.
• For adults, a total cholesterol level of 170 mg/dl or less is now
considered optimal, including an HDL of at least 50 mg/dl.
• The new 2013 guidelines no longer rely strictly on cholesterol
levels for advising patients or dosing medications.
• Instead the patient’s overall health is evaluated for treatment
decisions.
• The guidelines advise assessing factors such as age,
gender, race, whether a patient smokes, blood pressure
and whether it is being treated, whether a person has
diabetes, as well as blood cholesterol levels in
determining their risk.
• They also suggest that health care providers should
consider other factors, including family history.
• Only after that very personalized assessment is a
decision made on what treatment would work best.
• Risk calculator developed by the ACC/AHA expert panel
is available at http:// tools.acc.org/ASCVD-Risk-
Estimator
 I-3 Inflammatory Markers
• inflammatory markers are used to indicate the
presence of atherosclerosis in asymptomatic
individuals or the extent of atherosclerosis in
patients with symptoms. Several markers have
been suggested
• A recent study showed that the plasma levels of
(w3 fatty acids were inversely associated with
the inflammatory markers CRP, IL-6, fibrinogen,
and homocysteine (2010).
• In addition, genetic factors also play a role.
• An inflammatory marker specific to vascular
inflammation has recently become available.
• The PLAC™ test measures Lp-PLA2
• Lp-PLA2 levels indicate ASCVD risk independent
from other markers and provides information
on the relationship between inflammation and
atherosclerosis
 Fibrinogen
• Prospective studies have shown that plasma
fibrinogen is an independent predictor of CHD
risk.
• Factors associated with an elevated fibrinogen
are smoking, diabetes, hypertension, obesity,
sedentary lifestyle, elevated triglycerides, and
genetic factors
• Blood thrombogenicity increases with high
LDL cholesterol and in diabetes
C-Reactive Protein.
• C-Reactive Protein. C-reactive protein (CRP) is synthesized in the
liver as the acute-phase response to inflammation. Thus in a normal
individual without infection or inflammation, CRP levels are very
low <0.6 mg/dL.

• CRP has been shown to be elevated (>3 mg/dL) in people with

angina, MI, stroke, and peripheral vascular disease; the elevated
levels are independent of other risk factors
• Despite a lack of specificity for the cause of the inflammation, data
from more than 30 epidemiologic studies have shown significant
association between elevated blood levels of CRP and the
prevalence of atherosclerosis

• CRP has been found in arterial atheroma and therefore is now

considered both a risk factor and a causal agent for
atherothrombosis
• CRP levels are categorized for risk as low (,1
mg/L), average (2 to 3 mg/L), and high (.3
mg/L) after the average of two measurements
are taken at least 2 weeks apart.
• CRP levels have been shown to be inversely
correlated with a vegetable-based diet
• Table 33.3
 Homocysteine
• Elevated total homocysteine independently
increases the odds of stroke, especially in
younger individuals
• It was first observed that children who were
deficient in cystathionine B synthase, the
essential enzyme for breakdown of
homocysteine, had premature atherosclerosis
in some veins.
• Although evidence suggests that
homocysteine may promote atherosclerosis,
no causal link has been established.
• Homocysteine levels are influenced strongly
by genetic factors and diet.
• Giving supplemental vitamins B6 and B12,
which lower homocysteine levels, is being
investigated actively as a treatment for CVD
but as of now is not widely recommended.
• Trimethylamine-N-oxide. (TMAO)
• is a gut biota-dependent metabolite that
contributes to heart disease.
• TMAO has been shown to predict cardiac risk
in individuals not identified by traditional risk
factors and blood tests.
 Box 33.4
• Lifestyle Guidelines
• Lifestyle modification remains the backbone
of CVD prevention and treatment.
• Adhering to a heart-healthy diet, regular
exercising, avoidance of tobacco products, and
maintenance of a healthy weight are known
lifestyle factors that, along with genetics,
determine CVD risk.
• Diet
• The importance of diet and nutrition in modifying
the risk of CVD has been known for some time.
• However, in general, individual dietary
components have been the predominant focus.
• Because foods are consumed typically in
combinations rather than individually and
because of the possibility of synergist
relationships between nutrients, there has been
increasing attention to dietary patterns and their
relationship to health outcomes such as CVD.
• The Mediterranean Diet
• There is no uniform definition of the Mediterranean Diet
(MeD) in the published studies.
• Common features of the diet are greater number of
servings of fruits and vegetables (mostly fresh) with an
emphasis on root vegetables and greens, whole grains,
fatty fish (rich in omega-3 fatty acids), lower amounts of
red meat and with an emphasis on lean meats, lower fat
dairy products, abundant nuts and legumes, and use of
olive oil, canola oil, nut oil, or margarine blended with
rapeseed oil or flaxseed oil.
• The MeD dietary patterns that have been studied were
moderate in total fat (32% to 35%), relatively low in
saturated fat (9% to 10%), high in polyunsaturated fatty
acids (especially omega-3), and high in fiber (27 to 37 g per
day).
• The Dietary Approaches to Stop Hypertension (DASH)
Diet
• The DASH dietary pattern is high in fruits and
vegetables, low fat dairy products, whole grains, fish,
and nuts and low in animal protein and sugar.
• Two DASH variations were studied in the OmniHeart
(Optimal Macronutrient Intake Trial for Heart Health)
trial, one that replaced 10% of total daily energy from
carbohydrate with protein; the other that replaced the
same amount of carbohydrate with unsaturated fat.
• The former had showed better results than the latter in
lowering CVD risk
• Vegan Diet
• A vegan diet is a strict vegetarian diet that
includes no dietary sources from animal
origins
• It might reverse the ASCVD. Needs more
research to confirm that
• Physical Inactivity
• Physical inactivity and a low level of fitness are
independent risk factors for ASCVD.
• Physical activity is associated with ASCVD, independent of
the common cardiometabolic risk factors of obesity, serum
lipids, serum glucose and hypertension, in men and women
• With the high prevalence of obesity, physical activity is a
high priority.
• Physical activity lessens ASCVD risk by retarding
atherogenesis, increasing vascularity of the myocardium,
increasing fibrinolysis, increasing HDL cholesterol,
improving glucose tolerance and insulin sensitivity, aiding in
weight management, and reducing blood pressure
• Their recommendation based on the evidence
is for three to four sessions of aerobic exercise
per week for an average of 40 minutes
duration.
• Stress
• Stress activates a neurohormonal response in the body
that results in increased heart rate, blood pressure, and
cardiac excitability.
• The stress hormone angiotensin II is released after
stimulation of the sympathetic nervous system (SNS);
exogenous infusion of angiotensin II accelerates the
formation of plaque.
• The INTERHEART study found that the effect of stress
on CVD risk is comparable to that of hypertension.
• Stress management was not part of the 2013 ACC/AHA
lifestyle modification guidelines.
• Diabetes
• Diabetes is a disease that is an independent risk factor.
• The prevalence of diabetes mirrors that of obesity in the United
States.
• Type 2 diabetes has continued to increase in incidence
• Any form of diabetes increases the risk for ASCVD, with occurrence
at younger ages.
• Most people with diabetes die of CVD.
• Similarly, 75% of people with diabetes have more than two risk
factors for ASCVD
• Some of the increased risk seen in patients with diabetes is
attributable to the concurrent presence of other risk factors, such
as dyslipidemia, hypertension, and obesity.
• Thus diabetes is now considered an ASCVD risk factor
• Metabolic Syndrome
• Since the early findings of the Framingham
study, it has been known that a clustering of
risk factors markedly increases the risk of CVD
• Obesity
- Body mass index (BMI) and CHD are positively
related; as BMI goes up, the risk of CHD also
increases.
• The prevalence of overweight and obesity is the
highest that it has ever been in the United States;
65% of adults are overweight, and 31% are obese
- Carrying excess adipose tissue greatly affects the
heart through the many risk factors that are often
present
• hypertension, glucose intolerance, inflammatory
markers (IL-6, TNF-a, CRP), obstructive sleep
apnea, pro thrombotic state, endothelial
dysfunction, and dyslipidemia (small) LDL,
increased apo B, low HDL, high triglyceride levels
• Many inflammatory proteins are now known to
come from the adipocyte.
• These concurrent risk factors may help to explain
the high morbidity and mortality rates observed in
people who are obese.
• Weight distribution (abdominal versus gynoid) is
also predictive of CHD risk, glucose tolerance, and
serum lipid levels.
• Central adiposity has also been strongly related
to markers of inflammation, especially CRP
• Small weight losses (10 to 20 lb) can improve LDL
cholesterol, HDL cholesterol, triglycerides, high
blood pressure, glucose tolerance, and CRP levels,
even if an ideal BMI is not achieved.
• Weight loss also has been correlated with lower
CRP levels.
 Nonmodifiable Risk Factors
• Nonmodifiable Risk Factors
-1- Age and Sex
• Being older than 45 years of age is considered
a risk factor for men.
• For women the increased risk comes after the
age of 55 years, which is after menopause for
most women.
• Overall the increased risk for CHD parallels
Increase In age.
• 2- Family History and Genetics
• A family history is considered to be positive when
MI or sudden death occurs before the age of 55
years in a male first-degree relative or the age of
65 in a female first-degree relative
• 3- Menopausal status
• Loss of estrogen following natural or surgical
menopause is associated with increased CVD risk
• During menopausal period, LDL increase and HDL
decreases
 I-7 Medical Nutrition Therapy
• Diet + exercise and weight reduction →
patients can often reach serum lipid
goals and reduce body inflammation.
• Box 33.4
• The complexity of changes, number of changes,
and motivation of the patient will dictate how
many patient visits it will take for the adherent
client to be successful.
• An initial visit of 45 to 90 minutes followed by
two to six visits of 30 to 60 minutes each with the
RDN is recommended
• These interventions are tried before drug therapy
and also continue during pharmacologic
treatment to enhance effectiveness of the
medication
• Lifestyle Recommendations
• The ACC/AHA recommends diet and lifestyle changes to
reduce ASCVD risk in all people older than the age of 2
• The ACC/AHA recommendations are for a diet high in
vegetables, fruits, whole grains, low-fat poultry, fish, non
tropical vegetable oils, nuts, and low-fat dairy and low in
sweets, sugar-sweetened beverages, and red meat.
• The DASH diet pattern or USDA food pattern (MyPlate) is
recommended to achieve this diet.
• The Mediterranean Diet was not specifically recommended
but it does fit the “my plate guidelines’
• The Mediterranean Diet Score Tool was used (see Figure
33-5) to validate the dietary pattern.
• A Mediterranean diet may also reduce recurrent CVD by
50% to 70% and has been shown to affect lipoprotein levels
positively in high-risk populations
• Saturated Fatty Acids.
• Currently in the United States the average intake of
saturated fat is 11% of calories.
• The recommendation for decreasing LDL cholesterol is
5% to 6%.
• Trans fatty acids.
• They are produced in the hydrogenation process used
in the food industry to increase shelf life of foods and
to make margarines, made from oil, firmer
• Trans fat intake is inversely associated with HDL levels
• Monounsaturated Fatty Acids.
• Oleic acid (C18:1) is the most prevalent MUFA in
the American diet.
• Substituting oleic acid for carbohydrate has
almost no appreciable effect on blood lipids.
• Replacing SFAs with MUFAs (as would happen
when substituting olive oil for butter) lowers
serum cholesterol levels, LDL cholesterol levels,
and triglyceride levels.
• Oleic acid as part of the Mediterranean diet has
been shown to have antiinflammatory effects.
• PUFA
• Large amounts of LA decrease HDL serum
cholesterol levels.
• High intakes of omega-6 PUFAs may exert adverse
effects on the function of vascular endothelium
or stimulate production of proinflammatory
cytokines
• Overall, eliminating SFAs is twice as effective in
lowering serum cholesterol levels as increasing
PUFAs
• Omega-3 Fatty Acids.
• The main omega-3 fatty acids (eicosapentaenoic
acid [EPA] and docosahexaenoic acid [DHA]) are
high in fish oils, fish oil capsules, and ocean fish.
• Some studies have shown that eating fish is
associated with a decreased ASCVD risk.
• The recommendation for the general population
is to increase fish consumption specifically of fish
high in omega-3 fatty acids
• Patients who have hypertriglyceridemia need 2 to
4 g of EPA and DHA per day for effective lowering.
• Omega-3 fatty acids lower triglyceride levels by inhibiting VLDL
and apo B-100 synthesis, thereby decreasing postprandial
lipemia.
• Fish oil consumption has been associated with high levels of HDL
cholesterol
• An omega-3 fatty acid from vegetables, alpha-linolenic acid
(ALA), has antiinflammatory effects.
• CRP levels are reduced when patients consume 8 g of ALA daily
• Omega-3 fatty acids are thought to be cardioprotective because
they interfere with blood clotting and alter prostaglandin
synthesis.
• Omega-3 fat stimulates production of nitric oxide, a substance
that stimulates relaxation of the blood vessel wall (vasodilation).
• Unfortunately, high intakes prolong bleeding time,
• Dietary CT.
• The ACC/AHA 2013 guidelines no longer make this
recommendation (to reduce food rich in CT), and they
specifically state that dietary cholesterol does not raise
LDLs
• Food high in CT are high in SFA too!

• Fiber. High intake levels of dietary fiber are associated

with significantly lower prevalence of ASCVD and stroke
• The USDA MyPlate, the DASH diet, and the
Mediterranean diet pattern emphasize fruits, vegetables,
legumes, and whole grains, so they are innately high in
fiber
• (1) the fiber binds bile acids, which lowers serum cholesterol
and
• (2) bacteria in the colon ferment the fiber to produce acetate,
propionate, and butyrate, which inhibit cholesterol synthesis.
• The role of fiber, if any, on inflammatory pathways is not well
established.
• Minerals, vitamins, and antioxidants that are components of a
high-fiber diet further enrich the diet.
• Insoluble fibers such as cellulose and lignin have no effect on
• serum cholesterol levels.
• For the purpose of heart disease prevention, most of the
recommended 25 to 30 g of fiber a day should be soluble
fiber
• Antioxidants.
• Two dietary components that affect the oxidation
potential of LDL cholesterol are the level of LA in the
particle and the availability of antioxidants.
• Vitamins C, E, and beta carotene at physiologic levels
have antioxidant roles in the body.
• Vitamin E is the most concentrated antioxidant carried
on LDLs. A major function of vitamin E is to prevent
oxidation of PUFAs in the cell membrane.
• The AHA does not recommend vitamin E
supplementation for CVD prevention.
• A dietary pattern that includes increased amounts of
whole grains has increased amounts of vitamin E.
• Red grapes, red wine, tea (especially green tea),
berries, and broad beans (fava beans) are part of the
Mediterranean diet pattern.
• Stanols and Sterols.
• Since the early 1950s, plant stanols and sterols isolated
from soybean oils or pine tree oil have been known to
lower blood cholesterol by inhibiting absorption of
dietary cholesterol.
• Stanols and sterols should be part of dietary
recommendations for lowering LDL cholesterol in
adults
• These esters also can affect the absorption of and
cause lower beta-carotene, alpha-tocopherol, and
lycopene levels, further safety studies are needed
• Weight loss:
• Obesity is associated with increased risk in all-
cause and cardiovascular disease mortality
• Box 33.5 P.658
• Pharmacologic Management
• Guidelines for Treatment of Blood Cholesterol have updated
recommendations for prescribing statin drugs to be more
focused on overall patient risk than on specific serum
cholesterol targets.
• Many drugs are available for LDL lowering:
• The classes of drugs include the following:
• (1) bile acid sequestrants such as cholestyramine (adsorbs
bile acids);
• (2) nicotinic acid;
• (3) statins, or 3-hydroxy-3- methylglutaryl-coenzyme A
(HMG-CoA) reductase inhibitors, which inhibit the rate-
limiting enzyme in cholesterol synthesis;
• (4) fibric acid derivatives;
• and (5) probucol.
• Medical intervention
• Medical interventions such as percutaneous coronary
intervention (PCI) are now performed in patients with
asymptomatic ischemia or angina.
• PCI, is a procedure that uses a catheter with a balloon that,
once inflated, breaks up plaque deposits in an occluded
artery.
• Coronary stenting involves a wire mesh tube inserted to
hold an artery open; it can release medication that
prevents clotting
• PCI is often possible because of earlier detection of
blockages.
• The most common problem with PCI is restenosis of the
artery.
• Angioplasty did not appear to provide an additional
benefit versus lifestyle changes combined with
medication
• Because PCI is performed with the patient under local
anesthesia in a cardiac catheterization laboratory,
recovery is quicker than with coronary artery bypass
graft (CABG) surgery.
• In CABG surgery, an artery from the chest is used to
redirect blood flow around a diseased vessel.
• Candidates for CABG usually have more than two
occluded arteries.
• CABG does not cure atherosclerosis; the new grafts are
also susceptible to atherogenesis.
• Consequently, restenosis is common within 10 years of
surgery
 II- Hypertension
• Hypertension is persistently high arterial blood
pressure, the force exerted per unit area on the
walls of arteries.
• Hypertension: the systolic blood pressure
(SBP),the blood pressure during the contraction
phase of the cardiac cycle, has to be 120 mm Hg
or higher;
or the diastolic blood pressure (DBP), the
pressure during the relaxation phase of the
cardiac cycle, has to be 80 mm Hg or higher; this
is reported as more than 120/80 mm Hg
• Management of high blood pressure in adults
indicates that adults aged 60 years or older
should be treated with medication if their blood
pressure exceeds 150/90, which sets a higher bar
for treatment than the former guideline of
140/90
• The expert panel also recommends that
individuals with diabetes and chronic kidney
disease younger than 60 years be treated at the
same point as everyone else that age, when their
blood pressure exceeds 140/90.
• Until now, people with those chronic conditions
have been prescribed medication when their
blood pressure exceeded 130/80
• The recommendations are based on clinical
evidence showing that stricter guidelines for
these patients provided no additional benefit.
• Importantly, the guidelines emphasize that
people with high blood pressure should follow
a healthy diet and lifestyle along with
medication management.
• Diet and lifestyle modifications are important
part of primary prevention of hypertension.
• Untreated hypertension leads to many
degenerative diseases, including heart failure
(HF), end stage renal disease, and peripheral
vascular disease.
• It is often called a “silent killer” because people
with hypertension can be asymptomatic for years
and then have a fatal stroke or heart attack.
• Although no cure is available, hypertension is
easily detected and usually controllable.
• Some of the decline in CVD mortality during
the last two decades has been attributed to
the increased detection and control of
hypertension.
• The emphasis on lifestyle modifications has
given diet a prominent role in the primary
prevention and management of hypertension
• Of those persons with high blood pressure, 90% to 95%
have essential hypertension (hypertension of unknown
cause) or primary hypertension.
• The cause involves a complex interaction between poor
lifestyle choices and gene expression.
• Lifestyle factors that have been implicated include poor diet
(i.e., high sodium, low fruit and vegetable intake), smoking,
physical inactivity, stress, and obesity.
• Vascular inflammation has also been implicated
• Hypertension that arises as the result of another disease,
usually endocrine, is referred to as secondary
hypertension.
• Depending on the extent of the underlying disease,
secondary hypertension can be cured.
• Prevalence and incidence
• Approximately 78 million American adults age
20 and older have hypertension or are taking
antihypertensive medication (AHA, 2013).
• Projections show that by 2030, prevalence of
hypertension will increase by 7.2% from 2013
estimates.
• Prevalent more in black than white people
• A person of any age can have hypertension.
• Approximately 16% of boys and 9% of girls have
elevated blood pressure
• With aging, the prevalence of high blood pressure
increases
• Before the age of 45 more men than women have high
blood pressure, and after age 65 the rates of high
blood pressure among women in each racial group
surpass those of the men in their group
• The relationship between blood pressure and risk of
CVD events is continuous and independent of other
risk factors
• 28% of adults with hypertension have treatment-
resistant hypertension, which means that their
blood pressure remains high despite the use of
three or more antihypertensive drugs from
different classes
• Treatment-resistant hypertension puts an
individual at greater risk of target organ damage.
• Older age and obesity are two of the strongest
risk factors associated with the condition.
• American Diabetes Association (ADA, 2013), have
set the target blood pressure goal for
antihypertensive therapy for individuals with
diabetes lower than that recommended for the
general population, which is 140/90 mm Hg.
• Although hypertensive patients are often
asymptomatic, hypertension is not a benign
disease.
• Cardiac, cerebrovascular, and renal systems are
affected by chronically elevated blood pressure.
 II-1 Pathophysiology
• Blood pressure is a function of cardiac output
multiplied by peripheral resistance (the
resistance in the blood vessels to the flow of
blood).
• Diameter decreases→ Peripheral resistance
increases→ BP increases
• Diameter increases→ Peripheral resistance
decreases→ BP decreases
• The major regulators are the SNS for short-
term control and the kidney for long-term
control.
• Low blood pressure → SNS secretes
norepinephrine (vasoconstrictor)→ increase
BP
• Conditions that result in overstimulation of
the SNS : adrenal disorders or sleep apnea →
INCREASE in BP
• The kidney regulates blood pressure by
controlling the extracellular fluid volume and
secreting renin, which activates the renin-
angiotensin system (RAS)
• In most cases of hypertension, peripheral
resistance increases.
• This resistance forces the left ventricle of the
heart to increase its effort in pumping blood
through the system.
• With time, left ventricular hypertrophy (LVH) and
eventually HF can develop
Renal Regulation
ACE: angiotensin converting enzyme
• Hypertension often occurs with other risk factors
for CVD, including visceral (intraabdominal)
obesity, insulin resistance, high triglycerides, and
low HDL cholesterol levels.
• The coexistence of three or more of these risk
factors leads to metabolic syndrome.
• Accumulation of visceral fat synthesizes increased
amounts of angiotensinogen, which activates the
RAS and BP
• Also, angiotensin II, the primary mediator of
the RAS, promotes the development of large
dysfunctional adipocytes, which produce
increased amounts of leptin and reduced
quantities of adiponectin.
• Higher levels of leptin and lower amounts of
circulating adiponectin activate the SNS, a key
component of the hypertensive response
• Primary prevention:
• Changing lifestyle factors have documented efficacy in the
primary prevention and control of hypertension.
• These guidelines made a strong recommendation (i.e., high
benefit/risk ratio with supporting evidence) for reducing
intake of dietary sodium.
• A strong recommendation also was made for fruits and
vegetables and dietary patterns emphasizing these foods,
as well as weight management to lower blood pressure.
• Increasing physical activity was recommended, although
the ACC/AHA felt that data showing that physical activity
lowers blood pressure were limited in diverse populations.
• The ACC/AHA did not make a
recommendation for potassium, citing
insufficient evidence from RCTs to determine
whether increasing dietary potassium intake
without use of nutritional supplements lowers
blood pressure.
• Table 33.2
• Fats
• Although the total quantity of dietary fat, SFA, and
omega-6 PUFAs does not seem to affect blood
pressure, evidence from short-term feeding trials
documented that MUFA, when used as a replacement
for SFAs, PUFA, or carbohydrate, lowered blood
pressure in some individuals with hypertension
• In a recent meta-analysis, including 9 RCTs, examining
the effect of MUFA on blood pressure, SBP (net
change: - 2.26 mm Hg), and DBP (net change: -1.15 mm
Hg) reductions were significantly greater among
participants assigned to high MUFA diets compared
with those on control diets
• Supplementation with n-3 PUFAs (EPA DHA) in doses
higher than 2 g/day also can give modest reductions in
SBP and DBP, especially in untreated hypertensive
persons
• Protein supplementation in doses of 60 g/day reduced
SBP by 4.9 mm Hg and DBP by 2.7 mm Hg as compared
with 60 g/day of carbohydrate in overweight
individuals with prehypertension and untreated stage 1
hypertension
• Although soy protein may contribute to the lowering of
blood pressure, the effect of increased soy food intake
on blood pressure remains controversial
• The Dietary Approaches to Stop Hypertension (DASH)
controlled feeding study showed that a dietary pattern
emphasizing fruits, vegetables, low-fat dairy products,
whole grains, lean meats, and nuts significantly
decreased SBP in hypertensive and normotensive
adults.
• The DASH diet was found to be more effective than
just adding fruits and vegetables to a low-fat dietary
pattern and was equally effective in men and women
of diverse racial and ethnic backgrounds
• This dietary pattern serves as the core for the ACC/AHA
dietary recommendations for lowering blood pressure
• Although the DASH diet is safe and currently advocated
for preventing and treating hypertension, the diet is high
in potassium, phosphorus, and protein, depending on
how it is planned.
• For this reason the DASH diet is not advisable for
individuals with end-stage renal disease
• A hypocaloric DASH diet versus a low-calorie, low-fat diet
produces a greater reduction in SBP and DBP.
• More recently, the ENCORE study showed that the
addition of exercise and weight loss to the DASH diet
resulted in greater blood pressure reductions, greater
improvements in vascular function, and reduced left
ventricular mass compared with the DASH diet alone
• The MeD dietary pattern has many similarities
to the DASH diet but is generally higher in fat,
primarily MUFA from olive oil, nuts, and
seeds.
• A traditional MeD diet also contains fatty fish
rich in omega-3 fatty acids
• Weight Reduction
• There is a strong association between BMI and
hypertension among men and women in all race
or ethnic groups and in most age groups.
• It is estimated that at least 75% of the incidence
of hypertension is related directly to obesity
• Weight gain during adult life is responsible for
much of the rise in blood pressure seen with
aging
• Some of the physiologic changes proposed to explain the
relationship between excess body fat and blood pressure
are:
- overactivation of the SNS and RAS and vascular
inflammation
- Visceral fat in particular promotes vascular inflammation
by inducing cytokine release, proinflammatory
transcription factors, and adhesion molecules
• Low-grade inflammation occurs in the vasculature of
individuals with elevated blood pressure; whether it
precedes the onset of hypertension is unclear.
• Weight loss, exercise, and a MeD-style diet are beneficial.
• Virtually all clinical trials on weight reduction and
blood pressure support the efficacy of weight loss on
lowering blood pressure.
• Reductions in blood pressure can occur without
attainment of desirable body weight in most
participants.
• Possible synergistic effect of weight loss+ antiHTN
medications
• Although weight reduction and maintenance of a
healthy body weight is a major effort, interventions to
prevent weight gain are needed before midlife.
• In addition, BMI is recommended as a screening tool in
adolescence for future health risk
Sodium
• Several randomized trials have confirmed these positive
effects of sodium reduction on blood pressure and
cardiovascular outcomes
• According to the DASH diet a reduction of Na to 1500mg is
the most beneficial in reducing HTN
• The 2013 guidelines from the ACC/AHA advocate for
sodium reduction to 1500 mg/day in at-risk adults based on
evidence of improved blood pressure reduction
• Persons without HTN→ 2300mg of Na (6g of NaCl/ day)
• salt-sensitive hypertension : Persons who respond to a Na
restriction → BP decreases
• Salt –resistant HTN : Persons who don’t respond to a
significant Na restriction
• In general, individuals who are more sensitive
to the effects of salt and sodium tend to be
individuals who are black, obese, and middle-
aged or older, especially if they have diabetes,
chronic kidney disease, or hypertension.
Calcium
• Higher dairy versus supplemental calcium is
associated with lower risk of hypertension
• Peptides derived from milk decrease the
peripheral resistance
• Low Ca intake → secretion of PTH and activation
of Vit D→ influx of Ca into the vessels→ increase
peripheral resistance→ Increase in BP
• Dash diet found that: diet rich in fruits and
vegetables + 3 serving of dairy pdts→ decrease in
BP
• Cross-sectional studies suggests lower 25-hydroxy
vitamin D (25(OH)D) levels are associated with
higher blood pressure levels and higher rates of
incident hypertension
• Mechanistically, vitamin D has been shown to
improve endothelial function, reduce RAS activity,
and lower PTH levels.
• However, recent evidence suggests that
supplementation with vitamin D is not effective
as a blood pressure lowering agent and therefore
is not recommended as a antihypertension agent
Magnesium
• Potent inhibitor of vascular smooth-muscle
contraction and may play a role in blood
pressure regulation as a vasodilator
• Diet high in Mg (DASH) (green leafy
vegetables, nuts, and whole-grain breads and
cereals) → decrease BP
Potassium
• Diet high in K→ lower BP and stroke
• The effects of potassium are greater in those with higher
initial blood pressure, in blacks compared with whites, and
in those with higher intakes of sodium.
• Higher potassium intake also is associated with a lower risk
of stroke
• It might work in decreased vascular smooth muscle
contraction by altering membrane potential or restoring
endothelium-dependent vasodilation
• The large number of fruits and vegetables recommended in
the DASH diet makes it easy to meet the dietary potassium
recommendations—approximately 4.7 g/day
Physical activity
• Less active persons are 30% to 50% more
likely to develop hypertension than their
active counterparts.
• Increasing the amount of moderate-intensity
physical activity to a minimum of 40 minutes
3-4 times/week→ important strategy
 Alcohol consumption
• Excessive alcohol consumption→ responsible of
5-7% of the HTN cases
• 3 drinks/ day→ increase in 3mmHg of SBP
• For preventing high blood pressure, alcohol
intake should be limited to no more than two
drinks per day (24 oz of beer, 10 oz of wine, or 2
oz of 80-proof whiskey) in men, and no more
than one drink a day is recommended for lighter-
weight men and for women.
II-3 Medical Management
• Goal of HTN management:
- Reduce morbidity and mortality from stroke, hypertension-
associated heart disease, and renal disease.
• Objectives:
- 1- identify the possible causes
- 2- assess the presence or absence of target organ
disease and clinical CVD
- 3- identify other CVD risk factors that will help guide
treatment.
• The presence of risk factors and target organ damage
determines treatment priority
• Lifestyle modification is most important strategy
to begin with BEFORE the drug therapy
• Failure of lifestyle modification in the ttment of
HTN can still increase the efficacy of
pharmacologic agents and improve other CVD
risk factors
• Mngt of HTN : lifelong commitment
• Drug therapy is given after 6-12 months of
lifestyle modification failure
• In severe HTN, drug therapy is always required +
lifestyle modification
• The blood pressure target for initiating
pharmacologic treatment is 140/90 mm Hg in
adults with diabetes, kidney disease, and in the
general population of 60 years of age or less to
reduce risk of stroke, heart failure, and ASCVD.
• For individuals more than 60 years of age, the
blood pressure target is 150/90 mm Hg because
additional health benefits in lowering blood
pressure further have not been demonstrated
• Most patients with HTN more severe than stage 1 require
drug treatment; however, lifestyle modifications remain a
part of therapy in conjunction with medications.
• Recommended pharmacologic treatment includes thiazide-
type diuretics, calcium channel blockers (CCB), angiotensin-
converting enzyme inhibitors (ACEI), or angiotensin receptor
blockers (ARB)
• Thiazide-type diuretics and CCBs are recommended in black
populations, including those with diabetes, because they
have been shown to be more effective in improving CVD
outcomes compare to other classes of medications
• Diuretics lower blood pressure in some patients by
promoting volume depletion and sodium loss.
• At high doses other water soluble nutrients are also lost
and may have to be supplemented.
• Thiazide diuretics increase urinary potassium excretion,
especially in the presence of a high salt intake
• Except in the case of a potassium sparing diuretic such as
spironolactone or triamterene, additional potassium
usually is required.
• Grapefruits and grapefruit juice can affect the action of
many of the calcium channel blockers and should not be
consume while taking the medication.
• A number of medications either raise blood
pressure or interfere with the effectiveness of
antihypertensive drugs.
• These include oral contraceptives, steroids,
nonsteroidal anti-inflammatory drugs, nasal
decongestants and other cold remedies,
appetite suppressants, cyclosporine, tricyclic
antidepressants, and monoamineoxidase
inhibitors
II-4 Medical nutrition therapy
• 1- Energy intake
• For each 1Kg reduced → decrease in 1mmHg of
DBP and SBP
• Hypertensive patients who weigh more than 115%
of ideal body weight should be placed on an
individualized weight-reduction program that
focuses on hypocaloric dietary intake and exercise
• Weight loss diet + DASH diet BETTER results than
Weight loss diet + normal low fat diet
• Weight loss may decrease the use of
antihypertensive agents
• 2. DASH Diet
- Prevent and control BP
- High in fruits and vegetables (8-10 servings)
- Low SFA
- High MUFA
- High Mg
- High K
- High Ca
• Eight to 10 cups of fluids daily should be encouraged.
• Slow changes can reduce potential short-term gastrointestinal
disturbances associated with a high-fiber diet, such as bloating and
diarrhea.
• The DASH pattern is advocated in the 2013 ACC/ AHA nutrition
guidelines on lifestyle management to reduce CVD risk
• 3-Salt Restriction
• The Dietary Guidelines for Americans recommend that young adults
consume less than 2300 mg of sodium per day.
• Although further blood pressure improvements may be achieved by
reducing sodium to 1500 mg/day, patients with heart failure should
be cautioned against use of this dietary approach because adverse
health effects of very low sodium diets in these patients have been
reported
• 4- K-Ca- Mg
- DASH diet is rich in these nutrients
- Getting the DRI for these nutrients is enough
• 5- Fats
• Omega-3 fatty acids are not highlighted, because their
consumption does not appear to lower blood pressure although
intakes of fish oils exceeding 2 g/day may have blood pressure
benefits
• 6- Alcohol
• Limit it to no more than two drinks daily in men, which
is equivalent to 2 oz of 100-proof whiskey, 10 oz of
wine, or 24 oz of beer.
• Women or lighter-weight men should consume half
this amount.
• 7- Physical activity
• Moderate to-vigorous aerobic activity such as brisk
walking done at least three to four times per week,
lasting on average 40 minutes per session, is
recommended as an adjunct therapy in hypertension
management.
 II-5 Management of HTN in children
• Increase in obesity + HIGH cal diet + Na intake→ increase in
primary HTN in children
• Secondary HTN is more common in preadolescent because
of renal diseases and other disorders
• Hypertension tracks into adulthood and has been linked
with carotid intimal-medial thickness, LVH, and fibrotic
plaque formation.
• Secondary hypertension is more common in preadolescent
children, mostly from renal disease;
• Primary hypertension caused by obesity or a family history
of hypertension is more common in adolescents
Intrauterine growth retardation→ HTN in children
• HYPERTENSION:
- SBP and/or DBP > 95th percentile for age, sex and height
• PRE-HTN
- SBP and/or DBP > 90th percentile for age, sex and height
• Initial ttment for HTN and pre-HTN:
- Therapeutic lifestyle changement, it includes: regular PA
+ avoid extra weight gain + limiting sodium (DASH diet)
• Because weight loss is difficult to adhere in childhood→
at least DASH diet
• Weight reduction is considered the primary
therapy for obesity-related hypertension in
children and adolescents
• Unfortunately, sustained weight loss is difficult to
achieve in this age group.
• The Framingham Children’s Study showed that
children with higher intakes of fruits, vegetables
(a combination of four or more servings per day),
and dairy products (two or more servings per
day) had lower SBP compared with those with
lower intakes of these foods.
• Focus on “behaviorally oriented nutrition
intervention emphasizing the DASH diet”.
• Treatment of Blood Pressure in Older Adults
• Blood pressure should be controlled regardless of age,
initial blood pressure level, or duration of hypertension.
• Severe sodium restrictions are not adopted because these
could lead to volume depletion in older patients with renal
damage.
• Drug treatment in the older adult is supported by very
strong data.
• Additionally, the benefits of treating hypertensive persons
age 60 years and older to reach a blood pressure goal of
less than 150/90 mm Hg are well supported in the
literature
 Heart failure
• In heart failure (H F), formerly called congestive heart
failure, the heart cannot provide adequate blood flow
to the rest of the body, causing symptoms of fatigue,
shortness of breath (dyspnea), and fluid retention
• Diseases of the heart (valves, muscle, blood vessels)
and vasculature can lead to HF
• HF can be right-sided, left-sided, or can affect both
sides of the heart.
• It is further categorized as systolic failure when the
heart cannot pump, or eject, blood efficiently out of
the heart or diastolic failure, meaning the heart cannot
fill with blood
• The progression of HF is similar to that of
atherosclerosis because there is an
asymptomatic phase when damage is silently
occurring (stages A and B)
• HF is initiated by damage or stress to the heart
muscle either of acute MI or insidious
(hemodynamic pressure or volume overloading)
onset
• Check 671, fig 33.11
• The progressive insult alters the function and shape of the
left ventricle such that it hypertrophies in an effort to
sustain blood flow, a process known as cardiac remodeling.
• Symptoms do not usually arise until months or years after
cardiac remodeling begins
• In HF the heart can compensate for poor cardiac output by
(1) increasing the force of contraction,
(2) increasing in size,
(3) pumping more often, and
(4) stimulating the kidneys to conserve sodium and water
• Three symptoms—fatigue, shortness of breath, and fluid
retention—are the hallmarks of HF.
• Cardiac cachexia is a serious complication of HF with a poor
prognosis and mortality rate of 50% in 18 months
• Symptoms that reflect inadequate blood supply to the abdominal
organs include anorexia, nausea, a feeling of fullness, constipation,
abdominal pain, malabsorption, hepatomegaly, and liver
tenderness.
• All of these contribute to the high prevalence of malnutrition
observed in hospitalized patients with HF.
• Lack of blood flow to the gut leads to loss of bowel integrity;
bacteria and other endotoxins may enter the bloodstream and
cause cytokine activation.
• Proinflammatory cytokines such as TNF-alpha and adiponectin are
highest in patients with cardiac cachexia.
• An increased level of TNF-alpha is associated with a lower BMI,
smaller skinfold
• Medical Management
• Therapy recommendations correspond to the stage of
HF.
• For patients at high risk of developing HF (stage A),
treatment of the underlying conditions (hypertension,
dyslipidemia, thyroid disorders, arrhythmias),
avoidance of high-risk behaviors (tobacco, excessive
alcohol, illicit drug use), and lifestyle changes (weight
reduction, exercise, reduction of sodium intake, heart
healthy diet) are recommended.
• All these recommendations are carried through the
other stages.
• Pharmacologic treatment of HF is the hallmark of
therapy with progressive stages.
• The last stage also includes surgically implanted
ventricular assist devices, heart transplantation,
and continual intravenous therapy.
• The short-term goals for the treatment of HF are
to relieve symptoms, improve the quality of life,
and reduce depression if it is present.
• The long-term goal of treatment is to prolong life
by lessening, stopping, or reversing left ventricular
dysfunction
• Standard fluid restrictions are to limit total
fluid intake to 2 L (2000 ml) daily.
• When patients are severely decompensated, a
more restrictive fluid intake (1000 to 1500 ml
daily) may be warranted for adequate diuresis.
• A sodium-restricted diet should be maintained
despite low-sodium blood levels because in
this case the sodium has shifted from the
blood to the tissues.
• MNT
• Nutrition screening:
• Altered fluid balance complicates assessment of body
weight in the patient with HF.
• Weights should be taken before eating and after voiding at
the same time each day.
• A dry weight (weight without edema) should be
determined on the scale at home.
• Patients should record daily weights and advise their care
providers if weight gain exceeds more than 1 lb a day for
patients with severe HF, more than 2 lb a day for patients
with moderate HF, and more than 3 to 5 lb with mild HF.
• Restricting sodium and fluids along with diuretic therapy
may restore fluid balance and prevent full-blown HF.
• In overweight patients, caloric reduction must be
monitored carefully to avoid excessive and rapid
body protein catabolism.
• Nutrition education to promote behavior change
is a critical component of MNT.
• The benefits of MNT should be communicated to
patients
• For dyslipidemia or atherosclerosis, a heart-
healthy diet low in SFAs, trans fatty acids, and
cholesterol and high in fiber, whole grains, fruits,
and vegetables is recommended
• A 2-g sodium restriction is regularly prescribed for patients
with HF.
• Poor adherence to low-sodium diets occurs in part as a
result of lack of knowledge about sodium and lower-
sodium food choices by the patient, and perception that
the diet interferes with the social aspects of eating.
• Alcohol:Quantity, drinking patterns, and genetic factors
influence the relationship between alcohol consumption
and HF
• If alcohol is consumed, intake should not exceed one drink
per day for women and two drinks per day for men.
• Caffeine :Study in the Netherlands suggests that
moderate intake of either tea or coffee reduces
ASCVD risk; tea actually reduces ASCVD deaths
• Calcium: Patients with HF are at increased risk of
developing osteoporosis because of low activity
levels, impaired renal function, and prescription
drugs that alter calcium metabolism
• Ca supp may impair CVD function
• L arginine l-Arginine is converted to nitric oxide,
an endothelium-derived relaxing factor. More
studies are needed to confirm that
• Energy
• The energy needs of patients with HF depend on
their current dry weight, activity restrictions, and
the severity of the HF.
• Overweight patients with limited activity should
be encouraged to maintain an appropriate weight
that will not stress the myocardium.
• W3: Fats
• Fish consumption and fish oils rich in omega-3
fatty acids can lower elevated triglyceride levels
and may prevent atrial fibrillation in HF patients
• Folate, Vitamin B6, and Vitamin B12
• High dietary intakes of folate and vitamin B6 have
been associated with reduced risk of mortality
from HF and stroke in some populations
• Magnesium
• Magnesium deficiency is common in patients
with HF as a result of poor dietary intake and the
use of diuretics, including furosemide.
• As with potassium, the diuretics used to treat HF
increase magnesium excretion.
• Thiamin
• Thiamin
• Patients with HF are at risk for thiamin deficiency because
of poor food intake; use of loop diuretics, which increases
excretion; and advanced age.
• Thiamin is a required coenzyme in the energy-producing
reactions that fuel myocardial contraction.
• Vitamin D:
• As a steroid hormone, vitamin D regulates gene expression
and inversely regulates renins secretion.
• However, it remains unclear if vitamin D supplementation
truly is needed in HF patients.