Medical Nutrition Therapy for CVD PDF

Medical Nutrition Therapy for Cardiovascular Disease Dr. Öğr. Üyesi Yonca SEVİM Cardiovascular disease (CVD) is a group of interrelated diseases that include atherosclerosis, hypertension, ischemic heart disease, peripheral vascular disease, and heart failure (HF). Of all causes of dea...

Medical Nutrition Therapy for Cardiovascular Disease Dr. Öğr. Üyesi Yonca SEVİM Cardiovascular disease (CVD) is a group of interrelated diseases that include atherosclerosis, hypertension, ischemic heart disease, peripheral vascular disease, and heart failure (HF). Of all causes of death, CVD, 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. ATHEROSCLEROSIS AND CORONARY HEART DISEASE Anatomy and Physiology 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.  The endothelium functions as a protective barrier between tissues and circulating blood. It facilitates bidirectional passage of macromolecules and blood gases to and from tissues and blood. 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).  NO is a soluble gas continually synthesized from the amino acid l- arginine in endothelial cells. NO has a wide range of biologic properties that maintain vascular homeostasis. It appears to be involved in protection from injurious substances and plays a key role in vasodilation. 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.  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. This “remodeling” of the shape and size of the blood vessel may result in an aneurysm.  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. Arterial changes begin in infancy and progress asymptomatically throughout adulthood 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. Thus atherosclerosis is the underlying cause of many forms of CVD. Major clinical manifestations of atherothrombotic disease.  Dyslipidemia refers to a blood lipid profile that increases the risk of developing atherosclerosis. Three important biochemical measurements in ASCVD include lipoproteins, total cholesterol,and triglycerides.  Cholesterol is delivered into cell walls by low-density lipoprotein (LDL), especially smaller particles. To attract and stimulate the macrophages, the cholesterol must be released from the LDL particles and oxidized, a key step in the ongoing inflammatory process.  Additionally, macrophages must move excess cholesterol quickly into high-density lipoprotein (HDL) particles to avoid becoming foam cells and dying. The typical dyslipidemic condition is one in which LDL levels are elevated (hyperlipidemia) and HDL levels are low. Lipoproteins Lipoproteins measured in clinical practice—chylomicrons, very- lowdensity lipoprotein (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL)—consist of varying amounts of triglyceride, cholesterol, phospholipid, and protein. The ratio of protein to fat determines the density; thus particles with higher levels of protein are the most dense (e.g., HDLs have more protein than LDLs).  transporting lipid to cells for energy, storage, or use as substrate for synthesis of other compounds such as prostaglandins, thromboxanes, and leukotrienes.  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. Apolipoproteins carry lipids in the blood and also control the metabolism of the lipoprotein molecule. Apo C-II, one of theapolipoproteins, is a cofactor for LPL.  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 particles are synthesized in the liver to transport endogenous triglyceride and cholesterol. Triglyceride accounts for 60% of the VLDL particle. The large, buoyant 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 intermediatedensity lipoproteins (IDLs), are atherogenic and are taken up by receptors on the liver or converted to LDLs. Some of the smaller LDL particles stay in the blood, are oxidized, and are then taken into the arterial wall. Clinically, a total triglyceride level is a measurement of the triglycerides carried on the VLDL and the IDL remnants  LDL is the primary cholesterol carrier in blood, formed by the breakdown of VLDL. High LDL cholesterol is associated specifically with atherosclerosis. After LDL formation, 60% is taken up by LDL receptors on the liver, adrenals, and other tissues. The remainder is metabolized via nonreceptor pathways. The number and activity of these LDL receptors are major determinants of the LDL level in the blood.  Apolipoprotein B is the structural protein for all of the atherogenic lipoproteins (VLDL, IDL, LDL) and modulates the transport of lipids from the gut and liver to the tissues.  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 for excretion or repackaging. This process prevents the build-up and oxidation of cholesterol in the arteries.  Evaluation of apo A-I or the ratio of apo B to apo A-I has been proposed to assess risk and determine treatment. The lower the ratio, the lower the ASCVD risk.  High HDL levels are associated with low levels of chylomicrons; VLDL remnants; and small, dense LDLs. Epidemiologic studies have shown an inverse correlation between HDL levels and risk of cardiovascular events. Subsequently, high HDL implies lower atherosclerotic risk, except in patients with specific genetic causes of hypercholesterolemia who can have a triglyceride-enriched HDL3 fraction that is proatherogenic. 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. Triglycerides 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 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 (3 mg/dl) in people with angina, MI, stroke, and peripheral vascular disease.  CRP levels are categorized for risk as low (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. Homocysteine Homocysteine, an amino acid metabolite of methionine, is a risk factor for CVD. Elevated total homocysteine (tHcy) independently increases the odds of stroke, especially in younger individuals. 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 Trimethylamine-N-oxide (TMAO) is a gut biota-dependent metabolite that contributes to heart disease. It is produced by the liver after intestinal bacteria have digested animal protein. TMAO has been shown to predict cardiac risk in individuals not identified by traditional risk factors and blood tests. Malondialdehyde Malondialdehyde results from lipid peroxidation of polyunsaturated fatty acids. The degree of lipid peroxidation can be estimated by the amount of malondialdehyde in tissues. Reactive oxygen species degrade polyunsaturated lipids, forming malondialdehyde. This compound is a reactive aldehyde and is one of the many reactive electrophile species that cause toxic stress in cells and form covalent protein adducts referred to as advanced lipoxidation end- products (ALE), in analogy to advanced glycation end-products (AGE). The production of this aldehyde is used as a biomarker to measure the level of oxidative stress in an organism. Malondialdehyde is reactive and potentially mutagenic. It has been found in heated edible oils such as sunflower and palm oils. 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.  Three critical questions (CQs) were addressed in the 2013 ACC/AHA Lifestyle modification guidelines. CQ1 presents evidence on dietary patterns and macronutrients and their effect on blood pressure and lipids, CQ2 presents evidence on the effect of dietary sodium and potassium intake on blood pressure and CVD outcomes, and CQ3 presents the evidence on the effect of physical activity on lipids and blood pressure. Diet 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. Vegan Diet A vegan diet is a strict vegetarian diet that includes no dietary sources from animal origins. There is ongoing research to suggest only this type of very restricted diet can actually reverse ASCVD. 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. 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.  The 2013 ACC/AHA recommendations for exercise are based on studies on the role of exercise in preventing and treating CVD alone, not in combination with other interventions. 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. Diabetes Diabetes is a disease that is an independent risk factor. 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 Obesity has now reached epidemic levels in children and adults in many developed countries. Body mass index (BMI) and CVD are positively related; as BMI goes up, the risk of CVD also increases. Higher obese-years were associated with higher CVD risk in the study.  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, prothrombotic state, endothelial dysfunction, and dyslipidemia (small dense LDL, increased apo B, low HDL, high triglyceride levels).  Weight distribution (abdominal versus gynoid) is also predictive of CVD risk, glucose tolerance, and serum lipid levels. Central or abdominal length of adiposity also has 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 Age and Sex Family History and Genetics Menopausal Status Age and Sex With increasing age, higher mortality rates from CVD are seen in both genders. However, gender is a factor for the assessment of risk. The incidence of premature disease in men 35 to 44 years of age is three times as high as the incidence in women of the same age. Therefore 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 CVD parallels age. Family History and Genetics A family history of premature disease is a strong risk factor, even when other risk factors are considered. 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 (parents, siblings, or children). Menopausal Status Endogenous estrogen confers protection against ASCVD in premenopausal women, probably by preventing vascular injury. Loss of estrogen after natural or surgical menopause is associated with increased ASCVD risk. During the menopausal period total cholesterol, LDL cholesterol, and triglyceride levels increase; HDL cholesterol level decreases, especially in women who gain weight. Medical Nutrition Therapy Medical nutrition therapy (MNT), which includes discussion of physical activity, is the primary intervention for patients with elevated LDL cholesterol. 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 (American Dietetic Association [ADA]. Consequently these interventionsare tried before drug therapy and also continue during pharmacologic treatment to enhance effectiveness of the medication. Summary of ACC/AHA Recommendations for Lifestyle Management 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, nontropical 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.  Saturated Fatty Acids.- The recommendation for decreasing LDL cholesterol is 5% to 6%. It is recommended that intake of animal protein, especially red meat and high fat dairy be decreased. Trans Fatty Acids.-In 2013 the FDA made a decision to remove PHOs from the “generally recognized as safe” list. This was based on the mounting evidence that trans fats contributed to ASCVD and was associated with increased LDL cholesterol levels. Trans fat intake is inversely associated with HDL levels.  Monounsaturated Fatty Acids.-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. Polyunsaturated Fatty Acids.-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. Replacing PUFAs for carbohydrate in the diet results in a decline in serum LDL cholesterol. When SFAs are replaced with PUFAs in a low-fat diet, LDL and HDL cholesterol levels are lowered.  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 (salmon, tuna, mackerel, sardines). Patientswho 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.  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 (vasodilation). Unfortunately, high intakes prolong bleeding time, a common condition among Arctic Native populations.  Dietary Cholesterol.- Previous recommendations have been to decrease dietary cholesterol to decrease LDL cholesterol and reduce ASCVD risk. The ACC/AHA 2013 guidelines no longer make this recommendation, and they specifically state that dietary cholesterol does not raise LDLs. The 2015 US Dietary Guidelines also eliminate the recommendation to restrict cholesterol. However it is important to remember that most high cholesterol foods are also high in saturated fats that do raise LDL cholesterol. Fiber.- the DASH diet, and the Mediterranean diet. This combination of foods provides a combination of soluble and insoluble fiber. Proposed mechanisms for the hypocholesterolemic effect of soluble fiber include the following: (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.  Minerals, vitamins, and antioxidants that are componentsof 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 betacarotene at physiologic levels have antioxidant roles in the body. Vitamin E is the most concentrated antioxidant carried on LDLs, the amount being 20 to 300 times greater than any other antioxidant. 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. Foods with concentrated amounts of antioxidants are found in phytochemicals known as catechins and have been found to improve vascular reactivity. 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. Because these esters also can affect the absorption of and cause lower beta-carotene, alpha-tocopherol, and lycopene levels, further safety studies are needed for use in normocholesterolemic individuals, children, and pregnant women.  Weight Loss.- obesity raises the risk of hypertension, dyslipidemia, type 2 diabetes, ASCVD, and stroke. Obesity is associated with increased risk in all-cause and cardiovascular disease mortality. Recommendations from the AHA/ACC/TOS Obesity Guideline Medical Management Pharmacologic Management Determination of drug therapy depends on risk category and attainment of the LDL cholesterol goal. The primary treatment for those at risk of ASCVD are the HGM-CoA reductase inhibitors, of which there are many. 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. HYPERTENSION  Hypertension is persistently high arterial blood pressure. The systolic blood pressure (SBP), the upper reading in a blood pressure measurement, is the force exerted on the walls of blood vessels as the heart contracts and pushes blood out of its chambers. The lower reading, known as diastolic blood pressure (DBP), measures the force as the heart relaxes between contractions. Blood pressure is measured in millimeters (mm) of mercury (Hg). Adult blood pressure is considered normal at 120/80 mm Hg.  Hypertension is a common public health problem in developed countries. In the United States one in three adults has high blood pressure (AHA, 2013). Untreated hypertension leads to many degenerative diseases, including heart failure (HF), endstage 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.  Hypertension is easily detected and usually controllable. 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) Hypertension that arises as the result of another disease, usually endocrine, is referred to as secondary hypertension. 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. The prevalence of high blood pressure in blacks is one of the highest rates seen anywhere in the world. A person of any age can have hypertension. 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. More than half the older adult population (more than 65 years of age) in any racial group has hypertension Risk factors The relationship between blood pressure and risk of CVD events is continuous and independent of other risk factors. The higher the blood pressure, the greater is the chance of target organ damage, including left ventricular hypertrophy (LVH), HF, stroke, chronic kidney disease, and retinopathy. As many as 28% of adults with hypertension have treatment- resistant hypertension. Older age and obesity are two of the strongest risk factors associated with the condition. Risk Factors and Adverse Prognosis in Hypertension Pathophysiology Blood pressure is a function of cardiac output multiplied by peripheral resistance (the resistance in the blood vessels to the flow of blood). Thus the diameter of the blood vessel markedly affects blood flow. When the diameter is decreased (as in atherosclerosis) resistance and blood pressure increase. Conversely, when the diameter is increased (as with vasodilator drug therapy), resistance decreases and blood pressure is lowered. The major regulators are the sympathetic nervous system (SNS) for short-term control and the kidney for long-term control. In response to a fall in blood pressure, the SNS secretes norepinephrine, a vasoconstrictor, which acts on small arteries and arterioles to increase peripheral resistance and raise blood pressure. Conditions that result in overstimulation of the SNS (i.e., certain adrenal disorders or sleep apnea) result in increased blood pressure. The kidney regulates blood pressure by controlling the extracellular fluid volume and secreting renin, which activates the renin-angiotensin system (RAS) Abnormal blood pressure is usually multifactorial. 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.  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 increases blood pressure. 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 factors were systematically reviewed and categorized by the Academy of Nutrition and Dietetics (AND) in 2009 and more recently by the ACC and AHA in 2013.  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. Fats Although the total quantity of dietary fat, SFA, and omega-6 PUFAs do 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. Higher intake of dietary MUFA (,13 g/day), especially oleic acid from plant oils, was associated with significantly lower DBP. In a recent meta-analysis, examining the effect of MUFA on blood pressure, SBP (net change: -2.26 mm Hg), and DBP (net change: -1.15 mm Hg)  Taken together, these findings suggest that diets high in MUFA may be a useful component of blood pressure–lowering diets. Supplementation with n-3 PUFAs (EPA 1 DHA) in doses higher than 2 g/day also can give modest reductions in SBP and DBP, especially in untreated hypertensive persons Protein Replacement of protein for fat or carbohydrate in an isocaloric diet results in lowered blood pressure. Although soy protein may contribute to the lowering of blood pressure, the effect of increased soy food intake on blood pressure remains controversial. Dietary Patterns Emphasizing Fruits and Vegetables Plant-based dietary patterns have been associated with lower SBP in observational studies and clinical trials. Average SBP reductions of 5 to 6 mm Hg have been reported. Specifically, 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. 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.  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.  Because many hypertensive patients are overweight, hypocaloric versions of the DASH diet also have been tested for efficacy in promoting weight loss and blood pressure reduction. 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. A recent systematic review of the MeD diet and CVD risk factors, found that although limited, evidence from RCTs was suggestive of a blood-pressure lowering effect of this style dietary pattern in adults with hypertension. According to the ACC/AHA more studies on diverse populations are warranted before recommendations can be made related to the MeD diet for use in blood pressure management. 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 (AHA, 2013). Due to relationship between excess body fat and blood pressure are overactivation of the SNS and RAS and vascular inflammation Sodium Evidence from a variety of studies supports lowering blood pressure and CVD risk by reducing dietary sodium. A recent meta-analysis of 37 RCTs confirmed these positive effects of sodium reduction on blood pressure and cardiovascular outcomes for normotensive and hypertensive individuals.  The DASH sodium trials tested the effects of three different levels of sodium intake (1500 mg, 2400 mg, and 3300 mg/day) combined with either a typical U.S. diet or the DASH diet in persons with prehypertension or stage 1 hypertension. The lowest blood pressures were achieved by those eating the 1500- mg sodium level in the DASH diet. the lower the sodium, the lower the blood pressure  The 2013 ACC/AHA (Eckel et al, 2013) sodium guideline for adults with elevated blood pressure to consume no more than 2400mg/day. For those with normal blood pressure, the Dietary Guidelines for Americans recommend an intake of less than 2300 mg of sodium, the equivalent of 6 g of salt, each day (USDA, 2015). Nevertheless, 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.  Salt-sensitive hypertension has been used to identify persons with hypertension show a greater decrease in their blood pressures in response to reduced sodium intake than others. Salt-resistant hypertension refers to individuals with hypertension whose blood pressures do not change significantly with lowered salt intakes.  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 and Vitamin D Higher dairy versus supplemental calcium is associated with lower risk of hypertension (van Mierlo et al, 2008). In particular, low-fat dairy intake reduced the risk of hypertension by 13%, whereas supplemental calcium intake and high fat dairy sources had no effect. At least 2.5 servings of low-fat dairy per day are necessary for blood pressure improvement.  Mechanistically, dairy intake, a major source of dietary calcium, potentiates an increase in intracellular calcium concentration. This in turn increases 1, 25-vitamin D3 and parathyroid hormone levels, causing calcium influx into vascular smooth muscle cells and greater vascular resistance. Alternatively, peptides derived from milk proteins, especially fermented milk products, may function as ACEs, thereby lowering blood pressure.  A diet rich in fruits, vegetables, and low-fat dairy products (versus calcium supplements) for the prevention and management of elevated blood pressure. An intake of dietary calcium to meet the DRI is recommended.  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 Magnesium is a potent inhibitor of vascular smooth-muscle contraction and may play a role in blood pressure regulation as a vasodilator. High dietary magnesium often is correlated with lower blood pressure. The DASH dietary pattern emphasizes foods rich in magnesium, including green leafy vegetables, nuts, and whole-grain breads and cereals. Overall food sources of magnesium rather than supplemental doses of the nutrient are encouraged to prevent or control hypertension. Potassium Supplemental doses of potassium in the range of 1900 to 4700 mg/day lower blood pressure approximately 2 to 6 mm Hg DBP and 2 to 4 mm Hg SBP (Dickinson et al, 2006). 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. 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. Exercise is beneficial to blood pressure. Increasing the amount of moderate-intensity physical activity to a minimum of 40 minutes on 3 to 4 days per week is an important adjunct to other blood pressure–lowering strategies Alcohol Consumption Excessive alcohol consumption is responsible for 5% to 7% of the hypertension in the population. A three drink per day amount (a total of 3 oz of alcohol) is the threshold for raising blood pressure and is associated with a 3-mm Hg rise in 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. Medical Management The goal of hypertension management is to reduce morbidity and mortality from stroke, hypertension-associated heart disease, and renal disease. The three objectives for evaluating patients with hypertension are to (1) identify the possible causes, (2) assess the presence or absence of target organ disease and clinical CVD, and (3) identify other CVD risk factors that help guide treatment. Recommendations on Blood Pressure in Hypertensive Adults from Evidence Analysis Library (2009) and American College of Cardiology/American Heart Association (2013)  Lifestyle modifications are definitive therapy for some and adjunctive therapy for all persons with hypertension. Several months of compliant lifestyle modifications should be tried before drug therapy is initiated. Even if lifestyle modifications cannot completely correct blood pressure, these approaches help increase the efficacy of pharmacologic agents and improve other CVD risk factors. Management of hypertension requires a lifelong commitment.  Recommended pharmacologic treatment includes thiazide-type diuretics, calcium channel blockers (CCB), angiotensin-converting enzyme inhibitors (ACEI), or angiotensin receptor blockers (ARB)  Diuretics lower blood pressure in some patients by promoting volume depletion and sodium loss. At high doses other watersoluble 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, thus leading to potassium loss and possible hypokalemia. 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. Complementary and Alternative Approaches to Lowering Blood Pressure Medical Nutrition Therapy  The appropriate course of nutrition therapy for managing hypertension should be guided by data from a detailed nutrition assessment. Weight history; leisure-time physical activity; and assessment of intake of sodium, alcohol, fat type (e.g., MUFA versus SFA), and other dietary patterns (e.g., intake of fruits, vegetables, and low-fat dairy products) are essential components of the medical and diet history. Nutrition assessment should include evaluation of the individual in the following specific domains to determine nutrition problems and diagnoses: food and nutrient intake; knowledge, beliefs, and attitudes; behavior; physical activity and function; and appropriate biochemical data. Energy Intake For each kilogram of weight lost, reductions in SBP and DBP of approximately 1 mm Hg are expected. 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. A modest caloric reduction is associated with a significant lowering of SBP and DBP, and LDL cholesterol levels.  Another benefit of weight loss on blood pressure is the synergistic effect with drug therapy. Weight loss should be an adjunct to drug therapy because it may decrease the dose or number of drugs necessary to control blood pressure. DASH Diet Successful adoption of this diet requires many behavioral changes: eating twice the average number of daily servings of fruits, vegetables, and dairy products; limiting by one third the usual intake of beef, pork, and ham; eating half the typical amounts of fats, oils, and salad dressings; and eating one quarter the number of snacks and sweets. To achieve the 8 to 10 servings, two to three fruits and vegetables should be consumed at each meal. Importantly, because the DASH diet is high in fiber, gradual increases in fruit, vegetables, and whole-grain foods should be made over time. Eight to 10 cups of fluids daily should be encouraged. Salt Restriction The Dietary Guidelines for Americans recommend that young adults consume less than 2300 mg of sodium per day. In addition to advice to select minimally processed foods, dietary counseling should include instruction on reading food labels for sodium content, avoidance of discretionary salt in cooking or meal preparation (1 tsp salt = 2400 mg sodium), and use of alternative flavorings to satisfy individual taste  Because most dietary salt comes from processed foods and eating out, changes in food preparation and processing can help patients reach the sodium goal. Potassium-Calcium-Magnesium Consuming a diet rich in potassium may lower blood pressureand blunt the effects of salt on blood pressure in some individuals. The recommended intake of potassium for adults is 4.7 g/day. Potassium rich fruits and vegetables include leafy green vegetables, fruits, and root vegetables. Examples of such foods include oranges, beet greens, white beans, spinach, bananas, and sweet potatoes. Although meat, milk, and cereal products contain potassium, the potassium from these sources is not as well absorbed as that from fruits and vegetables.  Increased intakes of calcium and magnesium may have blood pressure benefits, although there are not enough data to support a specific recommendation for increasing levels of intake. recommendations suggest meeting the AI intake for calcium and the recommended dietary allowance for magnesium from food sources rather than supplements. The DASH diet plan encourages foods that would be good sources of both nutrients, including low-fat dairy products, dark green leafy vegetables, beans, and nuts. Lipids Current recommendations for lipid composition of the diet are recommended to help control weight and decrease the risk of CVD. Omega-3 fatty acids are not highlighted in blood pressure treatment guidelines, although intakes of fish oils exceeding 2 g/day may have blood pressure benefits. Alcohol The diet history should contain information about alcohol consumption. Alcohol intake should be limited to no more than two drinks daily in men, which is equivalent to 2 oz of 80-proof whiskey, 10 oz of wine, or 24 oz of beer. Women or lighter-weight men should consume half this amount. Exercise 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. For substantial health benefits, the dietary guidelines recommends at least 2 hours and 30 minutes a week of moderate-intensity physical activity as well as muscle-strengthening activities that include all major muscle groups on 2 or more days for all Americans. Treatment of Blood Pressure in Older Adults losing weight (8 to 10 lb) and reducing sodium intake (to 1.8 g/day) can lessen or eliminate the need for drugs in obese, hypertensive older adults Although losing weight and decreasing sodium in older adults are very effective in lowering blood pressure, knowing how to facilitate these changes and promote adherence remains a challenge for health professionals. HEART FAILURE  In heart failure (HF), 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. Pathophysiology The progression of HF is similar to that of atherosclerosis because there is an asymptomatic phase when damage is silently occurring. HF is initiated by damage or stress to the heart muscle either of acute MI or insidious (hemodynamic pressure or volume overloading) onset. 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.  Many compensatory mechanisms from the SNS, RAS, and cytokine system are activated to restore homeostatic function. Proinflammatory cytokines, such as TNF-alpha, IL-1, and IL-6, are increased in blood and the myocardium and have been found to regulate cardiac remodeling.  HF patients have elevated levels of norepinephrine, angiotensin II, aldosterone, endothelin, and vasopressin; all of these are neurohormonal factors that increase the hemodynamic stress on the ventricle by causing sodium retention and peripheral vasoconstriction. These neurohormones and the proinflammatory cytokines contribute to disease progression 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. For a time this compensation maintains near-normal circulation, but eventually the heart can no longer maintain a normal output (decompensation). Advanced symptoms can develop in weeks or months, and sudden death can occur at any time.  Cardiac cachexia is the end result of HF in 10% to 15% of patients. It is defined as involuntary weight loss of at least 6% of nonedematous body weight during a 6-month period Unlike normal starvation, which is characterized by adipose tissue loss, this cachexia is characterized by a significant loss of lean body mass  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. 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.  An increased level of TNF-alpha is associated with a lower BMI, smaller skinfold measurements, and decreased plasma total protein levels, indicative of a catabolic state. Risk Factors The Framingham Study showed the risk factors for HF were: hypertension, diabetes, ASCVD, and left ventricular hypertrophy (LVH) (enlargement of the left ventricle of the heart). Because long-term survival rates for persons with HF are low, prevention is critical. Medical Nutrition Therapy The RDN provides MNT, which includes assessment, a nutrition diagnosis, and interventions (education, counseling). As part of a multidisciplinary team (physician, pharmacist, psychologist, nurse, and social worker), the RDN positively affects patient outcomes. Reduced readmission to the hospital, fewer days in the hospital, improved compliance with restricted sodium and fluid intakes, and improved quality of life scores are the goals in HF patients.  The first step in screening is determination of body weight. 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.  Dietary assessments in HF patients reveal that more than half have malnutrition, usually related to the cardiac cachexia mentioned earlier. Negative energy balance and negative nitrogen balances can be noted. In overweight patients, caloric reduction must be monitored carefully to avoid excessive and rapid body protein catabolism.  underlying risk factors are often present; dietary changes to modify these risk factors are an important component of MNT. 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. For persons with hypertension, the DASH diet is recommended. Both of these dietary patterns emphasize lower-sodium foods and higher intake of potassium. Total energy expenditure is higher in HF patients because of the catabolic state, adequate protein and energy should be provided. Salt Restriction Excessive sodium intake is associated with fluid retention and edema. A 2-g sodium restriction is regularly prescribed for patients with HF. The Heart Failure Society of America recommends 2 to 3 g of sodium daily unless severe symptoms are present, then the recommendation is for 2 g. The updated AHA recommendation is for “moderate” sodium restriction. There is consensus that high sodium intake (above 3 g/day) is contraindicated for HF.  The first step is to minimize or eliminate the use of table salt and high-sodium foods. Food Labeling Guide for Sodium Top Ten Categories of High-Sodium Foods Alcohol In excess, alcohol contributes to fluid intake and raises blood pressure. Many cardiologists recommend avoiding alcohol. Chronic alcohol ingestion may lead to cardiomyopathy and HF. If alcohol is consumed, intake should not exceed one drink per day for women and two drinks per day for men. A drink is equivalent to 1 oz of alcohol (1 oz of distilled liquor), 5 oz of wine, or 12 oz of beer. Caffeine Until now caffeine has been considered detrimental to patients with HF because it contributes to irregular heartbeats. However, a study in the Netherlands suggests that moderate intake of either tea or coffee reduces ASCVD risk; tea actually reduces ASCVD deaths. The antioxidant effects of coffee and tea may be beneficial. 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. Cachectic HF patients have lower bone mineral density and lower calcium levels than HF patients without cachexia. Caution must be used with calcium supplements because they may aggravate cardiac arrhythmias. L-Arginine l-Arginine is convertedto nitric oxide, an endothelium-derived relaxing factor. At least four studies have showed some benefit with supplementation. The studies were small, and more research is needed to establish clear recommendations. Coenzyme Q10 Some studies on the use of coenzyme Q10 (CoQ10) supplementation in HF patients showed positive outcome. Outcomes included significantly improved exercise tolerance, decreased symptoms, and improved quality of life. Patients on statins (HMGCoA reductase inhibitors) may have a different reason to consider supplementation. HMG-CoA reductase inhibitors are a class of cholesterol-lowering drugs that are known to interfere with synthesis of CoQ10. Energy The energy needs of patients with HF depend on their current dry weight, activity restrictions, and the severity of the HF. This area requires more research. Standard nutritional assessment should be employed with careful monitoring. 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. Intake of at least 1 g daily of omega-3 fatty acids from either oily fish or fish-oil supplementswas used in the study. However, further studies are needed. Some evidence suggests that high saturated fat feeding in mild to moderate HF preserves contractile function and prevents the switch from fatty acid to glucose metabolism, thus serving a cardioprotective role. Meal Strategies* Patients with HF often tolerate small, frequent meals better than larger, infrequent meals because the latter are more tiring to consume, can contribute to abdominal distention, and markedly increase oxygen consumption. All these factors tax the already stressed heart. Caloric supplements can help to increase energy intake; however, this intervention may not reverse this form of malnutrition. 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. However, deficiencies of vitamin B12 and folate have been studied and found to be relatively rare in HF patients. 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. Magnesium deficiency aggravates changes in electrolyte concentration by causing a positive sodium and negative potassium balance. Magnesium supplementation (800 mg/day) produces small improvements in arterial compliance. Poor dietary intake of magnesium has been associated with elevated CRP, a product of inflammation. 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. Therefore, thiamin deficiency can cause decreased energy and weaker heart contractions.  Supplementation with thiamin has been shown to improve cardiac function, urine output, weight loss and signs and symptoms of HF. Thiamin supplementation (e.g., 100 mg/day) can improve left ventricular ejection fraction (fraction of blood pumped out of the ventricles with each heartbeat) and symptoms. Vitamin D Vitamin D may improve inflammation in HF patients. Supplementation with vitamin D (50 mcg or 2000 international units of vitamin D3 per day) for 9 months increased the anti-inflammatory cytokine and decreased the proinflammatory factors in HF patients. As a steroid hormone, vitamin D regulates gene expression and inversely regulates renin secretion. However, it remains unclear if vitamin D supplementation truly is needed in HF patients. CARDIAC TRANSPLANTATION Nutrition support before and after transplantation is crucial to decrease morbidity and mortality. Thus the nutrition care of the heart transplant patient can be divided into three phases: pretransplant, immediate posttransplant, long-term posttransplant. Pretransplant Medical Nutrition Therapy Recommended lifestyle changes before transplantation include restricting alcohol consumption, losing weight, exercising, quitting smoking, and eating a low-sodium diet. Extremes in body weight (less than 80% or more than 140% of ideal body weight) increase the patient’s risk for infection, diabetes, morbidity, and higher mortality. If oral intake is inadequate, an enteral feeding should be tailored to the nutritional and comorbid conditions of the patient. Immediate Posttransplant Nutrition Support The nutritional goals in the acute posttransplant patient are to (1) provide adequate protein and calories to treat catabolism and promote healing, (2) monitor and correct electrolyte abnormalities, (3) achieve optimal blood glucose control. In the immediate posttransplant period nutrient needs are increased, as is the case after any major surgery. Protein needs are increased because of steroid-induced catabolism, surgical stress, anabolism, and wound healing.  Patients progress from clear liquids to a soft diet given in small, frequent feedings. Enteral feeding may be appropriate in the short term, especially if complications arise. Nutrient intake is often maintained by using liquid supplements and foods of high caloric density, especially in patients with poor appetite. Weight gain to an ideal weight is the nutritional goal for patients who were cachectic before transplant. Hyperglycemia can be exacerbated by the stress of the surgery and the immunosuppressive drug regimen. Dietary adjustments can be made to aid in glucose control. Long-Term Posttransplant Nutrition Support Comorbid conditions that often occur after transplantation include hypertension, excessive weight gain, hyperlipidemia, osteoporosis, and infection. Hypertension is managed by diet, exercise, and medications. Minimizing excessive weight gain is important because patients who become obese after transplantation are at higher risk for rejection and lower rates of survival.  Increases in total LDL cholesterol and triglycerides are a consequence of immunosuppressive drug therapy and increase the risk of HF after transplantation. Along with a heart-healthy diet, patients also need a lipid-lowering drug regimen to normalize blood lipids. Statins are recommended in the early and long term postoperative periods. Because of their LDL-lowering effect, stanols or sterols may be helpful to reduce statin dosages.  Before transplantation, patients are likely to have osteopenia because of their lack of activity and cardiac cachexia. After transplantation, patients are susceptible to steroid-induced osteoporosis. Patients require optimal calcium and vitamin D intake to slow bone loss; weight-bearing exercise and antiresorptive drug therapy are often necessary. Infection must be avoided because of the necessity of lifelong use of immunosuppressive drugs. Food safety should be discussed.