Heart failure is the clinical syndrome resulting from the structural or functional inability of the heart to meet the body’s basic metabolic needs at normal pressures, specifically in the left ventricle.[1] It can be the consequence of any of a number of disorders that affect heart function. These disorders may be temporary or progressive and can affect the pericardium, myocardium, or endocardium. Examples include longstanding hypertension, valvular disease, genetic disorders, infections, and congenital diseases.

Heart failure can range from an asymptomatic condition to one requiring intensive hospital care. This condition may lead to inadequate perfusion to the body’s peripheral tissues as well as to pulmonary edema (left heart failure), build-up of pressure in the venous system (right heart failure), or both.

In the US, about 5.8 million people suffer from heart failure, and there about 1 million hospitalizations per year due to decompensated heart failure. About 30% of patients discharged from the hospital with heart failure will be readmitted within 90 days.[2] Heart failure incidence increases with age.

Heart failure is typically classified by ejection fraction which may be reduced (≤ 40%), preserved (≥ 50%), or ‘borderline’ (between 40% and 50%). The terms ‘systolic’ and ‘diastolic’ failure are no longer preferred.[1]

There are many good treatments for heart failure with reduced ejection fraction. However, there are significantly fewer evidence-based treatments for heart failure with preserved ejection fraction, and prognosis tends to be worse for these patients.

As noted above, heart failure can also be classified as primarily right-sided or left-sided. Signs and symptoms of right-sided failure include increased jugular venous pressure, right upper quadrant or abdominal discomfort, hepatomegaly, ascites and/or jaundice, and peripheral edema. Left-sided failure is characterized by dyspnea, orthopnea, and paroxysmal nocturnal dyspnea, attributable to elevated pulmonary pressure with or without pulmonary edema or effusion. Acute exacerbation of left-sided heart failure often presents with prominent dyspnea, diaphoresis, tachycardia, and pale, cold extremities.

Low-output heart failure is marked by decreased cardiac output and is most often caused by hypertension, myocardial infarction, or chronic coronary artery disease. High-output heart failure is often caused by anemia, sepsis, obesity[3] , or hyperthyroidism. In these cases, long term excessive demands on the heart due to a decrease in blood volume, oxygen carrying capacity, or systemic vascular resistance lead to a clinical syndrome similar to that seen with typical low-output heart failure. The heart may initially be able to respond with appropriate or increased cardiac output, but left untreated, ventricular remodeling and impaired ejection fraction can occur.

The most common etiology of heart failure with reduced ejection fraction is ischemic heart disease.[4] Heart failure with preserved ejection fraction is usually multifactorial, with the most common causes being uncontrolled hypertension, diabetes, and coronary artery disease. In this condition, myocardial stiffness and impaired relaxation lead to elevated ventricular filling pressures. The ventricle is still able to contract (and therefore the ejection fraction remains preserved), but stroke volume is reduced. To maintain or increase cardiac output, the heart rate must increase. If persistent, this increased stress on the heart can lead to failure. Heart failure with preserved ejection fraction accounts for approximately half of heart failure diagnoses and is more common in women.[5]

Complications of heart failure include activity-limiting symptoms, syncope, arrhythmias (which may be fatal), progressive systolic or diastolic dysfunction, thromboembolism (usually strokes), and circulatory collapse.

Risk Factors

Age. The incidence of heart failure and left-ventricular dysfunction increases with age.[6]

Race. There is a higher incidence of heart failure in African Americans, compared with white Americans. This is thought to be due to socioeconomic factors as well as higher prevalence of resistant hypertension and type 2 diabetes.[7]

History of coronary artery disease. Left ventricular dysfunction often results from ischemic injury to the myocardium.

History of cardiomyopathy. Family or personal history of dilated, hypertrophic, or restrictive cardiomyopathy.

Diabetes. Diabetes accelerates the progression of coronary artery disease as well as left ventricular remodeling, both of which contribute to systolic as well as diastolic dysfunction.

Use of thiazoladinediones. Rosiglitazone and pioglitazone raise the risk of heart failure in diabetes patients. Rosiglitazone is also associated with other cardiac risks.[8] ,[9]

Smoking. Smoking dramatically raises risk for ASCVD and thus heart failure.

History of rheumatic fever or valvular heart disease.

Hypertension. Pulmonary hypertension generally leads to right-sided heart failure, whereas systemic hypertension leads to left-sided heart failure.

Alcohol abuse. Alcohol may lead to dilated cardiomyopathy.

Pericardial disease.

Obesity. Hypertension, type 2 diabetes, and left ventricular hypertrophy are commonly found in obese patients. Heart failure incidence increases by 5% for men and 7% for women for every 1 point increase in BMI above 25 kg/m 2.[10] Surprisingly, however, BMI appears to have an inverse association with CHF-related mortality in most studies. In a study of more than 7,500 individuals, a linear increase in CHF mortality has been found to occur with a BMI below 30 kg/m². Persons with heart failure and a BMI of 25 to 29.9, 22.5 to 24.9, and < 22.5 had a mortality risk approximately 120%, 145%, and 170% greater than those with a BMI > 30 kg/m².[11]

Obstructive Sleep Apnea (OSA). Untreated obstructive sleep apnea causes frequent night-time apneic episodes, which in turn causes periods of deoxygenation. Over time, this process leads not only to irreversible pulmonary disease, but both right and left sided systolic failure. Systolic heart failure due to OSA is thought to be one of the least reversible causes of CHF.

Diagnosis

Diagnosis is based on history and physical examination. Imaging and lab results are used to support the diagnosis.[12] The New York Heart Association (NYHA) classification system describes the functional limitations of heart failure[13] :

Class I: Symptoms (e.g., fatigue, dyspnea, and palpitations) are experienced on heavy exertion.

Class II: Symptoms occur with mild to moderate levels of exertion.

Class III: Symptoms occur with less than ordinary exertion.

Class IV: Symptoms occur with any exertion or at rest.

Diagnostic Tools

2-D and Doppler echocardiogram is the most common imaging modality for assessing cardiac function. Echocardiography can evaluate left and right ventricular systolic function, diastolic function, valvular structure and function, and cardiac chamber sizes. It also identifies possible heart failure etiologies, such as MI, valvular disease, and cardiomyopathies.

Chest x-ray can identify intrinsic pulmonary disease, pulmonary edema, and pleural effusions. It can also estimate the degree of cardiac enlargement but is much less accurate than echocardiography.

Electrocardiogram may reveal MI, dysrhythmias, conduction abnormalities, or left ventricular hypertrophy.

Measurement of circulating concentrations of brain natriuretic peptide (BNP), which is produced by the heart, is increasingly used to diagnose and assess the degree of heart failure and monitor treatment effects.

Blood tests, such as a complete blood count and comprehensive metabolic panel, are usually standard. Additional tests should be ordered when clinically appropriate to help determine the etiology. Heart failure without an identifiable cause usually requires an evaluation for coronary heart disease, such as exercise stress testing, noninvasive imaging, or cardiac catheterization.

Treatment

Treatment of chronic heart failure should target the underlying disorder: hypertension, coronary artery disease, diabetes, etc. See relevant chapters for specific information. Certain medications (i.e., Calcium channel blockers, NSAIDs, metformin, and thiazolidinediones) may worsen heart failure.[14]

Heart failure with preserved ejection fraction is more difficult to treat. Treatment strategies overlap with systolic failure in some cases (i.e., treatment of hypertension, diuretic use for pulmonary symptoms, rate control in atrial fibrillation, and treatment of ischemic CHD), but additional treatment strategies are still being researched.[5]

Oral Drugs

Diuretics are first-line therapy for heart failure patients with symptoms of fluid retention and reduced ejection fraction, but they are less useful (and may be contraindicated) for heart failure with preserved ejection fraction. Loop diuretics (e.g., furosemide) are most commonly used, prevent volume overload, and have favorable vascular effects.

Angiotensin-converting enzyme inhibitors (ACEI) (e.g., enalapril, lisinopril) are first-line heart failure treatments. They decrease mortality in a broad range of heart failure patients by decreasing preload and afterload, as well as by several other mechanisms including reducing blood volume and preventing cardiac remodeling associated with heart failure.[15]

Beta-blockers are a first-line treatment for all categories of heart failure and are not limited to patients with coronary artery disease or hypertension. Carvedilol, metoprolol succinate, and bisoprolol have all been shown to decrease heart failure mortality.[16]

Angiotensin II receptor blockers (ARB) (e.g., losartan, candesartan, irbesartan) are generally equivalent to ACEIs and often used if side effects (usually cough) limit ACEI use. It is not recommended to combine an ACEI and an ARB as this can result in renal impairment and potentially dangerous electrolyte imbalances.[17]

Hydralazine and Nitrates. Evidence suggests that patients who self-identify as African American and have NYHA class III or IV heart failure may have improved response to the addition of hydralazine and isosorbide dinitrate when initial therapy is not successful.

Aldosterone blockers (e.g., spironolactone, eplerenone) have been shown to decrease heart failure mortality when added to usual therapy[18] ,[19] but patients must be monitored for hyperkalemia and impaired renal function.

Angiotensin Receptor Neprilysin Inhibitor (ARNi) (e.g. Sacubitril) – Sacubitril, in combination with valsartan, an ARB) was approved in 2015 for treatment of heart failure with reduced ejection fraction. It can be used in place of ACE-inhibitors to decrease mortality and heart failure hospitalizations (Paradigm-HF trial). Sacubitril must be used with caution in patients prone to renal failure or hypotension.

Anticoagulants (e.g., warfarin, Aspirin, Clopidogrel) are typically not recommended for routine use in cases of reduced ejection fraction unless there is a specific indication such as concomitant atrial fibrillation or left ventricular thrombus. In clinical trials, anticoagulation decreased the rate of thrombotic events but this benefit was outweighed by increased risk of significant bleeding.[20] When coronary artery disease is present along with left ventricular dysfunction, it is recommended to follow the CAD guidelines regarding anticoagulation.

Digoxin is an oral inotropic agent that provides symptomatic relief, but no improvement in overall mortality, in patients with decompensated heart failure.[21] Its therapeutic window is narrow, and high serum digoxin concentration may increase mortality and cause a wide array of arrhythmias.[22] It may be useful for patients who remain symptomatic despite optimal treatment with diuretics, ACEI or ARB, and beta-blockers, especially if atrial fibrillation is present. Digoxin is not useful for diastolic dysfunction. Dosage must be adjusted for older patients and those with renal dysfunction, as well as in the presence of many drugs that influence digoxin levels.

Calcium channel blockers (e.g., verapamil, amlodipine) are contraindicated for patients with significant impairment in ventricular function.

Statins. There are currently no studies showing any reduction in mortality or symptomatic improvement from statin therapy when prescribed solely for treatment of heart failure.

Intravenous Medications

In general, intravenous therapies for heart failure decompensation are intended to relieve symptoms and facilitate hospital discharge. They are not generally used for prolonging survival beyond the short term. The following drugs are used for treatment of decompensation:

Dobutamine is an inotropic and vasoactive agent administered intravenously for symptom relief and systolic function improvement. It requires close monitoring, as it may produce dysrhythmias or abrupt blood pressure changes. It is sometimes given to end-stage heart failure patients for home infusion, in conjunction with amiodarone, to provide symptomatic relief and to decrease the need for hospitalization.[23]

Phosphodiesterase inhibitors (e.g., amrinone, milrinone) increase contractility by modulating calcium influx into cardiac cells. They also facilitate both arterial and venous dilation, reducing preload and afterload. They are not used for chronic therapy, as this has resulted in increased mortality for heart failure patients.[24]

Surgical Procedures

Implantable cardioverter-defibrillator (ICD) use has been shown to decrease mortality from lethal dysrhythmias for high-risk patients, particularly those with documented dysrhythmias and/or severe systolic dysfunction, typically with ejection fraction less than 30%-35%.

Cardiac Resynchronization Devices (CRT) are implantable devices designed to allow the right and left ventricles to beat in synchrony, allowing for improved cardiac output, and in some cases, an increase in ejection fraction. These devices are often placed in conjunction with ICD’s (CRT-D) to reduce the hospitalization and mortality rates for people with heart failure with reduced ejection fraction).

Intra-aortic balloon pump (IABP) is used to treat refractory cases of cardiogenic shock, which can be due to acute, decompensated heart failure. IABP assists the heart by decreasing afterload and improving cardiac output. After insertion into the aorta via catheter, the balloon inflates at the beginning of diastole to enhance coronary perfusion. It deflates at the beginning of systole, thereby increasing cardiac output.

Cardiac transplant may be necessary for patients with end-stage heart failure. Left ventricular assist devices (LVAD) are used in extraordinary cases to bridge a severely ill patient to cardiac transplantation.

Other Treatments

Cardiac Rehabilitation should be approved by a physician and overseen by an exercise physiologist. Exercise and conditioning have been shown to improve functional status, decrease hospitalization, and improve quality of life, but has not been shown to reduce mortality.[25]

Leg elevation above the heart should be done during rest.

Compression stockings may help control leg edema and improve fluid removal. Results are variable, and a therapeutic trial will help determine usefulness for individual heart failure patients.

Nutritional Considerations

Previously, the mainstay of heart failure prevention and treatment was concerned mainly with the restriction of excess sodium intake in order to prevent fluid overload. While sodium remains important, macronutrient nutrition has appeared as more important in the prevention than previously, and a particular role for the avoidance of foods containing saturated fat has emerged. Healthy dietary patterns high in fruits and vegetables and the inclusion of fish also appear important in preventing heart failure, and the benefit of certain dietary supplements (thiamine, Coenzyme Q10) has been further confirmed.

Avoidance of saturated fat and fried foods. The risk for heart failure was shown to increase with higher amounts of red meat intake in the Physicians Health Study, with or without previous MI. Men in the highest compared to lowest intake groups had a roughly 25% greater risk for heart failure.[26] Similarly, daily consumption of eggs was found to increase the risk for heart failure by 30% when compared with individuals who didn’t eat eggs or limited these to three per month.[27] These results were similar to those of the Atherosclerosis Risk in Communities study that found a 23% greater risk for heart failure in individuals eating the most compared to the fewest eggs.[28] The Physicians Health Study also found a graded increase in risk for heart failure in persons consuming fried foods, with a two-fold risk for those consuming these at least daily compared with those eating these less than once per week.[29] Meat, eggs, and fried foods are all sources of advanced glycation end products, which have been related to the severity of HF and are an independent predictor for cardiac events in these patients.[30]

A health-promoting dietary pattern. Both Mediterranean[31] ,[32] and DASH (Dietary Approaches to Stop Hypertension) –style diets[33] as well as dietary patterns that are lower in meat[34] higher in unsaturated fat[35] and higher in fish 36 (discussed further below) have all been associated with significant reductions in the risk for heart failure.

Eating a minimum of five fruits and vegetables per day. Total fruit and vegetable consumption was inversely related to the incidence of heart failure in a study of over 34,000 women. Although vegetables appeared to be more protective against heart failure than fruits, the intake of five or more daily servings combined was associated with a 20% lower risk when compared to those eating half that amount.[36]

Fish consumption. Meta-analytic reviews[37] ,[38] have concluded that omnivores consuming the most fish have slightly (roughly 15%) lower risk for heart failure compared with individuals consuming the lowest amount. However, in omnivorous populations, the ratio of omega-6 to omega-3 fats is high (20:1), in contrast to that during much of human evolution (1:1). This ratio predisposes individuals to atherosclerosis and inflammation[39] that are often precursors of heart failure. Thus, these studies do not suggest that fish consumption is preferable to the avoidance of meat altogether, and are more indicative of the need to counterbalance a high omega-6 intake from animal products, an important consideration, given that plant-based are associated with improvements in major cardiac risk factors.

Sodium reduction. Restriction of excess sodium is important in reducing the risk for heart failure; however, the degree of sodium restriction in established CHF is a matter of some controversy. The most recent recommendations from the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) downgraded sodium restriction for patients with CHF from a class I (part of standard care) to a class IIa (reasonable to include in care) recommendation. In addition, the recommendation for stringent low salt intakes (to 1500 mg/d) was reserved for patients with Stage A and B CHF only.[40] The Heart Failure Society of America recommends a salt restriction to less than 2,000 mg/d for patients with moderate to severe CHF.[41]

Some experts are more permissive regarding sodium intake, because stringent sodium restriction can increase renin, aldosterone, epinephrine, and norepinephrine. Liberalizing sodium intake (while avoiding the high sodium intakes found on typical Western diets) may actually enhance response to diuretic therapy and predispose patients to more favorable long-term outcomes. 30 Thus, most evidence supports a more moderate level of salt restriction to 2,000-3,000 mg/day (half of typical daily American sodium intake).[42] This level of intake reduces hospital readmissions for CHF, while higher intakes increase the need for urgent transplantation. 30

Monitoring magnesium status. The importance of magnesium in patients with heart failure lies in its vasodilatory, anti-inflammatory, anti-ischemic, and antiarrhythmic properties, among others. The reported prevalence of hypomagnesemia in heart failure patients ranges from 7%-52%, and replacement therapy is not uncommon. However, a review of magnesium status in these patients indicated that high blood levels were associated with an almost 40% greater risk for cardiovascular mortality, when compared with those with normal levels.[43]

Thiamine supplements for patients treated with diuretics. Diuretic therapy, particularly furosemide, is responsible for increasing thiamine excretion.[44] High dose thiamine (300 mg/day) was found to significantly improve ejection fraction in heart failure patients.[45]

Moderation in alcohol consumption. A dose-response meta-analysis found a 10% lower risk for heart failure in persons consuming 3 drinks per week and a 13% and 14% lower risk respectively in persons consuming 7 and 10 drinks per week when compared with individuals who rarely or never consumed alcohol. No further benefit was found above this amount.[46]

Coenzyme Q10 supplementation. A previous meta-analysis of controlled clinical trials with coenzyme Q10 found significant improvements in stroke volume, cardiac output, cardiac index, and end-diastolic volume in patients with heart failure, regardless of etiology (e.g., idiopathic, dilated, ischemic, hypertension, valvular heart disease, and congenital heart disease).[47] More recently, the Q-SYMBIO study documented significantly fewer cardiovascular deaths and hospital admissions for heart failure in heart failure patients given 300 mg. Coq10 per day compared with placebo.[48]

Orders

Diet: When heart failure is the result of heart disease, a cardiovascular-specific diet should be ordered (see Coronary Heart Disease chapter).

Sodium and fluid restriction as appropriate.

Nutrition consultation to help the patient adjust to the above diet.

Exercise physiologist, physical therapist, and occupational therapist consultations to prescribe exercise regimen and provide appropriate support for activities of daily living.

What to Tell the Family

Heart failure is usually progressive. However, patients may be able to prolong survival, improve heart function, ameliorate chronic symptoms, avoid repeated episodes of decompensation, and decrease the need for hospitalization by following a low-sodium diet, restricting fluids, and taking medications as prescribed. Exercise conditioning is also important, as it can help improve exercise tolerance and oxygen uptake. The family may need to provide physical support as the patient attempts to recondition. Family support is also important to help the patient adhere to diet changes.

References

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Last updated: November 21, 2017

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TY - ELEC T1 - Heart Failure ID - 1342034 Y1 - 2017/11/21/ PB - Nutrition Guide for Clinicians UR - https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342034/all/Heart_Failure ER -