Other conditions that may lead to or contribute to HF, such as obesity, diabetes mellitus, tobacco use, and known cardiotoxic agents, should be controlled or avoided. The lifetime risk for development of hypertension is considerable and represents a major public health issue.
Choice of antihypertensive therapy should also follow guidelines, 27 with specific options tailored to concomitant medical problems, such as diabetes mellitus or CAD. Diuretic-based antihypertensive therapy has repeatedly been shown to prevent HF in a wide range of patients; ACE inhibitors, ARBs, and beta blockers are also effective. Data are less clear for calcium antagonists and alpha blockers in reducing the risk for incident HF.
Patients with known atherosclerotic disease are likely to develop HF. Clinicians should seek to control vascular risk factors in such patients according to guidelines. Obesity and overweight have been repeatedly linked to an increased risk for HF. Similarly, insulin resistance, with or without diabetes mellitus, is also an important risk factor for the development of HF. Additionally, standard therapies for diabetes mellitus, such as use of ACE inhibitors or ARBs, can prevent the development of other risk factors for HF, such as renal dysfunction, , and may themselves directly lower the likelihood of HF.
Despite the lack of supportive, prospective, randomized data, consensus exists that risk factor recognition and modification are vital for the prevention of HF among at-risk patients eg, obese patients or patients with diabetes mellitus. A substantial genetic risk exists in some patients for the development of HF. As noted in Section 6. Adequate therapy of AF is advisable, given a clear association between uncontrolled heart rate and development of HF.
Many therapeutic agents can exert important cardiotoxic effects, with consequent risk for HF, and clinicians should be aware of such risk. For example, cardiotoxic chemotherapy regimens particularly anthracycline based and trastuzumab may increase the risk for HF in certain patients — ; it may be reasonable to evaluate those who are receiving or who have received such agents for LV dysfunction. The use of advanced echocardiographic techniques or biomarkers to identify increased HF risk in those receiving chemotherapy may be useful but remain unvalidated as yet.
Tobacco use is strongly associated with risk for incident HF, 92 , , and patients should be strongly advised about the hazards of smoking, with attendant efforts at quitting. Cocaine and amphetamines are anecdotally but strongly associated with HF, and their avoidance is mandatory. Although it is recognized that alcohol consumption is associated with subsequent development of HF, 92 , , there is some uncertainty about the amount of alcohol ingested and the likelihood of developing HF, and there may be sex differences as well.
Nevertheless, the heavy use of alcohol has repeatedly been associated with heightened risk for development of HF.
Therefore, patients should be counseled about their alcohol intake. Although several epidemiological studies have revealed an independent link between risk for incident HF and biomarkers such as natriuretic peptides, , highly sensitive troponin, and measures of renal function such as creatinine, phosphorus, urinary albumin, or albumin-creatinine ratio, , , , , — it remains unclear whether the risk for HF reflected by any of these biomarkers is modifiable.
Although routine screening with BNP before echocardiography may be a cost-effective strategy to identify high-risk patients, routine measurement of biomarkers in stage A patients is not yet justified. See Table 12 for a summary of recommendations from this section. In all patients with a recent or remote history of MI or ACS and reduced EF, evidence-based beta blockers should be used to reduce mortality.
In all patients with a recent or remote history of MI or ACS, statins should be used to prevent symptomatic HF and cardiovascular events.
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In patients with structural cardiac abnormalities, including LV hypertrophy, in the absence of a history of MI or ACS, blood pressure should be controlled in accordance with clinical practice guidelines for hypertension to prevent symptomatic HF. Beta blockers should be used in all patients with a reduced EF to prevent symptomatic HF, even if they do not have a history of MI. Nondihydropyridine calcium channel blockers with negative inotropic effects may be harmful in asymptomatic patients with low LVEF and no symptoms of HF after MI. Patients with reduced LVEF may not have HF symptoms and are most often identified during an evaluation for another disorder eg, abnormal heart sounds, abnormal ECG, abnormal chest x-ray, hypertension or hypotension, an arrhythmia, acute MI, or pulmonary or systemic thromboembolic event.
However, the cost-effectiveness of routine periodic population screening for asymptomatic reduced LVEF is not recommended at this time. Echocardiographic evaluation should be performed in selected patients who are at high risk of reduced LVEF eg, those with a strong family history of cardiomyopathy, long-standing hypertension, previous MI, or those receiving cardiotoxic therapies. In addition, it should be acknowledged that many adults may have asymptomatic valvular abnormalities or congenital heart lesions that if unrecognized could lead to the development of clinical HF.
Although these asymptomatic patients are in stage B as well, the management of valvular and congenital heart disease is beyond the scope of this guideline. In general, all recommendations for patients with stage A HF also apply to those with stage B HF, particularly with respect to control of blood pressure in the patient with LV hypertrophy 27 , 94 , , and the optimization of lipids with statins.
In 1 study, losartan reduced adverse outcomes in a population with hypertension, and in another study of patients post-MI with low LVEF, valsartan was equivalent to captopril. In patients with previously established structural heart disease, the administration of agents known to have negative inotropic properties such as nondihydropyridine calcium channel blockers and certain antiarrhythmics should be avoided.
Elevations in both systolic and diastolic blood pressure are major risk factors for developing LV hypertrophy, another form of stage B. Consequently, long-term treatment of both systolic and diastolic hypertension reduces the risk of moving from stage A or B to stage C HF. Clinicians should lower both systolic and diastolic blood pressure in accordance with published guidelines. Diuretic-based antihypertensive therapy has been shown to prevent HF in a wide range of target populations.
http://bluetangent.org/tug-of-war.php ACE inhibitors and beta blockers are also effective in the prevention of HF. Patients with HF should receive specific education to facilitate HF self-care. The self-care regimen for patients with HF is complex and multifaceted. Education regarding these recommendations is necessary, albeit not always sufficient, to significantly improve outcomes.
After discharge, many patients with HF need disease management programs, which are reviewed in Section A systematic review of 35 educational intervention studies for patients with HF demonstrated that education improved knowledge, self-monitoring, medication adherence, time to hospitalization, and days in the hospital. See Online Data Supplement 14 for additional data on patient nonadherence. Social support is thought to buffer stress and promote treatment adherence and a healthy lifestyle.
Sodium restriction is reasonable for patients with symptomatic HF to reduce congestive symptoms. Dietary sodium restriction is commonly recommended to patients with HF and is endorsed by many guidelines. Observational data suggest an association between dietary sodium intake with fluid retention and risk for hospitalization. In most of these studies, patients were not receiving GDMT; no study to date has evaluated the effects of sodium restriction on neurohormonal activation and outcomes in optimally treated patients with HF.
These data are mostly from white patients; when the differences in cardiovascular and renal pathophysiology among races are considered, the effects of sodium restriction in nonwhite patients with HF cannot be ascertained from these studies. To make this more complicated, the 3 RCTs that assessed outcomes with sodium restriction have all shown that lower sodium intake is associated with worse outcomes in patients with HF r EF.
These limitations make it difficult to give precise recommendations about daily sodium intake and whether it should vary with respect to the type of HF eg, HF r EF versus HF p EF , disease severity eg, NYHA class , HF-related comorbidities eg, renal dysfunction , or other characteristics eg, age or race. Continuous positive airway pressure can be beneficial to increase LVEF and improve functional status in patients with HF and sleep apnea.
Sleep disorders are common in patients with HF. The decision to refer a patient to a sleep study should be based on clinical judgment. The primary treatment for obstructive sleep apnea is nocturnal continuous positive airway pressure. In a major trial, continuous positive airway pressure for obstructive sleep apnea was effective in decreasing the apnea—hypopnea index, improving nocturnal oxygenation, increasing LVEF, lowering norepinephrine levels, and increasing the distance walked in 6 minutes; these benefits were sustained for up to 2 years.
See Online Data Supplement 15 for additional data on the treatment of sleep disorders. A U-shaped distribution curve has been suggested in which mortality is greatest in cachectic patients; lower in normal, overweight, and mildly obese patients; and higher again in more severely obese patients.
Although there are anecdotal reports about symptomatic improvement after weight reduction in obese patients with HF, , large-scale clinical trials on the role of weight loss in patients with HF with obesity have not been performed. Because of reports of development of cardiomyopathy, sibutramine is contraindicated in HF. Exercise training or regular physical activity is recommended as safe and effective for patients with HF who are able to participate to improve functional status.
Cardiac rehabilitation can be useful in clinically stable patients with HF to improve functional capacity, exercise duration, HRQOL, and mortality. Exercise training in patients with HF is safe and has numerous benefits. Meta-analyses show that cardiac rehabilitation reduces mortality; improves functional capacity, exercise duration, and HRQOL; and reduces hospitalizations. See Online Data Supplement 16 for additional data on cardiac exercise.
Measures listed as Class I recommendations for patients in stages A and B are recommended where appropriate for patients in stage C. Levels of Evidence: A, B, and C as appropriate.
Figure 1. Diuretics are recommended in patients with HF r EF who have evidence of fluid retention, unless contraindicated, to improve symptoms. Diuretics inhibit the reabsorption of sodium or chloride at specific sites in the renal tubules. Bumetanide, furosemide, and torsemide act at the loop of Henle thus, the term loop diuretics , whereas thiazides, metolazone, and potassium-sparing agents eg, spironolactone act in the distal portion of the tubule.
Thiazide diuretics may be considered in hypertensive patients with HF and mild fluid retention because they confer more persistent antihypertensive effects. Controlled trials have demonstrated the ability of diuretic drugs to increase urinary sodium excretion and decrease physical signs of fluid retention in patients with HF.
Diuretics are the only drugs used for the treatment of HF that can adequately control the fluid retention of HF. Appropriate use of diuretics is a key element in the success of other drugs used for the treatment of HF. The use of inappropriately low doses of diuretics will result in fluid retention. Conversely, the use of inappropriately high doses of diuretics will lead to volume contraction, which can increase the risk of hypotension and renal insufficiency.
Diuretics should be prescribed to all patients who have evidence of, and to most patients with a prior history of, fluid retention. Diuretics should generally be combined with an ACE inhibitor, beta blocker, and aldosterone antagonist.
Few patients with HF will be able to maintain target weight without the use of diuretics. The most commonly used loop diuretic for the treatment of HF is furosemide, but some patients respond more favorably to other agents in this category eg, bumetanide, torsemide because of their increased oral bioavailability. In outpatients with HF, diuretic therapy is commonly initiated with low doses, and the dose is increased until urine output increases and weight decreases, generally by 0.
Further increases in the dose or frequency ie, twice-daily dosing of diuretic administration may be required to maintain an active diuresis and sustain weight loss. The ultimate goal of diuretic treatment is to eliminate clinical evidence of fluid retention. Diuretics are generally combined with moderate dietary sodium restriction.
Once fluid retention has resolved, treatment with the diuretic should be maintained in some patients to prevent the recurrence of volume overload. Patients are commonly prescribed a fixed dose of diuretic, but the dose of these drugs frequently may need adjustment. In many cases, this adjustment can be accomplished by having patients record their weight each day and adjusting the diuretic dosage if weight increases or decreases beyond a specified range.