Heart failure guidelines: What you need to know about the 2017 focused update

Cleveland Clinic Journal of Medicine. 2019 February;86(2):123-139 | 10.3949/ccjm.86a.18022
February 1, 2019|Cleveland Clinic Journal of Medicine
Lee Rodney Haselhuhn, MD;Daniel J. Brotman, MD;Ilan Shor Wittstein, MD
Author and Disclosure Information

Lee Rodney Haselhuhn, MD
Department of Medicine, Johns Hopkins University, Baltimore, MD

Daniel J. Brotman, MD
Department of Medicine, Johns Hopkins University, Baltimore, MD

Ilan Shor Wittstein, MD
Departments of Medicine and Cardiology, Johns Hopkins University, Baltimore, MD

Address: Lee Rodney Haselhuhn, MD, Division of General Internal Medicine, Johns Hopkins Hospitalist Program, Johns Hopkins Hospital, 600 N. Wolfe St., Meyer 8-134M, Baltimore, MD 21287; lhaselh1@jhmi.edu

Dr. Brotman has disclosed consulting for Portola Pharmaceuticals.

Release date: February 1, 2019
Expiration date: January 31, 2020
Estimated time of completion: 1 hour

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ABSTRACT

The 2017 focused update of the 2013 ACC/AHA guideline on heart failure contains new and important recommendations on prevention, novel biomarker uses, heart failure with preserved ejection fraction (HFpEF), and comorbidities such as hypertension, iron deficiency, and sleep-disordered breathing. Potential implications for management of acute decompensated heart failure will also be explored.

KEY POINTS

  • Despite advances in treatment, heart failure remains highly morbid, common, and costly. Prevention is key.
  • Strategies to prevent progression to clinical heart failure in high-risk patients include new blood pressure targets (< 130/80 mm Hg) and B-type natriuretic peptide screening to prompt referral to a cardiovascular specialist.
  • An aldosterone receptor antagonist might be considered to decrease hospitalizations in appropriately selected stage C HFpEF patients. Routine use of nitrates or phosphodiesterase-5 inhibitors in such patients is not recommended.
  • Outpatient intravenous iron infusions are reasonable in persistently symptomatic New York Heart Association stage II to III heart failure with reduced ejection fraction (HFrEF) to improve functional capacity and quality of life.
  • The new systolic blood pressure target is less than 130 mm Hg for stage A heart failure, stage C HFrEF, and stage C HFpEF.

New or modified recommendations on iron

The 2017 update1 makes recommendations regarding iron deficiency and anemia in heart failure for the first time.

A class IIb recommendation states that it might be reasonable to treat NYHA class II and III heart failure patients with iron deficiency with intravenous iron to improve functional status and quality of life. A strong recommendation has been deferred until more is known about morbidity and mortality effects from adequately powered trials, some of which are under way and explored further below.

The 2017 update also withholds any recommendations regarding oral iron supplementation in heart failure, citing an uncertain evidence base. Certainly, the subsequent IRONOUT-HF trial does not lend enthusiasm for this approach.

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Lastly, given the lack of benefit coupled with the increased risk of thromboembolic events evident in a trial of darbepoetin alfa vs placebo in non-iron deficiency-related anemia in HFrEF,40,41 the 2017 update provides a class III (no benefit) recommendation against using erythropoietin-stimulating agents in heart failure and anemia.

HYPERTENSION IN HEART FAILURE

The 2013 guidelines for the management of heart failure simply provided a class I recommendation to control hypertension and lipid disorders in accordance with contemporary guidelines to lower the risk of heart failure.1

SPRINT

The Systolic Blood Pressure Intervention Trial (SPRINT)42 sought to determine whether a lower systolic blood pressure target (120 vs 140 mm Hg) would reduce clinical events in patients at high risk for cardiovascular events but without diabetes mellitus. Patients at high risk were defined as over age 75, or with known vascular disease, chronic kidney disease, or a Framingham Risk Score higher than 15%. This multicenter, open-label controlled trial randomized 9,361 patients to intensive treatment (goal systolic blood pressure < 120 mm Hg) or standard treatment (goal systolic blood pressure < 140 mm Hg).

SPRINT was stopped early at a median follow-up of 3.26 years when a 25% relative risk reduction in the primary composite outcome of myocardial infarction, other acute coronary syndromes, stroke, heart failure, or death from cardiovascular causes became evident in the intensive-treatment group (1.65% vs 2.19% per year, HR 0.75, P < .0001).

All-cause mortality was also lower in the intensive-treatment group (HR 0.73, P = .003), while the incidence of serious adverse events (hypotension, syncope, electrolyte abnormalities, acute kidney injury, and noninjurious falls) was only slightly higher (38.3% vs 37.1%, P = .25). Most pertinent, a significant 38% relative risk reduction in heart failure and a 43% relative risk reduction in cardiovascular events were also evident.

Of note, blood pressure measurements were taken as the average of 3 measurements obtained by an automated cuff taken after the patient had been sitting quietly alone in a room for 5 minutes.

New or modified recommendations on hypertension in heart failure

Given the impressive 25% relative risk reduction in myocardial infarction, other acute coronary syndromes, stroke, heart failure, or death from cardiovascular causes in SPRINT,42 the 2017 update1 incorporated the intensive targets of SPRINT into its recommendations. However, to compensate for what are expected to be higher blood pressures obtained in real-world clinical practice as opposed to the near-perfect conditions used in SPRINT, a slightly higher blood pressure goal of less than 130/80 mm Hg was set.

Specific blood pressure guidelines have not been given for stage A heart failure in the past. However, as for other new approaches to prevent heart failure in this update and given the 38% relative risk reduction in heart failure seen in SPRINT, a class I recommendation is given to target a blood pressure goal of less than 130/80 mm Hg in stage A heart failure with hypertension (Table 4).

Although not specifically included in SPRINT, given the lack of trial data on specific blood pressure targets in HFrEF and the decreased cardiovascular events noted above, a class I (level of evidence C, expert opinion) recommendation to target a goal systolic blood pressure less than 130 mm Hg in stage C HFrEF with hypertension is also given. Standard guideline-directed medications in the treatment of HFrEF are to be used (Table 4).

Similarly, a new class I (level of evidence C, expert opinion) recommendation is given for hypertension in HFpEF to target a systolic blood pressure of less than 130 mm Hg, with special mention to first manage any element of volume overload with diuretics. Other than avoiding nitrates (unless used for angina) and phosphodiesterase inhibitors, it is noted that few data exist to guide the choice of antihypertensive further, although perhaps renin-angiotensin-aldosterone system inhibition, especially aldosterone antagonists, may be considered. These recommendations are fully in line with the 2017 ACC/AHA high blood pressure clinical practice guidelines,43 ie, that renin-angiotensin-aldosterone system inhibition with an angiotensin-converting enzyme (ACE) inhibitor or ARB and especially mineralocorticoid receptor antagonists would be the preferred choice (Table 4).

SLEEP-DISORDERED BREATHING IN HEART FAILURE

Sleep-disordered breathing, either obstructive sleep apnea (OSA) or central sleep apnea, is quite commonly associated with symptomatic HFrEF.44 Whereas OSA is found in roughly 18% and central sleep apnea in 1% of the general population, sleep-disordered breathing is found in nearly 60% of patients with HFrEF, with some studies showing a nearly equal proportion of OSA and central sleep apnea.45 A similar prevalence is seen in HFpEF, although with a much higher proportion of OSA.46 Central sleep apnea tends to be a marker of more severe heart failure, as it is strongly associated with severe cardiac systolic dysfunction and worse functional capacity.47

Not surprisingly, the underlying mechanism of central sleep apnea is quite different from that of OSA. Whereas OSA predominantly occurs because of repeated obstruction of the pharynx due to nocturnal pharyngeal muscle relaxation, no such airway patency issues or strained breathing patterns exist in central sleep apnea. Central sleep apnea, which can manifest as Cheyne-Stokes respirations, is thought to occur due to an abnormal ventilatory control system with complex pathophysiology such as altered sensitivity of central chemoreceptors to carbon dioxide, interplay of pulmonary congestion, subsequent hyperventilation, and prolonged circulation times due to reduced cardiac output.48

What the two types of sleep-disordered breathing have in common is an association with negative health outcomes. Both appear to induce inflammation and sympathetic nervous system activity via oxidative stress from intermittent nocturnal hypoxemia and hypercapnea.49 OSA was already known to be associated with significant morbidity and mortality rates in the general population,50 and central sleep apnea had been identified as an independent predictor of mortality in HFrEF.51

At the time of the 2013 guidelines, only small or observational studies with limited results had been done evaluating treatment effects of continuous positive airway pressure therapy (CPAP) on OSA and central sleep apnea. Given the relative paucity of data, only a single class IIa recommendation stating that CPAP could be beneficial to increase left ventricular ejection fraction and functional status in concomitant sleep apnea and heart failure was given in 2013. However, many larger trials were under way,52–59 some with surprising results such as a significant increase in cardiovascular and all-cause mortality (Table 5).54