Heart Failure: A guideline to optimizing care

Heart failure (HF) is a syndrome resulting from the structural or functional impairment of the ventricular filling or the ejection of blood. Approximately 1% to 2% of adults in developed countries are affected by HF. The risk of HF increases with age, and HF is thought to affect over 10% of adults above 70 years of age. Though common cardiovascular risk factors such as obesity, diabetes, and hyperlipidemia are all prevalent in patients with HF, hypertension is an important cause of HF. Common symptoms of HF include dyspnea, orthopnea, acute pulmonary edema, chest pain, tachycardia, fatigue, weight loss, nausea, and wheezing.

DIAGNOSIS

There are a few important steps that must be undertaken in order to correctly diagnose HF. First, the clinician should take a detailed clinical history including a history of coronary artery disease (CAD), history of arterial hypertension, exposure to cardiotoxic drugs/radiation, diuretic use, and orthopnea or paroxysmal nocturnal dyspnea. Additionally, the American College of Cardiology/American Heart Association (ACC/AHA) 2013 guidelines recommends that the clinician also takes a 3–generation family history. This may indicate potential causes of cardiomyopathy and is important in diagnosing familial syndromes, which occur in 20% to 35% of patients with apparent idiopathic dilated cardiomyopathy.

A thorough physical examination should be performed to check for rales, bilateral ankle edema, heart murmur, jugular venous dilatation, and laterally displaced or broadened apical beat.

Finally, electrocardiography (ECG) should be used to screen for abnormalities. If ≥1 positive factors from the history, examination or ECG are present, the clinician should obtain natriuretic peptide (NP) levels. HF is very unlikely with normal NP levels, but elevated NP levels indicate that echocardiography is required. A 12–lead electrocardiogram can be of use to determine whether or not arrhythmias, are present that may contribute to HF.

 

Acute heart failure (AHF) is a life–threatening condition. The first step in diagnosis is ruling out other causes of the symptoms (eg. pulmonary infection or acute renal failure). The 2016 ESC HF guidelines detail measures for the diagnosis and treatment of HF. They suggest that the clinician should identify immediately coexisting life-threatening clinical conditions and/or precipitants (according to the CHAMP acronym):

  • [acute] Coronary syndrome
  • Hypertension emergency
  • Arrhythmia
  • Mechanical cause
  • Pulmonary embolism

A clinical history, physical exam, and other tests such as X–ray, and echocardiography are required for diagnosis; however, in AHF, it is critical that treatment is started as soon as possible. Patients should be monitored continuously to ensure that ventilation, peripheral perfusion, oxygenation, heart rate, and blood pressure are maintained.

To gauge prognosis and select appropriate therapeutic options for patients with HF, clinicians can use one of the available classification systems.

The New York Heart Association (NYHA) system defines

Class I as no limitation of physical activity.

Class II as slight limitation of physical activity.

Class III as marked limitation of physical activity

Class IV as symptoms occurring even at rest or discomfort with any physical activity.

The ACC/AHA classification system has 4 stages.

Stage A means there is a high risk of HF but no structural heart disease or symptoms of HF.

Stage B means there is structural heart disease but no symptoms of HF.

Stage C indicates structural heart disease and symptoms of HF.

Stage D indicates refractory HF requiring specialized interventions.

The recent ESC guidelines incorporate updated terminology to describe patients with HF; patients with HF are now categorized according to their left ventricular ejection fraction (LVEF). Depending on the LVEF, patients may present with different etiologies and comorbidities and may respond differently to therapy.

The ESC has defined 3 different categories

  • HF with preserved ejection fraction (HFpEF): these patients have an LVEF ≥50%, elevated NP levels (B–type natriuretic peptide [BNP] >35 pg/mL and/or NT–proBNP >125 pg/mL), and either relevant structural heart disease or diastolic dysfunction
  • HF with midrange ejection fraction (HFmrEF): these patients have an LVEF of 40% to 49%, elevated NP levels (BNP >35 pg/mL and/or NT–proBNP >125 pg/mL), and either relevant structural heart disease or diastolic dysfunction
  • HF with reduced ejection fraction (HFrEF): these patients have an LVEF <40%

 

Risk stratification can aid in selecting the best treatment approach. Objective measures such as biomarker testing may provide more accurate prognostic information than clinical risk scores. BNP and NT–proBNP are the best-known biomarker in diagnosing HF and can reliably predict the probability of survival in patients with HF irrespective of age, gender, and the number of comorbidities. Other emerging biomarkers include galectin–3, ST, and hsCRP.

 

TREATMENT

ESC guidelines recommend the following to prevent or delay the development of overt HF (class I recommendations):

Treatment of hypertension, statin treatment for patients with or at high risk for coronary artery disease (CAD), Counseling for smoking cessation and alcohol intake reduction, and pharmacologic treatment as described below.

 

Lifestyle Modification:

One of this first steps to treat HF is through lifestyle modification. Patients should stop smoking, avoid secondhand smoke, and avoid alcohol. Alcohol may interact with medications, weaken the heart muscle, and increase the risk of abnormal heart rhythm. Patients should consume a healthy diet that is low in salt and includes lots of fruits and vegetables, lean proteins, and whole grains. Patients with HF should limit their consumption of fats and cholesterol.

 

Obesity is a risk factor for HF and complicates its diagnosis because it can cause dyspnea, exercise intolerance, and ankle swelling and may result in poor quality echocardiographic images. Obese individuals also have reduced NP levels. Obesity is more common in HFpEF than in HFrEF, although it is possible that misdiagnosis may explain at least some of this difference in prevalence. Obesity should be managed as recommended in the ESC guidelines on cardiovascular disease prevention if the aim is to prevent future development of HF. However, these guidelines do not refer to the HF patient in whom higher BMI is not adverse, and, although often recommended for symptom benefit and risk factor control, weight loss as an intervention has never been prospectively shown to be either beneficial or safe in HFrEF. When weight loss is occurring in HF, it is associated with high mortality and morbidity, worse symptom status, and poor quality of life. In patients with HF with moderate degrees of obesity (BMI <35 kg/m2), weight loss cannot be recommended. In more advanced obesity (BMI 35 to 45 kg/m2), weight loss may be considered to manage symptoms and exercise capacity.

 

For those patients at a stable weight, sudden weight gain may indicate fluid retention. Patients should check their extremities for swelling daily and know when to call their provider about weight gain since this may necessitate a change in treatment. If the clinician deems it safe, patients with HF can enroll in a cardiac rehabilitation program or perform moderate aerobic activity.

 

Pharmacologic Therapies

Patients with HF often require multiple concomitant medications to treat HF and manage other cardiovascular risk factors (eg. dyslipidemia, hypertension, and diabetes). In patients with HF, yearly vaccination against influenza and pneumonia should be considered.

  • Angiotensinconverting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are vasodilators that widen blood vessels, lower blood pressure, improve blood flow, and reduce the amount of work required by the heart. Drugs in this class include enalapril, lisinopril, captopril, losartan, and valsartan. The Guidelines recommend ACE inhibitor therapy for all symptomatic patients as well as for patients with asymptomatic LV systolic dysfunction (Class I). The guidelines note that many patients receive suboptimal doses of ACE inhibitors and caution clinicians to up–titrate ACE inhibitors to the maximum tolerated dose. The ESC recommends ARBs only for patients who cannot take ACE inhibitors.
  • Beta blockers block norepinephrine and epinephrine from binding to receptors and can control the symptoms of HF. Beta blockers widen blood vessels and reduce blood pressure, which is helpful in patients with both HF and hypertension. Beta-blockers can also be used to slow the heart rate, giving the heart more time to fill with blood and improving ejection fraction. Over time, this treatment can improve the heart’s pumping mechanism. Beta-blockers can reduce the risk of abnormal heart rhythms and decrease the chance of sudden cardiovascular death. Drugs in this class include carvedilol, metoprolol extended–release, nebivolol, and bisoprolol. The guidelines recommend that beta-blockers be initiated in stable patients at a low dose and then up–titrated to the maximum tolerated dose. Beta-blocker therapy is recommended by the ESC for patients with asymptomatic LV systolic dysfunction and a history of myocardial infarction (MI).

Loop diuretics such as furosemide, bumetanide, and torsemide prevent sodium reabsorption and help prevent fluid from collecting in the body (especially in the lungs). Loop diuretics are stronger than thiazide diuretics but have a shorter duration of effect. Thiazide diuretics are normally used to treat hypertension, while loop diuretics are used to treat edema. Clinicians should monitor potassium and magnesium levels in patients taking diuretics.

  • Mineralocorticoid/aldosterone antagonists (MRAs) are potassium–sparing diuretics. Blocking aldosterone decreases sodium and water retention by the kidneys to reduce blood pressure. Examples of drugs in this class include spironolactone and eplerenone. A potential adverse effect of these agents is elevated potassium, so patients may be required to avoid eating foods high in potassium, and clinicians should monitor renal function and serum potassium levels regularly.The Guidelines recommend MRAs for all symptomatic patients with HFrEF and LVEF ≤35%.

 

 

Novel Therapies

Angiotensin receptor neprilysin inhibitors (ARNIs) are the newest class of agents to treat HF. The first drug in this class is a combination tablet containing sacubitril and valsartan. Valsartan is an ARB that inhibits the renin–angiotensin–aldosterone system, Sacubitril inhibits neprilysin, which in turn slows down the rate at which NPs, bradykinin and other peptides break down. The resulting high concentrations of A–type natriuretic peptide (ANP) and BNP bind to NP receptors and increase cyclic guanosine monophosphate (cGMP) to improve diuresis, natriuresis, and myocardial relaxation. ANP and BNP also inhibit the secretion of renin and aldosterone.

Clinicians should be aware that this medication increases BNP values, but not NT–proBNP values; this may make it difficult for clinicians to interpret BNP levels in patients with HF who are taking this medication. The tablets are substituted for an ACE inhibitor or ARB and are usually given with other HF therapies. Simultaneous use of an ACE Inhibitor (or ARB) with sacubitril/valsartan is contraindicated. These drugs must be stopped 36 hours prior to initiation of sacubitril/valsartan.

Ivabradine is the second novel agent was approved by the FDA in April 2015 to reduce hospitalizations for HF. Based on the results of a retrospective analysis that showed ivabradine reduced the combined endpoint of mortality or hospitalization for in patients with symptomatic HFrEF or LVEF ≤35% who were in sinus rhythm and had a heart rate ≥70 bpm who had been hospitalized for HF within the previous 12 months, receiving treatment with an evidence-based dose of beta blocker (or maximum tolerated dose), an ACE inhibitor (or ARB) and an MRA. Ivabradine is a hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker that inhibits the cardiac pacemaker If the current to lower the heart rate. It does not affect myocardial contractility or ventricular repolarization, and it is the first approved drug in this class. It should only be used in patients who are in sinus rhythm. Ivabradine should not be used in patients with decompensated heart failure, blood pressure <90/50 mm Hg, sick sinus syndrome, resting heart rate <60 bpm before treatment, severe hepatic impairment, or in patients whose heart rate is maintained solely by a pacemaker.

 

The European Society of Cardiology, American College of Cardiology, the American Heart Association, as well as the Heart Failure Society of America have updated their HF guidelines to recommend the use of novel therapies in patients with stage C. These include the angiotensin receptor–neprilysin inhibitor (ARNI) sacubitril/valsartan, and the sinoatrial node modulator (If channel Inhibitor) ivabradine.

 

Device Treatment

Patients with HF may be treated with implantable cardioverter–defibrillators (ICDs) that can prevent bradycardia and correct dangerous ventricular arrhythmias to prevent sudden death due to electrical disturbances. The ESC guidelines recommend ICDs as primary prevention for patients with symptomatic HF (NYHA class II to III), an LVEF ≤35% despite ≥3 months of optimal therapy, and ischemic heart disease or dilated cardiomyopathy. Patients who are expected to survive for >1 year with good functional status are good candidates for ICDs (Class I). ICDs are also recommended as secondary prevention for patients who have recovered from a ventricular arrhythmia who are expected to survive for >1 year (class I). ICDs should not be used within 40 days of an MI since they will not improve prognosis. Wearable ICDs are appropriate for short–term use in patients at risk of sudden cardiac death or as a bridge therapy until an ICD can be implanted or when recovery of LV function is expected.

Cardiac resynchronization therapy (CRT) uses a biventricular pacemaker to send electrical impulses to the left and right ventricles so that they pump in a more coordinated fashion. The ESC guidelines recommend CRT for symptomatic patients with LVEF ≤35% despite optimal medical therapy. QRS width predicts CRT response and was the inclusion criterion in all randomized trials, but QRS morphology has also been related to a beneficial response to CRT. Several studies have shown that patients with left bundle branch block (LBBB) morphology are more likely to respond favorably to CRT, whereas there is less certainty about patients with non–LBBB morphology. CRT improves not only cardiac performance but also symptoms and quality of life while reducing morbidity and mortality. Certain patients, such as those with extensive myocardial scar tissue, may experience less improvement in LV function. It also appears that women may respond more favorably to CRT than men due to a smaller body and heart size. Patients in sinus rhythm with a QRS of 130 to 149 ms should be considered for a defibrillator CRT (CRT–D) instead of an ICD. CRT is recommended for patients with a QRS ≥150 ms and LBBB morphology (class I) as well as for patients with a QRS ≥150 ms and non–LBBB morphology (class IIa).

 

Dr. Zubair Ali Menon

Specialist Cardiologist

Aster Speciality Clinic, International City

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