Page created on August 24, 2021. Last updated on April 29, 2022 at 20:58
New ESC guidelines on HF were released in August 2021. I’ve updated this topic to reflect the new guidelines.
Diagnosis and evaluation
Physical examination is important for determining the volume status of the patient. A patient with peripheral pitting oedema, pulmonary crackles on auscultation, elevated jugular pressure, hepatosplenomegaly and/or a recent increase in body weight has fluid overload (hypervolaemia).
Assess the functional capacity
Assessing the functional capacity of the patient is important, as it allows us to stratify the patient into one of the four NYHA types. This is based on the patient history and/or a simple walk test.
Chest X-ray is essential for the evaluation of HF, as it’s a quick and low-impact tool which can give a lot of information. The most common findings are pulmonary congestion, pleural effusion, enlarged heart, etc.
Echo is also essential for the evaluation of HF, as it can directly show the systolic and diastolic function of the heart. It also gives us the information necessary to determine whether the HF is HFrEF, HFmrEF, or HFpEF, which is important for prognosis and treatment.
Echo can also give valuable information on the etiology. It can show valvular abnormalities, hypertrophy, regional hypo/akinesia (due to infarction), etc.
The most important biomarkers for heart failure are the natriuretic peptides, NT-proBNP and BNP. Of these, NT-proBNP is the most used. These biomarkers have high negative predictive value, so NT-proBNP in a normal range makes HF very unlikely. They also have prognostic value and value in monitoring progression.
The level of NT-proBNP correlates with the severity of the HF, and a high value is associated with a worse prognosis. However, while it’s a sensitive biomarker, it’s not a specific one. NT-proBNP can be elevated in other conditions, like renal failure, pulmonary embolism, etc.
There are no specific ECG findings for heart failure, but the ECG is abnormal in more than 90% of cases of LV systolic dysfunction. Findings may include conduction abnormalities, arrhythmias, ST-T changes, etc.
Treatment of HFrEF
The objectives of treatment in heart failure are to reduce the number of hospitalisations, increase survival and quality of life, and slow the progression of the disease while reducing the symptoms. For HFrEF, we know of many medications which achieve all these objectives.
For HFrEF, the four most important drugs are beta blockers, ACE inhibitors or ARNIs, MRAs, and SGLT2 inhibitors. The higher the dose, the greater the benefit. These drugs are initiated in a low dose which is then slowly increased over longer periods of time until the maximum tolerated dose by the patient is reached. Usually, side effects like bradycardia, hypotension, and/or hyperkalaemia prevent further increase. The patient taking all four of these drugs in the maximum tolerated dose is called optimal medical therapy (OMT).
Patient education is important. When they know the signs and symptoms of worsening HF, they can seek a physician earlier and treat the problem earlier rather than waiting until they’re in such poor condition that they’re admitted to the hospital, which unfortunately occurs in many cases due to poor education.
Self-weighing regularly is important. During an exacerbation patients become fluid overloaded, and one of the earliest signs of this is rapid unintentional weight gain.
Reducing risk factors for HF and cardiovascular disease is important, and includes weight loss, normalising blood pressure, alcohol restriction, smoking cessation, and physical activity.
To avoid fluid overload, salt and water restriction is often used. Guidelines recommend avoiding excessive salt and fluid intake, but where exactly to draw the line of what’s excessive is difficult. The evidence of the efficacy in salt and water restriction is weak. The European Society of Cardiology recommends eating less than 6 g salt daily and “avoiding excessive fluid intake”, with consideration of fluid restriction of 1,5 – 2 L daily in those with severe HF.
Any infection can cause a HF exacerbation. As such, taking the pneumococcal, COVID-19, and seasonal influenza vaccines is recommended.
Cardiac rehabilitation is as important for all types of HF as it is for AMI, as it improves quality of life and reduces mortality.
Iron deficiency, especially with anaemia, worsens outcomes in HF. Patients should be regularly screened for iron deficiency and anaemia, and managed with IV iron supplementation if present.
Beta blockers block the sympathetic nervous system overactivation which occurs in HF and is indicated in all patients with HF (class I recommendation).
Extended-release metoprolol (metoprolol depot), carvedilol, and bisoprolol are most frequently used.
ACE inhibitors block the RAAS overactivation which occurs in HF and is indicated in all patients with HF (class I recommendation). If ACE inhibitors are not tolerated due to angioedema or dry cough, ARBs should be used as an alternative.
Ramipril is most frequently used.
Mineralocorticoid receptor antagonists
MRAs like spironolactone block the aldosterone overproduction which occurs in HF and is indicated in all patients with HF who remain symptomatic despite beta blocker and ACE inhibitor treatment (class I recommendation).
Angiotensin receptor-neprilysin inhibitor
Sacubitril is a first-in-class neprilysin inhibitor. Neprilysin is an enzyme which degrades the vasoactive peptides (ANP, BNP) in the body. These peptides are beneficial in heart failure. Neprilysin inhibitors must be combined with an ARB, the combination of which is known as angiotensin receptor-neprilysin inhibitor (ARNI).
The only ARNI available at the time of writing is Entresto® (valsartan/sacubitril). In the 2021 guidelines it is recommended as a replacement for ACE-I (class IB recommendation) as part of optimal medical therapy, as they’re better than ACE inhibitors alone. Because ARNIs contain an ARB, they can’t be combined with an ACE inhibitor and must therefore replace it. However, they may be combined with MRAs.
Diuretics, most often loop diuretics like furosemide and bumetanide, are important in the management of heart failure, as fluid overload and congestion is a frequent problem. Research has not shown diuretics to improve survival in HF, but it does alleviate symptoms and reduce hospitalisations.
As such, diuretics are only recommended when there are signs or symptoms of congestion. They may also be used regularly to prevent fluid overload in patients who are prone to this.
Bumetanide has better and more predictable absorption from the GI tract, which is beneficial in heart failure as backward congestion can significantly impair absorption of furosemide.
Overuse of diuretics may cause prerenal AKI and/or a decline in cardiac output, and so care must be used.
SGLT2 inhibitors like dapagliflozin and empagliflozin were initially discovered as treatment of diabetes mellitus. Nowadays we have evidence that these drugs are effective in treating HF as well, even in the absence of DM.
As of the 2021 guidelines, SGLT2 inhibitors are recommended (class 1 recommendation) for the treatment of HFrEF as it reduces risk of hospitalisation and death.
An integral part of HF treatment is RAAS blockade, which increases the risk for hyperkalaemia. In the case of hyperkalaemia, rather than stopping these medications, other measures to prevent hyperkalaemia should be tried first. A potassium-reduced diet is always indicated.
Nowadays so-called potassium binders, drugs which bind to potassium in the food and prevents absorption, may also be used. These may be patiromer calcium or sodium zirconium cyclosilicate.
Cardiac resynchronisation therapy
CRT is indicated for patients with HF and left bundle branch block. Having a LBBB and heart failure worsens the heart failure because of the desynchronised contraction of the right and the left ventricle. You can read more about this in topic 5.
Primary prevention of sudden cardiac death with an ICD is indicated in all HF with an underlying ischaemic etiology and EF < 35% despite optimal medical therapy. This is a class I recommendation, as it’s effective in reducing SCD. In those with a non-ischaemic etiology, ICD implantation is a class IIa recommendation.
However, in reality, this is evaluated on a case-by-case basis, as ICDs are expensive and not risk-free to implant.
Digoxin is nowadays one of the last-line interventions for HF, as we know that it increases the risk for sudden cardiac death and the therapeutic range is very narrow. It may be considered in patients who remain symptomatic despite all the above mentioned therapies.
Heart transplantation is a last-line intervention for HF. It’s recommended for patient with medical and device-refractory advanced HF who have no contraindications to transplant.
Treatment of HFpEF
While there is much research on effective medications for HFrEF, the same cannot be said for HFpEF. For HFpEF and HFmrEF, we have much less research on effective treatment. For these patients, the only interventions which are known to be effective are:
- Controlling hypertension
- Controlling tachycardia
- Treating fluid retention
- Preventing myocardial ischaemia
- Exercise training
In fact, exercise training is the only intervention known to consistently improve quality of life in HFpEF.
Notably, ACE inhibitors, ARBs, ARNIs, and beta blockers have shown to have very little to not benefit in HFpEF. MRAs may provide a small benefit. Ongoing trials will reveal whether other drugs are useful for HFpEF, like SGLT2 inhibitors.
2 thoughts on “13. Diagnosis and therapy of heart failure”
Budesonide is a corticosteroid and not a loop diuretic. I think you meant Burinex, which is Bumetanid?
It’s hard to keep track of these stupid names, OKAY?