Pharmacology: Drugs for Heart Failure, Animation

Mechanisms of actions of ACE inhibitors, Angiotensin receptor blockers (ARBs), Beta-blockers, Aldosterone receptor antagonists (ARAs), Digoxin, Ivabradine, Angiotensin Receptor-Neprilysin Inhibitor, ARNIs (sacubitril/valsartan), Diuretics, Vasodilators. Role of RAAS, sympathetic system and natriuretic peptide system in pathophysiology of Congestive heart failure (CHF) and rational for treatment of HF.

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Voice by : Marty Henne

All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment.

Heart failure is when the heart is unable to pump effectively, called systolic heart failure; or unable to fill properly, called diastolic heart failure. In both cases, blood output is reduced. Ejection fraction is reduced in systolic heart failure, but typically preserved in diastolic heart failure.
The pathophysiology of heart failure involves a vicious cycle in which reduced cardiac output, as a compensatory response, activates the renin-angiotensin-aldosterone system (RAAS) and sympathetic system. However, these systems cause vasoconstriction, increase heart rate and blood pressure, making it even harder for the heart to pump. Increased aldosterone level also promotes ventricular remodeling, myocardial scarring, and vascular injury, worsening the disease.
On the other hand, the natriuretic peptide system is also activated. This system is protective to the heart. It promotes vasodilation, sodium and water excretion, and inhibits cardiac remodeling.
Most drugs used in heart failure therapy aim to inhibit RAAS and sympathetic activities, and/or promote the natriuretic system. Other drugs increase ventricular contractility or reduce water retention – a major heart failure symptom.
First-line therapy for patients with reduced ejection fraction typically includes an angiotensin-converting enzyme (ACE) inhibitor, and a beta-blocker.
– ACE inhibitors block the conversion of angiotensin-I to angiotensin-II in RAAS, thereby inhibiting RAAS activity. Common side effects include dry cough, headache, and hypotension. Rarely, ACE inhibitors may cause a swelling reaction known as angioedema.
– Angiotensin receptor blockers (ARBs) inhibit the effects of angiotensin-II. Their mechanism of action is similar to that of ACE inhibitors, but they do not usually cause a cough.
– Beta-blockers decrease heart rate by binding to β1-adrenergic receptor in the heart and blocking the sympathetic influences that act through these receptors. Adverse effects: hypotension, bradycardia and AV blocks.
– Vasodilators reduce blood pressure and are usually used for patients who cannot tolerate ACE inhibitors or ARBs.
– Diuretics are often prescribed to relieve fluid retention. Loop diuretics are most powerful and typically used for most patients. Thiazides are less effective, but they also have a vasodilation effect, and are thus preferred for patients with hypertension but only mild fluid retention.
– Aldosterone receptor antagonists block the action of aldosterone. Because aldosterone’s primary function is to promote sodium and water retention, and potassium excretion; aldosterone antagonists act as potassium-sparing diuretics. However, their effect in heart failure treatment is also attributed to the inhibition of aldosterone’s damaging impact on the heart and blood vessels.
– Digoxin increases cardiac contractility by inhibiting the sodium-potassium pump, causing intracellular sodium concentration to rise. This then leads to higher levels of intracellular calcium via the action of sodium-calcium exchanger. Higher calcium results in increased muscle contraction. Digoxin also decreases sympathetic activities, slowing down heart rate.
– Ivabradine slows the heart rate by inhibiting the “funny” channel responsible for spontaneous firing of the SA node. Adverse effects include bradycardia, atrial fibrillation, and vision problems.
– ARNIs are a new class of medications. ARNI therapy consists of a neprilysin inhibitor and an ARB.

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