ARB

Question 1

Why are ARBs used in heart failure?

Answer 1

For patients intolerant to ACEIs/ARNIs and to selectively block AT1 receptors, preventing harmful Ang II effects.

Question 2

What is “angiotensin II escape”?

Answer 2

Ang II production continues via non-ACE pathways during ACEI therapy (e.g., chymase), reducing ACEI effectiveness.

Question 3

What receptor do ARBs block?

Answer 3

AT1 receptors — responsible for vasoconstriction, aldosterone release, remodelling, and sodium retention.

Question 4

What is the effect of blocking AT1 receptors?

Answer 4

Vasodilation, ↓ SVR, ↓ aldosterone, ↓ preload, ↓ congestion, ↓ remodelling.

Question 5

How do ARBs improve symptoms of HF?

Answer 5

By reducing preload and afterload, improving cardiac output, and decreasing congestion.

Question 6

How do ARBs affect cardiac remodelling?

Answer 6

They reduce hypertrophy, fibrosis, and pathological structural change.

Question 7

Which ARBs are licensed for heart failure?

Answer 7

Candesartan, losartan, valsartan.

Question 8

When should ARBs be used in HF?

Answer 8

In HFrEF/HFmrEF patients intolerant to ACE inhibitors or sacubitril/valsartan.

Question 9

What are the main adverse effects of ARBs?

Answer 9

Hypotension, worsening renal function, hyperkalaemia.

Question 10

Which ACEI-related adverse effect does NOT occur with ARBs?

Answer 10

Cough, because ARBs do not increase bradykinin.
(Implicit from mechanism)

Question 11

Why do ARBs not cause cough like ACEIs?

Answer 11

They don’t inhibit ACE and therefore don’t increase bradykinin levels.

Question 12

Which provides stronger mortality evidence: ACEIs or ARBs?

Answer 12

ACEIs, which is why they are first-line.
(ARB = alternative when ACEIs are not tolerated.)