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General Medicine · Cardiology: ticagrelor dyspnoea
Sample itemA 58-year-old man takes aspirin and ticagrelor after a non-ST elevation myocardial infarction. Two weeks later he notes a feeling of breathlessness at rest, though his chest is clear, oxygen saturation is normal and BNP is normal. Which mechanism most likely explains this?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Adenosine accumulation, as ticagrelor blocks its cellular uptake
Dyspnoea is a recognised adverse effect of ticagrelor and is attributed to raised adenosine levels because the drug inhibits adenosine reuptake. It is often mild and does not signal heart failure or lung disease, so the drug usually need not be stopped.
Option by option
A. Leukotriene release triggered by cyclo-oxygenase inhibition
Leukotriene shift after cyclo-oxygenase inhibition is the mechanism of aspirin-exacerbated asthma, with wheeze.
B. Adenosine accumulation, as ticagrelor blocks its cellular uptake (correct)
Correct. Reduced adenosine reuptake raises its level and stimulates the sensation of dyspnoea.
C. Bradykinin accumulation from impaired kininase breakdown
Bradykinin accumulation causes the cough of ACE inhibitors, not breathlessness with ticagrelor.
D. Direct bronchial smooth muscle injury by the drug
Ticagrelor has no direct bronchial toxicity, and the chest is clear.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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