Modern role for clopidogrel in management of atrial fibrillation and stroke reduction

Figures & data

Figure 1 Mode of action of clopidogrel.

Clopidogrel irreversibly inhibits the ADP P2Y₁₂ receptor. P2X₁ mediates extracellular calcium influx and utilizes ATP as an agonist. The binding of ADP to the G-coupled P2Y₁₂ receptor liberates G protein subunits and results in stabilization of platelet aggregation. One subunit leads to inhibition of AC, which reduces cAMP levels. cAMP as well as the second subunit of the G protein lead to activation of the GP IIb/IIIa receptor.

Abbreviations: AC, adenylyl cyclase; ADP, adenosine diphosphate; ATP, adenosine triphosphate; Ca, calcium; cAMP, cyclic adenosine monophosphate; GDP, guanosine diphosphate; GP, glycoprotein; GTP, guanosine triphosphate.

Table 1 CHADS₂ score

C:	Congestive heart failure	= 1 point
H:	Hypertension (systolic > 160 mmHg)	= 1 point
A:	Age > 75 years	= 1 point
D:	Diabetes	= 1 point
S:	Prior transient ischemic attack or stroke	= 2 points

CHADS2 score	Adjusted stroke rate* (%) [95% CI]
0	1.9 (1.2–3.0)
1	2.8 (2.0–3.8)
2	4.0 (3.1–5.1)
3	5.9 (4.6–7.3)
4	8.5 (6.3–11.1)
5	12.5 (8.2–17.5)
6	18.2 (10.5–27.4)

Notes: The annual stroke rates for patients suffering from atrial fibrillation according to the CHADS₂ Score. Patients with a CHADS₂ Score of 0 are considered to have a low risk for cardioembolic stroke. Patients with a score of 1–2 are classified as having a moderate risk for stroke and should be medically treated with an antithrombotic agent. Patients with a score of 3 or higher have a high risk for thromboembolic complications and require optimal antithrombotic treatment as well.

* The adjusted stroke rate is the expected stroke rate per 100 person/years derived from the multivariable model assuming that aspirin is not taken.