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Review
. 2006 Jan;147 Suppl 1(Suppl 1):S241-51.
doi: 10.1038/sj.bjp.0706401.

Antiplatelet drugs

Gustav Born  1 , Carlo Patrono
Affiliations
Review

Antiplatelet drugs

Gustav Born et al. Br J Pharmacol. 2006 Jan.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
Haemostatic platelet plug forming in a cut arteriole (electron micrograph × 650).
Figure 2
Figure 2
Massive platelet aggregates on an atheromatous plaque fissure blocking a human coronary artery (from Dr Paris Constantinides in the 1950s).
Figure 3
Figure 3
Platelet embolus blocking an intramyocardial arteriole (from Professor Michael Davies in the 1980s).
Figure 4
Figure 4
Principle of optical platelet aggregometry: as platelets aggregate in plasma, transmitted light increases.
Figure 5
Figure 5
Optical aggregometry records of transmitted (upper trace) and scattered (lower trace) light. The initial deflections are due to the rapid shape change of platelets.
Figure 6
Figure 6
Postulated fibrinogen ‘bridges' between neighbouring platelets during aggregation (Born, 1965).
Figure 7
Figure 7
Electron-microscopic image of labelled fibrinogen molecules forming ‘bridges' between platelets (from Dr Alan Nurden in the 1980s).
Figure 8
Figure 8
First recording of platelet aggregation inhibition by adenosine (Born & Cross, 1962).
Figure 9
Figure 9
Recording of platelet aggregation by increasing concentrations of ADP: note the anomalous rises in the lower tracings (unpublished record made at the time of Born & Cross, 1962).
Figure 10
Figure 10
Inhibition by aspirin of second phase platelet aggregation induced by ADP, adrenaline, or thrombin (from Drs David Mills and Gordon Roberts in the late 1960s).
Figure 11
Figure 11
Main historical steps in understanding aspirin's mechanism of action in inhibiting platelet biochemistry and function. PG, prostaglandin; TX, thromboxane.
Figure 12
Figure 12
Crystal structure of the cyclooxygenase channel of PGH-synthase 1 and its modification by acetylsalicylic acid. Courtesy of Dr Patrick Loll.
Figure 13
Figure 13
Selective cumulative inhibition of platelet thromboxane production by low-dose aspirin in healthy subjects. Redrawn from Patrignani et al. (1982).
Figure 14
Figure 14
The change in optical density (Tmax) of the primary phase of the platelet aggregation response induced by ADP (2.5, 5.0, and 10.0 μM) ex vivo in five volunteers before receiving aspirin (control) on the 7th day of each dosage period and 7 days postdosage. Doses of 20, 40, 80, 160, 325, 650, 1300, and 2600 mg were administered, each dose for 7 days in sequential weeks. Differences are expressed from predosing control values. Redrawn from FitzGerald et al. (1983).
Figure 15
Figure 15
Nonlinear relationship between pharmacologic inhibition of platelet COX-1 activity, as measured ex vivo, and inhibition of platelet activation in vivo, as reflected by thromboxane metabolite excretion. COX, cyclooxygenase; TX, thromboxane. Redrawn from Reilly & FitzGerald (1987).
Figure 16
Figure 16
Low-dose aspirin (160 mg daily) reduces vascular mortality vs placebo in patients with an acute myocardial infarction treated within 24 h of the onset of symptoms. Redrawn from ISIS Collaborative Group (1988).
Figure 17
Figure 17
Inhibition of platelet aggregation and release of ATP by 10E5. Reproduced from Coller et al. (1983).
Figure 18
Figure 18
The oral GPIIb/IIIa antagonists, xemilofiban, orbofiban, sibrafiban and lotrafiban, do not reduce the rate of myocardial infarction or death when compared to aspirin or placebo in patients with acute coronary syndromes. EXCITE, Evaluation of oral Xemilofiban in Controlling Thrombotic Events; OPUS, Orbofiban in Patients with Unstable coronary Syndromes; SYMPHONY, Sibrafiban vs aspirin to Yield Maximum Protection from ischaemic Heart events pOst-acute coroNary sYndromes; BRAVO, Blockade of the GPIIb/IIIa Receptor to Avoid Vascular Occlusion.
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References

    1. BORN G.V.R. Quantitative investigations into the aggregation of blood platelets. J. Physiol. 1962a;162:7–68.
    1. BORN G.V.R. Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature (London) 1962b;194:927–929. - PubMed
    1. BORN G.V.R. Strong inhibition by 2-chloroadenosine of the aggregation of blood platelets by adenosine diphosphate. Nature (London) 1964;202:95–96. - PubMed
    1. BORN G.V.R. Platelets in thrombogenesis: mechanisms and inhibition of platelet aggregation. Ann. Roy. Coll. Surg. Engl. 1965;36:200–206. - PMC - PubMed
    1. BORN G.V.R. Observations on the change in shape of blood platelets brought about by adenosine diphosphate. J. Physiol. 1970;209:487–511. - PMC - PubMed

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