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Mode of DAPT cessation plays pivotal role

Issue: November 2013

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AMSTERDAM — Two-year results of the PARIS study suggest that the reasoning for dual antiplatelet therapy cessation may substantially influence cardiac risk.

Specifically, patients whose DAPT cessation was caused by disruption were at increased risk for MACE, whereas those who discontinued use were at decreased risk.

“These findings highlight the need for uniform approaches in classifying DAPT cessation, analogous to those currently used for bleeding and MI,” Roxana Mehran, MD, study investigator and professor of medicine at Mount Sinai Hospital, N.Y., who presented the data at ESC Congress 2013, said in a press conference.

 

Roxana Mehran

Mehran, who is also Associate Medical Editor of Cardiology Today’s Intervention, and colleagues conducted the PARIS study to determine whether risk after DAPT cessation depends on the underlying context or clinical circumstances in which antiplatelet therapy is stopped, including surgery, bleeding and physician guidance. They also sought to find out how long the risk persists after antiplatelet therapy is withdrawn and what the overall contribution of DAPT cessation is on adverse events in the contemporary PCI era.

The PARIS study was conducted at 15 clinical sites in the United States and Europe between July 1, 2009, and Dec. 2, 2010, and included patients (n=5,018) who were undergoing successful stent implantation in one or more native coronary arteries and discharged on DAPT. Patients were followed for 1, 6, 12, and 24 months after implantation.

At 2 years, follow-up was available in 93.2% of patients and indicated a 57.3% rate of any DAPT cessation. The causes for cessation were physician-recommended discontinuation (40.8%), interruption for surgery (10.5%) and disruption due to noncompliance or because of bleeding (14.4%).

The 2-year MACE rate — which included cardiac death, definite/probable stent thrombosis, spontaneous MI and clinically driven target lesion revascularizatoin — was 11.5%, and primarily occurred while patients were taking DAPT (74%). Further analysis revealed that, compared with patients on DAPT, there was a significantly increased risk for MACE in patients with disrupted DAPT usage (adjusted HR=1.5; 95%, 1.14-1.97; P=.004), a decreased risk in patients who discontinued DAPT (HR=0.63; 95% CI, 0.46-0.86; P=.004) and no significant difference in patients with interrupted DAPT (HR=1.41; 95% CI 0.94-2.12; P=.10).

Mehran and colleagues also found that timing of disruption played a key role, as the risk decreased with time: within 7 days, HR=7.04 (95% CI, 3.31-14.95); 8 to 30 days, HR=2.17 (95% CI, 0.97-4.88); and more than 30 days after disruption, HR=1.3 (95% CI, 0.97-1.76).

In conclusion, Mehran said, “The impact of DAPT cessation on cardiac risk after PCI is not uniform, but varies substantially by underlying mode, a novel finding with important implications for future study design and clinical practice. – by Brian Ellis

For more information:

Mehran R. Hot line: Late breaking trials on thrombosis. Presented at: the European Society of Cardiology Congress; Aug. 31-Sept. 4, 2013; Amsterdam.

Mehran R. Lancet. 2013;doi:10.1016/S0140-6736(13)61720-1.

Disclosure: See the study for a full list of researcher disclosures.