Improving outcomes after PCI: what can interventionalists learn from the ATPCI trial?
Reported from the European Society of Cardiology ESC Congress 2020
Professor Roberto Ferrari presented the results of the ATPCI trial on Sunday, August 30th, in a Hot Line session of the ESC Congress 2020 The Digital Experience. Dejan Milasinovic provides his analysis of this study.
Rationale
The clinical rationale behind the ATPCI trial was to address the issue of residual ischemia following successful PCI, more specifically whether Trimetazidine would be able to further decrease angina and improve outcomes in patients treated with PCI and on optimal medical therapy for coronary artery disease.
Here are the basic facts of the ATPCI trial that was simultaneously published in the Lancet
Population: 6007 PCI-treated patients with either chronic (58.1%) or acute coronary syndromes (41.9%, NSTE-ACS only) were included in the analysis.
Intervention: Trimetazidine 35mg twice daily for the duration of the study versus placebo.
Outcomes: There was no difference between the study groups in terms of the primary combined endpoint that included 4 components – a) cardiac death, b) hospital admission for a cardiac event (i.e. MI, angina or ischemia requiring revascularization, HF, sustained VT or cardiac arrest), c) angina leading modification of antianginal drugs, and d) angina leading to coronary angiography. Individual components of the primary endpoint were also similar in the Trimetazidine and placebo groups.
Time: Median follow-up duration was 47.5 months.
Interpretation
In the ATPCI trial, Trimetazidine did not reduce the occurrence of cardiac events or angina following successful PCI for chronic coronary syndromes or NSTE-ACS.
From the interventionalist’s perspective, there may be two interesting points. First, the included population may be in the lower risk spectrum of patients treated with PCI, judging from the cardiac death rate of 2.4% over a 4-year follow-up. Second, the rate of angina reported at 1-month was close to 20% and was unaffected by the treatment with Trimetazidine. Interestingly this rate is similar to the recently reported rates of residual ischemia post PCI as measured by FFR/iFR (e.g. the DEFINE-PCI study, JACC Cardiovasc Interv. 2019 Oct 28;12(20):1991-2001).
More specifically, the DEFINE-PCI study showed that in the majority of cases there is a potentially correctable, angiographically inapparent, focal lesion responsible for low iFR after PCI. From the interventionalists’ perspective, this may indicate that the lack of benefit of Trimetazidine in the ATPCI trial may be due to an entirely different mechanism of post-PCI ischemia than so far assumed, at least in some patients, namely unrecognized lesion in the stented coronary artery segment that may be detected with an increased use of intracoronary physiology/imaging, and consequently treated during the same procedure.
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