PCI vs. OMT for Stable IHD: What Part of the Term
‘Optimal Medical Therapy’ Is Confusing?
T
here have been several trials in the contemporary era comparing percutaneous
coronary intervention (PCI) versus optimal
medical therapy (OMT) for treating patients with
stable ischemic heart disease (SIHD), such as
COURAGE, BARI 2D, FAME 2, and ISCHEMIA.
None of these trial have shown a clear reduction
in death or MI with PCI, not even in patients with
diabetes (BARI 2D). Long-term follow-up did not
make a difference; in FAME 2, for example, there
was still no difference in death or MI at 2 years of
follow-up, nor at 5 years in BARI 2D or even at up
to 15 years in COURAGE.1 The latter is notable
given that at 4.6 years, there was a trend in the
COURAGE study suggesting better survival with
PCI versus OMT.
FAME 2 evaluated fractional flow reserve
(FFR)-guided PCI for SIHD and while there were
no significant between-group differences in the
rates of death and MI, landmark analysis indicated
that the rate of death or MI from 8 days to 2 years
was lower in the PCI group than in OMT group
(4.6% vs. 8.0%; p = 0.04), although
it should be noted that only a small
number of patients achieved that
duration of follow-up.
William E. Boden, MD, professor of medicine, Albany Medical
College, and chief of medicine,
Albany Stratton VA Medical Center, New York, NY, was the lead investigator of the COURAGE trial.2
He noted that FAME 2 randomized patients after catheterization;
physicians treating patients in the
OMT arm knew the anatomy and
FFR results. Dr. Boden explained
that if the primary endpoint of
COURAGE and BARI 2D included
revascularization procedures, there
would have been a significant difference between the arms. Also, he pointed out
that success of OMT/risk factor control in FAME 2
has not been reported.
So, is there any high-risk group of SIHD patients in whom revascularization improves death/
MI in the era of contemporary OMT that includes
intensive lifestyle intervention and aggressive,
multifaceted secondary prevention?
OMT ROCKS (AND STILL UNDERUTILIZED)
What about significant multivessel angiographic
coronary artery disease (CAD) and/or a proximal
left anterior descending (LAD) stenosis? In an
evaluation of COURAGE patients,2 PCI and proximal LAD stenosis did not influence any outcome.
Death was predicted by low LVEF (HR: 1.86;
p < 0.001) and the number of diseased vessels
(HR: 1.45; p < 0.001). MI and non-ST-segment
elevation (NSTE) ACS were predicted only by the
number of diseased vessels (HR: 1.53 for MI and
1.24 for NSTE-ACS; p = 0.007).
Dr. Boden noted that if you look at the broad
“OMT needs to be more widely embraced and utilized
by clinicians as both a best medical practice and
a universal standard of care in all patients with
coronary artery disease.”
swath of available data, comprising 16 RCTs in
8,820 patients (including diabetics with multivessel disease), there were no reductions in death,
MI, stroke, or other “hard events” with PCI in the
modern era of contemporary OMT. Having said
that, he quickly added that OMT remains underutilized in patients undergoing
revascularization.
In a recent editorial comment in JACC,3 Dr. Boden (and
David J. Maron, MD) wrote
that the data supporting OMT
“are compelling and argue persuasively that all patients with
To listen to an
SIHD should receive OMT,
interview with
William E. Boden,
regardless of whether they
MD, on the optimal
undergo revascularization.
management of
However, the use of OMT
patients with SIHD
in the modern era,
remains disappointingly low
scan the code.
in patients with SIHD.”
The interview was
conducted by James
The commentary was
H. Cheseboro, MD.
discussing findings of Bittner
et al.4 who, in the same issue
of JACC, provided powerful
evidence that simultaneous
control of multiple risk factors
improves survival and reduces
nonfatal MI and stroke. “For
that singular reason,” Boden
and Maron wrote, “OMT needs
to be more widely embraced
and utilized by clinicians as both a best medical
practice and a universal standard of care in all
patients with coronary artery disease.” ■
REFERENCES:
1. Sedlis SP, Hartigan PM, Teo KK, et al. N Engl J Med.
2015;373:1937-46.
2. Mancini GB, Hartigan PM, Bates ER, et al. Am Heart J.
2013;166:481-7.
3. Maron DJ, Boden WE. J Am Coll Car