This study evaluated the correlation between the occurrence and
morphology of VAs and LGE in patients with apparently normal hearts. The
results demonstrated that LGE is more common in patients with VAs than
those without VAs, especially in those with polymorphic VAs and
ST-segment depression. Moreover, polymorphic VAs and ST-segment
depression were associated with a 25.24-fold increase and an 8.83-fold
increase in the occurrence of LV-LGE, respectively. The frequency and
burden of VAs have no impact on the presence of LV-LGE. LV-LGE extent
tended to increase in patients with polymorphic VAs.
Our study demonstrated that patients with VAs were more prone to show
LGE which was similar to results seen in a previous study. Ghannam et
al.18 reported that one-quarter of the patients with
frequent PVCs were found to have myocardial scars. The presence of
myocardial fibrosis represents an increased risk of
death.1, 19 Moreover, a previous study reported that
patients with PVCs had an odds ratio (OR) of 1.72 for the combined
end-points of all-cause mortality, cardiovascular mortality, and sudden
cardiac death compared with those without PVCs.20 This
could be one reason why LGE was more common in patients with VAs.
The present analysis showed that VAs frequencies and burdens have no
impact on the presence of LGE. However, Adabag et
al.14 reported that myocardial fibrosis, detected on
CMR imaging in patients with hypertrophic cardiomyopathy, was associated
with an increased frequency of ventricular
tachyarrhythmias.14 That study showed that patients
with LGE had a 7-fold higher risk of NSVT than patients without LGE. In
our study, the constituent ratio of NSVT was 26.3% (5/19) versus 25.0%
(8/32) in patients with and without LGE, respectively. A similar
constituent ratio between the two groups could have been due to
selection bias because of the small number of enrolled patients. Further
studies with larger sample sizes are needed to clarify the association
between LGE and NVST. Moreover, the lower VAs burdens of our study could
also have contributed to the deviating results.
Regarding VAs morphology and LGE occurrence, the results of this study
showed that patients with polymorphisms and ST-segment depression were
more likely to have LGE. A previous study21 reported
that polymorphic PVCs (OR=4.25) were significantly associated with the
presence of LGE, consistent with this study. Moreover, Niemann et
al.22 reported LGE was eliminated when ST-segment
alterations were absent. Our study also showed that patients with
ST-segment depression had an 8.83-fold higher risk of having LV-LGE.
In terms of the extent of LGE between subgroups, inconsistent results
have been presented in previous studies.14, 18, 23Adabag et al.14 demonstrated that LGE was similar in
patients with hypertrophic cardiomyopathy with and without PVCs, while
Ghannam et al.18 reported that patients with inducible
VT had larger fibrotic volumes compared with non-inducible patients.
Similarly, our study showed no association between the extent of LV-LGE
and the presence or burdens of VAs. Nevertheless, patients with
polymorphic VAs tended to have increased LV-LGE extent. Most LV-LGE
(20/23, 87.0%) were distributed in the midmyocardium, in this study. A
previous study1 showed that LGE was also present in
the midmyocardium and were associated with increased risks for sudden
cardiac death, indicating that these patients should be followed up
closely.
In the multivariable analysis, polymorphisms and ST-segment depression
were associated with an increased incidence of LV-LGE. Muser et
al.21 reported that having multiple VAs morphologies
is a risk factor for the presence of concealed myocardial structural
abnormalities. Since they used CMR imaging and looked at LGE, the
conclusions of that study support the results of our study.
Some limitations should be acknowledged in this study. First, only a few
cases had LGE (23/78) that could lead to biased results. In future
studies, we plan to enroll a greater number of patients to strengthen
the results. Second, due to the particularity of CMR, the study only
focused on the influence of VAs on LV-LGE regardless of the influence on
right ventricular LGE. Third, in morphologic terms, the study only
analyzed the origins and ST-segments. Additional studies evaluating more
ECG details, such as QRS complexes, amplitudes, and durations, are
needed. Finally, the present study lacked follow-up regarding the
effects of having LGE on patient prognosis. Our team will perform
follow-up studies to further understand the influence of fibrosis in
patients without known structural heart disease.