Cardiovascular Journal of Africa: Vol 28 No 2 (March/April 2017)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 2, March/April 2017 102 AFRICA
Previous studies have reported the independent predictive
value of STEaVR for LM/3VD in NSTEACS. Barbares et al.9
reported that patients with STEaVR had a higher prevalence
of LM/3VD and increased risk of in-hospital death. Kosuge
et al.1 showed that STEaVR (≥ 0.05mV) was independently
associated with LM/3VD, and STEaVR and increased cTnT
level were independent predictors of death or MI only in patients
with NSTEMI. Rostoff et al.10 evaluated the prognostic role of
STEaVR in 134 patients with NSTEACS and reported that left
main coronary artery disease was independently associated with
STEaVR.
Atie et al.8 evaluated ECG changes in patients with left
main disease and showed that the most frequently observed
ECG finding was STD in leads V3, V4 and V5. In addition to
the predictive value for LM/3VD, STD carries a significant
prognostic value in patients with NSTEMI.11,12 Furthermore,
STD in leads V4–V 6 has been reported to be an independent
predictor for short-term mortality in patients with inferior
ST-elevation myocardial infarction (STEMI).13 In the present
study, STD in the anterior leads was another independent
predictor for a high SS.
Janata et al.14 has shown the prognostic value of STEaVR
in patients with acute pulmonary embolism. In our study
pulmonary embolism was excluded by echocardiographic and
biochemical findings. One of the most common causes of
STEaVR is left ventricular hypertrophy (LVH), which may
represent repolarisation abnormalities.15 In our study LVH was
excluded by echocardiographic evaluation.
Althoughmajor STEaVR (> 0.1mV) remained an independent
predictor of LM/3VD, minor (0.05–0.1 mV) and major STEaVR
were not independent predictors of in-hospital or six-month
death, after adjusting for other validated prognosticators in the
GRACE risk model.2 Taglieri et al.16 investigated the prognostic
significance of STEaVR in patients with NSTEMI. They
reported that STD plus STEaVR were associated with high-
risk coronary lesions and predicted in-hospital and one-year
cardiovascular death. Several studies have reported a close
relationship between STEaVR and in-hospital or one-year
cardiovascular death.1,9,16 In this study, we could not evaluate the
relationship with mortality due to lack of data.
SS, which is used in the evaluation of angiographic severity
and extent of coronary lesions, has been shown to predict
mortality in addition to its role in the decision-making process
of interventional procedure.6,17 SS predicted short- and long-
term adverse events following revascularisation in a study by
Valgimigli and co-workers.18 In our study, STEaVR was an
independent predictor of increased SS. It is well known that SS
predicts mortality after a revascularisation procedure.
Nabati et al.19 reported that STEaVR was independently
associated with severity of coronary artery atherosclerosis and
decreased LVEF in patients with NSTEACS. Although we
found a significant relationship between STEaVR and severity
and extent of coronary artery disease, there was no difference
regarding LVEF. Additionally, they have shown that this ECG
pattern had been associated with markers of myocardial necrosis
and high-risk coronary lesions, including multi- or three-vessel
coronary artery disease.19 Similarly, in our study, there was a
significant difference with regard to peak cTnT value in patients
with STEaVR.
Several studies have shown a different ratio of STEaVR in
patients with NSTEACS; Barrabés et al.9 reported 32.2%, Kosuge
et al.5 reported 27.4%, Taglieri et al.16 reported 15.7%, Misumida
et al.20 reported 26%, and Nabati et al.21 reported 40.3%. In
our study, the ratio of STEaVAR was 68.4%. Misumida et al .20
reported that patients with STEaVR had a significantly higher
rate of LM/3VD than those without STEaVR (39 vs 18%,
respectively, p < 0.001). Nabati et al.21 reported that patients with
STEaVR had a significantly higher rate of three- or multi-vessel
disease than those without STEaVR (53.8 vs 31.2%, respectively,
p = 0.01).
In our study, patients with STEaVR had a significantly higher
rate of LM/3VD than those without STEaVR (86.2 vs 72.9%,
respectively, p = 0.03). High rates of STEaVR and LM/3VD
in our study are thought to have resulted from the inclusion of
CABG patients into the study.
There are several limitations in this study. First, our study
was a retrospective, observational study. Second, the sample
size was small. Third, we did not exclude patients with posterior
infarction presenting with STD in V1–V4, which is equivalent of
STEMI. Therefore, our study group may have included patients
with posterior STEMI. Fourth, we could not access death
records in our country, therefore we could not evaluate mortality
rates in this study.
Conclusion
This study demonstrates that STEaVR and STD in the anterior
leads were independent predictors of a higher SS and higher rate
of LM/3VD in patients with NSTEACS.
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