DISCUSSION
In our study we found that PSS is more sensitive and specific for
coronary arterial lesion than PLS in patients with stable CAD. We also
found that GLS was lower in patients with severe coronary artery disease
but there was no correlation with ischemic risk area. It has been shown
that in different clinical and experimental studies, that PSS is
superior to conventional methods, such as wall thickening and peak
longitudinal systolic strain in detecting acute coronary ischemia and
coronary artery disease (4,17,18). We also tested the capability of PSS
and PLS to predict coronary lesions in patients scheduled for coronary
angiography as a result of a stress test and confirmed the results with
coronary angiography.
It has been proven in a vast number of studies that strain is highly
correlated with severity of coronary artery disease (3-10) and that PLS
and PSS can detect acute coronary ischemia (4,12,15). Additionally, it
is also known that PSS can be seen in around 15% of normal healthy
people, particularly in basal segments. We applied the criteria from
previous studies for PSS assessment to avoid false positive results (5).
PSS was mostly seen in the basal and mid segments in our study too.
Similarly, it has been shown that PSS is more common in basal segments
(5), and contraction anomalies are seen in apical segments rather than
temporal anomalies (19).
Experimental animal studies have also demonstrated that PLS and PSS are
significantly reduced in coronary artery occlusion (20-22). PSS
continued while systolic strain recovered rapidly after reperfusion.
Even after 2 minutes of occlusion, PSS was persisting (23, 24). These
findings depicted that PSS can be more sensitive and specific in
detecting intermittent mild ischemia. Mechanism of PSS is still
speculative. Some studies claimed that it is due to prolonged
contraction and delayed relaxation (25) while some others suggested that
fatty acid metabolism is responsible fot that, which is suppressed
during ischemia (26,27). This may also be a combination of active and
passive processes (28,29).
Stable CAD and low-risk unstable angina are most commonly caused by
atheromatous plaques in the coronary arteries that obstruct blood flow
and may lead to the silent ischemia (30). Silent ischaemia is common and
prognostically important entity (31). There is also evidence that silent
myocardial ischemia is seen more frequently than anginal attacks in
patients with coronary artery disease (32). It has been already found
that more than 70% of patients with stable angina have frequent
episodes of silent ischemia (33). In different studies silent myocardial
ischemia has been indicated to occur frequently even during treatment
with conventional anti-anginal drugs (33, 34). Both an increase in
myocardial oxygen demand and abnormalities of coronary vasomotor tone
appear to play a significant role in the genesis of silent ischemia
(34). For this reasons, we consider that silent ischemia is present in
stable coronary artery patients and we suggest that PSS may detect
serious coronary artery disease without performing stress test.
GLS was lower in patients with severe coronary artery disease, similar
to previous studies (7-10). However, segmental analysis was not
performed in these above mentioned studies. Unlike previous studies, we
performed segmental analysis and also investigated the relationship
between PLS and the area at risk as well. No relation was found between
the area with severe coronary artery disease and PLS in our study.
Although strain values are within normal limits, PSS was seen in
ischemic segments in patients with severe coronary lesion. Similarly, a
recent published study demonstrated that PLS could be a sensitive but
nonspecific imaging method to determine significant CAD at rest (35).
Figure 3