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