P1590 Regional differences in longitudinal strain and response to adenosine stress in patients with myocardial infarction and ST-segment elevation. Results from Extreme trial
Authors: Manfredonia L , Locorotondo G , Graziani F , Ravenna S E , Ruscio E , Filice M , Ingrasciotta G , Palma F , Addamo E , Lombardo A , Lanza G A , Crea F 
Published: January 2020

Abstract

Background
Global longitudinal strain (LS) is a sensitive marker of ischemic myocardial damage and predicts adverse left ventricular (LV) remodeling and outcome, independently of infarct size. In healthy subjects, regional LS increases from LV base to apex and enhances under physical or pharmacological stress, while in ST-elevation myocardial infarction (STEMI), response to dobutamine depends on transmurality of necrosis. It is known that coronary flow reserve during adenosine (ADN) is impaired both in ischemic and remote myocardium, but effect of ADN on strain reserve has never been investigated. Similarly, LS response to ADN in ischemic (iLS) and remote (rLS) myocardium and their relative contribution to LV function and remodeling are still unknown.

Methods
61 consecutive patients with first STEMI (26 anterior, 29 inferior, 6 lateral), treated by successful primary percutaneous coronary intervention (PCI) followed by PCI of non-culprit coronary arteries, underwent rest and stress ADN (140 mcg/kg/minutes in 90 seconds) echocardiography at discharge (7 ± 2 days after admission). LV end-diastolic volume indexed for body surface area (EDV), ejection fraction (EF) and wall motion score index (WMSI) were measured at rest, while GLS, iLS and rLS analysis was performed both at rest and during stress. Ischemic and remote myocardium was allocated, by standard LV segmentation, basing on the culprit coronary artery.

Results
Significant differences existed among anterior, inferior and lateral STEMI in median (iQr) EDV [52 (45-59) vs 45 (36-51) vs 48 (45–56) ml, respectively, p=.034 overall], EF [47 (37-58) vs 58 (53–61) vs 56 (46-60)%, respectively, p=.002 overall], WMSI [1.63 (1.38–2) vs 1.25 (1.19-1.47) vs 1.41 (1.30-1.75), respectively, p=.001 overall]. GLS differed among anterior, inferior and lateral STEMI both at rest [13.75 (11.63-16.1) vs 19.5 (17.15-22.4) vs 17.85 (17.02-19), respectively, p&lt;.001 overall] and during ADN [14 (12.35-16.15) vs 19.5 (17.9–22.05) vs 15.95 (14.40-19.48), respectively, p&lt;.001], but did not change within groups. No differences were found between rest and stress iLS in any group. Similarly, rLS remained unchanged in anterior and inferior STEMI, and impaired after ADN in lateral STEMI [15.90 (11.45-18) at stress vs 16.8 (15.25-19.2) at rest, p=.043]. Inferior STEMI showed better iLS than anterior STEMI both at rest [17 (15.1–19.9) vs 13.75 (11.46-16.92), respectively, p=.001] and during stress [16.2 (15–20.4) vs 14.42 (12.67-15.83), respectively, p=.001].

Conclusions
In the subacute phase of STEMI, GLS, iLS and rLS are heterogeneous and depend on infarct site. After ADN, there is no strain reserve in ischemic neither in remote myocardium. This may reflect regional differences in the response of microcirculation and myocardium to ischemia or may underlie pre-existing pathophysiological differences in the coronary circulation