AIMS: The anatomical correlates of perfusion defect (PD) at myocardial contrast echocardiography (MCE) in the subacute phase of ST-elevation myocardial infarction (STEMI) are currently unknown. The study aimed at assessing whether, in the subacute phase of STEMI, within MCE PD microvessels are anatomically damaged or if some vasodilation can be still elicited and if the PD correlates with the extent of myocardial necrosis. METHODS AND RESULTS: Twenty-two post-percutaneous coronary intervention (PCI) patients underwent MCE 7 ± 1 days after STEMI, at baseline and after adenosine (ADN) administration. An area of completely non-opacified myocardium, corresponding to the area of the PD, was quantitated by planimetry. The area of the PD on MCE was compared with biochemical and imaging measures of myocardial necrosis: cardiac Troponin T peak (cTnT peak) and hyperenhanced area at gadolinium-enhanced cardiac magnetic resonance (Gd-CMR), respectively. After vasodilator stimulus, the area of the PD remained significantly unchanged when compared with the baseline value (P = 0.09 vs. baseline). The MCE index correlated at baseline with cTnT peak and Gd-CMR assessments of myocardial necrosis (P < 0.001). Also after ADN infusion, correlations between PD and extent of myocardial necrosis were similar to that assessed at baseline. CONCLUSION: When assessed in the subacute phase of STEMI, the extent of the PD on MCE represents an area of both myocardial and microvascular necrosis.
AIMS: The anatomical correlates of perfusion defect (PD) at myocardial contrast echocardiography (MCE) in the subacute phase of ST-elevation myocardial infarction (STEMI) are currently unknown. The study aimed at assessing whether, in the subacute phase of STEMI, within MCE PD microvessels are anatomically damaged or if some vasodilation can be still elicited and if the PD correlates with the extent of myocardial necrosis. METHODS AND RESULTS: Twenty-two post-percutaneous coronary intervention (PCI) patients underwent MCE 7 ± 1 days after STEMI, at baseline and after adenosine (ADN) administration. An area of completely non-opacified myocardium, corresponding to the area of the PD, was quantitated by planimetry. The area of the PD on MCE was compared with biochemical and imaging measures of myocardial necrosis: cardiac Troponin T peak (cTnT peak) and hyperenhanced area at gadolinium-enhanced cardiac magnetic resonance (Gd-CMR), respectively. After vasodilator stimulus, the area of the PD remained significantly unchanged when compared with the baseline value (P = 0.09 vs. baseline). The MCE index correlated at baseline with cTnT peak and Gd-CMR assessments of myocardial necrosis (P < 0.001). Also after ADN infusion, correlations between PD and extent of myocardial necrosis were similar to that assessed at baseline. CONCLUSION: When assessed in the subacute phase of STEMI, the extent of the PD on MCE represents an area of both myocardial and microvascular necrosis.