Vol 15, No 1 (2008)
Original articles
Published online: 2007-12-17

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Predictive factors of myocardial reperfusion in patients with anterior wall acute myocardial infarction

Maria Olszowska, Wiesława Tracz, Magdalena Kostkiewicz, Piotr Podolec
Cardiol J 2008;15(1):57-62.

Abstract

Background: The no-reflow phenomenon due to microvasculature damage is sometimes observed in patients despite patency of the infarct-related artery. The study aimed to assess the predictive value of clinical, hemodynamic and electrocardiographic parameters for the development of the no-reflow phenomenon in patients after successful coronary reperfusion.
Methods: Eighty-six patients, mean age 58.4 ± 11.2, underwent primary percutaneous coronary intervention (PCI) for acute anterior myocardial infarction (AMI). Angiographic parameters, i.e. TIMI grade flow, cTFC, TMPG, wall motion score index (WMSI), ST-segment resolution and segmental perfusion, were estimated by myocardial contrast echocardiography (MCE).
Results: As evidenced by MCE, 54 patients were classified as the reflow ones and 32 as no- reflow. Patients from the no-reflow group showed a higher creatine kinase peak (p = 0.0034), higher kinase-MB (p = 0.0033) and higher troponin level (p = 0.062), longer time span between the onset of pain and reperfusion (p = 0.0003), worse baseline WMSI (p = 0.0022), inferior flow in the infarct-related artery and ST-segment resolution. Univariate analysis revealed that age, time span between the onset of chest pain to PCI, all angiographic parameters, WMSI and ST-segment resolution were related to the no-reflow phenomenon. Multivariate logistic regression analysis revealed that lack of preservation of normal or nearnormal flow before PCI and significant impairment of left ventricle contractility were independent predictive factors of the no-reflow phenomenon. Conclusions: MCE yields vital information about the outcome of coronary intervention in patients with AMI. Development of a no-reflow phenomenon is correlated with the severity of myocardial damage and poor flow through the infarct-related artery before PCI. (Cardiol J 2008; 15: 57-62)

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