ISSN 1016-5169 | E-ISSN 1308-4488
Effects of Preinfarction Angina on Infarct Size, Postinfarct Left Ventricular Systolic Function and Early Prognosis [Turk Kardiyol Dern Ars]
Turk Kardiyol Dern Ars. 1997; 25(5): 281-286

Effects of Preinfarction Angina on Infarct Size, Postinfarct Left Ventricular Systolic Function and Early Prognosis

Coşku TURAN1, Seçkin PEHLİVANOĞLU1, Rasim ENAR1

There are some inconsistencies between the results of the studies which were carried out to investigate the role of preinfarction angina (PA) on infarct size and early prognosis of acute myocardial infarction (AMI). For that reason, we investigated the effects of PA that occured in the last 72 hours before the index AMI on early prognosis in postinfarction period. We evaluated 55 patients with AMI that was admitted to our hospital with chest pain of less than 6 hours of duration and received thrombolytic therapy. There were 32 patients in PA group (Group A) and 23 patients in the control group (Group B). There were no statistically significant difference between the groups in terms of age, sex, atherosclerotic risk factors, duration of chest pain, infarct location, multivessel disease, collateral circulation. infarct complications both in hospital and 3 months' period and revascularisation procedures (PTCA and CABG). Determinants of left ventricular function; QRS score (7.58±2.67 vs 6.95±3.58), left ventricular ejection fraction (% EF) (44.2±8.57 vs 44. 1±9. 16) and wall motion score index ( 1.36±0.29 vs 1.36±0.29) were not different between the groups. But still, in group A patients had smaller infarct size (peak hydroxibutyrate dehydrogenase: 554 ± 252 U/L vs 782±402 U/L, p=O.O1) and less patients had EF?45% (46% vs 78%, p=0.02). These differences between the groups were more prominent in the patients with anterior infarction; in group A, pcak hydroxibutyrate dehydrogenase level (528 ± 158 U/L) and QRS score (7.8±1.7) were significantly less than group B (932 ± 453 U/L and 9.6 ± 1.8) (p=0.005 anel p=0.03). The salutary effects of PA may be due to the acquired myocardial resistance to the ischemia is possibly via ischemic preconditioning and stress proteins.



Manuscript Language: Turkish
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