![]() ![]() Development and prognosis of non-Q-wave myocardial infarction in the thrombolytic era. Guidelines for the diagnosis and management of unstable angina and non-Q-wave myocardial infarction: Proposed revisions. The authors have no relationships relevant to the contents of this manuscript. The changes in the definition of Q-wave MI have also made older and more contemporary studies mutually incomparable because they resulted in different incidences of Q versus non-Q MIs. The standard concept of a “window” of infarcted tissue was challenged by MRI and autopsy studies, which have shown that infarction scars are rarely homogenous and contain regions of viable tissue. The reasons for these challenges include inconsistent methodology of Q wave definition (different versions of the so-called universal MI definitions were reported to result in Q-wave IM incidences ranging between 28% and 58% ) and doubtful pathologic basis of Q wave formation. Traditionally, MI patients have been and still are conventionally classified as Q and non-Q MI, although the clinical utility of this distinction has repeatedly been challenged. Importantly, 20 ms represents only 0.5 mm of ECG recordings with the standard recording speed of 25 mm/s, which places the definition at the border of human ability of interpreting and diagnosing customary paper printed ECGs. Since the first universal MI definition (UDMI) of 2007, the pathologic Q wave definition has been based mostly on its duration of at least 20 or 30 ms ( Table 1). Since then, the definition of Q wave infarction has undergone several changes. The presence of pathological Q waves was firstly described by Harold Pardee in 1930. p-level < 0.05 was considered statistically significant. ![]() Statistical analyses were performed using IBM SPSS Statistics for Windows, Version 25, and in Statistica package, Version 6.1. The subpopulations dichotomized by medians of age, BMI, BNP, and LVEF were then further dichotomized by the addition of presence or absence of 72 h Q and presence or absence of 72 h Selvester score ≥6, respectively. The Kaplan–Meier curves were calculated (together with their confidence bands based on 1000 bootstrap repetitions) in subpopulations defined by presence or absence of 72 h Q wave, presence or absence of acute Selvester score ≥6, presence or absence of 72 h Selvester score ≥6, and other clinical variables (age, BMI, TnT, BNP, and LVEF) dichotomized at population medians. Time-dependent all-cause mortality probabilities were displayed by Kaplan–Meier curves and compared by the log-rank and chi-square tests. Two separate backwards stepwise regression analysis models were used to predict death with continuous variables dichotomized at population medians (“median model”) and at the following cut-off values (“conventional model”): age ≥ 70 years, TnT ≥ 3 μg/L, BNP ≥ 500 ng/L, LVEF ≤ 40%, BMI ≥ 25 kg/m 2, acute Selvester score ≥ 6, and 72 h Selvester score ≥ 6. ![]() Differences between continuous variables were compared using a two-tail two-sample t-test assuming different variances between compared samples. Categorical data are presented as absolute and relative incidences. On the contrary, the prognostic value of Q-wave presence appears limited in contemporarily treated STEMI patients.Ĭontinuous data are presented as mean ± standard deviation (SD) and as median with interquartile ranges (IQR). In contemporarily treated STEMI patients, Selvester score is a strong independent predictor of long-term all-cause mortality. On the contrary, the additional risk-prediction by 72 h Q presence was either absent or only borderline. In high-risk subpopulations defined by clinical and laboratory variables, the differences in total mortality were highly significant ( p < 0.01 for all subgroups) when stratified by 72 h Selvester score ≥6. Multivariably, 72 h Selvester score ≥6 was a strong independent predictor of death, while a predictive value of the 72 h Q wave was absent. A 72 h Q presence and 72 h Selvester score ≥6 was observed in 184 (65.02%) and 143 (50.53%) patients, respectively. The results were related to total mortality and to clinical and laboratory variables. ![]() The Selvester score was evaluated in acute ECGs (acute Selvester score) and in the pre-discharge ECGs (72 h Selvester score). The presence of pathological Q wave was evaluated in pre-discharge electrocardiograms (ECGs) recorded ≥72 h after the chest pain onset (72 h Q). Data of 283 consecutive STEMI patients (103 females) treated by PPCI were analysed. In this study, we investigated long-term mortality of STEMI patients treated by primary percutaneous coronary intervention (PPCI) and compared predictive values of Q waves and of Selvester score for infarct volume estimation. The development of pathological Q waves has long been correlated with worsened outcome in patients with ST elevation myocardial infarction (STEMI). ![]()
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