IJCS | Volume 31, Nº2, March / April 2018

140 Barros et al. Acute pulmonary edema. Coronary artery disease. Int J Cardiovasc Sci. 2018;31(2)133-142 Original Article In the study by Figueras et al., 2 acute myocardial infarction with ST elevation was present in 30% of patients admitted with this pathology. Classifying serial troponin measurements, increased in APE, as secondary to an acute coronary event is not reasonable in this model and brings costly consequences for the health system, 8 since the presence of CAD in acute HF increases the time and costs of hospitalization, according Purek et al. 9 It is noteworthy the fact that alterations in the electrocardiogram, which may suggest ischemia, such as changes in ST (depression) and T wave, were not part of the predictor model, suggesting that such changes can be found with or without obstructive CAD. 10 This was verified in the series of nine cases by Littmann, 11 in which negative and deep T waves and QT increase were not associatedwith coronary disease at the electrocardiogram after 24 hours of APE. Onemust always consider that other causes of ST depressionmay occur, such as left ventricular hypertrophy and drug use (such as digoxin) and, perhaps, the relative ischemia itself, which may occur during an episode of APE, where hypoxia is invariably present and, when associatedwith an increase in troponin, can be considered a type-2 acute myocardial infarction. 10 The exact mechanism of the found alterations is poorly defined, attributing the electrophysiological responses of myocardial cells to adrenergic stimulation and myocardial hypoxia, which usually accompany the clinical condition of APE. In this series, only four patients underwent invasive investigation. That study was not intended to evaluate mortality, but it was 15% over a one-year period – emphasizing that contact was established with only 48% of the study population. In the study by Figueras et al., 2 mortality at 30 days was 14%. That demonstrates disease severity, even in the present day. Severe valvular disease occurred in 15 cases (10%). It is worth remembering that no prior valvulopathy was known and that 11 cases (73%) had severe aortic stenosis, which is characteristic of the study population’s profile, whose mean age was 65.4 ± 10.2. This study shows that severe obstructive coronary disease was present in most patients with acute pulmonary edema, but variables commonly used in the emergency room to identify its presence failed, such as the interpretation of troponin levels and chest pain preceding the clinical picture. Of course, we expect to find the predictors related to this condition – such as history of coronary disease and the segmental deficit at the echocardiogram – in this pathology. Study limitations and prospects The present study showed that obstructive coronary disease is prevalent in patients with APE: 59% of patients had some artery with severe obstructive lesion as demonstrated by the invasive hemodynamic study. Percutaneous intervention was not performed in most individuals with this condition, that is, increased troponin and obstructive CAD; as previouslymentioned, the research was not designed to answer this question. Moreover, considering the high frequency of troponin positivity in all the acute conditions affecting the heart, and the intersection of symptoms in the different etiologies, one expects a misdiagnosis when there is no specific marker for a given disease, such as the electrocardiogram in acute myocardial infarction with ST elevation and total atrioventricular block. This has occurred in clinical practice, in which symptoms associated with myocardial ischemia and positive troponin have elicited the request for a CA, interpreting the whole set as an acute ischemic syndrome. Another limitation would be the CAD progression in patients who were submitted to CA in less than 1 year and the disease occurred during this period. It is assumed, however, that any research process restricted to a single research center results in limitations, considering the differences of conduct and clinical interpretations found in health units. Conclusion In hospitalized individuals with acute pulmonary edema of unclear origin, prior history of coronary artery disease and segmental myocardial contractility deficit were the independent predictors of obstructive coronary disease. Of these two predictors, the previous history of coronary artery disease is the main probabilistic determinant, practically guaranteeing the presence of obstructive coronary disease. However, in the absence of a previous history of coronary artery disease or stroke, the probability of obstructive coronary disease is an intermediate one, being modulated by two independent predictors: ejection fraction andmyocardial contractility