IJCS | Volume 31, Nº2, March / April 2018

134 Barros et al. Acute pulmonary edema. Coronary artery disease. Int J Cardiovasc Sci. 2018;31(2)133-142 Original Article cost among the modalities of acute HF, with the first one being cardiogenic shock. 1 APE 30-day mortality is still considered high. In the study by Figueras et al., 2 it was observed that the mortality rate in 216 consecutive patients admitted with APE in a single center was 14.1%. Severe Coronary Artery Disease (CAD) is often the anatomical substrate in patients with APE, as shown by Graham et al. 3 in a study of 119 patients with APE, of which 71 (60%) had a significant coronary lesion; 35 (49%), lesion in three epicardial vessels; and 7 (10%), left coronary trunk lesion. Ischemic heart disease is the most frequent etiology of chronicHFworldwide 4 and inBrazil. 5 APE is a severe clinical expressionof acuteHF andobstructiveCAD(arterial lumen mostly occluded) is often related to this clinical syndrome. The present study aimed to determine the predictors of obstructive CAD in this extreme HF clinical condition. We believe that we can contribute to the decision‑making concerning patients who have this syndrome and with a suspected ischemic substrate for its occurrence. Methods An observational, cross-sectional, diagnostic study with prospective data collection was performed, analyzing 149 patients between 40 and 80 years of age, consecutively admitted to a public emergency unit, specialized in cardiology, after registration in the hospital admission authorization form and patient history was reviewed by the research team. If the APE etiology was not clearly defined, such as uremic syndrome, previously knownvalvulopathy, well-defined cardiomyopathy at the echocardiogram and ST-segment elevation myocardial infarction, the patient was invited to participate in the study. Kidney dysfunction with creatinine >2 mg% was an exclusion criterion. Creatinine values ​above 2mg% were included in the study if a coronary angiography (CA) had been requested by the attending physician prior to the study protocol evaluation. After signing the Free and Informed Consent form (CAAE 05503912.6.0000.5544), the CAwas requested, aiming at defining the degree of coronary obstruction. Patientswho hadundergone the examination 1 year prior to the study and had normal results or had CAD definition without new therapeutic possibilities were not submitted to a new examination. The CA was analyzed by a single physician who was only aware of the reason for the hospitalization, APE. Obstructive CAD was considered severe if more than two-thirds (70%) of the arterial lumen, including total vessel occlusion, were occupied and if an epicardial vessel was affected: right coronary artery and its branches, circumflex artery and its branches, anterior descending artery, diagonal artery and 50% if the left main coronary artery was affected. The CAwas part of the research protocol because, as part of the primary objective, it was necessary to determine the predictors of severe obstructive coronary disease, and this is the gold standard examination for the investigation of this pathology. The electrocardiogram was performed on the first and second days, and was analyzed by an arrhythmologist, a specialist on the subject. All patients underwent Doppler echocardiography. Ultrasensitive troponin (Roche laboratory equipment) was performed on the first and second days and two cardiologists were asked to interpret the results if the obtainedvalueswere compatiblewithAPE precipitated by or associatedwith an acute coronary event. The diseases considered to be present, such as systemic arterial hypertension, diabetes mellitus, prior stroke, valvulopathy, asthma and chronic obstructive pulmonary disease, were taken into account based on the information provided by the patient. Smoking was considered when the patient was a current smoker, or when the patient had been an ex-smoker for less than 2 years. Statistical analysis To create the explanatory model for the occurrence of obstructive coronary disease, the following variables were collected: age, gender, presence of chest pain on admission, suggestive of myocardial ischemia prior to dyspnea, presence of previous dyspnea, history of coronary disease (classic angina pectoris, history of acute myocardial infarction, surgical or percutaneousmyocardial revascularization); electrocardiographic alteration suggestiveofmyocardialischemia(STdepression≥0.05mV −ornegativeTwave≥2mminleadscorrelatedtoacoronary artery occlusionon admission and/or electrocardiographic evolution of an acute ischemic event, such as a new q wave and/or dynamic change in ST or T); high-sensitivity troponin T value and its evolution in the first 48 hours, with measurements made on the first and second days; ejection fraction at the echocardiogram and myocardium segmental deficit at the echocardiogram; blood pressure at admission, and risk factors for atherosclerotic disease and atherosclerosis-related diseases, such as peripheral obstructive arterial disease and stroke, systemic arterial hypertension, diabetes mellitus and smoking.