ABC | Volume 113, Nº5, November 2019

Viewpoint Souza & Herdy Exercise-related SCAD in young people Arq Bras Cardiol. 2019; 113(5):988-998 Table 1 – List of pathologies and procoagulant markers surveyed with negative results Researched procoagulant pathologies and markers Leiden V Factor Rheumatoid factor Antithrombin III ANF Prothrombin Gene Mutation Anti-Ro Protein C and S Anti-La Activated protein C resistance Anti DNA Homocysteine β2 glycoprotein IgG and IgM MTHFR Research VDRL Lupus anticoagulant Anti-HIV IgG and IgM anticardiolipin Anti-HCV pANCA HBsAg cANCA Anti-HBc IgG and IgM ANF: antinuclear factor; MTHRF: methylenetetrahydrofolate reductase; pANCA: perinuclear neutrophil anti-cytoplasm antibody; cANCA: cytoplasmic neutrophil anti-cytoplasmic antibody; HbsAg: hepatitis B detection antibody; anti-HCV: hepatitis C detection antibody; anti‑HIV: HIV detection antibody; anti-HBc: hepatitis B detection antibody. Case Descriptions Case 1 Patient PS, male, 20 years old, amateur athlete, without risk factors for early CAD, does not use medication, anabolic, ergogenic, illicit or anorectic drugs. Negative family history for CAD, cardiomyopathy or thrombotic disease which began. Presents oppressive and burning chest pain, with irradiation to the left upper limb and chin, associated with nausea and insidious diaphoresis with six months of evolution. Symptoms appear after 30 min to 1h of high‑intensity exercise, or sometimes only in the morning after strenuous physical activity and the night before, during a long period (up to 4h), once or twice a week. During six months, the patient sought emergency care several times. At times, during precordium pain episodes, the resting electrocardiogram (ECG) showed altered ventricular repolarization (ARV) in the lower wall with small Q waves and T wave inversion (Figure 1); when asymptomatic and at rest, it also presented a conduction disorder in the right branch and apical anterior septum T waves, considered at the time as changes that are compatible with a young individual that practices physical activities (Figure 2). Therewere no changes inmyocardial necrosismarkers (MNM). Continuing the investigation, a transthoracic echocardiogram (ECO-TT) was performed at the outpatient center, which showed a slight segmental disturbance in the left ventricular (LV) wall contractility at rest, with normal systolic function (LV ejection 64% fraction), as well as dilation in the right coronary artery (DCA), initially suggesting a coronary anomaly or fistula, and was advised to perform a CATE at the outpatient center (Figure 3). The next morning, he sought emergency care once again presenting chest pain typically occurring when resting and with progressive chacteristics. There were 10 hours of evolution associated with diaphoresis. During hospital admission, the patient presented regular general conditions, eupneic in ambient air, normalized, feverless and was anicteric. He presented high systolic blood pressure (220/140mmHg). His weight was 78 kg; 1.78 m high and had a heart rate of 70 bpm. Therewere no changes in cardiac and pulmonary auscultation. Pulses were symmetrical with normal amplitudes and there was no peripheral edema. Serial ECGs demonstrated the same changes as those described in the previous resting ECG during typical chest pain crises. After morphine and nitrate analgesic measures, there was a partial response. It evolved with a slight change in MNM, characterizing the condition as non-ST-segment acutemyocardial infarction (STEMI). After risk stratification, the patient underwent CATE, which showed a large, large, a non-lesioned anterior descending artery (ADA) with major extensions and thick caliber that reached the middle third of the posterior interventricular sulcus, originating part of the posterior descending branch; non-dominant, non-injured circumflex artery (ACX) with a short extension and large caliber leading to a moderately important atrioventricular branch; Large SCAD with a large caliber apparently ectasized occluded with multiple thrombus images (Figure 4) and collateral circulation (CC) present with other uninjured arteries (Figure 5). Primary coronary transluminal angioplasty (TCA) was performed using Pronto® Extraction Catheter and a Power Line® balloon catheter, with the removal of a large number of thrombi, a lesion with 100% occlusion began demonstrating some irregularities and a final TIMI 2 flow. In the absence of CAD, other causes for coronary obstruction, such as thrombophilia, rheumatologic, inflammatory and connective tissue diseases, were investigated, but the results were negative. P.S. was discharged one week after the event with no further symptoms. Simvastatin 40 mg was prescribed once a day to the patient; 50 mg atenolol was prescribed once per day, clopidogrel 75 mg once a day (as I was allergic to acetylsalicylic acid [AAS]); and enalapril 10 mg, 1 time/day. He remained using medication for two and a half years, and after that period discontinued use of the medication on his own. He remained asymptomatic and practicing moderate- intensity exercise for another two and a half years. After completing five years since the primary event, there was a recurrence of chest pain and associated symptoms, a few hours after intense and strenuous physical activity (jiu‑jitsu and running). When admitted, the patient was nauseated and had moderate to progressive chest pain, beginning 3 hours 989