A man in his early 40s presented to our hospital’s emergency department with a 16-hour history of continuous stomach colic. Physical examination and questioning at a county hospital revealed that the patient had severe left lower abdominal colic without an apparent cause, along with dizziness, nausea, vomiting, palpitations, and dyspnea. He had no chest pain, cough, sputum production, fever, dysphagia, hematemesis, hematochezia, melena, diarrhea, or abdominal distension. His blood pressure was 210/140 mmHg. Emergency ECG revealed sinus tachycardia and ST-segment elevation in leads II, III, aVF, V7, V8, and V9. The patient was diagnosed with acute myocardial infarction of the inferior and posterior wall. He was treated by 300 mg each of oral aspirin and clopidogrel. With no contraindications to thrombolysis, thrombolytic treatment was also administered, beginning with an intravenous injection of 20 mg of recombinant human prourokinase within 3 minutes and progressing to 30 mg within 30 minutes. After receiving this thrombolytic treatment, the patient experienced a minor improvement in his abdominal colic. Subsequent ECG revealed sinus rhythm, atrial premature beats, and lower ST-segment elevation in leads II, III, and aVF than previously observed. Following the patient’s transfer to a cardiovascular hospital, ECG revealed sinus rhythm and lower ST-segment elevation in leads II, III, aVF, V7, V8, and V9 than observed in the first two ECG examinations. Echocardiography revealed paradoxical systolic motion of the apex, inferior wall, left ventricular anterior wall, and interventricular septum as well as a left ventricular end-diastolic diameter of 57 mm and a left ventricular ejection fraction of 35%. As shown in Table, the levels of the myocardial enzymes cardiac troponin-I and creatine kinase-MB were higher than the reference range. Table shows the blood pressure changes that occurred during the patient’s stay in the cardiovascular hospital; his blood pressure was higher than the reference range on four instances. The same diagnosis of acute myocardial infarction was made, and nitroglycerin was administered for treatment. The patient was then sent to our hospital’s emergency department. Figure shows the results of the ECG examination on admission: elevated ST-segment returning to baseline; Q-wave deepening in lead III; Q-wave forming in lead IVF; and inverted T-waves in leads V3, V4, V5, and V6. The patient’s medical history included 3 years of paroxysmal hypertension (maximum blood pressure of 230/146 mm Hg) and 10 months of undiagnosed hyperglycemia. Assessment of his vital signs revealed a temperature of 36.5°C, heart rate of 94 beats/minute, respiratory rate of 20 breaths/minute, and blood pressure of 100/64 mmHg. Physical examination revealed left lower abdominal pain, cyanosis of the lips, low breath tones in both lungs, and a slight amount of moist rales. Figure shows the emergency plain and enhanced abdominal computed tomography scans, which revealed masses and mixed low-density shadows on both sides of the abdominal aorta. The larger mass was located on the left side and measured 4.01×3.94 cm, had visibly thin walls and partitions, and had a computed tomography value of approximately 14 HU. The enhanced scan revealed annular enhancement of this mass, which was classified as PGL. Emergency coronary angiography, shown in Fig., revealed the following: Left main (LM) had no obvious stenosis; proximal and middle segment of left anterior descending (LAD) artery and left circumflex (LCX) artery had diffuse ectasia with rough endangium, forward blood flow grade TIMI 2, conformed to Markis type I diagnosis standard []. The obtuse marginal (OM) artery had irregular stenosis and forward blood flow grade TIMI 2. The patient ultimately received thrombolysis agents, antiplatelet therapy, atorvastatin, and myocardial protection agents. His glycosylated hemoglobin A1c concentration was 10.3%, and an oral glucose tolerance test revealed that his plasma glucose level was 15.0 mmol/L after 2 hours. As a result, we were able to determine that he had diabetes mellitus, though it was likely secondary. The results of the laboratory tests for PGL are shown in Table. The patient’s free normetanephrine level was significantly elevated in both plasma and 24-hour urine, his normetanephrine + metanephrine level was elevated in plasma, and his 3-methoxytyramine and vanillylmandelic acid levels were elevated in urine. PGL was diagnosed and treated by phenoxybenzamine; surgery was recommended, but the patient declined. Table shows the results of myocardial enzymology performed while the patient was hospitalized. The patient’s health gradually but clearly improved. His systolic blood pressure ranged from 104 to 136 mmHg, and his diastolic blood pressure fluctuated between 66 and 82 mmHg during the 6-month post-discharge follow-up. His fasting plasma glucose level varied from 4.2 to 5.8 mmol/L, and another oral glucose tolerance test showed that his plasma glucose level after 2 hours was <11.0 mmol/L. Another physical examination revealed no cyanosis of the lips, normal breath tones in both lungs, no moist rales, no discomfort in the left lower abdomen, and no other bothersome symptoms, all indicating a good overall clinical condition. Another echocardiography examination after 6 months revealed normal systolic motion of the apex, inferior wall, left ventricular anterior wall, and interventricular septum; a left ventricular end-diastolic diameter of 50 mm; and a left ventricular ejection fraction of 66%. Therefore, according to the European guidelines [], the patient had no red flags of acute infectious myocarditis, and was retrospectively diagnosed with TTS combined with the echocardiographical findings at the cardiovascular hospital and the after 6 months of follow-up. Finally, we were able to validate the efficacy of phenoxybenzamine for the PGL; thrombolysis, antiplatelet therapy, and lipid modulation for the CAE; and myocardial protection for the TTS. Consent for all treatments was obtained from the patient. He was ultimately diagnosed with TTS produced by PGL combined with Markis type I CAE.