Introduction: Acute coronary syndrome (ACS) presenting as non-ST-elevation myocardial infarction (NSTEMI) in a very young Filipina female with a maternal history of premature coronary artery disease and no comorbidities is a rare occurrence and seldom suspected. An integral approach using clinical presentation, information derived from ECG, cardiac troponin and risk assessment criteria should be used in order to arrive at the proper diagnosis and management. The other challenges encountered were angioedema secondary to clopidogrel hypersensitivity and financial constraints. These factors should be taken into consideration when deciding the short and long-term treatment especially after percutaneous coronary intervention and stenting. Case presentation: A 27-year-old active, female, Filipino, single, with a normal body mass index, non-smoker nonalcoholic drinker, no use of recreational drugs, no history of previous hospitalization, and comorbidities presented with sudden onset severe angina accompanied by diaphoresis and dyspnea. She was immediately brought to a local hospital, 12LECG showed T wave inversion on the inferior leads, troponin I was positive at 0.51ng/ml (0-.08) She was given aspirin, followed by clopidogrel in which she developed periorbital edema, dyspnea and was treated immediately with intravenous hydrocortisone and maintained on cetirizine and prednisone for five days. The clopidogrel was shifted to cilostazol. A coronary angiogram was done which showed a severe coronary artery disease at proximal right coronary artery. She underwent percutaneous coronary with stenting and was discharged stable and improved. Conclusion A delay in diagnosis and management may happen in a very young Filipino female presenting with acute chest pain and no comorbidities. A family history of premature coronary artery disease is a clinical marker of risk for acute coronary syndrome. A genetic testing may further establish this relationship. The clinical presentation of typical angina, T-wave inversions on inferior leads, highly abnormal cardiac troponin and very-high-risk criteria of recurrent or ongoing chest pain refractory to medical treatment warrants an immediate invasive strategy of coronary angiogram with revascularization. An angioedema secondary to clopidogrel hypersensitivity is a rare complication and can cause reluctance in a patient. The financial capacity to maintain long term treatment of dual antiplatelet should be considered for better compliance. A shared decision making between the physician and patient is a valuable tool in facing these challenges.
Myocardial Infarction ; Young Adult ; Cilostazol

OBJECTIVES: The plateau environment is characterized by low oxygen partial pressure, leading to the reduction of oxygen carrying capacity in alveoli and the reduction of available oxygen in tissues, and thus causing tissue damage. Cilostazol is a phosphodiesterase III inhibitor that has been reported to increase the oxygen release of hemoglobin (Hb) in tissues. This study aims to explore the anti-hypoxic activity of cilostazol and its anti-hypoxic effect. METHODS: A total of 40 male BALB/C mice were randomly divided into a low-dose cilostazol (6.5 mg/kg) group, a medium-dose (13 mg/kg) group, a high-dose (26 mg/kg) group, and a control group. The atmospheric airtight hypoxia experiment was used to investigate the anti-hypoxic activity of cilostazol and to screen the optimal dosage. Twenty-four male Wistar rats were randomly divided into a normoxia control group, a hypoxia model group, an acetazolamide (22.33 mg/kg) group, and a cilostazol (9 mg/kg) group. After 3 days of hypoxia in the 4 010 m high altitude, blood from the abdominal aorta was collected to determine blood gas indicators, the levels of IL-6 and TNF-α in plasma were determined by enzyme-linked immunosorbent assay, and the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutataione (GSH) were measured. The degree of pathological damage for rat tissues was observed with HE staining. RESULTS: Compared with the control group, the survival time of mice in the low, medium, and high dose group of cilostazol was significantly prolonged, and the survival time of mice in the medium dose group was the longest, with an extension rate at 29.34%, so the medium dose was the best dose. Compared with the hypoxia model group, the P50 (oxygen partial pressure at Hb oxygen saturation of 50%) value of rats in the cilostazol group was significantly increased by 1.03%; Hb and Hct were significantly reduced by 8.46% and 8.43%, and the levels of IL-6 and TNF-α in plasma were reduced by 50.65% and 30.77%. The MDA contents in heart, brain, lung, liver, and kidney tissues were reduced by 37.12%, 29.55%, 25.00%, 39.34%, and 21.47%, respectively. The SOD activities were increased by 94.93%, 9.14%, 9.42%, 13.29%, and 20.80%, respectively. The GSH contents were increased by 95.24%, 28.62%, 28.57%, 20.80%, and 44.00%, respectively. The results of HE staining showed that compared with the hypoxia model group, cilostazol significantly improved the damage of heart, lung, and kidney tissues in rats after hypoxia. CONCLUSIONS Cilostazol can significantly improve the oxidative stress and inflammatory reaction caused by rapid altitude hypoxia, and it has a significant protective effect on tissue damage caused by hypoxia, suggesting that it has obvious anti-hypoxic activity.
Altitude Sickness ; Animals ; Cilostazol/therapeutic use* ; Hypoxia/drug therapy* ; Interleukin-6/pharmacology* ; Male ; Mice ; Mice, Inbred BALB C ; Oxidative Stress ; Oxygen ; Rats ; Rats, Wistar ; Superoxide Dismutase/metabolism* ; Tumor Necrosis Factor-alpha/pharmacology*