A 76-year-old man was brought to the emergency department (ED) while undergoing cardiopulmonary resuscitation (CPR) due to cardiac arrest. The patient had hypertension, diabetes, and stage 5 chronic kidney disease (estimated glomerular filtration rate, 13 mL/min). He used aspirin, clopidogrel, an angiotensin-converting enzyme inhibitor (perindopril 4 mg), a beta-blocker (carvedilol 25 mg), and oral hypoglycemic agents (linagliptin 5 mg and glimepiride 4 mg). Before arriving at the ED, the patient reported chest pain and dyspnea. He then lost consciousness. His initial troponin I level had increased to 0.28 μg/L. After CPR for 12 minutes in the ED, the patient achieved return of spontaneous circulation (ROSC). After ROSC, his electrocardiogram (EKG) showed T-wave inversion at the anterior leads (Fig. 1A). The TIMI risk score was 9, and we decided to perform emergency coronary angiography (CAG) based on the suspicion of AMI as the cause of the arrest. However, because his family members strongly opposed CAG and signed a ‘do not resuscitate’ (DNR) document, the patient was admitted to the intensive care unit without undergoing CAG. The next day, the patient remained unconscious, but his vital signs were stable. However, his troponin I level had increased to 5.02 μg/L, and the echocardiogram showed regional wall motion abnormalities from the base to the mid inferior wall with reduced systolic function (ejection fraction, 45%). At that time, his family members changed their previous opinion and demanded CAG. Consequently, we performed CAG, which showed three-vessel disease with 80%–90% diffuse stenosis in the left anterior descending artery (LAD), diffuse near-total stenosis at the distal circumflex artery, and 70% tubular stenosis at the proximal right coronary artery (RCA). In addition, mid-RCA CTO with collateral flow from the distal LAD and septal branch was observed (Fig. 1B, C). Because the patient’s vital signs remained stable during CAG, we decided to treat the RCA CTO rather than the feeding vessel (the LAD). A wire (Gaia 1st; Asahi Intecc Co. Ltd., Tokyo, Japan) was loaded into a microcatheter (Corsair, Asahi Intecc Co. Ltd.) and passed through the proximal cap of the CTO lesion; however, it failed to penetrate the distal cap. Subsequently, we changed the wire to a Gaia 2nd wire (Asahi Intecc Co. Ltd.), which was successfully passed (Fig. 1D). Thereafter, predilatation was repeatedly performed with a 1.0×6-mm balloon with 14 atm of pressure, followed by sequential ballooning with a 2.0×15-mm balloon with nominal pressure. Afterward, the blood flow was recovered. Consequently, we implanted a 2.75×32-mm stent (SYNERGY; Boston Scientific, Marlborough, MA, USA) (Fig. 1E). However, contrast leakage was observed in the proximal part of the stent, and the patient experienced cardiac arrest (Fig. 1F). All procedures were stopped and 1 mg of epinephrine and 0.5 mg of atropine were administered intravenously during CPR. After 30 seconds of CPR, the patient achieved ROSC and was returned to the intensive care unit. There was no covered stent in the angiography room at that time; therefore, we focused on stabilizing his vital signs instead of prolonging the procedure time. The patient’s family members already agreed with the DNR order; therefore, we did not recommend any other procedures such as pericardiocentesis or bypass surgery. The patient died 4 days after the procedure.

A 56-year-old man visited the ED and reported chest pain. He had hypertension and diabetes and used aspirin. He had experienced dyspnea 3 days previously, but he did not visit the hospital at that time. The dyspnea became worse, and new chest pain occurred 6 hours before visiting the ED. On admission, the EKG showed ST segment elevation at the aVR and V1–3 leads and reciprocal changes at the lateral leads (Fig. 2A). The patient’s TIMI risk score was 5. We performed emergency CAG for ST-segment elevation MI. The emergency coronary angiogram revealed tight stenosis with heavy calcification at the distal left main coronary artery and proximal LAD, diffuse disease at the mid-to-distal LAD, tubular stenosis of 80% at the proximal RCA, and CTO at the mid-RCA, with collateral flow from the LAD (Fig. 2B, C). Because of the EKG findings, we inserted a wire (Runthrough NS; Terumo Interventional Systems, Somerset, NJ, USA) in the LAD after engaging the guiding catheter. Even though only one wire was inserted, the blood flow became very slow. Although the flow slightly recovered to nominal pressure after rapid ballooning with a 2.0×15-mm balloon, the dilatation was not enough to implant a stent because of heavy calcification (Fig. 2D). Suddenly, the patient’s blood pressure decreased; therefore, we immediately administered norepinephrine and dopamine. The patient’s vital signs became stable with inotropes, and we tried to insert a stent. However, the guiding catheter was pushed back because of poor support, and we inserted another wire (Sion; Asahi Intecc Co. Ltd.) to acquire greater back-up force. Nonetheless, we could not pass the stent through the lesion (Fig. 2E). Subsequently, ventricular fibrillation suddenly occurred due to flow disturbance created by the stent. We immediately retrieved the stent and started CPR (Fig. 2E). After ROSC, we used an extra backup 3.5 guiding catheter and performed ballooning of the lesion with a 2.5×15-mm balloon. We then successfully inserted the stent in the lesion. However, afterward, a second arrest suddenly occurred. The cardiothoracic surgery team was called to start extracorporeal membrane oxygenation (ECMO). After performing and controlling ECMO completely, we recommended emergency coronary artery bypass grafting (CABG) because the patient’s condition was unstable and arrest occurred 2 times during the procedure. After emergency CABG, the ECMO catheters were removed on postoperative day 4. The patient was still alive at the time of writing this article.