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This case report represents Kinase Inhibitor Library high throughput successful LMCA stenting under intravascular ultrasound (IVUS) guidance in a patient with cardiogenic shock due to TAAD with LMCA dissection. This procedure, particularly in terms of the use of IVUS, may be effective for rapid hemodynamic stabilization in patients in critical condition. INTRODUCTION Acute myocardial infarction (AMI) concomitant with acute type A aortic dissection (TAAD) is associated with a high hospital mortality rate despite improvements in TAAD surgical outcomes[1-3]. In particular, TAAD involving the left main coronary artery (LMCA) is a rare but lethal condition associated with low output syndrome, which results from extensive myocardial necrosis regardless of whether an aortic repair surgery is successful. Early coronary revascularization should be performed to minimize cardiac dysfunction[3]. The treatment of dissected coronary arteries with stent implantation achieves prompt and adequate myocardial blood flow and helps prevent extensive myocardial damage. However, an accurate diagnosis of TAAD prior to treatment for AMI is difficult, particularly in patients with hemodynamic instability[4,5]. Furthermore, percutaneous coronary intervention for LMCA obstruction due to TAAD is a complicated procedure unless the mechanism of the LMCA obstruction has been clarified[6]. Here, we describe a case of successful coronary intervention under intravascular ultrasound (IVUS) guidance in a patient with shock due to an unusually localized TAAD with LMCA obstruction. CASE REPORT A 65-year-old man was admitted due to sudden-onset chest pain accompanied with click here cold sweats. The patient had Isotretinoin previously undergone a drug-eluting stent implantation in the left anterior descending artery (LAD) 5 years earlier to treat stable angina. His hypertension and hyperlipidemia were well controlled with medication, and he had continued dual antiplatelet therapy (DAPT) since the stent implantation. The patient was transported by ambulance to our hospital within an hour of onset, and his status on arrival included an unmeasurable blood pressure below 60 mmHg and a heart rate of 50 beats/min. The initial electrocardiogram demonstrated bradycardia with an idioventricular rhythm, wide QRS complexes, and ST elevation in the lead aVR (Figure ?(Figure1).1). Transthoracic echocardiography (TTE) revealed marked left ventricular dysfunction and a left ventricular ejection fraction of