Atrial Tachycardia in the Coronary Sinus Communicating With Circumflex Artery Aneurysm.

Coronary artery fistula is a rare anomaly, and localized re-entrant atrial tachycardia (AT) in the coronary sinus (CS) has rarely been reported. We report a case in a patient with a left circumflex artery aneurysm associated with the CS fistula who underwent radiofrequency catheter ablation for localized re-entrant AT, which originated from the CS.

Single-Cell RNA Sequencing Reveals an Immune Landscape of CD4+ T Cells in Coronary Culprit Plaques With Acute Coronary Syndrome in Humans-Brief Report.

BACKGROUND: Acute coronary syndrome (ACS) involves plaque-related thrombosis, causing primary ischemic cardiomyopathy or lethal arrhythmia. We previously demonstrated a unique immune landscape of myeloid cells in the culprit plaques causing ACS by using single-cell RNA sequencing. Here, we aimed to characterize T cells in a single-cell level, assess clonal expansion of T cells, and find a therapeutic target to prevent ACS. METHODS: We obtained the culprit lesion plaques from 4 patients with chronic coronary syndrome (chronic coronary syndrome plaques) and the culprit lesion plaques from 3 patients with ACS (ACS plaques) who were candidates for percutaneous coronary intervention with directional coronary atherectomy. Live CD45+ immune cells were sorted from each pooled plaque samples and applied to the 10× platform for single-cell RNA sequencing analysis. We also extracted RNA from other 3 ACS plaque samples and conducted unbiased TCR (T-cell receptor) repertoire analysis. RESULTS: CD4+ T cells were divided into 5 distinct clusters: effector, naive, cytotoxic, CCR7+ (C-C chemokine receptor type 7) central memory, and FOXP3 (forkhead box P3)+ regulatory CD4+ T cells. The proportion of central memory CD4+ T cells was higher in the ACS plaques. Correspondingly, dendritic cells also tended to express more HLAs (human leukocyte antigens) and costimulatory molecules in the ACS plaques. The velocity analysis suggested the differentiation flow from central memory CD4+ T cells into effector CD4+ T cells and that from naive CD4+ T cells into central memory CD4+ T cells in the ACS plaques, which were not observed in the chronic coronary syndrome plaques. The bulk repertoire analysis revealed clonal expansion of TCRs in each patient with ACS and suggested that several peptides in the ACS plaques work as antigens and induced clonal expansion of CD4+ T cells. CONCLUSIONS: For the first time, we revealed single cell-level characteristics of CD4+ T cells in patients with ACS. CD4+ T cells could be therapeutic targets of ACS. REGISTRATION: URL: https://upload.umin.ac.jp/cgi-open-bin/icdr_e/ctr_view.cgi?recptno=R000046521; Unique identifier: UMIN000040747.

Efficacy of Native T1 Mapping for Patients With Non-Ischemic Cardiomyopathy and Ventricular Functional Mitral Regurgitation Undergoing Transcatheter Edge-to-Edge Repair.

BACKGROUND: We investigated the efficacy of left ventricular (LV) myocardial damage by native T1mapping obtained with cardiac magnetic resonance (CMR) for patients undergoing transcatheter edge-to-edge repair (TEER).Methods and Results: We studied 40 symptomatic non-ischemic heart failure (HF) patients and ventricular functional mitral regurgitation (VFMR) undergoing TEER. LV myocardial damage was defined as the native T1Z-score, which was converted from native T1values obtained with CMR. The primary endpoint was defined as HF rehospitalization or cardiovascular death over 12 months after TEER. Multivariable Cox proportional hazards analysis showed that the native T1Z-score was the only independent parameter associated with cardiovascular events (hazard ratio 3.40; 95% confidential interval 1.51-7.67), and that patients with native T1Z-scores <2.41 experienced significantly fewer cardiovascular events than those with native T1Z-scores ≥2.41 (P=0.001). Moreover, the combination of a native T1Z-score <2.41 and more severe VFMR (effective regurgitant orifice area [EROA] ≥0.30 cm2) was associated with fewer cardiovascular events than a native T1Z-score ≥2.41 and less severe VFMR (EROA <0.30 cm2; P=0.002). CONCLUSIONS: Assessment of baseline LV myocardial damage based on native T1Z-scores obtained with CMR without gadolinium-based contrast media is a valuable additional parameter for better management of HF patients and VFMR following TEER.

Excimer laser coronary atherectomy with distal protection for neoatherosclerosis rupture: a case report.

Background: Neoatherosclerosis, a prominent contributor to in-stent restenosis (ISR), persists as a formidable challenge during percutaneous coronary intervention. Excimer laser coronary atherectomy (ELCA) and embolic protection devices may help reduce coronary flow disturbance from procedure-related distal embolization. Case summary: A 71-year-old man experienced in-stent neoatherosclerosis rupture-related non-ST segment elevation myocardial infarction. Multidisciplinary intracoronary imaging, including intravascular ultrasound and optical coherence tomography (OCT), suggested that the ISR was caused by a neoatherosclerosis rupture that can potentially lead to distal embolization. Excimer laser coronary atherectomy (fluence, 45 mJ/mm2 and frequency, 25 pulse/s) using a 1.7 mm concentric catheter was performed with distal protection using Filtrap (Nipro Corporation, Tokyo, Japan), which significantly reduced the volume of the neoatherosclerosis. However, subsequent ELCA on the highest setting (fluence, 60 mJ/mm2 and frequency, 40 pulse/s) led to a filter no-reflow phenomenon, although OCT revealed a further effective vaporization of the neoatherosclerosis and an apparent reduction of soft tissue compatible with the thrombus. After removing the embolic protection device, drug-coated balloon angioplasty provided optimal results without coronary flow disturbance. Discussion: Excimer laser coronary atherectomy reduces soft plaque and thrombus burden, which can reduce the occurrence of distal embolization in select cases. In the case of this patient, procedure-related distal embolization may have been induced by the heightened photomechanical effects resulting from the use of the highest setting in ELCA under increased intracoronary arterial pressure caused by continuous saline injection during ELCA. Concomitant distal protection during ELCA may be more feasible for preventing coronary flow disturbance in patients with a large amount of neoatherosclerosis.

Bailout MitraClip therapy for deteriorated systolic anterior motion-related severe mitral regurgitation post-alcohol septal ablation: a case report.

Background: Percutaneous alcohol septal ablation (ASA) is a non-surgical treatment for symptomatic hypertrophic obstructive cardiomyopathy. It has a potential risk for systolic anterior motion (SAM)-related mitral regurgitation (MR) deterioration, leading to acute congestive heart failure. In such clinical scenarios, additional surgical interventions for SAM-MR are risky. Case summary: A 70-year-old man experienced acutely deteriorated heart failure caused by SAM-related MR following ASA, for which venous-arterial extracorporeal membrane oxygenation (ECMO) and a percutaneous left ventricular assist device (Impella CP, Abiomed, MA, USA) were required. Transoesophageal echocardiography showed that an interventricular septal oedematous protrusion led to a large coaptation gap of mitral leaflets with a pseudo-prolapse of the posterior mitral leaflet (PML). Because of his prohibitive surgical risks, we opted for transcatheter edge-to-edge mitral valve repair with MitraClip therapy. After removing the Impella device, an XT clip (Abbott Vascular, CA, USA) was located to cover the pseudo-prolapsed PML, resulting in optimal MR reduction with an acceptable mean transmitral valve-pressure gradient. Thereafter, his heart failure was well controlled, and venous-arterial ECMO was successfully removed on post-MitraClip Day 2. Discussion: This case demonstrated that MitraClip therapy rescued the patient from a rare complication of severe acute heart failure with haemodynamic collapse caused by massive SAM-related MR following ASA. MitraClip therapy can be a feasible, less-invasive interventional therapy for SAM-related MR in cases with acceptable severity of iatrogenic mitral stenosis post-MitraClip implantation.

Rapidly progressive infective endocarditis after MitraClip therapy: A rare complication of transcatheter edge-to-edge mitral valve repair.

Infective endocarditis (IE) is a rare, life-threatening complication of MitraClip (Abbott, Abbott Park, IL, USA) therapy. We report a case of an 84-year-old male who underwent transcatheter edge-to-edge mitral valve (MV) repair using MitraClip (Abbott, Abbott Park, IL, USA) 4 weeks prior for ventricular functional mitral regurgitation (MR) and returned with unstable hemodynamics and high-grade fever. Transthoracic echocardiography (TTE) on emergency admission showed thickening of the anterior mitral leaflet (AML) without apparent MR deterioration. TTE and transesophageal echocardiography (TEE) performed the next day showed severe MR due to rapidly progressing AML degeneration with aneurysmal formation. During the TEE examination, exacerbated heart failure due to severe MR caused cardiogenic shock and subsequent ventricular fibrillation, necessitating emergency extracorporeal cardiopulmonary resuscitation. Considering the positive findings of methicillin-resistant Staphylococcus aureus (MRSA) in blood cultures and degenerative MV findings, MitraClip-related IE was diagnosed; finally, MV replacement was performed. Retrospective consideration suggested that the potential causes of this MitraClip-related IE were valve injuries caused by multiple full-close procedures and insufficient prophylaxis for preoperatively detected MRSA. MitraClip-related IE has destructive characteristics that necessitate surgical intervention despite high risks; therefore, we should prevent procedure-related MV injuries and implement preoperative infection precautions to prevent catastrophic complications, particularly in patients with preoperative nasal MRSA-positive findings. Learning objectives: MitraClip-related infective endocarditis (IE) is a rare but fatal condition. IE caused by methicillin-resistant Staphylococcus aureus (MRSA), in particular, has an inferior prognosis with high mortality rates due to its destructive nature. Therefore, interventionalists should consider preventive strategies to avoid procedure-related valve injuries and adequately prepare for prophylaxis of patients who are carriers of MRSA to prevent MitraClip-related IE caused by MRSA.