Consecutive electrocardiographic changes during percutaneous coronary intervention for acute coronary syndrome with high-grade atrioventricular block: a case report.

BACKGROUND: Acute coronary syndrome (ACS) with high-grade atrioventricular block (HAVB) still has a poor mortality risk, even in the current percutaneous coronary intervention (PCI) era. However, early PCI for ACS with HAVB is associated with improved in-hospital survival and a 6-month survival similar to that of ACS without HAVB. CASE PRESENTATION: A 70-year-old man was admitted to our hospital for ACS with HAVB. ECG showed complete AV block, complete right bundle branch block (CRBBB), and left axis deviation. Cardiac enzymes were elevated. He underwent temporary pacemaker insertion and coronary angiography, which showed severe stenosis of the proximal right coronary artery (RCA), 99% stenosis of the distal RCA with Thrombolysis in Myocardial Infarction (TIMI) grade 2 flow, and total occlusion of the proximal left anterior descending artery (LAD). We performed primary PCI in both the RCA and LAD, which resulted in TIMI grade 3 flow in both. After PCI, the HAVB recovered to normal sinus rhythm with CRBBB; a normal QRS interval returned within three days. The patient was discharged from the hospital without complications. CONCLUSION: In this case of ACS with HAVB, early intensive coronary artery reperfusion resulted in long-term patient survival. The blood supply to the AV node and bilateral bundle branches is complex. Multivessel ischemia may compromise both primary and collateral blood flows to the AV node and septum, resulting in severe conduction impairment. Clinicians performing PCI should be aware of this anatomy and physiology.

Acute myocardial infarction with "wrap around" right coronary artery mimicking Takotsubo cardiomyopathy: a case report.

BACKGROUND: Takotsubo cardiomyopathy (TC) is a cardiomyopathy that shows distinctive clinical conditions first described more than 20 years ago. Because clinical features of TC mimic those of anterior acute myocardial infarction (AMI), the differential diagnosis is important in selecting the appropriate treatment strategy in the acute phase. But it was difficult to differentiate those two diseases because the TC-like findings; such as the electrocardiogram (ECG) changes and left ventricular wall motion abnormality can occur in AMI especially with the anatomical variance of the coronary artery. CASE PRESENTATION: A 63-year-old man was admitted due to sudden onset of chest pain and was in a cardiogenic shock state. His ECG showed ST-segment elevation in precordial (V2-6) and inferior leads (II, III, and aVF) and ST-segment depression in lead aVR. Blood biochemistry showed that cardiac enzymes were not elevated. Ultrasonic cardiography showed that the left ventricular apical level was akinetic, papillary muscle level was severely hypokinetic, and basal level was hyperkinetic, mimicking TC. However, coronary angiogram showed total occlusion of his right coronary artery wrapping around the cardiac apex. Successful percutaneous coronary intervention reversed his critical status. CONCLUSION: To our knowledge, the present case is the first report described AMI with wrap-around RCA, mimicking TC. Although TC is increasingly recognized as a true but relatively infrequent clinical entity, it is still important to carefully rule out obstructive coronary artery disease.

Paracrine osteogenic signals via bone morphogenetic protein-2 accelerate the atherosclerotic intimal calcification in vivo.

OBJECTIVE: Vascular calcification is an important risk factor for cardiovascular diseases. Here, we investigated a role of dedifferentiated vascular smooth muscle cells (VSMCs) in the atherosclerotic intimal calcification. METHODS AND RESULTS: We prepared human cultured VSMCs in either redifferentiatiated or dedifferentiated state and analyzed the gene expressions of bone-calcification regulatory factors. Expression of bone morphogenetic protein-2 (BMP-2), a potent initiator for osteoblast differentiation, was significantly enhanced in dedifferentiated VSMCs. Furthermore, endogenous BMP-2 antagonists, such as noggin, chordin, and matrix gamma-carboxyglutamic acid protein, were all downregulated in the dedifferentiated VSMCs. Conditioned medium from dedifferentiated VSMCs, but not from redifferentiated VSMCs, stimulated the osteoblastic differentiation of the mesenchymal progenitor C2C12 cells, which was abolished by BMP-2 knockdown. In atherosclerotic intima from apolipoprotein (apo)E-deficient mice, αSM-actin-positive cells, presumably dedifferentiated VSMCs, expressed BMP-2. We generated BMP-2-transgenic mice using αSM-actin promoter and crossed them with apoE-deficient mice (BMP-2-transgenic/apoE-knockout). Significantly accelerated atherosclerotic intimal calcification was detected in BMP-2-transgenic/apoE-knockout mice, although serum lipid concentration and atherosclerotic plaque size were not different from those in apoE-knockout mice. Enhanced calcification appeared to be associated with the frequent emergence of osteoblast-like cells in atherosclerotic intima in BMP-2-transgenic/apoE-knockout mice. CONCLUSIONS: Our findings collectively demonstrate an important role of dedifferentiated VSMCs in the pathophysiology of atherosclerotic calcification through activating paracrine BMP-2 osteogenic signals.

Replicative senescence of vascular smooth muscle cells enhances the calcification through initiating the osteoblastic transition.

Medial artery calcification, which does not accompany lipid or cholesterol deposit, preferentially occurs in elderly population, but its underlying mechanisms remain unclear. In the present study, we investigated the potential role of senescent vascular smooth muscle cells (VSMCs) in the formation of senescence-associated medial calcification. Replicative senescence was induced by the extended passages (until passages 11-13) in human primary VSMCs, and cells in early passage (passage 6) were used as control young cells. VSMC calcification was markedly enhanced in the senescent cells compared with that in the control young cells. We identified that genes highly expressed in osteoblasts, such as alkaline phosphatase (ALP) and type I collagen, were significantly upregulated in the senescent VSMCs, suggesting their osteoblastic transition during the senescence. Knockdown of either ALP or type I collagen significantly reduced the calcification in the senescent VSMCs. Of note, runt-related transcription factor-2 (RUNX-2), a core transcriptional factor that initiates the osteoblastic differentiation, was also upregulated in the senescent VSMCs. Knockdown of RUNX-2 significantly reduced the ALP expression and calcification in the senescent VSMCs, suggesting that RUNX-2 is involved in the senescence-mediated osteoblastic transition. Furthermore, immunohistochemistry of aorta from the klotho(-/-) aging mouse model demonstrated in vivo emergence of osteoblast-like cells expressing RUNX-2 exclusively in the calcified media. We also found that statin and Rho-kinase inhibitor effectively reduced the VSMC calcification by inhibiting P(i)-induced apoptosis and potentially enhancing matrix Gla protein expression in the senescent VSMCs. These findings strongly suggest an important role of senescent VSMCs in the pathophysiology of senescence-associated medial calcification, and the inhibition of osteoblastic transition could be a new therapeutic approach for the prevention of senescence-associated medial calcification.

The potential hazard of a non-slip element balloon causing distal longitudinal stent deformation: the first clinical experience and in vitro assessment.

BACKGROUND: A new complication, longitudinal stent deformation (LSD), is increasingly reported with recent intracoronary stent designs. There have been experiences of unusual cases of distal LSD caused by entrapment of a Lacrosse® non-slip element (NSE) balloon (Goodman Co., Ltd., Nagoya, Japan), which has three flexible nylon elements to prevent slippage. Accordingly, the aim of this study is to report the clinical experience of distal LSD caused by the NSE in the documented center and to investigate the incidence and mechanisms involved. METHODS: Coronary intervention cases were retrospectively reviewed using the NSE balloon in hospital between May 2014 and June 2017. In bench testing, distal LSD was reproduced in a silicon tube model to identify its mechanism. RESULTS: A total of 95 patients with 107 lesions underwent coronary interventions with NSE. Of these, 72 lesions (12 de-novo lesions and 60 in-stent restenosis) were treated using in-stent dilatation. Two distal LSD cases occurred, representing an incidence of 2.78% (2/72) among all procedures; 16.7% (2/12) of the de-novo lesions developed LSD. In vitro experimentation allowed indentification of the mechanisms involved and bailout strategies. CONCLUSIONS: This is the first study to evaluate NSE balloon catheter entrapment complicated by distal LSD in which reconstruction of the deformed stent and retrieval of the NSE could be achieved successfully. There is a potential hazard for distal LSD during post-dilatation using the NSE balloon due to its structural characteristics. Careful assessment is needed to prevent this complication.

Clinical significance of induced left atrial macro-reentrant tachycardia after pulmonary vein isolation.

BACKGROUND: The clinical significance of induced left atrial macro-reentrant tachycardia (LA-AT) after encircling pulmonary vein isolation (EPVI) is unclear. Our objective was to determine whether induced LA-ATs are associated with the clinical recurrence of ATs. METHODS: We studied 185 consecutive patients with paroxysmal atrial fibrillation (PAF) who underwent their first EPVI with an 8-mm tip, nonirrigated catheter approach. AT was induced by atrial burst pacing after the completion of EPVI, and the atrial activation pattern was evaluated using EnSite NavX. Induced LA-ATs were ablated only in patients with clinical ATs of suspected LA origin. The factors associated with occurrence of AT after the procedure were examined. RESULTS: LA-ATs were induced in 38 patients and ablated in 5 patients. During a follow-up of 23 ± 7 months, the occurrence of AT did not differ between patients with nonablated LA-ATs (4/33, 12 %) and those without any inducible ATs (16/113, 14 %, p > 0.99). In multivariate analysis, the number of ablation points for completing EPVI was the only independent predictor of AT occurrence (odds ratio 1.07, p < 0.01). A repeat procedure was performed in 22 of 26 patients who developed AT. Nineteen patients became free from AT and AF after ablation of the conduction gaps (EPVI, n = 17; another line, n = 4), extra PV firing (n = 4), focal AT (n = 4), and induced LA-ATs (n = 3). CONCLUSIONS: In patients who had EPVI for PAF using an 8-mm tip, nonirrigated catheter, the occurrence of AT after EPVI was mainly due to conduction gaps in the ablation line or extra PV triggers. In patients with PAF, LA-ATs induced during the first procedure did not require ablation if they were not associated with clinical AT.