Amyloid Deposition Mainly Localized in the Basal Area of the Left Ventricle in a Patient with Amyloid Transthyretin Cardiac Amyloidosis.

A 74-year-old Japanese man was admitted to our hospital for catheter ablation of paroxysmal atrial fibrillation. Transthoracic echocardiography revealed basal interventricular septal hypertrophy without apical sparing. Cardiac magnetic resonance imaging revealed late gadolinium enhancement in the hypertrophic lesions. The Kumamoto criteria was one point, and the patient had no carpal tunnel syndrome. However, technetium-99m pyrophosphate scintigraphy revealed an accumulation in the basal region of the left ventricle. A skin biopsy revealed transthyretin (TTR) amyloid deposition. A TTR gene examination revealed no variants. This case suggests that amyloid deposition in TTR may occur in the basal area of the interventricular septum.

Circulating intermediate CD14++CD16+monocytes are increased in patients with atrial fibrillation and reflect the functional remodelling of the left atrium.

AIMS: A recent large clinical study demonstrated the association between intermediate CD14++CD16+monocytes and cardiovascular events. However, whether that monocyte subset contributes to the pathogenesis of atrial fibrillation (AF) has not been clarified. We compared the circulating monocyte subsets in AF patients and healthy people, and investigated the possible role of intermediate CD14++CD16+monocytes in the pathophysiology of AF. METHODS AND RESULTS: This case-control study included 44 consecutive AF patients without systemic diseases referred for catheter ablation at our hospital, and 40 healthy controls. Patients with systemic diseases, including structural heart disease, hepatic or renal dysfunction, collagen disease, malignancy, and inflammation were excluded. Monocyte subset analyses were performed (three distinct human monocyte subsets: classical CD14++CD16-, intermediate CD14++CD16+, and non-classical CD14+CD16++monocytes). We compared the monocyte subsets and evaluated the correlation with other clinical findings. A total of 60 participants (30 AF patients and 30 controls as an age-matched group) were included after excluding 14 AF patients due to inflammation. Atrial fibrillation patients had a higher proportion of circulating intermediate CD14++CD16+monocytes than the controls (17.0 ± 9.6 vs. 7.5 ± 4.1%, P < 0.001). A multivariable logistic regression analysis demonstrated that only the proportion of intermediate CD14++CD16+monocytes (odds ratio: 1.316; 95% confidence interval: 1.095-1.582, P = 0.003) was independently associated with the presence of AF. Intermediate CD14++CD16+monocytes were negatively correlated with the left atrial appendage flow during sinus rhythm (r= -0.679, P = 0.003) and positively with the brain natriuretic peptide (r = 0.439, P = 0.015). CONCLUSION: Intermediate CD14++CD16+monocytes might be closely related to the pathogenesis of AF and reflect functional remodelling of the left atrium.

A Simultaneous Evaluation of Occupational Stress and Depression in Patients with Lifestyle-related Diseases.

Objective Karoshi, which is the Japanese term for death from over-work, is usually the extreme result of cardiovascular diseases, and occupational stress plays a pivotal role in the pathogenesis. Depression is closely associated with atherosclerotic cardiovascular disease. The present study was undertaken to examine the relationship between occupational stress and depression. Methods We enrolled 231 consecutive outpatients with lifestyle-related diseases such as diabetes, hyperlipidemia and hypertension were enrolled. Occupational stress was measured by qualitative constructs assessing job control, job demands, and worksite social support using a job content questionnaire (JCQ). The job strain index measured by the ratio of job demands to job control was used as an indicator of the occupational stress. Depression was evaluated by the Self-rating Depression Scale (SDS). Results A univariate linear regression analysis showed the SDS scores to be positively correlated with job demands and the job strain index and negatively correlated with job control and worksite social support. Multiple regression analyses to predict the SDS scores demonstrated that job demands were positively associated with SDS scores and job control and worksite social support were negatively associated with SDS scores after controlling for other variables. The job strain index was positively related to SDS scores. Conclusion Occupational stress expressed as the job strain index was strongly associated with depression. By simultaneously using the SDS and JCQ, the health conditions of patients could be classified based on occupational stress and mental stress, and this classification could help to promote a healthy work environment and guide individual workers.

Coconut atrium in long-standing rheumatic valvular heart disease.

BACKGROUND: Complete calcification of the left atrium (LA) is called "coconut atrium", which decreases the compliance of LA, leading to the elevation of LA pressure that is transmitted to the right-side of the heart. The pathogenesis of LA calcification in patients with rheumatic heart disease is unknown; however, possible mechanisms include chronic strain force in the atrial wall and inflammation. We report here a patient with long-standing rheumatic valvular heart disease with coconut atrium. CASE REPORT: A 76-year-old man presented with breathlessness and leg edema due to right-sided heart failure. He was diagnosed with rheumatic fever at 8 years of age. Mitral commissurotomy and the mitral and aortic valve replacement were previously performed to treat mitral and aortic valvular stenosis. The profile view of the chest X-ray indicated a diffuse calcified outline of the LA wall. A transthoracic echocardiogram revealed pulmonary hypertension and dilatation of both atria. Moreover, computed tomography showed nearly circumferential calcification of the LA wall. Despite intense medical treatment, he succumbed to heart failure. An autopsy demonstrated that the LA was markedly dilated, its wall was calcified, and its appearance was similar to the surface of an atherosclerotic aorta. Microscopic examination revealed intensive calcification in the endocardium. Minimal accumulation of inflammatory cells was noted. Although slight fibrosis was observed, the cardiac musculature was preserved. CONCLUSIONS: To the best of our knowledge, this is the first report that identifies the histological changes of LA calcification associated with long-standing rheumatic valvular heart disease.

Reduction in coronary microvascular resistance through cardiac resynchronization and its impact on chronic reverse remodelling of left ventricle in patients with non-ischaemic cardiomyopathy.

AIMS: Left bundle branch block (LBBB) induces mechanical dyssynchrony, thereby compromising the coronary circulation in non-ischaemic cardiomyopathy. We sought to examine the effects of cardiac resynchronization therapy (CRT) on coronary flow dynamics and left ventricular (LV) function. METHODS AND RESULTS: Twenty-two patients with non-ischaemic cardiomyopathy (New York Heart Association class, III or IV; LV ejection fraction, ≤35%; QRS duration, ≥130 ms) were enrolled. One week after implantation of the CRT device, coronary flow velocity and pressure in the left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCx) were measured invasively, before and after inducing hyperemia by adenosine triphosphate administration, with two programming modes: sequential atrial and biventricular pacing (BiV) and atrial pacing in patients with LBBB or sequential atrial and right ventricular pacing in patients with complete atrioventricular block (Control). We assessed hyperemic microvascular resistance (HMR, mean distal pressure divided by hyperemic average peak velocity) and the relationship between the change in HMR and mid-term LV reverse remodelling. Hyperemic microvascular resistance was lower during BiV than during Control (LAD: 1.76 ± 0.47 vs. 1.54 ± 0.45, P < 0.001; LCx: 1.92 ± 0.42 vs. 1.73 ± 0.31, P = 0.003). The CRT-induced change in HMR of the LCx correlated with the percentage change in LV ejection fraction (R = -0.598, P = 0.011) and LV end-systolic volume (R = 0.609, P = 0.010) before and 6 months after CRT. CONCLUSION: Cardiac resynchronization therapy improves coronary flow circulation by reducing microvascular resistance, which might be associated with LV reverse remodelling.

Impact of adenosine-provoked acute dormant pulmonary vein conduction on recurrence of atrial fibrillation.

INTRODUCTION: Adenosine can be associated with acute recovery of conduction to the pulmonary veins (PVs) immediately after isolation. The objective of this study was to evaluate whether the response to adenosine predicts atrial fibrillation (AF) recurrence after a single ablation procedure in patients with paroxysmal AF. METHODS AND RESULTS: A total of 109 consecutive patients (61 ± 10 years; 91 males) with drug-refractory paroxysmal AF who underwent AF ablation were analyzed. After PV antrum isolation (PVAI), dormant PV conduction was evaluated by an administration of adenosine in all patients. No acute reconnections were provoked by the adenosine in 70 (64.2%) patients (Group-1), but they were provoked in at least one side of the ipsilateral PVs in 39 (35.8%) patients (Group-2). All adenosine-provoked dormant conductions were successfully eliminated by additional ablation applications. By 12 months after the initial procedure, 72 (66.1%) patients were free of AF recurrences without any antiarrhythmic drugs. A Cox regression multivariate analysis of the variables including the adenosine-provoked reconductions, age, gender, duration of AF, presence of hypertension or structural heart disease, left atrial size, left ventricular ejection fraction, and body mass index demonstrated that adenosine-provoked reconductions were an independent predictor of AF recurrence after a single ablation procedure (hazard ratio: 1.387; 95% confidence interval: 1.018-1.889, P = 0.038). At the repeat session for recurrent AF, conduction recovery was observed similarly in both groups (P = 0.27). CONCLUSION: Even after the elimination of any adenosine-provoked dormant PV conduction, the appearance of acute adenosine-provoked reconduction after the PVAI was an independent predictor of AF recurrence after a single AF ablation procedure.

Prevalence, electrophysiological properties, and clinical implications of dissociated pulmonary vein activity following pulmonary vein antrum isolation.

The objective of this study was to investigate the prevalence, electrophysiologic properties, and clinical implications of dissociated pulmonary vein (PV) activity after PV antrum isolation (PVAI) in patients with paroxysmal atrial fibrillation (AF). One hundred seventy-three consecutive patients (61 ±10 years old, 141 men) with drug-refractory paroxysmal AF who underwent AF ablation were analyzed. After identification of arrhythmogenic foci, PVAI was performed in all patients. Of the total 346 isolated ipsilateral PVs, 97 (28.0%) were silent, 35 (10.1%) demonstrated isolated ectopic beats, 209 (60.4%) demonstrated a regular ectopic rhythm, and 5 (1.4%) demonstrated fibrillatory activity. The culprit thoracic vein was identified in 77 patients (44.5%). After isolation of ipsilateral PVs, venous activity was observed in 68 (79.1%) and 178 (68.5%) PVs among the 86 PVs with AF triggers and 260 PVs without AF triggers, respectively (p = 0.06). There was no significant difference in the incidence of acute PV reconnections exposed by adenosine triphosphate between the 97 silent ipsilateral PVs and 209 ipsilateral PVs with dissociated PV activity after the PVAI (20.6% vs 19.1%, p = 0.78). After a mean follow-up of 48.7 ± 7.9 months there was no significant difference in rates of freedom from atrial tachyarrhythmias after a single procedure between patients with and those without dissociated activity (62.1% vs 63.3%, p = 0.74, log-rank test). In conclusion, although dissociated PV activity appearing after PV isolation is an important electrophysiologic finding to prove bidirectional conduction block between the left atrium and the PV during the procedure, the clinical implications might be limited.

Catheter ablation of atrial fibrillation in patients with valvular heart disease: long-term follow-up results.

UNLABELLED: AF Ablation in Patients With Valvular Heart Disease. BACKGROUND: The purpose of this study is to evaluate the efficacy of atrial fibrillation (AF) ablation in patients with moderate valvular heart disease (VHD). METHODS: In total, 534 consecutive patients who underwent AF ablation were enrolled. Patients with a history of valve surgery or other structural heart disease were excluded. Patients with clinically moderate VHD (group-1, n = 45) were compared with those without VHD (control group-2, n = 436). Ipsilateral pulmonary vein antrum isolation (PVAI) was performed with a double Lasso technique in all the patients. Left atrial (LA) linear ablation was undertaken in persistent AF patients, if AF was inducible after PVAI. RESULTS: Patients in group-1 were significantly older and had a larger LA. PVAI was successfully achieved in all the patients. Patients in group-1 received LA linear ablation more frequently during the index procedure. After a median of 26 months from the index procedure, the freedom from AF was significantly lower in group-1 than group-2 off antiarrhythmic drugs (AADs) (47% vs 69%, P = 0.002). Although there were more number of total procedures in group-1 than group-2, the freedom from AF was lower at median 24 months after the last procedure (78% vs 87%, P = 0.038). There was no significant difference in the freedom from AF on AADs (91% vs 95%, P = 0.356) or complication rate between the 2 groups. Atrial tachycardia following the index procedure was observed more frequently in group-1 (P = 0.001). CONCLUSION: The patients with VHD undergoing AF ablation are less likely to remain in sinus rhythm at long term without AADs than those without VHD.

Electrophysiological characteristics of localized reentrant atrial tachycardia occurring after catheter ablation of long-lasting persistent atrial fibrillation.

BACKGROUND: Mapping of recurrent atrial tachycardia (AT) after extensive ablation for long-lasting persistent atrial fibrillation (AF) is complex. We sought to describe the electrophysiological characteristics of localized reentry occurring after ablation of long-lasting persistent AF. METHODS: Out of 70 patients undergoing catheter ablation of long-lasting persistent AF, 9 patients (13%, 55 +/- 8 years, 8 males) in whom localized reentry was demonstrated in a repeat ablation were studied. Localized reentry was defined as reentry in which the circuit was localized to a small area and did not have a central obstacle. The mechanism of AT was determined by electroanatomical and entrainment mapping. RESULTS: Nine localized reentries with cycle length of 243 +/- 41 ms were mapped in 9 patients. The location of AT was the left atrial appendage in 4 patients, anterior left atrium in 2, left septum in 2, and mitral isthmus in 1. In all ATs, a critical isthmus of <10 mm in width was identified in the vicinity of the prior linear lesions or ostia of isolated pulmonary veins. Ablation of the critical isthmus, which was characterized by continuous low-voltage activity (median voltage: 0.15 mV, mean duration: 117 +/- 31 ms), terminated AT and rendered it noninducible. Additionally, ablation was performed for all of inducible ATs. At 11 +/- 7 months after the procedure, 8 of 9 patients (89%) were free from any arrhythmias. CONCLUSIONS: After ablation of long-lasting persistent AF, localized reentry may arise from a site in the vicinity of the prior ablation lesions. Ablation of the critical isthmus eliminates the arrhythmia.

Adenosine triphosphate exposes dormant pulmonary vein conduction responsible for recurrent atrial tachyarrhythmias: importance of evaluating the dormant conduction during the re-do ablation procedure.

A 61-year-old man suffered from atrial tachycardia (AT) following pulmonary vein isolation (PVI) treatment of atrial fibrillation. During a re-do procedure, all pulmonary veins (PVs) were isolated from the left atrium (LA) and programmed stimulation could not induce any atrial arrhythmias. Adenosine triphosphate exposed dormant PV-LA conduction at the right superior PV. PV firing during the reconnection caused AT with the same P-wave morphology as clinical AT. For 6 months after the elimination of that dormant PV conduction, the patient has been free of any AT. Evaluation of dormant PV conduction was effective in curing the recurrent AT after PVI.

Expression of Toll-like receptors on human platelets.

INTRODUCTION: Platelets play a crucial role in arterial thrombosis, which is the main cause of acute coronary syndrome. Some mycobacteriums, such as Chlamydia pneumoniae, were associated with progression of atherosclerosis and they are interacted with Toll-like receptors (TLRs), which have been defined as pathogen-associated molecular pattern recognition molecules in innate immunity. In the present study, we examined whether human platelets express TLRs. MATERIALS AND METHODS: Human platelets were obtained from healthy volunteers and the mRNA and protein level of TLRs on platelets and Meg-01 cells, megakaryoblastic cell line, were investigated. RESULTS: Reverse transcription-polymerase chain reaction (RT-PCR) demonstrated that TLR1 and TLR6 mRNA were expressed in platelets and Meg-01 cells. Furthermore, interferon-gamma up-regulated their mRNA levels in dose and time dependent manners after stimuli. Both TLR1 and TLR6 proteins in platelets were detected by Western blotting, and their expression of platelets was more than that of Meg-01 cells. Flow cytometry analysis revealed the expression of TLR1 and TLR6 on the cell surface of Meg-01 cells. Furthermore, immunohistochemical analysis using human coronary thrombi obtained from patients with acute coronary syndrome confirmed the expression of TLR1 and TLR6 on platelets. CONCLUSION: In summary, we demonstrated that human platelets and Meg-01 cells expressed a family of TLRs for the first time, and our findings indicated that platelets might recognize antigens directly via TLRs. Our findings suggest a possibility that platelets have the ability to recognize the antigens via TLRs and that there are mechanistic relations between infectious inflammation and atherosclerotic vascular diseases.