A case of coronary artery compression syndrome resulting from peri-valvular regurgitation and long-standing atrial fibrillation.

A man in his 70s with a history of mitral valve replacement (MVR) and long-standing persistent atrial fibrillation (AF) presented with effort angina. Coronary angiography revealed severe stenosis of the left main coronary artery (LMCA). As it was an emergent case, PCI (percutaneous coronary intervention) was selected for treatment. Intravascular ultrasonography revealed no atherosclerotic lesions in the LMCA. The LMCA was effectively dilated by the drug-eluting stent. No elevation in intracardiac pressure was observed in cardiac catheterization after PCI. Computed tomography scan indicated potential compression of the LMCA by the surrounding structures. In cases of long-standing persistent AF and an enlarged atrium after MVR, the possibility of LMCA stenosis due to anatomical changes should be considered. Learning Objectives: ◾Peri-valvular regurgitation and long-standing persistent atrial fibrillation can potentially cause atrial enlargement.◾Coronary artery stenosis without atherosclerosis can occur due to compression from surrounding structures or shifting of the coronary artery.◾Stent therapy provides a temporary solution and coronary artery bypass grafting or switching should be considered if re-stenosis occurs.

A randomized controlled trial of eicosapentaenoic acid in patients with coronary heart disease on statins.

BACKGROUND: There is a residual risk of coronary heart disease (CHD) despite intensive statin therapy for secondary prevention. The aim of this study was to investigate whether coronary plaque regression and stabilization are reinforced by the addition of eicosapentaenoic acid (EPA) to high-dose pitavastatin (PTV). METHODS: We enrolled 193 CHD patients who underwent percutaneous coronary intervention (PCI) in six hospitals. Patients were randomly allocated to the PTV group (PTV 4mg/day, n=96) or PTV/EPA group (PTV 4mg/day and EPA 1800mg/day, n=97), and prospectively followed for 6-8 months. Coronary plaque volume and composition in nonstenting lesions were analyzed by integrated backscatter intravascular ultrasound (IB-IVUS). RESULTS: The PTV/EPA group showed a greater reduction in total atheroma volume compared to PTV group. IB-IVUS analyses revealed that lipid volume was significantly decreased during follow-up period in only PTV/EPA group. The efficacy of additional EPA therapy on lipid volume reduction was significantly higher in stable angina pectoris (SAP) patients compared to acute coronary syndrome patients. EPA/AA ratio was significantly improved in PTV/EPA group compared to PTV group. There was no significant difference in the incidence of major adverse cardiovascular events and side effects. CONCLUSIONS: Combination EPA/PTV therapy significantly reduced coronary plaque volume compared to PTV therapy alone. Plaque stabilization was also reinforced by EPA/PTV therapy in particular SAP patients. The addition of EPA is a promising option to reduce residual CHD risk under intensive statin therapy.

Impact of Serum Uric Acid Levels on Coronary Plaque Stability Evaluated Using Integrated Backscatter Intravascular Ultrasound in Patients with Coronary Artery Disease.

AIM: Because the prevalence of hyperuricemia is lower in females than in males, the association between hyperuricemia and cardiovascular disease has been frequently reported in females. Increased serum uric acid levels are associated with the presence of cardiovascular risk factors such as hypertension, renal dysfunction, insulin resistance, and metabolic syndrome. However, it is controversial whether hyperuricemia is an independent risk factor for coronary artery disease in both the genders. The purpose of this study was to investigate the relationship between serum uric acid levels and coronary plaque components assessed using integrated backscatter intravascular ultrasound (IB-IVUS) in males and females. METHODS: In total, 385 patients (298 males and 87 females) who underwent percutaneous coronary intervention using IB-IVUS were divided into three groups in each gender according to their serum uric acid levels. We characterized tissue from coronary plaques in culprit lesions. RESULTS: Serum uric acid levels significantly correlated with percent lipid volume (r=0.37) and inversely correlated with percent fibrous volume (r=－0.35). Multivariate analysis showed that the uric acid level was independently associated with lipid-rich plaques (odds ratio 2.43, 95%, confidence interval 1.75-3.47). The prevalence of lipid-rich plaques increased with increasing uric acid levels in both genders. CONCLUSION: Increased serum uric acid levels were associated with larger lipid content plaques in both genders.

Deficiency of Long Pentraxin PTX3 Promoted Neointimal Hyperplasia after Vascular Injury.

AIM: Pentraxin 3 (PTX3) is a novel marker for the primary local activation of innate immunity and inflammatory responses. Although clinical and experimental evidence suggests that PTX3 is associated with atherosclerosis, the relationship between PTX3 and vascular remodeling after wall injury remains to be determined. We investigated the effects of PTX3 on neointimal hyperplasia following wire vascular injury. METHODS: PTX3 systemic knockout (PTX3-KO) mice and wild-type littermate (WT) mice were subjected to wire-mediated endovascular injury. At four weeks after wire-mediated injury, the areas of neointimal and medial hyperplasia were evaluated. RESULTS: The PTX3-KO mice exhibited higher hyperplasia/media ratios than the WT mice after wire injury, and the degree of Mac-3-positive macrophage accumulation was significantly higher in the PTX3-KO mice than in the WT mice. Furthermore, the PTX3-KO mice showed a much greater increase in the number of PCNA-stained cells in the vascular wall than that observed in the WT mice. CONCLUSIONS: A deficiency of PTX3 results in deteriorated neointimal hyperplasia after vascular injury via the effects of macrophage accumulation and vascular smooth muscle cell proliferation and migration.

A combination of plaque components analyzed by integrated backscatter intravascular ultrasound and serum pregnancy-associated plasma protein a levels predict the no-reflow phenomenon during percutaneous coronary intervention.

AIMS: Previous studies reported that integrated backscatter intravascular ultrasound (IB-IVUS) provides high diagnostic accuracy for tissue characterization of coronary plaques and that pregnancy-associated plasma protein A (PAPP-A) could be a marker of adverse cardiac outcome in patients with cardiovascular disease. We examined whether IB-IVUS and PAPP-A levels could predict the incidence of no-reflow during percutaneous coronary intervention (PCI) METHODS AND RESULTS: About 176 consecutive patients (138 men, mean age 68 ± 11 years) who underwent PCI with IB-IVUS were prospectively enrolled. Combined no-reflow, including transient filter no-reflow by using distal protection devices, was observed in 31 patients. The percentages of coronary lipid volume (%LV) analyzed by IB-IVUS and serum PAPP-A were significantly higher in patients with combined no-reflow than normal-reflow. To predict no-reflow, a receiver operating characteristic (ROC) analysis determined cut-off values of %LV as 62% and serum PAPP-A as 7.71 ng/mL. The multivariate logistic regression analysis showed that %LV (hazard ratio 4.5, 95% confidence interval 1.6-13.4, P < 0.01) and PAPP-A (hazard ratio 4.32, 95% confidence interval 1.5-12.7, P < 0.01) were independent predictors of combined no-reflow CONCLUSIONS: %LV analyzed by IB-IVUS and serum PAPP-A levels were closely associated with the coronary no-reflow phenomenon. © 2014 Wiley Periodicals, Inc.

Prognostic value of myocardial damage markers in patients with chronic heart failure with atrial fibrillation.

OBJECTIVE: The aim of the present study was to examine the relationship between myocardial damage caused by atrial fibrillation (AF) and subsequent cardiovascular events in AF patients with chronic heart failure (CHF). METHODS AND RESULTS: We measured the serum levels of heart-type fatty acid binding protein (H-FABP) and high-sensitivity troponin T in 402 consecutive CHF patients with chronic AF (CHF-AF, n=201) or sinus rhythm (CHF-SR, n=201). The patients with CHF-AF had higher H-FABP and troponin T levels than those with CHF-SR. In order to examine the prognostic value of myocardial damage markers in CHF-AF and CHF-SR patients, we followed the above patients and analyzed their clinical outcomes. A multivariate Cox proportional hazard analysis revealed that both the serum H-FABP and troponin T levels independently predicted subsequent cardiovascular events. A Kaplan-Meier analysis demonstrated that the rate of cardiovascular events was higher in the patients with elevated H-FABP and troponin T levels. The optimal cut-off values for the myocardial damage markers of cardiovascular events were higher in the CHF-AF patients than in the CHF-SR patients (H-FABP, 5.4 vs. 4.6 ng/mL and troponin T, 0.030 vs. 0.013 ng/mL). CONCLUSION: Myocardial damage advances in association with the presence of AF and is associated with subsequent cardiovascular events in both CHF-AF and CHF-SR patients. In this study, the cut-off values for the myocardial damage markers were higher in the CHF-AF patients than in the CHF-SR patients.

Role of epicardial adipose tissue in coronary artery disease in non-obese patients.

BACKGROUND: Epicardial adipose tissue (EAT) surrounding the heart may contribute to the development of coronary artery disease (CAD) through its local secretion of adipocytokines. Although the quantity of EAT is associated with obesity and metabolic syndrome, the role of EAT in the development of CAD in non-obese patients remains to be determined. METHODS: This study included 41 patients with CAD who underwent coronary artery bypass graft surgery and 28 patients without CAD who underwent other cardiac surgery. EAT volume was measured by 64-slice multi-detector computed tomography before the surgery. We obtained pericardial fluid and epicardial and subcutaneous adipose tissue samples at the surgery. We investigated the relationship between EAT volume and adiponectin levels in pericardial fluid and incident CAD in patients with and without obesity (body mass index>25 kg/m(2)). RESULTS: There was no significant difference in EAT volume between obese patients with and without CAD (55.5 ± 40.2 mL vs. 40.1 ± 19.7 mL, p=0.323). However, EAT volume was significantly greater in non-obese patients with CAD compared to those without CAD (35.0 ± 18.8 mL vs. 15.7 ± 11.0 mL, p<0.001). Adiponectin concentrations in pericardial fluid were significantly lower in non-obese patients with CAD compared to those without CAD (2.7 ± 2.0 µg/mL vs. 4.3 ± 3.7 µg/mL, p=0.049), whereas the adiponectin levels were decreased in obese patients regardless of the presence of CAD. Non-obese patients with CAD had significantly larger size adipocytes in EAT but not subcutaneous adipose tissue compared to those without CAD. Multiple logistic regression analysis showed that increased EAT volume was independently associated with incident CAD in non-obese patients. CONCLUSION: Increased EAT may play a crucial role in development of CAD through impairment of adiponectin secretion in non-obese patients.

Electrocardiographic left ventricular hypertrophy Cornell product is a feasible predictor of cardiac prognosis in patients with chronic heart failure.

BACKGROUND: Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular disease and is associated with heart failure development. The Cornell product is an easily measured electrocardiographic parameter for assessing LVH. However, it is undetermined whether the Cornell product can predict the cardiac prognosis of chronic heart failure (CHF) patients. METHODS AND RESULTS: We performed standard 12-lead electrocardiography and calculated the Cornell product in 432 consecutive CHF patients. LV geometry was assessed as normal, concentric remodeling, concentric or eccentric hypertrophy. The Cornell product was significantly higher in patients with eccentric hypertrophy, and increased with advancing New York Heart Association functional class. During a median follow-up of 660 days, there were 121 cardiac events including 36 cardiac deaths and 85 re-hospitalizations for worsening heart failure. Multivariate Cox proportional hazard analysis showed that the Cornell product was an independent predictor of cardiac events in CHF patients. Patients in the highest quartile of Cornell product had a higher prevalence of LV eccentric hypertrophy (22, 29, 33 and 67 % for quartiles one through four). Kaplan-Meier analysis demonstrated that the highest quartile of Cornell product was associated with the greatest risk among CHF patients. CONCLUSION: The Cornell product is associated with LV eccentric hypertrophy and can be used to predict future cardiac events in CHF patients.

A novel mouse model of aortic valve stenosis induced by direct wire injury.

OBJECTIVE: The response-to-tissue-injury theory is currently the favorite paradigm to investigate valve pathology. To the best of our knowledge, there are currently no in vivo valve injury models. There are few calcific aortic valve stenosis (AVS) models that develop hemodynamically significant stenosis. Here, we investigated the effect of direct mechanical injury on aortic valves in vivo and developed a novel mouse model of calcific AVS. APPROACH AND RESULTS: Aortic valve injury was created by inserting and moving a spring guidewire under echocardiographic guidance into the left ventricle of male C57/BL6 mice via right common carotid artery. Serial echocardiographic measurements revealed that aortic velocity was increased 1 week after injury and persistently increased until 16 weeks after injury. AVS mice showed a higher heart weight/body weight ratio and decreased left ventricular fractioning shortening 4 weeks after injury, compared with sham mice. We found remarkable proliferation of valve leaflets 4 weeks after injury. Proliferative valves showed increased production of reactive oxygen species and expression of inflammatory cytokines and osteochondrogenic factors. Alizarin red staining showed valvular calcification 12 weeks after injury. CONCLUSIONS: We report a novel calcific AVS model to support the response-to-tissue-injury theory. This model may be a valuable tool for analyzing the mechanism of AVS and assessing therapeutic options.

Prognostic importance of objective nutritional indexes in patients with chronic heart failure.

BACKGROUND: Although malnutrition indicates an unfavorable prognosis in some clinical settings, the association between nutritional indexes and outcomes for patients with chronic heart failure (CHF) is unclear. METHODS AND RESULTS: All the previously established objective nutritional indexes were evaluated. The controlling nutritional status score (CONUT), prognostic nutritional index (PNI), and geriatric nutritional risk index (GNRI) were determined for 388 consecutive patients with CHF (mean age 69.6±12.3 years). The prevalence of malnutrition in this cohort was 60-69%. Patients were followed prospectively, with the endpoints being death due to a cardiovascular event or re-hospitalization. There were 130 events, including 33 deaths and 97 re-hospitalizations, during a mean follow-up period of 28.4 months. Patients experiencing cardiovascular events showed impaired nutritional status, higher CONUT scores, lower PNI scores, and lower GNRI scores, compared with those who did not experience cardiovascular events. CONUT score [hazard ratio 40.9, 95% confidence interval (CI) 10.8-154.8], PNI score (hazard ratio 6.4, 95% CI 5.4-25.1), and GNRI score (hazard ratio 11.6, 95% CI 3.7-10.0) were independently associated with cardiovascular events. Kaplan-Meier analysis showed that there was a significantly higher incidence of cardiovascular events in patients who were malnourished than in those who were not. CONCLUSION: Malnutrition was common in patients with CHF. Evaluation of nutritional status may provide additional prognostic information in patients with CHF.

The impact of renal tubular damage, as assessed by urinary ß2-microglobulin-creatinine ratio, on cardiac prognosis in patients with chronic heart failure.

BACKGROUND: Renal dysfunction was reported to be closely associated with clinical outcomes in patients with chronic heart failure (CHF). Renal tubulointerstitial damage has been shown to be an important factor in the development of renal dysfunction as well as glomerular damage. However, the impact of renal tubular damage on clinical outcomes in patients with CHF remains to be determined. METHODS AND RESULTS: Urinary ß2-microglobulin-creatinine ratio was measured in 315 patients with CHF. Renal tubular damage was defined as a urinary ß2-microglobulin-creatinine ratio ≥ 300 µg/g, as previously reported. Patients were prospectively followed up for a median period of 1097 days. There were 91 cardiac events, including 16 cardiac deaths and 75 rehospitalizations for worsening heart failure. Log10 urinary ß2-microglobulin-creatinine ratio was increased with worsening New York Heart Association functional class. Multivariate analysis revealed that renal tubular damage was an independent predictor of cardiac events. Kaplan-Meier analysis demonstrated that the rate of cardiac events was higher in patients with renal tubular damage compared with those without it. Patients were divided into 4 groups according to the presence of chronic kidney disease and renal tubular damage. The Cox proportional hazard analysis revealed that comorbidity of chronic kidney disease and renal tubular damage was associated with the highest risk for cardiac events compared with other groups. CONCLUSIONS: Renal tubular damage was related to the severity of heart failure and was associated with poor outcomes in patients with CHF. Renal tubular damage could add clinical information to chronic kidney disease in patients with CHF.

Acidic urine is associated with poor prognosis in patients with chronic heart failure.

Renal dysfunction is reported to be associated with poor outcomes in patients with chronic heart failure (CHF). A recent study showed that acidic urine is related to chronic kidney disease, which is a risk factor for the development of CHF. However, it remains to be determined whether acidic urine is associated with poor outcomes in patients with CHF. We measured urine pH using dipsticks in 537 patients with CHF. Acidic urine was defined as urine pH ≤5.5. Patients were prospectively followed during a median follow-up period of 556 days. There were 145 cardiac events. Prevalence of acidic urine was increased with advancing stage of chronic kidney disease. Patients with acidic urine had a more severe New York Heart Association functional class compared with those with normal urine. In the multivariate Cox proportional hazard analysis, acidic urine was independently associated with poor outcomes in patients with CHF after adjustment of confounding factors. A Kaplan-Meier analysis demonstrated that the rate of cardiac events was higher in patients with acidic urine than in those with normal urine. The presence of acidic urine can reliably identify patients at high risk of future cardiac events in patients with CHF.

Renal tubulointerstitial damage is associated with short-term cardiovascular events in patients with myocardial infarction.

BACKGROUND: Urinary ß2 microglobulin (U-ß2MG) is a more sensitive and accurate marker of tubulointerstitial damage. The etiology of glomerular damage is related to the occurrence of major adverse cardiovascular events (MACE) in patients with myocardial infarction (MI); however, the prognostic importance of tubulointerstitial damage in patients with ST-segment elevation MI (STEMI) has not been established. The aim of this study was to elucidate whether renal tubulointerstitial damage is associated with the occurrence of MACE in patients after STEMI undergoing percutaneous coronary intervention. METHODS AND RESULTS: The degree of renal tubulointerstitial damage was evaluated by measuring the U-ß2MG level in 89 consecutive STEMI patients. There were 22 MACEs during the follow-up period. Patients with MACE had higher U-ß2MG levels than those without MACE, and the U-ß2MG level was an independent predictor for MACE. A Kaplan-Meier analysis revealed that the group with higher U-ß2MG levels corrected for urinary creatinine was associated with a greater risk for MACE. CONCLUSIONS: An elevated U-ß2MG level was associated with the occurrence of MACE in STEMI patients who underwent PCI. Renal tubulointerstitial damage is therefore considered to be associated with the occurrence of MACE.

Impact of insulin resistance on silent and ongoing myocardial damage in normal subjects: the Takahata study.

BACKGROUND: Insulin resistance (IR) is part of the metabolic syndrome (Mets) that develops after lifestyle changes and obesity. Although the association between Mets and myocardial injury is well known, the effect of IR on myocardial damage remains unclear. METHODS AND RESULTS: We studied 2200 normal subjects who participated in a community-based health check in the town of Takahata in northern Japan. The presence of IR was assessed by homeostasis model assessment ratio, and the serum level of heart-type fatty acid binding protein (H-FABP) was measured as a maker of silent and ongoing myocardial damage. H-FABP levels were significantly higher in subjects with IR and Mets than in those without metabolic disorder regardless of gender. Multivariate logistic analysis showed that the presence of IR was independently associated with latent myocardial damage (odds ratio: 1.574, 95% confidence interval 1.1-2.3) similar to the presence of Mets. CONCLUSIONS: In a screening of healthy subjects, IR and Mets were similarly related to higher H-FABP levels, suggesting that there may be an asymptomatic population in the early stages of metabolic disorder that is exposed to myocardial damage and might be susceptible to silent heart failure.

Ongoing myocardial damage in patients with heart failure and preserved ejection fraction.

BACKGROUND: The relationship between ongoing myocardial damage and heart failure with preserved left ventricular systolic function (HF-PEF) is still unclear. To investigate this relationship, we measured the cardiac-specific cytosolic marker, heart-type fatty acid binding protein (H-FABP), and a myofibrillar component (troponin T), and analyzed clinical outcomes. METHODS AND RESULTS: Consecutive heart failure patients (n=151) with echocardiographic left ventricular ejection fraction >50% were prospectively enrolled. The cut-off values for myocardial membrane injury (H-FABP >4.3 ng/mL) and myofibrillar injury (troponin T >0.01 ng/mL) were defined using receiver operating characteristic curves. Myocardial membrane injury was observed more frequently than myofibrillar injury (41% vs. 26% of patients, p<0.05). Patients were followed up for a median of 694 days, with the end-points being cardiovascular death or re-hospitalization. By multivariate analysis, the serum H-FABP level was an independent predictor of cardiovascular events (hazard ratio 1.165 per 1 ng/mL increase, 95% confidence interval 1.034-1.314, p=0.012). CONCLUSIONS: Latent myocardial injury was frequently observed in patients with HF-PEF. The circulating H-FABP level was an independent predictor of subsequent cardiovascular events.

Circulating heart-type fatty acid binding protein levels predict the occurrence of appropriate shocks and cardiac death in patients with implantable cardioverter-defibrillators.

BACKGROUND: The association between ongoing myocardial damage and outcomes in patients who have received an implantable cardioverter-defibrillator (ICD) is unclear. METHODS AND RESULTS: Consecutive patients with cardiomyopathy, who had received an ICD (n = 107, mean age 65 ± 11 years), were prospectively enrolled. Myocardial membrane injury (heart-type fatty acid binding protein [H-FABP] >4.3 ng/mL) and myofibrillar injury (troponin T >0.01 ng/mL) were defined using receiver operating characteristic curves. Patients were followed for a median of 33.6 months, to an end point of appropriate ICD shock or cardiac death. Myocardial membrane injury (45%) and myofibrillar injury (41%) were equally prevalent among patients with cardiomyopathy who had received ICDs. Appropriate ICD shocks or cardiac death occurred in 31% and 15% of patients, respectively. Multivariate Cox regression analysis showed that serum H-FABP levels >4.3 ng/mL, but not troponin T levels, were a significant independent prognostic factor for cardiac events (hazard ratio 5.502, 95% confidence interval 1.705-17.75, P = .004). Subgroup analysis revealed that measuring H-FABP levels was valuable for anticipating event-free survival among patients with ICDs who were receiving amiodarone. High H-FABP levels also predicted subsequent outcomes in patients who had received ICDs for primary or secondary prevention. CONCLUSION: Evaluating myocardial damage using H-FABP may be a promising tool for predicting outcomes in patients with cardiomyopathy who have received ICDs.

Elevated plasma brain natriuretic peptide levels predict left atrial appendage dysfunction in patients with acute ischemic stroke.

BACKGROUND: It is well known that left atrial appendage (LAA) dysfunction plays an important role in the occurrence of cardioembolic stroke. The atrium is the main source of brain natriuretic peptide (BNP) in patients with atrial fibrillation (AF). We hypothesized that the plasma BNP level would be a sensitive predictor of LAA dysfunction in patients with acute ischemic stroke. METHODS AND RESULTS: Transesophageal echocardiography was performed and plasma BNP levels were measured in 223 patients (145 males, age 69 ± 14 years), within 7 days after the onset of acute ischemic stroke. None of the patients had a history of congestive heart failure. LAA thrombus was detected in 23 of 77 (30%) patients with AF. Plasma BNP levels were markedly higher in patients with cardioembolic stroke compared to those without (144 pg/ml vs. 35 pg/ml, p<0.05). Plasma BNP levels were significantly correlated with LAA emptying flow velocity regardless of sinus rhythm (R=-0.352) or AF (R=-0.436). Furthermore, among patients with cardioembolic stroke, plasma BNP levels were markedly higher in patients with cardiogenic stroke, as diagnosed by transesophageal echocardiography, than in those with cryptogenic stroke (193 pg/ml vs. 14 pg/ml, p<0.05). Multivariate logistic regression analysis showed that a BNP concentration >90 pg/ml was an independent predictor of cardiogenic stroke (odds ratio 41.39, 95% confidence interval 1.28-138; p=0.0358). CONCLUSION: Elevated plasma BNP concentrations may be a reliable surrogate marker for the prediction of LAA dysfunction and cardiogenic stroke in patients with acute ischemic stroke.

Prognostic value of low left atrial appendage wall velocity in patients with ischemic stroke and atrial fibrillation.

BACKGROUND: It is important to evaluate left atrial appendage (LAA) dysfunction for primary and secondary prevention of stroke in patients with atrial fibrillation (AF). LAA dysfunction can reportedly be evaluated by LAA wall velocity (LAWV) measured by transthoracic echocardiographic (TTE) imaging. The aim of this study was to examine whether TTE-LAWV can predict long-term cerebrovascular events in patients with ischemic stroke with AF. METHODS: TTE imaging and transesophageal echocardiographic imaging were performed <7 days after onset in 179 consecutive patients with stroke with AF. TTE-LAWV was measured using Doppler tissue imaging at the LAA tip from the parasternal short-axis view on TTE imaging, as previously reported. All patients were followed up prospectively. RESULTS: Cerebrovascular events were defined as cerebrovascular death and/or recurrent ischemic stroke requiring hospitalization. There were 32 cerebrovascular events during a median follow-up period of 397 days. TTE-LAWV was significantly lower in patients with cerebrovascular events than in patients without (8.3 ± 2.8 vs 11.3 ± 4.0 cm/sec, P < .01). Cox multivariate hazard analysis showed that low TTE-LAWV (<8.7 cm/sec) was an independent predictor of cerebrovascular events (hazard ratio, 3.460; P < .05). Kaplan-Meier analysis showed that cerebrovascular event rates were significantly higher in patients with low TTE-LAWV (<8.7 cm/sec) compared with those with high TTE-LAWV (34% vs 7%, P < .01). CONCLUSIONS: Impaired LAA function was associated with long-term cerebrovascular events in patients with stroke with AF. TTE-LAWV may be a feasible parameter for risk stratification in patients with AF.

Device troubleshooting: cross connection of ventricular leads in a patient with decreased right ventricular electrical activity.

A patient with cardiac sarcoidosis showed low R-wave amplitude in the entire right ventricle (RV). To troubleshoot this, a left ventricular (LV) lead was implanted in the coronary vein. The pace/sense terminal of the defibrillation lead was connected to LV:IS-1 of the defibrillator. Conversely, the LV lead was connected to RV:IS-1. Induced ventricular fibrillation was successfully terminated without any undersensing.

Difference of clinical course after catheter ablation of atrioventricular nodal reentrant tachycardia between younger and older patients: atrial vulnerability predicts new onset of atrial fibrillation.

BACKGROUND: The aim of this study was to compare the long-term procedural outcomes, the stability of atrioventricular conduction, and the new onset of atrial fibrillation (AF), after ablation of atrioventricular nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: Consecutive patients with AVNRT (n=109), who underwent slow-pathway ablation, were divided into two groups based on the median age of the studied patients: the younger group aged <55 years and the older group aged ≥55 years. During a mean follow-up period of 60.6 months, the rate of change in the PR interval from before ablation to follow-up was significantly greater in older patients compared with younger patients. However, there was no delayed-onset high-degree AV block during follow-up in either group. No patients in the younger group suffered from persistent AF, whereas persistent AF occurred in 5/54 (9.3%) older patients. Multivariate Cox analysis revealed that atrial vulnerability, with induction of AF during the electrophysiological study, was the only predictor of the development of AF (Hazard ratio: 13.9, 95% confidence interval: 1.62-119.2, p<0.01). CONCLUSION: Slow-pathway ablation of AVNRT is a reliable strategy even in older patients. However, physicians should consider regular long-term follow-up of older patients with atrial vulnerability, in order to assess the subsequent development of AF.