Masahiro Wanezaki

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.

Left atrial strain as evaluated by two-dimensional speckle tracking predicts left atrial appendage dysfunction in patients with acute ischemic stroke

Background Left atrial appendage (LAA) dysfunction predisposes patients with atrial fibrillation (AF) to cardioembolic stroke. Two-dimensional (2D) speckle tracking was reported to be useful for evaluating left atrial (LA) regional function, as well as left ventricular function. However, it remains unclear whether 2D speckle tracking is useful for evaluating LAA dysfunction. Therefore, we investigated whether decreased LA strain may predict LAA dysfunction and thrombus formation in patients with acute ischemic stroke. Methods We performed transthoracic and transesophageal echocardiography in 120 patients (83 males, mean age 72 ± 11 years) within 7 days of onset of an acute ischemic stroke. Longitudinal LA strain was evaluated using 2D speckle tracking imaging at each LA segment, and peak systolic strain was calculated by averaging the results for each segment. Results Forty-eight patients had LAA dysfunction as defined by the presence of LAA thrombus and/or severe spontaneous echo contrast. LA peak systolic strain was significantly decreased in patients with LAA dysfunction compared to those without (32.3 ± 13.7% vs. 12.1 ± 7.2%, p < 0.0001). LA peak systolic strain was significantly correlated with LAA emptying flow velocity (r = 0.693, p < 0.0001). The optimum LA peak systolic strain cut-off value for predicting LAA dysfunction was 19%. Multivariate logistic regression analysis showed that LA peak systolic strain was an independent predictor of LAA dysfunction (odds ratio 0.059, 95% confidence interval 0.018–0.146; p < 0.0001). Conclusion Decreased LA peak systolic strain was independently associated with LAA dysfunction in patients with acute ischemic stroke.

Rapid decline in renal function after acute myocardial infarction

AIM To investigate the long term effects of cardiac events on renal function, a prospective study of patients with acute myocardial infarction was conducted. METHODS A total of 137 patients with acute myocardial infarction were followed for 1 year. The change of estimated glomerular filtration rate (eGFR) in cardiac patients was compared with that in background-matched controls, and the factors associated with eGFR changes were analyzed. RESULTS The eGFR decrease was much larger after myocardial infarction, from 73.7 ± 1.9 ml/min/1.73 m2 (mean ± SEM) at baseline to 64.7 ± 1.7 at 1 year, (p < 0.001), compared with that of controls (from 72.8 ± 1.2 to 72.1 ± 1.3, p = 0.305). Multiple regression analysis showed that eGFR change was associated negatively with age, baseline eGFR, proteinuria, and positively with the administration of angiotensin converting enzyme inhibitors or angiotensin II receptor blockers, but not the severity of cardiac damage and comorbidities. Longitudinal analysis 1 year before and 2 years after myocardial infarction showed that eGFR decrease was larger during baseline and 6 months after the event (-7.0 ± 1.0). CONCLUSIONS Renal decline was rapid after myocardial infarction and was affected by clinical characteristics of patients. Careful follow-up of renal function is recommended to prevent the progression of renal and cardiac disease.

Trends in the incidences of acute myocardial infarction in coastal and inland areas in Japan: The Yamagata AMI Registry

BACKGROUND It has been reported that there are regional differences in the incidence of acute myocardial infarction (AMI) in Japan. The purpose of this study was to investigate trends in regional differences in AMI incidence and dyslipidemia between coastal and inland areas. METHODS We investigated trends in AMI incidence and risk factors in 5325 first-ever AMI patients residing in a coastal area (n=1817), a rural inland area (n=1959), or an urban inland area (n=1549) for the periods 1994-2002, and 2003-2010, using data from the Yamagata AMI Registry. RESULTS Patients in the coastal area were significantly older than those in rural and urban inland areas and had a lower prevalence of dyslipidemia. The age-adjusted incidence rate of AMI was significantly lower in coastal and rural inland areas patients than those from urban inland area (males: 43.3, 42.2, and 51.3/10(5) person-years; females: 17.4, 20.0, and 23.7/10(5) person-years, respectively) during 2 observation periods. Due to a large increase in AMI incidence in younger males of the coastal area and a decrease in AMI incidence in late elderly females of the urban inland area, no significant regional differences in the age-adjusted incidence rates of AMI were observed during the 2003-2010 period in both genders. The increase in AMI incidence in males in the coastal area was associated with an increasing prevalence of dyslipidemia. CONCLUSION There were no longer any regional differences observed in AMI incidence, which was considered to be associated with increased dyslipidemia especially in the coastal area.

Association of plasma thioredoxin-1 with renal tubular damage and cardiac prognosis in patients with chronic heart failure.

BACKGROUND Thioredoxin-1 (Trx-1) is an abundant 12.5 kDa redox protein expressed in almost all eukaryotic cells that protect against the development of heart failure and kidney dysfunction. Plasma Trx-1 levels are considered as a reliable marker for oxidative stress. However, it remains to be determined whether plasma Trx-1 levels can predict cardiac prognosis in patients with chronic heart failure (CHF). METHODS AND RESULTS We measured plasma Trx-1 levels and urinary β2-microglobulin-creatinine ratio (UBCR), a marker for renal tubular damage, in 156 consecutive patients with CHF and 17 control subjects. The patients were prospectively followed for a median follow-up period of 627 days and 46 cardiac events were observed. The patients with cardiac events had significantly higher plasma Trx-1 levels and UBCR levels than the cardiac event-free patients. Multivariate Cox proportional hazard analysis revealed that an elevated Trx-1 level was independently associated with poor outcome in patients with CHF after adjustment for confounding factors (hazard ratio, 1.74; 95% confidence interval, 1.33-2.29; p < 0.0001). UBCR was increased with higher plasma Trx-1 levels. Kaplan-Meier analysis demonstrated that the highest Trx-1 tertile was associated with the highest risk of cardiac events. CONCLUSION Plasma Trx-1 level was associated with renal tubular damage and cardiac prognosis, suggesting that it could be a useful marker to identify patients at high risk for comorbid heart failure and renal tubular damage.

Electroanatomical mapping of the atrialized right ventricle: Placement of a transvenous implantable cardioverter-defibrillator in a patient with Ebstein’s anomaly

A 47‐year‐old woman with Ebsteins anomaly suffered from an out‐of‐hospital cardiac arrest caused by ventricular fibrillation. Electroanatomical activation mapping showed an atrialized right ventricle. Atrial electrocardiogram, normal atrioventricular node conduction delay, and ventricular electrocardiogram were confirmed in the right atrium. Relatively preserved ventricular amplitude was found in the septal wall. Based on these findings, a transvenous dual‐chamber implantable cardioverter‐defibrillator was implanted for the prevention of sudden cardiac death. The patient has fared well, without any lead malfunctions, lead dislodgement, or inappropriate shocks. Sufficiently high atrial and ventricular amplitudes were confirmed during 18 months of follow‐up.

Increased plasma xanthine oxidoreductase activity deteriorates coronary artery spasm

Increased reactive oxygen species (ROS) contributes to the development of endothelial dysfunction, which is involved in coronary artery spasm (CAS). Xanthine oxidoreductase (XOR) plays a pivotal role in producing both uric acid and ROS. However, the association between plasma XOR activity and CAS has not been elucidated. The aim of this study was to investigate whether plasma XOR activity is associated with CAS. We measured XOR activity in 104 patients suspected for CAS, who presented without significant coronary artery stenosis and underwent intracoronary acetylcholine provocation tests. CAS was provoked in 44 patients and they had significantly higher XOR activity as compared with those without CAS. The patients were divided into three groups based on the XOR activity. The prevalence rate of CAS was increased with increasing XOR activity. A multivariate logistic regression analysis showed that the 3rd tertile group exhibited a higher incidence of CAS as compared with the 1st tertile group [odds ratio (OR) 6.9, P = 0.001) and the 2nd tertile group (OR 3.2, P = 0.033) after adjustment for conventional CAS risk factors, respectively. The C index was significantly improved by the addition of XOR activity to the baseline model based on CAS risk factors. Furthermore, the 3rd tertile group had the highest incidence of severe spasm defined as total obstruction, flow-limiting stenosis, diffuse spasm, multivessel spasm, and/or lethal arrhythmia. This is a first report to elucidate the association of plasma XOR activity with CAS. Increased plasma XOR activity is significantly associated with CAS.

Ruptured Right Sinus of Valsalva Aneurysm Caused by Suspected Takayasu's Arteritis.

A sinus of Valsalva aneurysm (SVA) is a rare aortic anomaly. The most common complication is a rupture into the right ventricle and atrium. An SVA rupture into the left ventricle is a rare event. A 42-year-old man visited an outpatient clinic due to worsening exertional dyspnea. A loud to-and-fro heart murmur was detected, and echocardiography revealed a right SVA that had ruptured into the left ventricle, inducing acute heart failure. Computed tomography imaging allowed us to determine that the right SVA had been caused by asymptomatic Takayasus arteritis. The patient was treated with prednisolone and the right SVA rupture was surgically repaired.