Masakazu Ohno

Tolvaptan reduces the risk of worsening renal function in patients with acute decompensated heart failure in high-risk population

BACKGROUND Although tolvaptan is a recently approved drug for heart failure and causes aquaresis without affecting renal function, its clinical efficacy for patients with acute decompensated heart failure (ADHF) is yet to be elucidated. METHODS AND RESULTS We conducted a prospective observational study in patients with ADHF and high risk for worsening renal function (WRF). Risk stratification for WRF was done by scoring system. Of 174 patients, 114 patients were included as high-risk population for WRF. Incidence of WRF, urine output within 24h and 48 h, and changes in brain natriuretic peptide (BNP) were recorded in 44 patients treated with tolvaptan plus conventional therapy, and 70 patients with only conventional therapy. Urine output at 24h and 48 h after admission were both significantly higher in the tolvaptan group (p=0.001 and <0.001, respectively), and changes in BNP were not significantly different (p=0.351). However, the incidence of WRF was significantly lower in the tolvaptan group compared to the conventional group (22.7% vs 41.4%, p=0.045). Logistic regression analysis showed that treatment with tolvaptan was an independent factor for reducing WRF (hazard ratio 0.28, 95% confidence interval; 0.10-0.84; p=0.023). CONCLUSION In patients with ADHF with high risk of WRF, treatment with tolvaptan could prevent WRF compared to conventional therapy.

Endothelial dysfunction measured by peripheral arterial tonometry predicts prognosis in patients with heart failure with preserved ejection fraction

BACKGROUND There is need for risk stratification of adverse events in patients with heart failure with HFpEF as the number of patients is increasing and prognosis of this population is poor. This study was performed to determine whether endothelial dysfunction measured by peripheral artery tonometry (PAT) can predict prognosis of patients with heart failure with preserved ejection fraction (HFpEF). METHODS We included 159 patients with HFpEF, and log-transformed reactive hyperemia index (L_RHI) was measured. Patients were followed-up for HF-related events, which including HF-related death and re-hospitalization due to congestive heart failure for 300 days. RESULTS A total of 32 HF-related events occurred during follow-up, including 4 deaths due to HF and 28 cases of re-hospitalization due to acute decompensated HF. Cox regression analysis indicated that L_RHI (HR 0.56, 95% CI: 0.39-0.80 for an increase of 0.1) was an independent predictor of HF-related events. Receiver operating characteristic analysis was performed for L_RHI, and the area under the curve was 0.73 (95% CI: 0.62-0.83). Moreover, a value of 0.49 was suggested as the optimal cut-off value for prediction of adverse events in this population. CONCLUSION L_RHI measured by non-invasive PAT is a predictor of poor prognosis in patients with HFpEF.

Prognostic implications of chronic kidney disease and anemia after percutaneous coronary intervention in acute myocardial infarction patients

Anemia is a common complication of chronic kidney disease (CKD), and a few studies suggest that both CKD and anemia have a marked impact on the prognosis of patients with cardiovascular disease. We retrospectively analyzed the prevalence of CKD and anemia in 312 patients with acute myocardial infarction (AMI). The patients were divided into four groups according to the presence of CKD and anemia. Chronic kidney disease was defined as estimated glomerular filtration rate <60 ml/min/1.73 m2, and anemia was defined according to the World Health Organization definition. Of 312 AMI patients, 166 (53.2%) had CKD and 87 (27.8%) had anemia. A powerful relationship was observed between both CKD and anemia and major adverse cardiac and cerebrovascular events (MACCE) or death by any cause. After adjustment for comorbidities, the hazard ratio (HR) for MACCE was significantly higher in the anemia-only group (HR 5.42, 95% confidence interval (CI) 1.38–21.27, P = 0.015), the CKD-only group (HR 6.4, 95% CI 2.09–19.58, P = 0.001), and the CKD and anemia group (HR 11.61, 95% CI 3.65–36.89, P < 0.001). With respect to death by any cause, the HR was significantly higher in the CKD-only group (HR 2.68, 95% CI 1.02–7.02, P = 0.045) and the CKD and anemia group (HR 4.40, 95% CI 1.56–12.43, P = 0.005). One-half of the patients with AMI had CKD as well. Furthermore, when anemia coexisted with CKD, these conditions had a multiplicative amplification effect on the risk of MACCE and death by any cause in patients with AMI.

Beta-blocker prevents sudden cardiac death in patients with hemodialysis

BACKGROUND Beta blockers were shown to prevent SCD in cardiomyopathy or coronary artery disease patients. Dialysis patients show elevated mortality rates, predominantly due to cardiovascular disease. SCD is now one of the leading causes of death in this population. However, the prevention of SCD remains to be elucidated. METHODS We conducted a retrospective study of 316 patients from a database of all patients undergoing maintenance hemodialysis and followed up for 4.9 years. All patients were followed-up until death. Cox regression analysis was used to adjust the hazard ratio for beta blocker use with time until death. RESULTS SCD occurred during the study period in 3 (3.8%) patients in the beta blocker group and in 27 (11.4%) patients in the non-beta blocker group (P=0.047). Death from all causes occurred in 15 (18.8%) patients in the beta blocker group and in 97 (41.3%) patients in the non-beta blocker group (P<0.001). Kaplan-Meier curve showed that the rates of both SCD and all-cause death were lower in the beta blocker group (log-rank test, P=0.028 and P<0.001, respectively). In the Cox regression model, beta blocker use was significantly associated with lower adjusted risk of SCD (multivariate adjusted hazard ratio, 0.201; 95% confidence interval, 0.058-0.693; P=0.011). CONCLUSION In hemodialysis patients, beta blocker use was associated with lower risks of SCD and death from all causes. Thus, beta blocker use in this high-risk population may substantially improve outcome.

A case of giant cell arteritis with massive pericardial effusion

Giant cell arteritis (GCA) is a chronic inflammatory disease of the medium and large blood vessels. The early symptoms of this disease are nonspecific, and pericardial effusion is a rare manifestation of GCA. Recently, we investigated a case of GCA in which massive pericardial effusion was the initial symptom, and active aortitis was observed on positron emission tomography with fluorine-18 fluorodeoxyglucose. These observations indicated that pericardial effusion could occur in patients with GCA.

Peripheral microvascular dysfunction predicts residual risk in coronary artery disease patients on statin therapy

OBJECTIVE Although lowering of low-density lipoprotein cholesterol (LDL-C) by statins is essential in treatment of coronary artery disease (CAD) patients, there is considerable residual risk of secondary coronary artery events (CAE). We examined whether microvascular dysfunction (MiD), measured by peripheral artery tonometry (PAT), can predict prognosis of CAD patients previously treated with statins. METHODS We measured log-transformed reactive hyperemia index (L_RHI) in 213 CAD patients who had already achieved LDL-C <100 by statin therapy. Patients were followed-up for secondary CAE for a median of 2.7 years. Patients were divided into two groups: L_RHI ≥ 0.54 (n = 99) and L_RHI < 0.54 (n = 114). RESULTS During follow-up, CAE occurred in 4 (4.0%) patients in the L_RHI ≥ 0.54 group and 18 (15.8%) patients in the L_RHI < 0.54 group (P = 0.006). Cox regression analysis indicated that L_RHI was an independent predictor for CAE even after adjustment by Framingham traditional risk factors (FRF; age, T-C/HDL-C ratio, systolic blood pressure, diabetes, current smoker, and gender) and estimated glomerular filtration rate (eGFR) for secondary CAE (HR 0.79, 95% CI: 0.66-0.95). ROC analysis for CAE prediction showed that the AUC for models including FRF only, FRF + eGFR, and FRF + eGFR + L_RHI were 0.60, 0.71, and 0.77, respectively. Moreover, adding eGFR to FRF only (0.63, P = 0.003) and adding L_RHI to the FRF + eGFR model were associated with significant improvement of net reclassification improvement (0.79, P = 0.007). CONCLUSION MiD measured by non-invasive PAT adds incremental predictive ability to traditional risk factors for prognosis of CAD patients successfully treated with statins.

Three-dimensional echocardiography could distinguish a ventricular septal defect adjacent to asymptomatic ruptured sinus of Valsalva aneurysm

Sinus of Valsalva aneurysm (SVA) arises frequently in the right coronary sinus, and ventricular septal defect (VSD) is a prevalent coexistent cardiac abnormality. A 38-year-old asymptomatic male diagnosed with VSD on cardiac catheterization in his childhood, was referred to our hospital for the change in intensity of his cardiac murmur pointed out by his family physician. A grade V continuous murmur was auscultated with a thrill loudest at the forth left sternal border. Although, transthoracic and transesophageal echocardiography and cardiac catheterization have showed the ruptured right coronary sinus aneurysm, it was difficult to demonstrate coexistence of a doubly committed subarterial VSD. Three-dimensional echocardiography could provide clear images for diagnosis of the VSD closely adjacent to the ruptured SVA. The defect was confirmed at surgery.

Mechanisms of Diuresis for Acute Decompensated Heart Failure by Tolvaptan

Tolvaptan, a vasopressin type 2 receptor antagonist, does not affect kidney circulation or cause worsening of renal function (WRF) in patients with acute decompensated heart failure (ADHF). Bioelectrical impedance analysis (BIA) can be used to evaluate intravascular volume by calculating the ratio of extracellular water (ECW) to intracellular water (ICW). There have been no reports examining the mechanisms of tolvaptan-induced diuresis using BIA. We investigated whether tolvaptan decreases excess volume while maintaining intravascular volume in ADHF patients.Study patients included 29 ADHF patients (age 48-95, men 69%) diagnosed between April 2013 and May 2016 and who underwent BIA before and after treatment. Fifteen patients were treated with tolvaptan in addition to conventional diuresis therapy (tolvaptan group), and 14 patients were treated with conventional diuresis therapy only (control group). In the control group, the numerical value of serum creatinine (Cre) significantly increased from 0.89 ± 0.22 mg/ dL to 1.07 ± 0.29 mg/dL (P = 0.004), and the ECW/ICW significantly decreased from 0.696 ± 0.036 to 0.673 ± 0.032 (P = 0.004). These values were not significantly different from those obtained for the tolvaptan group. Furthermore, regression analysis showed a negative correlation between ΔCre and ΔECW/ICW, which are the differences between values before and after treatment (ΔCre = -0.002-5.668 × ΔECW/ICW, r2 = 0.306, P = 0.002).Our findings suggest that WRF is caused by a reduction in intravascular volume and that tolvaptan treatment can decrease the excess volume while maintaining intravascular volume.

Occurrence of Focal Atrial Tachycardia During the Ablation Procedure Is Associated With Arrhythmia Recurrence After Termination of Persistent Atrial Fibrillation

Catheter ablation can terminate persistent atrial fibrillation (AF). However, atrial tachycardia (AT) often arises after termination of AF.

A Case of Atrial Lead Dislodgement after Surgery for Lung Cancer

Case is a 77 years-old female. She started having episodes of palpitations followed by pre-syncope from 3 months ago. Holter ECG was performed which revealed runs of paroxysmal atrial fibrillation followed by sinus pause up to 4.3 seconds, which was consistent with the symptoms. With the diagnosis of bradycardia-tachycardia syndrome, DDD pacemaker implantation was performed. Tined leads were implanted to right atrial appendage and right ventricular apex without any complications. Shortly after the pacemaker implantation, patient was found to have left lung cancer. Left upper lobe resection and broad partial left lower lobe resection was performed 3 months after the pacemaker implantation. Two days after the surgery, monitor ECG revealed atrial lead sensing and pacing failure, and atrial lead dislodgement was observed on chest rentogenography. The left lung resection caused the mediastinum to shift leftward, resulting in advancement of the leads which lead to the dislodgement. Atrial lead repositioning was performed which only needed a short pull of the lead. We report a case of atrial lead dislodgement after surgery for lung cancer due to the shift of the mediastinum.