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It is unclear whether afterload mismatch occurs during the initial stage of essential hypertension (EHT). Additionally, critical left ventricular hypertrophy (LVH) between preserved and reduced systolic functions in hypertension is also unclear. Thus, we aimed to clarify these points.Forty-five normal control subjects (NCS) and 140 EHT patients participated. EHT patients were subdivided into three groups: group I, without LVH (n = 37); group II, with LVH (n = 80); and group III, with LVH and LV heart failure (LVHF) (n = 23). Routine electrocardiographic and echocardiographic parameters, V5R/V6R ratio, relative wall thickness (RWT), LV mass (LVM) index, and peak systolic wall stress (PSWS) were measured.In group I, LV systolic functions were preserved despite the increase of PSWS. In group II, LVH advanced, but LV systolic functions remained normal. A negative T-wave was observed in 69% of group II and 100% of group III. A significant correlation between RWT and LVM index was seen in NCS and groups I and II (rAfterload mismatch did not occur in group I, but it was observed in group III due to the exhaustion of preload reserve.

We herein report two cases of potentially life-threatening arrhythmia due to hyperkalemia triggered by the excessive consumption of "Hoshi-Imo" (dried sweet potato). Both patients with chronic renal disease on renin-angiotensin-aldosterone system inhibitors presented at the emergency room with non-specific symptoms. Electrocardiograms revealed potentially life-threatening arrhythmia due to hyperkalemia in both cases: sinus arrest with a ventricular escape rhythm, tall and peaked T waves; and a widened QRS complex in a nearly sine-wave configuration without discernible P wave. Both patients fully recovered after intensive care for hyperkalemia. Physicians should recognize the excessive consumption of "Hoshi-Imo" may lead to the development of life-threatening arrhythmia, especially in patients with risk factors for hyperkalemia.

Our aim was to evaluate the ability of adenosine triphosphate (ATP)-stress myocardial computed tomography perfusion (CTP) imaging to detect myocardial ischemia in the left anterior descending artery (LAD) territory, and to compare this method with coronary flow velocity reserve (CFVR) measured by transthoracic Doppler echocardiography (TTDE).ATP-stress CTP and CFVR were performed in 50 patients with stable angina pectoris. Myocardial ischemia assessed from CTP imaging was defined as qualitative visual perfusion defects and reduced myocardial blood flow (MBF) based on quantitative assessment. A cut-off value of CFVR of 2.0 was used.The mean CFVR was 1.9 ± 0.6 in ischemic regions by CTP, whereas it was 2.9 ± 0.8 in non-ischemic regions (p 0.001). CTP imaging could accurately predict CFVR2.0 with 84.0% diagnostic accuracy (94.7% sensitivity, 77.4% specificity, 72.0% positive predictive value, and 96.0% negative predictive value). When receiver operating characteristic curve analysis of the MBF data was performed to detect CFVR2.0, the area under the curve was 0.89, and the optimal MBF cut-off value was 1.43 mL/g/min.This study suggests that qualitative and quantitative assessment of ATP-stress CTP exhibits a good correlation with CFVR for evaluation of myocardial ischemia.

The cardiac phenotype of laminopathies is characterized by cardiac conduction disorders (CCDs) and dilated cardiomyopathy (DCM). Although laminopathies have been considered monogenic, they exhibit a remarkable degree of clinical variability. This case series aimed to detect the causal mutation and to investigate the causes of clinical variability in a Japanese family with inherited CCD and DCM.Of the five family members investigated, four had either CCD/DCM or CCD alone, while one subject had no cardiovascular disease and acted as a normal control. We performed targeted resequencing of 174 inherited cardiovascular disease-associated genes in this family and pathological mutations were confirmed using Sanger sequencing. The degree of clinical severity and variability were also evaluated using long-term medical records. We discovered a novel heterozygous truncating lamin A/C (LMNA) mutation (c.774delG) in all four subjects with CCD. Because this mutation was predicted to cause a frameshift mutation and premature termination (p.Gln258HisfsTer222) in LMNA, we believe that this LMNA mutation was the causal mutation in this family with CCD and laminopathies. In addition, gender-specific intra-familiar clinical variability was observed in this Japanese family where affected males exhibited an earlier onset of CCD and more severe DCM compared to affected females. Using targeted resequencing, we discovered a novel truncating LMNA mutation associated with CCD and DCM in this family characterized by gender differences in clinical severity in LMNA carriers. Our results suggest that in patients with laminopathy, clinical severity may be the result of multiple factors.

PURPOSE Hypertrophic cardiomyopathy (HCM) impairs left ventricular (LV) diastolic function leading to left atrial (LA) dilatation. Because Doppler echocardiography cannot accurately assess LV diastolic function in hearts with heterogeneous hypertrophy, assessment of LA function might be useful for risk stratification of patients with HCM. This study aimed to elucidate the impact of LA function on outcome in patients with patients. METHODS Seventy-six patients with HCM who underwent echocardiographic and cardiac magnetic resonance imaging were retrospectively enrolled. Twenty-six control subjects were also included. Using speckle tracking echocardiography, LA function was divided into active and passive strain indices based on the timing of the second positive peak of LA strain rate that occurred during LV systole. RESULTS Left atrial strain indices of active and passive function were significantly impaired concomitantly with increased LA volume index in HCM patients compared with controls. During follow-up (2.6 ± 1.7 years), 14 patients with HCM developed cardiac events (heart failure hospitalization or atrial fibrillation). The association of LA active strain with cardiac events was independent of and incremental to clinical and echocardiographic parameters (age, gender, E/e', LV global longitudinal strain, and LA volume index) in sequential models. Cardiac events were more frequent in HCM patients with LA active strain

To evaluate the feasibility of myocardial blood flow (MBF) by computed tomography from dynamic CT perfusion (CTP) for detecting myocardial ischemia and infarction assessed by cardiac magnetic resonance (CMR) or single-photon emission computed tomography (SPECT). Fifty-three patients who underwent stress dynamic CTP and either SPECT (n = 25) or CMR (n = 28) were retrospectively selected. Normal and abnormal perfused myocardium (ischemia/infarction) were assessed by SPECT/CMR using 16-segment model. Sensitivity and specificity of CT-MBF (mL/g/min) for detecting the ischemic/infarction and severe infarction were assessed. The abnormal perfused myocardium and severe infarction were seen in SPECT (n = 90 and n = 19 of 400 segments) and CMR (n = 223 and n = 36 of 448 segments). For detecting the abnormal perfused myocardium, sensitivity and specificity were 80 % (95 %CI, 71-90) and 86 % (95 %CI, 76-91) in SPECT (cut-off MBF, 1.23), and 82 % (95 %CI, 76-88) and 87 % (95 %CI, 80-92) in CMR (cut-off MBF, 1.25). For detecting severe infarction, sensitivity and specificity were 95 % (95 %CI, 52-100) and 72 % (95 %CI, 53-91) in SPECT (cut-off MBF, 0.92), and 78 % (95 %CI, 67-97) and 80 % (95 %CI, 58-86) in CMR (cut-off MBF, 0.98), respectively. Dynamic CTP has a potential to detect abnormal perfused myocardium and severe infarction assessed by SPECT/CMR using comparable cut-off MBF. • CT-MBF accurately reflects the severity of myocardial perfusion abnormality. • CT-MBF provides good diagnostic accuracy for detecting myocardial perfusion abnormalities. • CT-MBF may assist in stratifying severe myocardial infarction in abnormal perfusion myocardium.

The cardiac phenotype of laminopathies is characterized by cardiac conduction disorders (CCDs) and dilated cardiomyopathy (DCM). Although laminopathies have been considered monogenic, they exhibit a remarkable degree of clinical variability. This case series aimed to detect the causal mutation and to investigate the causes of clinical variability in a Japanese family with inherited CCD and DCM.Of the five family members investigated, four had either CCD/DCM or CCD alone, while one subject had no cardiovascular disease and acted as a normal control. We performed targeted resequencing of 174 inherited cardiovascular disease-associated genes in this family and pathological mutations were confirmed using Sanger sequencing. The degree of clinical severity and variability were also evaluated using long-term medical records. We discovered a novel heterozygous truncating lamin A/C (LMNA) mutation (c.774delG) in all four subjects with CCD. Because this mutation was predicted to cause a frameshift mutation and premature termination (p.Gln258HisfsTer222) in LMNA, we believe that this LMNA mutation was the causal mutation in this family with CCD and laminopathies. In addition, gender-specific intra-familiar clinical variability was observed in this Japanese family where affected males exhibited an earlier onset of CCD and more severe DCM compared to affected females. Using targeted resequencing, we discovered a novel truncating LMNA mutation associated with CCD and DCM in this family characterized by gender differences in clinical severity in LMNA carriers. Our results suggest that in patients with laminopathy, clinical severity may be the result of multiple factors.

Aortic prosthetic graft infection detected by F-fluorodeoxyglucose positron emission tomography/computed tomography Tamami Kono ⁎, Akiyoshi Ogimoto , Chiharuko Iio , Kaori Fujimoto , Akira Fujii , Teruyoshi Uetani , Takayuki Nagai , Kazuhisa Nishimura , Katsuji Inoue , Jun Suzuki , Go Hiasa , Hideki Okayama , Takafumi Okura , Masao Miyagawa , Teruhito Mochizuki , Hironori Izutani , Jitsuo Higaki a

AIM Atrial fibrillation is a potent risk factor for stroke, and the administration of anticoagulant therapy is important for preventing thromboembolism. Dabigatran is the first new oral anticoagulant developed as an alternative to warfarin. However, serious major gastrointestinal bleeding events have been observed in elderly patients in post-market case reports. We therefore retrospectively investigated elderly cases of the use of anticoagulant therapy with dabigatran. METHODS Twenty-eight patients over 80 years of age were treated with anticoagulant therapy at our satellite hospital. Nine of the patients received dabigatran, and all others received warfarin. We evaluated the CHADS2 score, HAS-BLED score, renal function and incidence of adverse effects in nine patients treated with dabigatran. RESULTS All of the nine patients received 220 mg/day of dabigatran, with no antiplatelet agents. Seven patients continued to receive dabigatran. One patient had an impaired renal function (Cr 1.55 mg/dl, Ccr 30 ml/min). However, the activated partial thromboplastin time (APTT) was not prolonged and neither major bleeding nor stroke were noted in seven patients. Although two patients were unable to continue dabigatran treatment due to APTT prolongation, no serious complications were observed during the administration of dabigatran. CONCLUSIONS No serious adverse effects of dabigatran anticoagulant therapy were detected in our elderly patients. Although it is necessary to monitor the risk of bleeding, renal dysfunction, effects of drug combination and so on, some elderly patients with atrial fibrillation are good candidates for dabigatran treatment.

A 32-year-old man with Duchenne muscular dystrophy (DMD) was admitted to the hospital because of worsening dyspnea and general fatigue. He had received medication therapy for cardiomyopathy with heart failure and home mechanical ventilation for respiratory failure. An electrocardiogram on admission showed intermittent third-degree atrioventricular block. Echocardiography showed global mild left ventricular systolic dysfunction with dyssynchrony (ejection fraction: 45%). He underwent implantation of a cardiac resynchronization therapy-defibrillator. His B-type natriuretic peptide level was improved after cardiac resynchronization therapy-defibrillator implantation, and he remains asymptomatic. The incidence of cardiomyopathy increases with age. By adulthood, 100% of patients have cardiac involvement.

Cardiacmagnetic resonance imaging for assessment of steroid therapy in a patient with cardiac sarcoidosis and a magnetic resonance-conditional pacemaker Tamami Kono ⁎, Akiyoshi Ogimoto , Makoto Saito , Kaori Fujimoto , Akira Fujii , Teruyoshi Uetani , Takayuki Nagai , Kazuhisa Nishimura , Katsuji Inoue , Jun Suzuki , Takafumi Okura , Tomoyuki Kido , Masao Miyagawa , Teruhito Mochizuki , Jitsuo Higaki a

Coronary angioscopy is a useful tool for understanding plaque characteristics through the plaque color and surface thrombus formation. We experienced an interesting case of a newly developed yellow neointima 400 days after a sirolimus-eluting stent implantation. A 72-year-old woman suffering from angina pectoris was admitted to our hospital. Coronary angiography revealed severe stenosis at the proximal left descending artery and she was implanted with a sirolimus-eluting stent. Coronary angioscopic observation immediately after stent implantation revealed the presence of yellow plaque only at the most severe stenosis lesion in the stent placement site. We performed a coronary angiography 400 days after the sirolimus-eluting stent implantation and did not find an in-stent restenosis. An intravascular ultrasound indicated minimum neointimal formation. By coronary angioscopy, we could clearly observe that the neointima had covered the surface of the stent struts; the stent struts were barely visible under the neointima. Surprisingly, neointima formed in response to the sirolimus-eluting stent was entirely yellow. Precise mechanisms of producing yellow neointima was unknown, we may observe a pathologic neointima induced by sirolimus-eluting stent.

A rare case of primary pulmonary hypertension was observed in a 73-year-old man. Angina pectoris was diagnosed at the age of 67 and he received several percutaneous coronary interventions because of refractory restenosis. He also had coronary artery bypass surgery at the age of 69. After 4 years, he again suffered from dyspnea and chest pain upon physical exertion. On admission to our hospital, a chest radiograph showed dilatation of bilateral pulmonary arteries. Moreover, echocardiography showed right ventricular dilatation and tricuspid regurgitation. Continuous wave Doppler imaging revealed a pressure gradient of 82.1 mmHg. Pulmonary capillary wedge pressure was normal, but pulmonary artery pressure was elevated upon cardiac catheterization. Because there was no apparent etiology of pulmonary hypertension, primary pulmonary hypertension was diagnosed and appropriate conventional therapy was started.

Fractional flow reserve (FFR) is specifically related to the severity of a coronary stenosis to the amount of myocardium to be perfused. Recently, we became able to estimate the myocardial area at risk (MAAR) using coronary computed tomography angiography (CTA) and Voronoi algorithm-based myocardial

Coronary angioscopy is a useful tool for understanding plaque characteristics through the plaque color and surface thrombus formation. We experienced an interesting case of a newly developed yellow neointima 400 days after a sirolimus-eluting stent implantation. A 72-year-old woman suffering from angina pectoris was admitted to our hospital. Coronary angiography revealed severe stenosis at the proximal left descending artery and she was implanted with a sirolimus-eluting stent. Coronary angioscopic observation immediately after stent implantation revealed the presence of yellow plaque only at the most severe stenosis lesion in the stent placement site. We performed a coronary angiography 400 days after the sirolimus-eluting stent implantation and did not find an in-stent restenosis. An intravascular ultrasound indicated minimum neointimal formation. By coronary angioscopy, we could clearly observe that the neointima had covered the surface of the stent struts; the stent struts were barely visible under the neointima. Surprisingly, neointima formed in response to the sirolimus-eluting stent was entirely yellow. Precise mechanisms of producing yellow neointima was unknown, we may observe a pathologic neointima induced by sirolimus-eluting stent.