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Resistant hypertension is an important cardiovascular risk factor. This analysis of the JAMP study (Japan Ambulatory Blood Pressure Monitoring Prospective) data investigated the effects of uncontrolled resistant hypertension diagnosed using ambulatory blood pressure (BP) monitoring on the risk of heart failure (HF) and overall cardiovascular events. The JAMP study patients with hypertension and no HF history were included. They had true resistant hypertension (24-hour BP ≥130/80 mm Hg), pseudoresistant hypertension (24-hour BP P =0.012 and 2.24 [95% CI, 1.17–4.30]; P =0.015, respectively) and versus uncontrolled nonresistant hypertension (1.51 [1.03–2.20]; P =0.034 and 3.03 [1.58–5.83]; P Registration: URL: https://www.umin.ac.jp/ctr ; Unique identifier: UMIN000020377.

The effect of rosuvastatin was investigated on complicated aortic arch plaque (CAP) morphology and lipid profiles in acute cerebral embolism (CE) patients with normal low-density lipoprotein-cholesterol (LDL-c) levels. Transesophageal echocardiography (TEE) studies were performed in 56 consecutive CE patients with LDL-c less than 140 mg/dL who were not taking lipid-lowering agents at baseline. CAP observed by TEE was defined as the presence of greater than 4-mm diameter, ulcerated, or mobile aortic plaque. Patients were divided into those with CAP versus without CAP (group A, n=24, age 69±8 years) and without CAP (group B, n=32, age 62±10 years). Of the 24 group A patients, 18 received 5 mg/d of rosuvastatin for 6 months and had follow-up TEE studies. In Group A, the baseline values of high-density lipoprotein-cholesterol (HDL-c) and apolipoprotein A-1 (ApoA-1) were significantly lower than in Group B (44±15 versus 55±15 mg/dL, P=.0059; 103±19 versus 137±25 mg/dL, P=.0006, respectively) and age and serum high-sensitivity C-reactive protein concentration were significantly higher (69±8 vs. 62±10 years, P=.0080; 2.34±3.05 vs. 0.67±1.00 mg/dL, P=.0054, respectively). By multivariate logistic regression analysis, ApoA-1 was shown to be an independent predictor of CAP (odds ratio=.894, 95% confidence intervals .800-.996, P=.0483). In the 18 group A patients receiving rosuvastatin for 6 months, aortic arch plaque diameter and serum LDL-c were significantly decreased (5.8±2.2 to 5.1±2.1 mm, P=.0377; 110±23 to 81±23 mg/dL, P=.0008, respectively), whereas serum HDL-c and ApoA-1 concentrations were significantly increased (42±8 to 52±9 mg/dL, P=.0002; 109±22 to 135±15 mg/dL, P=.0002, respectively). Plaques were morphologically improved in 11 patients, unchanged in 6, and worsened in 1. These data suggest that rosuvastatin improves plaque morphology concomitant with improving lipid profiles in CE patients with normal LDL-c levels.

To evaluate left atrial appendage (LAA) dysfunction using left atrial pulse-wave tissue Doppler imaging (PW-TDI) in acute cerebral embolism (ACE) patients with sinus rhythm (SR), transthoracic (TTE) and transesophageal echocardiograhy (TEE) were performed in 60 consecutive patients with SR without obvious left ventricular dysfunction within 2 weeks after ACE. Two groups were identified: LAA dysfunction [LAA emptying peak flow velocity (LAA-eV)

Background Elevated aortic stiffness determined by transesophageal echocardiography (TEE), and presence of complicated aortic plaque provide prognostic information about cerebrovascular disease risk. Recently, pulse-wave tissue Doppler imaging (PW-TDI) has offered a new technique for assessing aortic wall stiffness. Methods The following aortic long-axis view TEE measurements were carried out in 103 consecutive acute ischemic stroke patients and 72 controls (stroke-free patients requiring TEE for conditions such as atrial fibrillation and valvular heart disease): (a) PW-TDI motion velocities measured as expansion peak velocity during systole (Vs) and contraction peak velocity during diastole (Vd); (b) aortic arch stiffness parameter β (Aoβ), defined as β = ln (systolic blood pressure/diastolic blood pressure)/([Dmax − Dmin]/Dmin), where ln is the natural logarithm, Dmax is maximum aortic lumen diameter, and Dmin is minimum aortic lumen diameter. The PW-TDI of Vs and Vd was compared with conventional vessel parameters brachial-ankle pulse wave velocity (baPWV) and cardio-ankle vascular index (CAVI, calculated from blood pressure and PWV). Results Comparing acute ischemic stroke patients versus controls, Vs and Vd were significantly decreased (3.3 ± 1.6 vs. 3.9 ± 2.0 cm/sec, P

The case of a 57-year-old man, who had a brother suddenly died at 62 years of age, admitted to other hospital with palpitation. Because his Holter ECG showed non-sustained ventricular tachycardia, and ultrasound cardiography showed left ventricular hypertrophy with normal cardiac function, he was introduced to our hospital for further cardiac examination of hypertrophic cardiomyopathy. Although his coronary angiography showed no organic stenosis, and his magnetic resonance imaging demonstrated asymmetrical septal hypertrophy and delayed enhancement on inferolateral wall of left ventricle compatible with hypertrophic cardiomyopathy, his biopsied tissue from cardiac muscle revealed cardiac Fabry disease. He received enzyme replacement therapy after implantation of implantable cardioverter defibrillator (ICD) for primary prevention. After 7 months from implantation, he had an appropriate ICD therapy for sustained ventricular tachycardia. Primary prevention of ICD implantation for patients with Fabry disease has not been established, while some cases of cardiac Fabry disease show fatal ventricular tachyarrhythmia in their lives. Primary prevention of ICD could be a considerable therapeutic option in some patients with cardiac Fabry disease, especially who demonstrated a family history of sudden death or ventricular tachyarrhythmias.