Abstract-Adiponectin is one of the key molecules in the metabolic syndrome, and its concentration is decreased in obesity, type-2 diabetes, and coronary artery disease. Genetic investigation has revealed that 2 polymorphisms (I164T and G276T) are related to adiponectin concentration and diabetes. To examine whether adiponectin affects hypertension genetically or biologically, we performed a case-control study. A total of 446 diagnosed cases of hypertension (HT) in men and 312 normotensive (NT) men were enrolled in this study. Plasma adiponectin concentration was measured using an enzyme-linked immunosorbent assay system. Single nucleotide polymorphisms were determined by TaqMan polymerase chain reaction method. After adjustment for confounding factors, adiponectin concentration was significantly lower in HT (HT: 5.2Ϯ0.2 g/mL; NT: 6.1Ϯ0.2 g/mL; PϽ0.001). Furthermore, multiple regression analysis indicated that hypoadiponectinemia was an independent risk factor for hypertension (PϽ0.001). Blood pressure was inversely associated with adiponectin concentration in normotensives regardless of insulin resistance. In subjects carrying the TC genotype of the I164T polymorphism, adiponectin concentration was significantly lower (TC: 2.6Ϯ0.9 g/mL; TT: 5.5Ϯ0.1 g/mL; PϽ0.01), and most of them had hypertension. In contrast, the G276T polymorphism was not associated with adiponectin concentration or hypertension. In conclusion, hypoadiponectinemia is a marker for predisposition to hypertension in men.

Renal denervation is a promising new non-pharmacological treatment for resistant hypertension. However, there is a lack of data from Asian patients. The REQUIRE trial investigated the blood pressure-lowering efficacy of renal denervation in treated patients with resistant hypertension from Japan and South Korea. Adults with resistant hypertension (seated office blood pressure ≥150/90 mmHg and 24-hour ambulatory systolic blood pressure ≥140 mmHg) with suitable renal artery anatomy were randomized to ultrasound renal denervation or a sham procedure. The primary endpoint was change from baseline in 24-hour ambulatory systolic blood pressure at 3 months. A total of 143 patients were included (72 renal denervation, 71 sham control). Reduction from baseline in 24-hour ambulatory systolic blood pressure at 3 months was not significantly different between the renal denervation (−6.6 mmHg) and sham control (−6.5 mmHg) groups (difference: −0.1, 95% confidence interval −5.5, 5.3; p = 0.971). Reductions from baseline in home and office systolic blood pressure (differences: –1.8 mmHg [p = 0.488] and −2.0 mmHg [p = 0.511], respectively), and medication load, did not differ significantly between the two groups. The procedure-/device-related major adverse events was not seen. This study did not show a significant difference in ambulatory blood pressure reductions between renal denervation and a sham procedure in treated patients with resistant hypertension. Although blood pressure reduction after renal denervation was similar to other sham-controlled studies, the sham group in this study showed much greater reduction. This unexpected blood pressure reduction in the sham control group highlights study design issues that will be addressed in a new trial. Clinical trial registration NCT02918305 (http://www.clinicaltrials.gov).

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2990ARIMURA T et al. Circulation JournalOfficial Journal of the Japanese Circulation Society http://www. j-circ.or.jp ilated cardiomyopathy (DCM) is a primary cardiac disorder caused by functional abnormalities in cardiomyocytes and is characterized by ventricular chamber dilation with decreased contractility. DCM is a major cause of chronic heart failure and the most common indication for cardiac transplantation. Various etiologies include genetic abnormalities, viral infections, alcohol, mitochondrial dysfunction and metabolic disorders. 1,2 Most of the genetic causes are mutations in genes for sarcomeric proteins, including contractile elements, sarcolemma elements, Z-disc elements, and Z-I region components, which play key roles in the generation and transmission of contractile force. 2 Editorial p 2879Formin homology 2 domain containing 3 (FHOD3) is a member of the formin family. We have previously reported that FHOD3 is a sarcomeric protein that is predominantly expressed in the heart and plays an essential role in the regulation of actin assembly and sarcomeric organization during myofibrillogenesis. 3 FHOD3 contains multiple domains, including GTPase-binding and diaphanous inhibitory domains at the Nterminus, formin homologous 1 (FH1), formin homologous 2 (FH2) and diaphanous autoregulation (DA) domains at the Cterminus. 4 The FH2 domain mediates actin filament nucleation and polymerization, which are accelerated by FH1-mediated Background: Dilated cardiomyopathy (DCM) is characterized by a dilated left ventricular cavity with systolic dysfunction manifested by heart failure. It has been revealed that mutations in genes for cytoskeleton or sarcomere proteins cause DCM. However, the disease-causing mutations can be found only in far less than half of patients with a family history, indicating that there should be other disease genes for DCM. Formin homology 2 domain containing 3 (FHOD3) is a sarcomeric protein expressed in the heart that plays an essential role in sarcomere organization during myofibrillogenesis. The purpose of this study was to explore a possible novel disease gene for DCM.

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