Objective-To examine the effects of pulmonary hypertension on left ventricular diastolic function and to relate the findings to possible mechanisms of interdependence between the right and left sides of the heart in ventricular disease.Design-A retrospective and prospective analysis of echocardiographic and Doppler studies.Setting-A tertiary referral centre for both cardiac and pulmonary disease.Patients-29 patients with pulmonary hypertension (12 primary pulmonary hypertension, 10 pulmonary fibrosis, five atrial septal defect (ASD), and two scleroderma) were compared with a control group of 10 patients with an enlarged right ventricle but normal pulmonary artery pressure (six ASD, one after ASD closure, one ASD and pulmonary valvotomy, one tricuspid valve endocarditis and repair, and one pulmonary fibrosis). None Conclusions-Prolonged decline of right ventricular tension, the direct result of severe pulmonary hypertension, may appear as prolonged tricuspid regurgitation. It persists until after mitral valve opening on the left side of the heart, where events during isovolumic relaxation are disorganised, and subsequent filling is impaired. These effects are likely to be mediated through the interventricular septum, and this right-left ventricular asynchrony may represent a hitherto unrecognised mode of ventricular interaction.The right and left ventricles cannot be considered independently of one another, and there is evidence of interaction in isolated perfused hearts,' whole animals,2 3 4 and humans.56 Experimental studies and animal models of acute and chronic right ventricular pressure overload have shown that the shape of both ventricles is altered as a result of leftward displacement of the interventricular septum. Also, some echocardiographic studies have shown that patients with right ventricular pressure or volume overload often have impaired left ventricular diastolic function that has been related to the geometrical distortion of the left ventricle.789The aim of this study was to show the abnormalities of left ventricular diastolic function present in a group of patients with right ventricular pressure overload secondary to severe pulmonary hypertension, and to compare these with a control group of patients with right ventricular dilatation but normal pulmonary artery pressures. In this way we hoped to study the possibility of right ventricular disease affecting left ventricular diastolic function, and in particular to separate any direct effects of pulmonary hyper-16

Phaeodactylum tricornutum (P. tricornutum) comprise several lipophilic constituents with proposed anti-obesity and anti-diabetic properties. We investigated the effect of an ethanolic P. tricornutum extract (PTE) on energy metabolism in obesity-prone mice fed a high fat diet (HFD). Six- to eight-week-old male C57BL/6J mice were switched to HFD and, at the same time, received orally placebo or PTE (100 mg or 300 mg/kg body weight/day). Body weight, body composition, and food intake were monitored. After 26 days, blood and tissue samples were collected for biochemical, morphological, and gene expression analyses. PTE-supplemented mice accumulated fucoxanthin metabolites in adipose tissues and attained lower body weight gain, body fat content, weight of white adipose tissue (WAT) depots, and inguinal WAT adipocyte size than controls, independent of decreased food intake. PTE supplementation was associated with lower expression of Mest (a marker of fat tissue expandability) in WAT depots, lower gene expression related to lipid uptake and turnover in visceral WAT, increased expression of genes key to fatty acid oxidation and thermogenesis (Cpt1, Ucp1) in subcutaneous WAT, and signs of thermogenic activation including enhanced UCP1 protein in interscapular brown adipose tissue. In conclusion, these data show the potential of PTE to ameliorate HFD-induced obesity in vivo.

The effect of right ventricular pacing on left ventricular relaxation was studied in 13 patients (age 62 +/- 3 years), with the atrial sensing ventricular pacing mode (VDD). A control group of similar age (64 +/- 4 years) consisted of 11 patients with atrial pacing (AAI). The timing of events was determined in both groups at similar R-R intervals (921 +/- 77 ms vs 967 +/- 37 ms). The loading conditions as estimated by peak systolic wall stress (afterload) and end-diastolic left ventricular dimensions (preload) were approximately the same in both groups. The ratio of late to early filling velocities were similar in both groups. Dominant changes were: increased preejection period (142 +/- 13 ms vs 95 +/- 15 ms); and higher velocities of isovolumic relaxation flow (60 +/- 34 cm/s vs 25 +/- 4 cm/s) in patients with ventricular pacing. The isovolumic relaxation time was longer in patients with VDD pacing (127 +/- 14 ms vs 108 +/- 12 ms). Anterior systolic interventricular septal motion (paradoxal motion) was recorded in nine patients with VDD pacing and in none of the patients with AAI pacing. Isovolumic relaxation flow was detected during atrial pacing in five (45%) patients and in 13 (100%) patients during atrial sensing ventricular pacing, indicating asynchronous left ventricular relaxation. This data shows that VDD pacing compared to atrial pacing resulted in an altered activation pattern of the left ventricle, associated with delayed onset, asynchronous contraction with interventricular septal motion abnormalities and prolonged asynchronous left ventricular relaxation with abnormal motion manifested by the presence of isovolumic relaxation flow.

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