RV mechanics is worse in night-time and daytime-night-time hypertensive patients than in normotensive controls and isolated daytime hypertensive patients. A 24-h SBP is independently associated with right heart mechanics.

BackgroundA biomarker that is of great interest in relation to adverse cardiovascular events is soluble ST2 (sST2), a member of the interleukin family. Considering that metabolic syndrome (MetS) is accompanied by a proinflammatory state, we aimed to assess the relationship between sST2 and left ventricular (LV) structure and function in patients with MetS.MethodsA multicentric, cross-sectional study was conducted on180 MetS subjects with normal LV ejection fraction as determined by echocardiography. LV hypertrophy (LVH) was defined as an LV mass index greater than the gender-specific upper limit of normal as determined by echocardiography. LV diastolic dysfunction (DD) was assessed by pulse-wave and tissue Doppler imaging. sST2 was measured by using a quantitative monoclonal ELISA assay.ResultsLV mass index (β=0.337, P<0.001, linear regression) was independently associated with sST2 concentrations. Increased sST2 was associated with an increased likelihood of LVH [Exp (B)=2.20, P=0.048, logistic regression] and increased systolic blood pressure [Exp (B)=1.02, P=0.05, logistic regression]. Comparing mean sST2 concentrations (adjusted for age, body mass index, gender) between different LV remodeling patterns, we found the greatest sST2 level in the group with concentric hypertrophy. There were no differences in sST2 concentration between groups with and without LV DD.ConclusionsIncreased sST2 concentration in patients with MetS was associated with a greater likelihood of exhibiting LVH. Our results suggest that inflammation could be one of the principal triggering mechanisms for LV remodeling in MetS.

The obtained results suggest that even slightly elevated risk for developing diabetes mellitus may be related to impaired HRV.

The authors sought to investigate the association between different hypertensive phenotypes and left atrial (LA) function assessed by the volumetric method and the strain method in patients with untreated hypertension. This cross-sectional study involved 236 untreated patients who underwent 24-hour ambulatory blood pressure monitoring and two-dimensional echocardiographic examination. Our findings showed that LA function gradually deteriorated from patients with normotension, across patients with daytime hypertension, to patients with night-and day-nighttime hypertension. LA reservoir and conduit functions were particularly deteriorated in patients with nighttime and day-nighttime hypertension compared with patients with normotension and patients with daytime hypertension, whereas LA pump function was compensatorily increased only in the participants with day-nighttime hypertension. Only nighttime hypertension and day-nighttime hypertension were independently associated with the reduced reservoir and conduit LA function. The difference between patients with daytime and nighttime hypertension was found in reservoir and conduit LA but not LA pump function. | INTRODUCTIONLeft atrial (LA) enlargement represents a very important and wellknown risk factor for cardiovascular and overall morbidity and mortality.1,2 LA phasic function has long been considered as unimportant.The number of studies that demonstrate the importance of LA reservoir, conduit, and active pump function is increasing. The existing data show that nondipping BP pattern is associated with deterioration of LA function and mechanics, which follows LV remodeling in these patients. 10,11A new classification of hypertensive phenotypes on daytime, nighttime, and day-nighttime hypertension reveals that nighttime hypertension rather than nondipping pattern represents an independent factor associated with LV mass index (LVMI) and LV hypertro- LA remodeling has been reported in patients with hypertension who have asymptomatic diastolic dysfunction. 16,17 Although LA enlargement could be a potential mechanism for compensating the impairment of LV compliance and progression of LV diastolic

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