The rapid technological developments of the past decade and the changes in echocardiographic practice brought about by these developments have resulted in the need for updated recommendations to the ...previously published guidelines for cardiac chamber quantification, which was the goal of the joint writing group assembled by the American Society of Echocardiography and the European Association of Cardiovascular Imaging. This document provides updated normal values for all four cardiac chambers, including three-dimensional echocardiography and myocardial deformation, when possible, on the basis of considerably larger numbers of normal subjects, compiled from multiple databases. In addition, this document attempts to eliminate several minor discrepancies that existed between previously published guidelines.
In normal subjects, left ventricular (LV) dimensions have been shown to decrease over time, while wall thickness is increasing. The aim of this study was to investigate LV remodeling in a cohort of ...patients with type 2 diabetes mellitus during a 3-year follow-up period and its potential association with decreased longitudinal systolic strain (εL).
One hundred seventy-two patients with type 2 diabetes without overt heart disease were prospectively enrolled and underwent echocardiography with speckle-tracking imaging to assess global LV εL at baseline and at 3 years. The associations between alteration in εL (defined as |εL| < 18%), LV geometry at baseline, and LV remodeling over time were evaluated.
Among the 172 enrolled patients, 154 completed 3-year follow-up. At baseline, patients with εL alteration had higher LV end-systolic volumes (28 ± 11 vs 23 ± 9 mL, P < .001) and relative wall thicknesses (RWT; 0.44 ± 0.06 vs 0.40 ± 0.07, P = .008) compared with those with normal εL. At 3-year follow-up, RWTs remained stable in both groups. LV volumes significantly decreased in patients with normal εL but not in patients with εL alteration. Multivariate analysis showed that εL alteration was independently associated with LV end-systolic volume (β = 5.0, P = .006) and RWT (β = 0.03, P = .03) at baseline and with changes in both LV end-diastolic volume (β = 19.1, P = .001) and LV end-systolic volume (β = 2.6, P = .047) over 3 years.
In patients with type 2 diabetes, εL alteration was associated with higher RWT and LV volumes and with the absence of decreases in LV volumes over time, which might be an early sign of adverse LV remodeling.
Diastolic dysfunction is considered the first marker of diabetic cardiomyopathy. However, preclinical systolic alteration was also recently described by strain, but its association with diastolic ...dysfunction has never been investigated.
One hundred fourteen patients with type 2 diabetes mellitus (DM) with controlled blood pressure and without overt heart disease were prospectively enrolled and compared with 88 age-matched controls. All subjects underwent comprehensive echocardiography, including diastolic evaluation according to current recommendations and speckle-tracking imaging. The prevalence of diastolic dysfunction, the determinants of diastolic parameters, and the association between preclinical systolic and diastolic dysfunctions were studied.
Diastolic parameters were altered in patients compared with controls, with lower E/A ratios, longer mitral deceleration and isovolumic relaxation times, and higher E/e' ratio. Diastolic dysfunction occurred in 47% of patients with DM (33% and 14% with grade I and II diastolic dysfunction, respectively) and systolic alteration (longitudinal strain ≥ -18%) in 32% of patients. Whereas longitudinal systolic strain was independently associated with DM and gender, diastolic parameters were influenced by many factors, including age, rate-pressure product, history of hypertension, and body mass index. Systolic alteration occurred in 28% of patients with DM with normal diastolic function and in 35% with diastolic dysfunction.
Diastolic dysfunction diagnosed according to current recommendations is frequent in patients with DM but is also influenced by other factors. Systolic strain alteration may exist despite normal diastolic function, indicating that diastolic dysfunction should not be considered the first marker of a preclinical form of diabetic cardiomyopathy.
Abstract Brown adipose tissue (BAT) has well recognized thermogenic properties mediated by uncoupling protein 1 (UCP1); more recently, BAT has been demonstrated to modulate cardiovascular risk ...factors. To investigate whether BAT also affects myocardial injury and remodeling, UCP1-deficient (UCP1−/− ) mice, which have dysfunctional BAT, were subjected to catecholamine-induced cardiomyopathy. At baseline, there were no differences in echocardiographic parameters, plasma cardiac troponin I (cTnI) or myocardial fibrosis between wild-type (WT) and UCP1−/− mice. Isoproterenol infusion increased cTnI and myocardial fibrosis and induced left ventricular (LV) hypertrophy in both WT and UCP1−/− mice. UCP1−/− mice also demonstrated exaggerated myocardial injury, fibrosis, and adverse remodeling, as well as decreased survival. Transplantation of WT BAT to UCP1−/− mice prevented the isoproterenol-induced cTnI increase and improved survival, whereas UCP1−/− BAT transplanted to either UCP1−/− or WT mice had no effect on cTnI release. After 3 days of isoproterenol treatment, phosphorylated AKT and ERK were lower in the LV's of UCP1−/− mice than in those of WT mice. Activation of BAT was also noted in a model of chronic ischemic cardiomyopathy, and was correlated to LV dysfunction. Deficiency in UCP1, and accompanying BAT dysfunction, increases cardiomyocyte injury and adverse LV remodeling, and decreases survival in a mouse model of catecholamine-induced cardiomyopathy. Myocardial injury and decreased survival are rescued by transplantation of functional BAT to UCP1−/− mice, suggesting a systemic cardioprotective role of functional BAT. BAT is also activated in chronic ischemic cardiomyopathy.
Right ventricular function is a strong determinant of prognosis in severe pulmonary hypertension.
The aim of this study was to evaluate the prognostic value of estimates of right ventricular function ...obtained by echocardiography and Doppler tissue imaging and of functional class and 6-min walk distance (6MWD) in 142 patients with either pulmonary arterial hypertension (n = 104) or chronic thromboembolic pulmonary hypertension (n = 38). Echocardiography was prospectively performed, and demographics, medications, associated medical conditions, New York Heart Association class, and 6MWD at inclusion in addition to vital status, transplantation, and hospital admission related to pulmonary hypertension at follow-up were then collected by review of the medical records.
Variables associated with overall survival by univariate analysis were 6MWD (P = .009), functional class (P = .024), tricuspid annular plane systolic excursion (P = .03) and isovolumic peak velocity at the tricuspid annulus (IVCv) (P = .003). On multivariate analysis, IVCv (P = .015) and 6MWD (P = .016) were the only independent predictors of survival. Kaplan-Meier estimates of survival at 1 year were 95% in patients with IVCv > 9 cm/sec and 80% in those with IVCv ≤ 9 cm/sec (P = .002). Intraobserver and interobserver variability of IVCv measurement were 5% and 9%, respectively.
Measurement of right ventricular function by Doppler tissue imaging, an easy, noninvasive, and reproducible method, is an independent predictor of clinical outcomes in patients with severe pulmonary hypertension.
Abstract
Aim
Long-term high-fat diet (HFD) induces both cardiac remodelling and myocardial dysfunction in murine models. The aim was to assess the time course and mechanisms of metabolic and cardiac ...modifications induced by short-term HFD in wild-type (WT) mice.
Methods and results
Thirty-three WT mice were subjected to HFD (60% fat, n = 16) and chow diet (CD, 13% fat, n = 17). Metabolic and echocardiographic data were collected at baseline and every 5 weeks for 20 weeks. Invasive haemodynamic data and myocardial samples were collected at 5 and 20 weeks. Echocardiographic data included left ventricular (LV) diameters and thickness, and systolic function using radial strain rate (SR). Histological assessment of cardiomyocyte and adipocyte sizes, interstitial fibrosis, and apoptosis index were performed. During follow-up, body weight, and glycaemia levels were higher in HFD than in CD mice, in association with an early adipose tissue remodelling. Despite no difference between both groups in blood pressure and LV mass at 5 weeks, an early LV dysfunction was observed in HFD mice as assessed by radial SR (21 ± 0.8 vs. 27 ± 0.8 unit/s, P < 0.001) and haemodynamic assessment. During follow-up, both groups demonstrated a progressive systolic and diastolic LV dysfunction and remodelling including dilatation and hypertrophy, which were more severe in HFD mice. Compared with CD mice, the early LV impairment in HFD mice was coupled with a higher cardiomyocyte apoptosis level (0.95 vs. 0.02%, P < 0.05) associated with an interstitial fibrosis process (2.3 vs. 0.2%, P < 0.05), which worsen during follow-up.
Conclusion
The HFD promoted early metabolic and cardiac dysfunctions, and adipose and myocardial tissues remodelling.
Diabetic cardiomyopathy has been characterized by an early impairment of left ventricular (LV) longitudinal function as opposed to preserved LV radial function.
Conventional echocardiography and ...longitudinal (ε(L)) and radial (ε(R)) systolic strain assessed by speckle-tracking imaging were obtained in 114 type 2 diabetic patients and 88 age-matched controls.
LV ejection fraction was similar in diabetic patients and controls. The presence of subclinical LV systolic dysfunction in diabetic patients was demonstrated by lower values of midwall fractional shortening (18% ± 3% vs 20% ± 3%, P = .006), ε(L) (-19% ± 3% vs -22% ± 2%, P < .001), and ε(R) (50% ± 16% vs 56% ± 12%, P = .003) compared with controls. On multivariate analysis, factors predicting strain values were diabetes (P = .001) and gender (P = .001) for ε(L) and diabetes (P = .003) for ε(R).
Diabetic patients without overt heart disease display subclinical alteration of both radial and longitudinal LV systolic function even after adjustment for blood pressure, age, and body mass index.
Abstract
Aims
Diastolic dysfunction is frequent in patients with type 2 diabetes mellitus (DM2) and associated with a poor prognosis. This study aimed to describe diastolic function changes over time ...in DM2 patients and to identify predictive factors of diastolic function deterioration.
Methods and results
Diastolic function was assessed by echocardiography according to the EACVI/ASE recommendations at baseline and 3-year follow-up in a prospective cohort of 310 DM2 patients without overt heart disease. Predictors of diastolic function deterioration were identified using logistic regression analysis. During the 3-year follow-up, prevalence of diastolic dysfunction increased from 49% to 67% (P = 0.001). Only 32% of the patients had a normal diastolic function both at baseline and 3 years and 27% of the patients presented diastolic function deterioration. At multivariable analysis, age (OR = 1.05 1.01–1.09, P < 0.01), retinopathy (OR = 2.00 1.10–3.63, P = 0.02), and increase in systolic blood pressure during follow-up (OR = 1.03 1.01–1.04, P < 0.01) were predictive of diastolic function deterioration.
Conclusion
Age, retinopathy, and increase in blood pressure over time are associated with an increased risk of diastolic function deterioration in DM2 patients. The presence of these co-factors might help to early identify patients at risk of heart failure.
When activated by the sympathetic nervous system, brown adipose tissue (BAT) increases energy expenditure to produce heat. Augmenting BAT mass or increasing BAT activation could potentially be used ...to decrease obesity. Noninvasive methods to detect and monitor BAT mass are needed. Contrast ultrasound can estimate BAT blood flow and is able to measure the perfused volume of an organ and thus its mass. The objective of this study was to evaluate whether contrast ultrasound could characterize BAT mass in two mouse models of obesity: wild-type mice fed a high-fat diet and mutant db/db mice.
Contrast ultrasound of BAT (Definity 2 μL/min; 14-MHz linear probe) was performed before and after stimulation of BAT with norepinephrine (NE). BAT replenishment curves were obtained, and blood flow was estimated by the product of the curve's plateau and slope. Additionally, consecutive two-dimensional images of perfused BAT were acquired at 1-mm intervals after stimulation with NE and used to assess BAT volume and mass.
BAT blood flow increased after NE infusion in all mice studied. Blood flow response to NE was similar in wild-type mice fed either a low-fat diet or a high-fat diet. BAT blood flow was lower in db/db mice than in wild-type mice (P = .02). Contrast ultrasound-derived BAT mass was correlated with BAT mass obtained at necropsy (R(2) = 0.83, P < .001). BAT mass was higher in mice fed a high-fat diet than in those fed a low-fat diet.
Contrast ultrasound can be used to estimate BAT mass in mice when BAT vascularization is not significantly impaired. This noninvasive technique may potentially allow the serial evaluation of therapies designed to augment BAT mass.
Bone morphogenetic protein (BMP) signaling contributes to the development of cardiac hypertrophy. However, the identity of the BMP type I receptor involved in cardiac hypertrophy and the underlying ...molecular mechanisms are poorly understood. By using quantitative PCR and immunoblotting, we demonstrated that BMP signaling increased during phenylephrine-induced hypertrophy in cultured neonatal rat cardiomyocytes (NRCs), as evidenced by increased phosphorylation of Smads 1 and 5 and induction of Id1 gene expression. Inhibition of BMP signaling with LDN193189 or noggin, and silencing of Smad 1 or 4 using small interfering RNA diminished the ability of phenylephrine to induce hypertrophy in NRCs. Conversely, activation of BMP signaling with BMP2 or BMP4 induced hypertrophy in NRCs. Luciferase reporter assay further showed that BMP2 or BMP4 treatment of NRCs repressed atrogin-1 gene expression concomitant with an increase in calcineurin protein levels and enhanced activity of nuclear factor of activated T cells, providing a mechanism by which BMP signaling contributes to cardiac hypertrophy. In a model of cardiac hypertrophy, C57BL/6 mice treated with angiotensin II (A2) had increased BMP signaling in the left ventricle. Treatment with LDN193189 attenuated A2-induced cardiac hypertrophy and collagen deposition in left ventricles. Cardiomyocyte-specific deletion of BMP type I receptor ALK2 (activin-like kinase 2), but not ALK1 or ALK3, inhibited BMP signaling and mitigated A2-induced cardiac hypertrophy and left ventricular fibrosis in mice. The results suggest that BMP signaling upregulates the calcineurin/nuclear factor of activated T cell pathway via BMP type I receptor ALK2, contributing to cardiac hypertrophy and fibrosis.
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