Background: Variable results of cardiac resynchronization therapy (CRT) on diastolic function have been described. We investigated 3 and 12 months' effect of CRT on diastolic function and left ventricular (LV) filling pressures and their relation to LV reverse remodeling.
Methods: Fifty-two patients' (36 male, 69 +/- 8 years, QRS duration 170 +/- 29 milliseconds) echo-Doppler was performed before and 3 and 12 months after CRT. Tissue Doppler early diastolic annular (Em) and color M-mode-derived flow propagation (Vp) velocities were used to estimate LV filling pressures by E/Em and E/Vp ratios.
Results: After 12 months, LV reverse remodeling (end-systolic volume decrease >15%) was observed in 58%. Despite a significantly more compromised baseline diastolic function of patients without LV reverse remodeling, multivariate analysis revealed that only LV dyssynchrony could predict LV reverse remodeling. Grades 2 and 3 diastolic function improved only in LV reverse remodeling patients (from 34% to 13% to 10%), whereas a nonsignificant increase from 59% to 67% to 72% was observed in patients without reverse remodeling. Irrespective of LV volume response, short-term symptomatic benefit was related to decreased filling pressure. However, after 12 months, E/Em and E/Vp only significantly decreased in patients with LV reverse remodeling (from 16.0 +/- 6 to 10.4 +/- 4 and 2.2 +/- 0.6 to 1.5 +/- 0.4, respectively).
Conclusions: Left ventricular reverse remodeling induced by CRT is accompanied by improvement in diastolic function and estimated LV filling pressure. Short-term symptomatic benefit was related to decreased filling pressure. However, for longer-term symptomatic improvement and decreased filling pressures, LV reverse remodeling appeared mandatory.
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http://dx.doi.org/10.1016/j.ahj.2007.02.033 | DOI Listing |
Introduction: To determine the effects of atorvastatin on cardiac function and hemodynamics and to investigate its functional mechanism on cardiac fibrosis in acute myocardial infarction (AMI) rats.
Methods: Cardiac functions and hemodynamic changes were evaluated in each group on day 28. Quantitative reverse transcription-polymerase chain reaction, Western blot, and immunohistochemistry were performed to detect the expression of notch1, transforming growth factor-β (TGF-β), Smad2, Smad7, as well as myocardial fibrosis factors (i.
Front Cardiovasc Med
January 2025
Department of Clinical Sciences and Community Health, Cardiovascular Section, University of Milan, Milan, Italy.
World J Cardiol
January 2025
Chinese Academy Medical Sciences, Fuwai Yunnan Hospital, Kunming 650000, Yunnan Province, China.
Sodium-glucose cotransporter-2 (SGLT-2) inhibitors represent a cutting-edge class of oral antidiabetic therapeutics that operate through selective inhibition of glucose reabsorption in proximal renal tubules, consequently augmenting urinary glucose excretion and attenuating blood glucose levels. Extensive clinical investigations have demonstrated their profound cardiovascular efficacy. Parallel basic science research has elucidated the mechanistic pathways through which diverse SGLT-2 inhibitors beneficially modulate pulmonary vascular cells and arterial remodeling.
View Article and Find Full Text PDFMol Cell Endocrinol
January 2025
Shanghai University of Sport, School of Health and Exercise, Shanghai 200438, China. Electronic address:
To clarify the roles and mechanisms of adipokine chemerin in exercise-induced bone improvements in type 2 diabetes mellitus (DM) mice and mice fed on high fat diet (HFD). DM mice were established by HFD+streptozotocin injection, exogenous chemerin was supplemented prior to running, and found that exogenous chemerin reversed 6-week exercise-induced improvements in cancellous bone parameters in DM mice. While adipose-specific chemerin knockout improved microstructure and mass of cancellous bone in HFD mice and further increased exercise-induced bone improvements, accompanied with promoted osteogenesis and inhibited osteoclasis represented as the changes of RANKL, M-CSF, Runx2, Osterix, OPG, ALP and CTSK.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Biomedical Sciences, Grand Valley State University, Allendale, MI 49401, USA.
Background: Diabetes mellitus is associated with morphological and functional impairment of the heart primarily due to lipid toxicity caused by increased fatty acid metabolism. Extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) have been implicated in the metabolism of fatty acids in the liver and skeletal muscles. However, their role in the heart in diabetes remains unclear.
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