Assessment of systolic function by atrioventricular plane displacement in patients with diastolic dysfunction

2004 ◽  
Vol 59 (4) ◽  
pp. 409-415 ◽  
Author(s):  
Dursun DUSUNOǦLU ◽  
Bülent POLAT ◽  
Harun EVRENGUL ◽  
Halil TANRIVERDI ◽  
Asuman KAFTAN ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Systolic Function ◽  
Atrioventricular Plane Displacement ◽  
Plane Displacement

scholarly journals Diastolic dysfunction in a pre-clinical model of diabetes is associated with changes in the cardiac non-myocyte cellular composition

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Charles D. Cohen ◽  
Miles J. De Blasio ◽  
Man K. S. Lee ◽  
Gabriella E. Farrugia ◽  
Darnel Prakoso ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
Diastolic Dysfunction ◽  
Systolic Function ◽  
Cardiac Fibroblasts ◽  
Detailed Examination ◽  
Diabetic Mice ◽  
Cellular Mechanisms ◽  
Clinical Model ◽  
Cardiac Ventricles

Abstract Background Diabetes is associated with a significantly elevated risk of cardiovascular disease and its specific pathophysiology remains unclear. Recent studies have changed our understanding of cardiac cellularity, with cellular changes accompanying diabetes yet to be examined in detail. This study aims to characterise the changes in the cardiac cellular landscape in murine diabetes to identify potential cellular protagonists in the diabetic heart. Methods Diabetes was induced in male FVB/N mice by low-dose streptozotocin and a high-fat diet for 26-weeks. Cardiac function was measured by echocardiography at endpoint. Flow cytometry was performed on cardiac ventricles as well as blood, spleen, and bone-marrow at endpoint from non-diabetic and diabetic mice. To validate flow cytometry results, immunofluorescence staining was conducted on left-ventricles of age-matched mice. Results Mice with diabetes exhibited hyperglycaemia and impaired glucose tolerance at endpoint. Echocardiography revealed reduced E:A and e’:a’ ratios in diabetic mice indicating diastolic dysfunction. Systolic function was not different between the experimental groups. Detailed examination of cardiac cellularity found resident mesenchymal cells (RMCs) were elevated as a result of diabetes, due to a marked increase in cardiac fibroblasts, while smooth muscle cells were reduced in proportion. Moreover, we found increased levels of Ly6Chi monocytes in both the heart and in the blood. Consistent with this, the proportion of bone-marrow haematopoietic stem cells were increased in diabetic mice. Conclusions Murine diabetes results in distinct changes in cardiac cellularity. These changes—in particular increased levels of fibroblasts—offer a framework for understanding how cardiac cellularity changes in diabetes. The results also point to new cellular mechanisms in this context, which may further aid in development of pharmacotherapies to allay the progression of cardiomyopathy associated with diabetes.

scholarly journals Atrioventricular plane displacement versus mitral and tricuspid annular plane systolic excursion: A comparison between cardiac magnetic resonance and M‐mode echocardiography

2021 ◽  
Vol 41 (3) ◽  
pp. 262-270
Author(s):  
Alvaro Sepúlveda‐Martínez ◽  
Katarina Steding‐Ehrenborg ◽  
Mérida Rodríguez‐López ◽  
Ellen Ostenfeld ◽  
Brenda Valenzuela‐Alcaráz ◽  
...  
Keyword(s):  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Atrioventricular Plane Displacement ◽  
Plane Displacement

Long-term levosimendan treatment improves systolic function and myocardial relaxation in mice with cardiomyocyte-specific disruption of the Serca2 gene

2013 ◽  
Vol 115 (10) ◽  
pp. 1572-1580 ◽  
Author(s):  
Vigdis Hillestad ◽  
Frank Kramer ◽  
Stefan Golz ◽  
Andreas Knorr ◽  
Kristin B. Andersson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Cardiac Function ◽  
Diastolic Dysfunction ◽  
Systolic Function ◽  
Cytosolic Calcium ◽  
Left Ventricular ◽  
Pressure Measurements ◽  
Human Heart Failure

In human heart failure (HF), reduced cardiac function has, at least partly, been ascribed to altered calcium homeostasis in cardiomyocytes. The effects of the calcium sensitizer levosimendan on diastolic dysfunction caused by reduced removal of calcium from cytosol in early diastole are not well known. In this study, we investigated the effect of long-term levosimendan treatment in a murine model of HF where the sarco(endo)plasmatic reticulum ATPase ( Serca) gene is specifically disrupted in the cardiomyocytes, leading to reduced removal of cytosolic calcium. After induction of Serca2 gene disruption, these mice develop marked diastolic dysfunction as well as impaired contractility. SERCA2 knockout (SERCA2KO) mice were treated with levosimendan or vehicle from the time of KO induction. At the 7-wk end point, cardiac function was assessed by echocardiography and pressure measurements. Vehicle-treated SERCA2KO mice showed significantly diminished left-ventricular (LV) contractility, as shown by decreased ejection fraction, stroke volume, and cardiac output. LV pressure measurements revealed a marked increase in the time constant (τ) of isovolumetric pressure decay, showing impaired relaxation. Levosimendan treatment significantly improved all three systolic parameters. Moreover, a significant reduction in τ toward normalization indicated improved relaxation. Gene-expression analysis, however, revealed an increase in genes related to production of the ECM in animals treated with levosimendan. In conclusion, long-term levosimendan treatment improves both contractility and relaxation in a heart-failure model with marked diastolic dysfunction due to reduced calcium transients. However, altered gene expression related to fibrosis was observed.

Abstract 12622: Western Diet for One Month Impairs Myocardial Energetics and Both Systolic and Diastolic Pump Function in the Mouse Heart

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Ivan Luptak ◽  
Aaron L Sverdlov ◽  
Aly Elezaby ◽  
Edward J Miller ◽  
David R Pimentel ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Mitochondrial Dysfunction ◽  
Systolic Function ◽  
Atp Synthesis ◽  
Contractile Reserve ◽  
31P Nmr Spectroscopy ◽  
Pump Function ◽  
High Workload ◽  
Myocardial Energetics ◽  
Intact Heart

Background and Significance: Metabolic heart disease(MHD) is common in patients with obesity, type 2 diabetes and/or metabolic syndrome. We found cardiac mitochondrial dysfunction in mice with obesity-related MHD due to consumption of a high fat high sucrose (HFHS) diet. The effects of diet-induced obesity on cardiac energetics and pump function in the intact organ are largely unknown. Hypothesis: We tested the hypothesis that cardiac mitochondrial dysfunction due to HFHS diet for one month impairs energetic and contractile reserve in the intact heart. Methods and Results: Mice were fed a HFHS or control diet (CD) for 1 month. In isolated cardiac mitochondria from HFHS-fed mice (vs. CD) the maximal rate of ATP synthesis was decreased for complex I (down by 42%; p<0.05) and II (down by 37%; p<0.05) substrates. We measured myocardial energetics in isolated perfused hearts using 31P NMR spectroscopy at baseline (450 bpm, 2 mM Ca++) and high workload (600 bpm, 4 mM Ca++) in HFHS (n=7) and CD (n=8) hearts. In HFHS-fed hearts, myocardial ATP concentration was the same at baseline (10.5±0.4 vs 10.4±0.5 mM) and high workload (7.4±0.9 vs. 7.5±0.5 mM) as that of CD hearts. However, in HFHS-fed hearts the concentration of phosphocreatine, which reflects energy reserve, was decreased at baseline (13±0.7 vs. 17.5±0.8 mM; p<0.01) and decreased further at high workload (down to 7.3±0.7; p<0.01 vs. baseline and p<0.01 vs. CD at 10.5±0.4 mM) - indicating a mismatch between ATP production and utilization. In HFHS hearts, the diastolic pressure-volume relationship was shifted upward and leftward at baseline, indicative of diastolic dysfunction. In HFHS hearts, baseline systolic function was preserved (rate pressure product 41,600±2,200 vs. 41,000±2,000 mmHg/min), but was decreased at high workload (54,800±7,200 vs. 85,300±4,300 mmHg/min; p<0.01 vs. CD), reflecting an impaired contractile reserve. Conclusion: Consumption of a HFHS diet for one month causes cardiac mitochondrial dysfunction with reduced ATP synthesis leading to impaired energetic reserve in the intact heart. Diastolic dysfunction at rest and the impaired ability to increase systolic function with increased work demands may result from impaired energetics in MHD.

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