scholarly journals Experimental Studies on Myocardial Contractility : Direct Measurements of the Contractility of Left Ventricular Myocardium with the Strain Gauge Arch

1968 ◽  
Vol 32 (5) ◽  
pp. 789-801 ◽  
Author(s):  
SUMIO HISADA
Keyword(s):  
Strain Gauge ◽  
Myocardial Contractility ◽  
Experimental Studies ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Direct Measurements

Pressure-Circumference Relations of Left Ventricle

1956 ◽  
Vol 186 (1) ◽  
pp. 115-121 ◽  
Author(s):  
Robert F. Rushmer
Keyword(s):  
Left Ventricle ◽  
Myocardial Contractility ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Work Output ◽  
External Work ◽  
Cardiac Adaptation

Changes in left ventricular pressure and left ventricular circumference of intact animals have been recorded simultaneously during spontaneous and induced cardiovascular responses. Mechanisms by which the left ventricular myocardium alters its ‘work output’ are indicated by pressure-circumference loops displayed on a cathode ray oscilloscope. Evidence is presented that the external work of the heart is not necessarily related to the diastolic dimensions in accordance with Starling's law of the heart. Instead, changes in both myocardial contractility and distensibility may play important roles in cardiac adaptation to various conditions.

P6398Peculiarities of the dynamics of fibrosis markers at the in-hospital stage in myocardial infarction patients with preserved left ventricular ejection fraction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A V Osokina ◽  
V N Karetnikova ◽  
O M Polikutina ◽  
Y U S Slepynina ◽  
O V Gruzdeva ◽  
...  
Keyword(s):  
Ejection Fraction ◽  
Myocardial Contractility ◽  
Myocardial Dysfunction ◽  
Ventricular Myocardium ◽  
Serum Markers ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Left Ventricular Myocardium ◽  
Ventricular Ejection Fraction

Abstract Purpose To identify the peculiarities of the dynamics of fibrosis markers in patients with STEMI and preserved myocardial contractility and to determine the relationship between the studied biomarkers and EchoCG indicators characterizing the violation of left ventricular myocardium diastolic function. Material and methods The study included 120 patients with STEMI. The final analysis included 83 patients with preserved left ventricular myocardial contractility measured. The preserved ejection fraction was considered to be ≥50%. Echocardiographic examination was performed using Sonos 2500. In addition to the standard laboratory and instrumental examinations, all the patients underwent the estimation of the concentrations of PICP and PIIINP by enzyme-linked immunoassay using BCM Diagnostics laboratory kits (USA) on the 1st and the 12th days of disease. To compare the obtained values of the studied markers, a control group of healthy volunteers matched by age and gender with the main sample of the patients, was recruited, n=20 (100%). In this group the following values were obtained: PIIINP 7.2 [6.8; 7.5] ng/ml, PICP 179.2 [163.5; 194.9] ng/ml. Statistical processing of the obtained data was performed using Statistica 6.0 software. Results The mean age of the patients was 58.8 years; LVEF was 59.0% [54; 62]. According to EchoCG data, LV dysfunction at normal dimensions was registered in 59 (72%) patients, dilatation – in 22 (27%) patients and regional contractility violation – in 43 (52.4%) cases. The increased values of Tei index 0.70 [0.63; 0.76] and myocardial mass 241.0 g [206.5; 272.0] stand out. The values of serum markers concentrations obtained on the 1st day of STEMI, significantly exceeded the values of the control group and were as follows: PIIINP 26.0 (18.9; 34.9) ng/ml (p=0.047), PICP – 609.0 (583.0; 635.0) ng/ml (p=0.049). On the 12th day the concentration of PICP - 588.0 (580.0; 621.0) ng/ml, PIIINP – 24.2 (18.6; 30.3) ng/ml. No statistically significant differences were obtained in comparison of the markers' concentrations on the 1st and 12th days of the disease. As a result of the correlation analysis between the values of the studied serum markers and EchoCG indicators the following statistically significant relationships were identified: E/Em the 1st day - PICP the 12th day: r=0.55, p=0.005; E/A the 12th day - PICP the 1st day: r=−0.42, p=0.033; E/Em the 12th day - PICP the 12th day: r=0.48, p=0.015; EDV the 12th day - PIIINP the 1st day: r=0.62, p=0.001; EDI the 12th day - PIIINP the 1st day: r=0.43, p=0.034; Age - PIIINP the 1st day: r=0.558, p=0.016. Conclusion The presence of statistically significant correlations between the concentrations of PIIINP, PICP with EchoCG indicators evidence the role of fibrosis in the formation of diastolic myocardial dysfunction and reflect the potential use of procollagen to predict heart failure in long-term post-infarction period.

scholarly journals Effects of Telmisartan on Myocardial Protein Profiles in Hypertensive Rats

2021 ◽  
Vol 34 (3) ◽  
pp. 299-299
Author(s):  
Yu Feng ◽  
Man-li Zhou ◽  
Jian-zhang Wang ◽  
Jia-qi Zhang ◽  
Shu-le Qian ◽  
...  
Keyword(s):  
Heat Shock ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Sterile Water ◽  
Protein Profiles ◽  
Related Protein ◽  
Hypertensive Rats ◽  
Treatment Groups ◽  
Proteasome 26S

Abstract Background To investigate the effects of telmisartan on the protein profiles of the left ventricular myocardium in spontaneously hypertensive rats (SHR). Methods Sixteen SHR were randomly divided into control and telmisartan treatment groups. Rats were treated with sterile water (10 ml/kg) or telmisartan (4.33 mg/kg) by gavage for 12 weeks. Wistar-Kyoto (WKY) rats treated with sterile water (10 ml/kg) as controls. At the end of 12 weeks of control or telmisartan treatment, rats were sacrificed, and hearts were collected for protein preparations, isotope labeling, and mass spectrometric analysis. Results In total, there were 23 differentially expressed proteins in the left ventricular myocardium between control and telmisartan treatment groups in SHR. Compared with the telmisartan group, the upregulated proteins in the SHR were dual-specificity mitogen-activated protein kinase kinase 3-like, transgelin, and haptoglobin subtype 2. The downregulated proteins in the SHR were as follows: von Willebrand factor (fragment), kininogen 1, small ribonucleoprotein-related protein, fibrinogen beta chain, protein mass 3 (fragment), proteasome 26s, heat shock protein 27-related protein 1, tenascin X, fibronectin subtype 2, transferrin receptor protein, platelets 1, cathepsin L1, complement factor B, isoform CRA_b, fibrinogen isomer, immunoglobulin heavy chain (γ polypeptide), and α 1 antiprotease. Conclusions Telmisartan differentially regulates myocardial protein expression in hypertensive rats including heat shock protein 27, fibrinogen, fibronectin, proteasome 26s and transgelin, as well as proteins in biochemical, metabolic, and signal transduction pathways. These changes in protein expression may contribute to the antihypertrophic effects of telmisartan in hypertension.

scholarly journals Remodeling of t-system and proteins underlying excitation-contraction coupling in aging versus failing human heart

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yankun Lyu ◽  
Vipin K. Verma ◽  
Younjee Lee ◽  
Iosif Taleb ◽  
Rachit Badolia ◽  
...  
Keyword(s):  
Heart Function ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Excitation Contraction Coupling ◽  
Transverse Tubular System ◽  
Contraction Coupling ◽  
Senescent Phenotype ◽  
Cellular Microstructure ◽  
T System

AbstractIt is well established that the aging heart progressively remodels towards a senescent phenotype, but alterations of cellular microstructure and their differences to chronic heart failure (HF) associated remodeling remain ill-defined. Here, we show that the transverse tubular system (t-system) and proteins underlying excitation-contraction coupling in cardiomyocytes are characteristically remodeled with age. We shed light on mechanisms of this remodeling and identified similarities and differences to chronic HF. Using left ventricular myocardium from donors and HF patients with ages between 19 and 75 years, we established a library of 3D reconstructions of the t-system as well as ryanodine receptor (RyR) and junctophilin 2 (JPH2) clusters. Aging was characterized by t-system alterations and sarcolemmal dissociation of RyR clusters. This remodeling was less pronounced than in HF and accompanied by major alterations of JPH2 arrangement. Our study indicates that targeting sarcolemmal association of JPH2 might ameliorate age-associated deficiencies of heart function.

scholarly journals Myxomatous Mitral Valve Disease with Mitral Valve Prolapse and Mitral Annular Disjunction: Clinical and Functional Significance of the Coincidence

2021 ◽  
Vol 8 (2) ◽  
pp. 9
Author(s):  
Nina C. Wunderlich ◽  
Siew Yen Ho ◽  
Nir Flint ◽  
Robert J. Siegel
Keyword(s):  
Mitral Valve ◽  
Mitral Valve Disease ◽  
Morphological Changes ◽  
Morphological Characteristics ◽  
Mitral Annulus ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Valve Disease ◽  
Left Ventricular Myocardium ◽  
Basal Portion

The morphological changes that occur in myxomatous mitral valve disease (MMVD) involve various components, ultimately leading to the impairment of mitral valve (MV) function. In this context, intrinsic mitral annular abnormalities are increasingly recognized, such as a mitral annular disjunction (MAD), a specific anatomical abnormality whereby there is a distinct separation between the mitral annulus and the left atrial wall and the basal portion of the posterolateral left ventricular myocardium. In recent years, several studies have suggested that MAD contributes to myxomatous degeneration of the mitral leaflets, and there is growing evidence that MAD is associated with ventricular arrhythmias and sudden cardiac death. In this review, the morphological characteristics of MAD and imaging tools for diagnosis will be described, and the clinical and functional aspects of the coincidence of MAD and myxomatous MVP will be discussed.

β-blockade abolishes the augmented cardiac tPA release induced by transactivation of heterodimerised bradykinin receptor-2 and β2-adrenergic receptor in vivo

2014 ◽  
Vol 112 (11) ◽  
pp. 951-959 ◽  
Author(s):  
Morten Eriksen ◽  
Arnfinn Ilebekk ◽  
Alessandro Cataliotti ◽  
Cathrine Rein Carlson ◽  
Torstein Lyberg ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Sympathetic Nerves ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Adrenergic Stimulation ◽  
Β2 Adrenergic Receptor ◽  
Β Blocker

SummaryBradykinin (BK) receptor-2 (B2R) and β2-adrenergic receptor (β2AR) have been shown to form heterodimers in vitro. However, in vivo proofs of the functional effects of B2R-β2AR heterodimerisation are missing. Both BK and adrenergic stimulation are known inducers of tPA release. Our goal was to demonstrate the existence of B2R-β2AR heterodimerisation in myocardium and to define its functional effect on cardiac release of tPA in vivo. We further investigated the effects of a non-selective β-blocker on this receptor interplay. To investigate functional effects of B2R-β2AR heterodimerisation (i. e. BK transactivation of β2AR) in vivo, we induced serial electrical stimulation of cardiac sympathetic nerves (SS) in normal pigs that underwent concomitant BK infusion. Both SS and BK alone induced increases in cardiac tPA release. Importantly, despite B2R desensitisation, simultaneous BK infusion and SS (BK+SS) was characterised by 2.3 ± 0.3-fold enhanced tPA release compared to SS alone. When β-blockade (propranolol) was introduced prior to BK+SS, tPA release was inhibited. A persistent B2R-β2AR heterodimer was confirmed in BK-stimulated and nonstimulated left ventricular myocardium by immunoprecipitation studies and under non-reducing gel conditions. All together, these results strongly suggest BK transactivation of β2AR leading to enhanced β2AR-mediated release of tPA. Importantly, non-selective β-blockade inhibits both SS-induced release of tPA and the functional effects of B2R-β2AR heterodimerisation in vivo, which may have important clinical implications.

scholarly journals Heart transplantation in an adult patient with isolated noncompaction of the left ventricular myocardium

Medicina ◽  
2010 ◽  
Vol 46 (3) ◽  
pp. 193 ◽  
Author(s):  
Sigita Glaveckaitė ◽  
Kęstutis Ručinskas ◽  
Jelena Čelutkienė ◽  
Vytė Maneikienė ◽  
Diana Zakarkaitė ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Adult Patient ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Important Process ◽  
Ventricular Noncompaction ◽  
Myocardial Development ◽  
Myocardial Fibers ◽  
Heart Lesions

Isolated noncompaction of the ventricular myocardium is defined as a rare cardiomyopathy caused by intrauterine arrest of compaction of the myocardial fibers and meshwork, an important process in myocardial development, in absence of any coexisting congenital heart lesions. A lot of controversies exist about diagnostic criteria, nomenclature, origin, pathogenesis, and prognosis of this disease. Here, we describe an adult patient with isolated left ventricular noncompaction who presented with worsening congestive heart failure and was successfully treated with heart transplantation.

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