scholarly journals Titin-Isoform Dependence of Titin-Actin Interaction and Its Regulation by S100A1/Ca2+in Skinned Myocardium

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Hideto Fukushima ◽  
Charles S. Chung ◽  
Henk Granzier
Keyword(s):  
Left Ventricle ◽  
Left Atrium ◽  
Left Ventricular ◽  
Intermediate Level ◽  
Passive Stiffness ◽  
Differential Splicing ◽  
Myocardial Stiffness ◽  
Viscous Component

Titin, also known as connectin, is a large filamentous protein that greatly contributes to passive myocardial stiffness. In vitro evidence suggests that one of titin's spring elements, the PEVK, interacts with actin and that this adds a viscous component to passive stiffness. Differential splicing of titin gives rise to the stiff N2B and more compliant N2BA isoforms. Here we studied the titin-isoform dependence of titin-actin interaction and studied the bovine left atrium (BLA) that expresses mainly N2BA titin, and the bovine left ventricle (BLV) that expresses a mixture of both N2B and N2BA isforms. For comparison we also studied mouse left ventricular (MLV) myocardium which expresses predominately N2B titin. Using the actin-severing protein gelsolin, we obtained evidence that titin-actin interaction contributes significantly to passive myocardial stiffness in all tissue types, but most in MLV, least in BLA, and an intermediate level in BLV. We also studied whether titin-actin interaction is regulated by S100A1/calcium and found that calcium alone or S100A1 alone did not alter passive stiffness, but that combined they significantly lowered stiffness. We propose that titin-actin interaction is a “viscous break” that is on during diastole and off during systole.

scholarly journals 1112 Discovering the origin of a mysterious heart cavity

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
V Vidal Urrutia ◽  
P Garcia Gonzalez ◽  
J L Perez Bosca ◽  
D Escribano Alarcon ◽  
J M Simon Machi ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Left Atrium ◽  
Left Atrial ◽  
Left Atrial Appendage ◽  
Contrast Echocardiography ◽  
Left Ventricular ◽  
Atrial Appendage ◽  
Invasive Approach ◽  
Cardiovascular Morbidity And Mortality ◽  
Doppler Color

Abstract Left atrial appendage aneurysm is an infrequent cardiac malformation, with less than 150 cases reported in the literature. It is a congenital anomaly in the majority of cases, related to a dysplasia of pectinate muscles and atrial muscle bands, which tends to grow with age. At the present time, and despite of being not considered in current guidelines, surgical resection is the standard of treatment in the current literature, even in asymptomatic cases, based on cardiovascular morbidity and mortality by predisposing to atrial tachyarrhythmia, thromboembolism, and other rare conditions as coronary or left ventricular compression and rupture of the aneurysm. We report the case of a 53-year-old male patient presenting an episode of supraventricular paroxysmal tachycardia with the casual finding of a mysterious cavity in the transthoracic echocardiography. We found out the presence of a 50 mm cavity adjacent to the left atrium and left ventricle, with a bidirectional blood flow between the left atrium and the cavity when applying Doppler color and with contrast echocardiography. Given this finding, several differential diagnosis had to be considered, including vascular and structural disorders. In order to clarify the diagnosis, a cardiac magnetic resonance was performed. It revealed the presence of a huge aneurysm of the left atrial appendage (50 x 53 mm) causing a mild compression of the left ventricle, with no thrombus and no other significant findings. Due to its size, the compression of the left ventricle and the history of atrial arrhythmia we decided to manage it with an invasive approach by performing a middle thoracotomy, in order to prevent potentially serious complications. Abstract 1112 Figure. CMR 3D reconstruction; echocardiography

P1501Can we measure the stiffening of hypertensive hearts non-invasively? A shear wave imaging study using ultra-high frame rate echocardiography

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Cvijic ◽  
P Santos ◽  
A M Petrescu ◽  
S Bezy ◽  
M Orlowska ◽  
...  
Keyword(s):  
Left Atrium ◽  
Shear Wave ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Frame Rate ◽  
Volume Index ◽  
Healthy Controls ◽  
Myocardial Stiffness ◽  
High Frame Rate ◽  
Concentric Hypertrophy

Abstract Background Cardiac shear wave (SW) elastography is a novel technique based on high-frame-rate (HFR) echocardiography which has been shown to be related to myocardial stiffness. In this study we explore the relation between myocardial SW velocity and myocardial remodelling in remodelled hearts of patients with arterial hypertension (AH). Methods We prospectively included 33 treated AH patients with hypertrophic left ventricular (LV) remodelling (59±14 years, 55% male) and 26 aged matched healthy controls (55±15 years, 77% male). AH patients were further divided according to their LV geometric pattern into a concentric remodelling (CR) group (13 patients) and a concentric hypertrophy (CH) group (20 patients). LV parasternal long axis views were acquired with an experimental HFR ultrasound scanner (HD-PULSE) at 1266±317 frames per seconds. Myocardial acceleration maps were created from the HFR-datasets and an anatomical M-mode line was drawn along the midline of the interventricular septum (IVS). The propagation velocity of natural SWs occurring at mitral valve closure (MVC) was measured on these M-modes (Figure A) in order to assess passive myocardial stiffness. Standard echocardiography using a commercial scanner was performed to evaluate LV remodelling. Results SW velocities at MVC differed significantly between AH patients and controls (5.83±1.20 m/s vs. 4.04±0.96 m/s; p<0.001). Within the patient group, patients with CH had highest SW velocities at MVC (p<0.001), whereas values between controls and patients with CR were comparable (p=0.075) (Figure B). In AH patients, significant positive correlations were found between SW velocity at MVC and parameters of LV remodelling (IVS thickness: r=0.728, p<0.001; LV mass index: r=0.780, p<0.001, LV end-diastolic volume: r=0.604, p=0.008) (Figure C) and also parameters of diastolic function (E/e': r=0.495, p=0.005, left atrium diameter: r=0.866, p<0.001, left atrium volume index: r=0.661, p<0.001). Figure A, B, C Conclusions SW velocity – and therefore myocardial stiffness – is higher in AH patients compared to healthy controls and increases with increasing severity of hypertensive heart disease. Patients with concentric remodelling have still close-to-normal passive myocardial properties while patients with concentric hypertrophy show significant stiffening. Echocardiographic shear wave elastography is a promising new technique for the non-invasive assessment of myocardial stiffness and might provide valuable new insights into myocardial function and the pathophysiology of myocardial disease.

scholarly journals Discrete effects of A57G-myosin essential light chain mutation associated with familial hypertrophic cardiomyopathy

2013 ◽  
Vol 305 (4) ◽  
pp. H575-H589 ◽  
Author(s):  
Katarzyna Kazmierczak ◽  
Ellena C. Paulino ◽  
Wenrui Huang ◽  
Priya Muthu ◽  
Jingsheng Liang ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Light Chain ◽  
Left Ventricular ◽  
Compensatory Hypertrophy ◽  
Familial Hypertrophic Cardiomyopathy ◽  
Heart Weight ◽  
Myocardial Stiffness ◽  
Essential Light Chain

The functional consequences of the familial hypertrophic cardiomyopathy A57G (alanine-to-glycine) mutation in the myosin ventricular essential light chain (ELC) were assessed in vitro and in vivo using previously generated transgenic (Tg) mice expressing A57G-ELC mutant vs. wild-type (WT) of human cardiac ELC and in recombinant A57G- or WT-protein-exchanged porcine cardiac muscle strips. Compared with the Tg-WT, there was a significant increase in the Ca2+ sensitivity of force (ΔpCa50 ≅ 0.1) and an ∼1.3-fold decrease in maximal force per cross section of muscle observed in the mutant preparations. In addition, a significant increase in passive tension in response to stretch was monitored in Tg-A57G vs. Tg-WT strips indicating a mutation-induced myocardial stiffness. Consistently, the hearts of Tg-A57G mice demonstrated a high level of fibrosis and hypertrophy manifested by increased heart weight-to-body weight ratios and a decreased number of nuclei indicating an increase in the two-dimensional size of Tg-A57G vs. Tg-WT myocytes. Echocardiography examination showed a phenotype of eccentric hypertrophy in Tg-A57G mice, enhanced left ventricular (LV) cavity dimension without changes in LV posterior/anterior wall thickness. Invasive hemodynamics data revealed significantly increased end-systolic elastance, defined by the slope of the pressure-volume relationship, indicating a mutation-induced increase in cardiac contractility. Our results suggest that the A57G allele causes disease by means of a discrete modulation of myofilament function, increased Ca2+ sensitivity, and decreased maximal tension followed by compensatory hypertrophy and enhanced contractility. These and other contributing factors such as increased myocardial stiffness and fibrosis most likely activate cardiomyopathic signaling pathways leading to pathologic cardiac remodeling.

scholarly journals Effects of the absence of procollagen C-endopeptidase enhancer-2 on myocardial collagen accumulation in chronic pressure overload

2012 ◽  
Vol 303 (2) ◽  
pp. H234-H240 ◽  
Author(s):  
Catalin F. Baicu ◽  
Yuhua Zhang ◽  
An O. Van Laer ◽  
Ludivine Renaud ◽  
Michael R. Zile ◽  
...  
Keyword(s):  
Cardiac Fibroblasts ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Bone Morphogenic Protein ◽  
Collagen Content ◽  
Fibrillar Collagen ◽  
Collagen Deposition ◽  
Myocardial Stiffness ◽  
Collagen Accumulation

Cardiac interstitial fibrillar collagen accumulation, such as that associated with chronic pressure overload (PO), has been shown to impair left ventricular diastolic function. Therefore, insight into cellular mechanisms that mediate excessive collagen deposition in the myocardium is pivotal to this important area of research. Collagen is secreted as a soluble procollagen molecule with NH2- and COOH (C)-terminal propeptides. Cleavage of these propeptides is required for collagen incorporation to insoluble collagen fibrils. The C-procollagen proteinase, bone morphogenic protein 1, cleaves the C-propeptide of procollagen. Procollagen C-endopeptidase enhancer (PCOLCE) 2, an enhancer of bone morphogenic protein-1 activity in vitro, is expressed at high levels in the myocardium. However, whether the absence of PCOLCE2 affects collagen content at baseline or after PO induced by transverse aortic constriction (TAC) has never been examined. Accordingly, in vivo procollagen processing and deposition were examined in wild-type (WT) and PCOLCE2-null mice. No significant differences in collagen content or myocardial stiffness were detected in non-TAC (control) PCOLCE2-null versus WT mice. After TAC-induced PO, PCOLCE2-null hearts demonstrated a lesser collagen content (PCOLCE2-null TAC collagen volume fraction, 0.41% ± 0.07 vs. WT TAC, 1.2% ± 0.3) and lower muscle stiffness compared with WT PO hearts [PCOLCE2-null myocardial stiffness (β), 0.041 ± 0.002 vs. WT myocardial stiffness, 0.065 ± 0.001]. In addition, in vitro, PCOLCE2-null cardiac fibroblasts exhibited reductions in efficiency of C-propeptide cleavage, as demonstrated by increases in procollagen α1(I) and decreased levels of processed collagen α1(I) versus WT cardiac fibroblasts. Hence, PCOLCE2 is required for efficient procollagen processing and deposition of fibrillar collagen in the PO myocardium. These results support a critical role for procollagen processing in the regulation of collagen deposition in the heart.

Unusual presentation during childhood of left ventricular myxoma

1998 ◽  
Vol 8 (1) ◽  
pp. 126-127 ◽  
Author(s):  
A. Kapoor ◽  
S. Radhakrishnan ◽  
N. Sinha
Keyword(s):  
Left Ventricle ◽  
Left Atrium ◽  
Febrile Illness ◽  
Left Ventricular ◽  
Unusual Presentation ◽  
Cardiac Tumors ◽  
History Of ◽  
Primary Cardiac Tumors

AbstractAmongst all primary cardiac tumors, myxomas are the commonest, and their commonest site of origin is the left atrium. Myxomas originating in the left ventricle are rare. When seen, they usually present with a history of systemic embolisation and/or syncopal episodes, with constitutional symptoms being absent. We report here a child with left ventricular myxoma who presented with a prolonged febrile illness.

Miscellaneous valvar pathology: Mitral stenosis, pulmonary stenosis, and tricuspid regurgitation

2018 ◽  
Author(s):  
Kazem Rahimi
Keyword(s):  
Mitral Valve ◽  
Left Ventricle ◽  
Left Atrium ◽  
Tricuspid Regurgitation ◽  
Mitral Stenosis ◽  
Left Atrial ◽  
Pulmonary Stenosis ◽  
Left Ventricular ◽  
Cor Triatriatum

Mitral stenosis is obstruction to inflow of blood from left atrium to left ventricle at the level of the mitral valve. Non-valvar causes of left ventricular inflow obstruction include left atrial tumours and cor triatriatum.

scholarly journals P777 Effects of chronic cigarette smoking on left ventricle, left atrium and right ventricle strain parameters with 2D speckle tracking echocardiography

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
B Yaman ◽  
L Cerit ◽  
H Kemal Gunsel ◽  
E Acikgoz ◽  
S Usalp ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Cigarette Smoking ◽  
Left Atrium ◽  
Speckle Tracking ◽  
Speckle Tracking Echocardiography ◽  
Left Ventricular ◽  
Smoking History ◽  
Healthy Participant ◽  
Diastolic Velocity ◽  
2D Speckle Tracking

Abstract Funding Acknowledgements None Background Cigarette smoking effects myocardium with several mechanisms such as sympathetic nervous system activation, oxidative stress and endothelial dysfunction. Chronic smokers have an increased risk of morbidity and mortality associated with adverse cardiac events. Echocardiography is the well-established non-invasive diagnostic tool for the assessment of cardiac systolic and diastolic functions. 2D speckle tracking echocardiography (STE) has been widely used for this purpose in recent years. Purpose The aim of this study is to compare the left ventricle, left atrium and right ventricle systolic functions with 2D speckle tracking echocardiography in chronic smokers and non-smoker healthy population. Method 40 healthy participant (mean age 33.4 ± 10.0) without smoking history, 42 healthy participant (mean age 33.9 ± 9.2) who had smoking history at least 3 years without history of cardiac disease or any other chronic diseases such as hypertension, diabetes mellitus, kidney failure were prospectively included. In addition to Standard 2D echocardiographic measurements, left ventricular global longitidunal strain (LvGLS), right ventricular global longitidunal strain (RvGLS), left atrial strain and strain rate were analyzed with Vivid E9, offline using a customized software package. Results Smokers had lower peak early diastolic velocity (E) and E/A (late diastolic velocity) ratio in mitral inflow (0.70 ± 0.13 vs 0.77 ± 0.13, p = 0.023; 1.47 ± 0.44 vs 1.73 ± 0.44, p = 0.011; respectively). Peak early diastolic velocity of mitral valve medial annulus and E’/A’ ratio (0.11 ± 0.02 vs 0.12 ± 0.02, p = 0.023; 1.20 ± 0.37 vs 1.40 ± 0.46, p = 0.039; respectively) was lower in smokers. LvGLS and RvGLS were significantly impaired in smokers (-17.65 ± 3.01 vs -19.21 ± 2.52, p = 0.013; -18.96 ± 4.47 vs -21.06 ± 4.58, p = 0.039; respectively). Although εs, reservoir phase strain of left atrium; εe, conduit phase strain of left atrium; εa, contractile phase strain of left atrium were similar between two groups, εe/εa was significantly lower in smokers than non-smokers (1.32 ± 0.59, 1.63 ± 0.63, p = 0.026). Conclusion Impaired RV deformation was found in chronic cigarette smokers. Besides standardized diastolic dysfunction parameters εe/εa might be used for the early indicator of diastolic dysfunction. Although there was no statistically significant difference with left ventricular ejection fraction between smokers and non-smokers, LvGLS which is the early indicator of LV systolic dysfunction in chronic smokers might be used for the early assesment of LV systolic impairment. Abstract P777 figure 1

Impact of exercise training on ventricular properties in a canine model of congestive heart failure

1997 ◽  
Vol 272 (3) ◽  
pp. H1382-H1390 ◽  
Author(s):  
K. Todaka ◽  
J. Wang ◽  
G. H. Yi ◽  
M. Knecht ◽  
R. Stennett ◽  
...  
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Heart Function ◽  
Systolic Pressure ◽  
Cardiac Pacing ◽  
Left Ventricular ◽  
Lv Function ◽  
Myocardial Stiffness

Exercise training improves functional class in patients with chronic heart failure (CHF) via effects on the periphery with no previously documented effect on intrinsic left ventricular (LV) properties. However, because methods used to evaluate in vivo LV function are limited, it is possible that some effects of exercise training on the failing heart have thus far eluded detection. Twelve dogs were instrumented for cardiac pacing and hemodynamic recordings. Hearts were paced rapidly for 4 wk. Six of the dogs received daily treadmill exercise (CHF(EX), 4.4 km/h, 2 h/day) concurrent with rapid pacing, while the other dogs remained sedentary (CHFs). Hemodynamic measurements taken in vivo at the end of 4 wk revealed relative preservation of maximum rate of pressure rise (2,540 +/- 440 vs. 1,720 +/- 300 mmHg/s, P < 0.05) and LV end-diastolic pressure (9 +/- 5 vs. 19 +/- 4 mmHg, P < 0.05) in CHF(EX) compared with CHFs. The hearts were then isolated and cross perfused for in vitro measurement of isovolumic pressure-volume relations; these results were compared with those of six normal dogs (N). Systolic function was similarly depressed in both groups of pacing animals [end-systolic elastance (Ees) values of 1.66 +/- 0.47 in CHFs, 1.77 +/- 0.38 in CHF(EX), and 3.05 +/- 0.81 mmHg/ml in N, with no changes in volume axis interceptors of the end-systolic pressure-volume relationship]. The diastolic myocardial stiffness constant, k, was elevated in CHFs and was normalized by exercise training (32 +/- 3 in CHFs, 21 +/- 3 in CHF(EX), 20 +/- 4 in N). Thus daily exercise training preserved in vivo hemodynamics during 4 wk of rapid cardiac pacing and was accompanied by a significant change in diastolic myocardial stiffness in vitro. These findings suggest that changes in heart function may contribute to the overall beneficial hemodynamic effects of exercise training in CHF by a significant effect on diastolic properties.

scholarly journals P695 Is reference value of left atrial strain using 2D echocardiography really reliable?

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
M Takeuchi ◽  
K Negishi ◽  
Y Nabeshima ◽  
K Otani ◽  
Y Otsuji
Keyword(s):  
Left Ventricle ◽  
Left Atrium ◽  
Healthy Subjects ◽  
Left Atrial ◽  
Speckle Tracking ◽  
Paired Comparison ◽  
Reference Value ◽  
Left Ventricular ◽  
2D Echocardiography ◽  
Longitudinal Length

Abstract Funding Acknowledgements MT received research grant from GE Healthcare. Background Left atrial (LA) longitudinal strain (LALS) assessed by two-dimensional echocardiography (2DE) speckle tracking analysis is increasingly popular for the estimation of left ventricular diastolic dysfunction and the prediction of adverse outcome. Since standard apical 4-chamber and 2-chamber views often maximize the long-axis of the left ventricle, and the long axis of the left ventricle and that of the left atrium do not lie on the same 2D cutting plane, these views have a risk for the foreshortening of the left atrium. It may cause overestimation of LALS due to the reduction of initial perimeter of region of interest that is a denominator for the strain calculation. Purpose The aim of this study was to compare LALS values between 2DE and 3D echocardiography (3DE) in healthy subjects, and investigate whether 2DE speckle tracking analysis overestimates reference value of LALS. Methods LALS and LA longitudinal length were measured by both 2DE and 3DE in 105 healthy subjects (median age, 42 years; 59 men). For 2DE, LA longitudinal length from the mitral annulus to the roof of the left atrium were measured on apical 4-chamber and 2-chamber views at end-diastole and at end-systole, and the values were averaged. Apical 4-chamber and 2-chamber LALS was also measured using 2DE speckle tracking software (EchoPac PC, GE Healthcare) for calculating biplane LALS. 3DE LALS was measured using new 3DE LA strain software (4D Auto LAQ, GE Healthcare). 3DE determined LA longitudinal length at both end-diastole and end-systole was also measured using the same 3DE datasets. Results Mean values of biplane LALS was 39.6 ± 11.8%. 2DE LA longitudinal length at both end-diastole (r=-0.43) and end-systole (r=-0.54) was negatively correlated with biplane LALS. Multivariable regression analysis revealed that both end-diastolic and end-systolic LA longitudinal length had a significant negative association for biplane LALS after adjusting anthropometric and echocardiography image quality parameters. 3DE LALS analysis was not possible in 11 subjects due to the erroneous LA border determination (Feasibility: 90%). 3DE LALS (23.7 ± 7.6%) was significantly lower than biplane LALS (39.5 ± 12.0%, p &lt; 0.001) with a weak correlation (r = 0.33) in 94 subjects who were possible in both analyses. Paired comparison of LA longitudinal length between 2DE and 3DE revealed that 2DE determined LA length at end-diastole (3.51 ± 0.72 cm vs. 4.85 ± 0.56 cm, p &lt; 0.001) and at end-systole (4.63 ± 0.69 cm vs. 5.84 ± 0.54 cm, p &lt; 0.001) was significantly shorter than that obtained from 3DE. Conclusions Our results highlighted that LA cavity visualizing on the standard apical 4-chamber and 2-chamber views are often longitudinally foreshortened, and this is a potential cause for the overestimation of LALS. 3DE may overcome this limitation.

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