Evaluation of Myocardial Stiffness in Hypertensive Patients by Intrinsic Wave Propagation of the Myocardial Stretch

2020 ◽  
Vol 46 (10) ◽  
pp. 2683-2691
Author(s):  
Jun Zhang ◽  
Youbin Deng ◽  
Qiaoying Tang ◽  
Jie Sun ◽  
Lingying Huang ◽  
...  
Keyword(s):  
Wave Propagation ◽  
Hypertensive Patients ◽  
Myocardial Stiffness ◽  
Myocardial Stretch

Intrinsic Wave Propagation of Myocardial Stretch, A New Tool to Evaluate Myocardial Stiffness: A Pilot Study in Patients with Aortic Stenosis and Mitral Regurgitation

2017 ◽  
Vol 30 (11) ◽  
pp. 1070-1080 ◽  
Author(s):  
Cristina Pislaru ◽  
Mahmoud M. Alashry ◽  
Jeremy J. Thaden ◽  
Patricia A. Pellikka ◽  
Maurice Enriquez-Sarano ◽  
...  
Keyword(s):  
Wave Propagation ◽  
Pilot Study ◽  
Mitral Regurgitation ◽  
Aortic Stenosis ◽  
Myocardial Stiffness ◽  
Myocardial Stretch

scholarly journals Wave propagation of myocardial stretch: correlation with myocardial stiffness

2014 ◽  
Vol 109 (6) ◽  
Author(s):  
Cristina Pislaru ◽  
Patricia A. Pellikka ◽  
Sorin V. Pislaru
Keyword(s):  
Wave Propagation ◽  
Myocardial Stiffness ◽  
Myocardial Stretch

Abstract 210: Titin Phosphorylation by Protein Kinase G as a Novel Mechanism of Diastolic Adaptation to Acute Hemodynamic Overload

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
João Almeida-Coelho ◽  
André M Leite-Moreira ◽  
João S Neves ◽  
Manuel Neiva-Sousa ◽  
Ricardo Castro-Ferreira ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Statistical Significance ◽  
Protein Kinase G ◽  
Control Group ◽  
Passive Tension ◽  
Papillary Muscles ◽  
Progressive Decrease ◽  
Myocardial Stiffness ◽  
Myocardial Stretch ◽  
Hemodynamic Overload

Titin is the main determinant of myocardial passive tension and its distensibility is increased via phosphorylation by protein kinase G (PKG), activated by nitric oxide (NO) and natriuretic peptides (NP) upon acute overload. We hypothesized whether myocardial stretch led to decreased stiffness, optimizing diastolic filling along with the usual increase in contractility. Intact rat Langendorff hearts, strips dissected from the LV or right atrium of cardiac surgery patients and rabbit papillary muscles were acutely stretched for 15min. Passive tension (PT) was measured in skinned cardiomyocytes extracted from the LV of control and stretched rat hearts for sarcomere lengths (SL) 1.8-2.3μm before and after incubation with PKG. Rabbit muscles were incubated with a PKG inhibitor or, simultaneously, a NO synthase inhibitor, a NO scavenger, a NP receptor A antagonist. All-total titin phosphorylation was stained with Pro-Q Diamond and indexed to total-protein signals using SYPRO Ruby. Values are given as mean±SEM and statistical significance was set to p<0.05. After acute stretch there was a progressive decrease in passive tension/diastolic pressure over 15min: 27±8% and 27±6% in human atrium and ventricular muscles, respectively, and 43±2% in rabbit papillary muscles and isolated hearts. This decrease in myocardial stiffness was significantly blunted by PKG inhibition (40%) and NO/NP pathway inhibition (29%). PT of cardiomyocytes was significantly lower (≈60%) in the previously stretched group for all SL. A similar effect, only significant in the control group, was observed after incubation with PKG. Titin phosphorylation increased markedly 15 minutes after acute myocardial stretch in human (atrial: 11±1% vs 41±8%; LV: 27±8% vs 71±21%) and rabbit (13±2% vs 23±3%) myocardium. The progressive decrease in myocardial stiffness after acute hemodynamic overload is preserved at the myofilamental level and seems to depend on PKG activity, representing a potential therapeutic target in patients with pathologically rigid myocardium. Moreover, blocking PKG activation seems to attenuate this adaptive diastolic response. Therefore, titin phosphorylation by this kinase is probably involved in this new myocardial response to stretch in both animals and humans.

MYOCARDIAL STIFFNESS IN THE MIDDLE-AGED HYPERTENSIVE PATIENTS IN THE PRESENCE OF OVERWEIGHT OR OBESITY

2018 ◽  
Vol 36 (Supplement 1) ◽  
pp. e189
Author(s):  
O. Ostroumova ◽  
A. Kochetkov
Keyword(s):  
Middle Aged ◽  
Hypertensive Patients ◽  
Myocardial Stiffness ◽  
Overweight Or Obesity

[PP.14.16] MYOCARDIAL STIFFNESS IN THE MIDDLE-AGE HYPERTENSIVE PATIENTS

2017 ◽  
Vol 35 ◽  
pp. e202
Author(s):  
O. Ostroumova ◽  
A. Kochetkov ◽  
V. Vikentiev ◽  
M. Lopukhina
Keyword(s):  
Middle Age ◽  
Hypertensive Patients ◽  
Myocardial Stiffness

MYOCARDIAL STIFFNESS AND LEFT VENTRICULAR HYPERTROPHY IN THE MIDDLE-AGED HYPERTENSIVE PATIENTS

2018 ◽  
Vol 36 (Supplement 1) ◽  
pp. e59
Author(s):  
O. Ostroumova ◽  
A. Kochetkov ◽  
M. Lopukhina ◽  
G. Piksina ◽  
V. Vikentiev
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Middle Aged ◽  
Hypertensive Patients ◽  
Myocardial Stiffness

Abstract 17078: Myocardial Stiffness by Intrinsic Wave Propagation Method: Comparison With End-Diastolic Pressure-Volume Relationship

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Orawan Anupraiwan ◽  
Filip Ionescu ◽  
Ioana Petrescu ◽  
Patricia A Pellikka ◽  
Martha Grogan ◽  
...  
Keyword(s):  
Wave Propagation ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Frame Rate ◽  
Doppler Imaging ◽  
Wave Method ◽  
Myocardial Stiffness ◽  
Volume Relationship ◽  
Pressure Volume Relationship

Introduction: Intrinsic wave propagation is a novel approach to measure myocardial stiffness (MS) as validated in animal studies. Aims and Hypothesis: 1) To compare MS measured by the wave method with chamber stiffness (CS) derived from noninvasively estimated end-diastolic pressure-volume relationship (EDPVR) in patients; 2) To test the hypothesis that MS is superior to CS for predicting outcomes in patients with cardiac amyloidosis (CA). Methods: Prospective study in 56 patients with amyloidosis (CA: 38, noncardiac amyloidosis, NCA: 18; 90% AL-type; age 63 ± 10 yrs; ejection fraction 57 ± 11%) and 36 normal subjects (age 49 ± 13 years). Intrinsic velocity propagation of myocardial stretch (iVP), a measure of MS, was measured by ultra-high frame rate (250-465Hz) tissue Doppler imaging. Left ventricular (LV) EDPVR were reconstructed using the noninvasive single-beat method (Fig.A). Stiffness coefficients (α, β, load-independent) and CS (dP/dV) were calculated. End-diastolic pressure (EDP) was estimated from E/e’. Adverse events at follow-up (death, heart failure, stroke, significant arrhythmia) were recorded. Results: iVP was higher in CA compared to NCA and controls, indicating higher MS (Fig. B). This was confirmed by EDPVR, which were steeper and shifted leftward (Fig. A). The slope (β) of EDPVR and CS (dP/dV) were higher and LV capacitance (V 30 , volume at 30 mmHg) was lower in CA (Fig. A) and correlated with iVP (β: r = 0.59; CS dP/dV, r = 0.43; EDP, r = 0.61; all p<0.0001). Patients with higher LV thickness (r = 0.66), lower LV longitudinal strain (r = -0.57) and elevated NT-proBNP (r = 0.69) had higher iVP. At follow-up (median 2.5 years), after adjusting for relevant confounders, an iVP >2.7 m/s was strongly associated with excess events (p<0.0001; Fig. C) and was superior to measures of CS (dP/dV: p = 0.28; β >6.5: p = 0.03; Fig. D). Conclusions: Myocardial stiffness by intrinsic wave method shows similar findings to chamber stiffness by EDVPR, but is more strongly related to outcomes in patients with amyloidosis.

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