scholarly journals Clinical Assessment of Ventricular Wall Stress in Understanding Compensatory Hypertrophic Response and Maladaptive Ventricular Remodeling

2021 ◽  
Vol 8 (10) ◽  
pp. 122
Author(s):  
Takeshi Tsuda
Keyword(s):  
Ventricular Remodeling ◽  
Clinical Medicine ◽  
Oxygen Demand ◽  
Left Ventricular Pressure ◽  
Wall Stress ◽  
Left Ventricular ◽  
Feedback Signal ◽  
Myocardial Oxygen Demand ◽  
Ventricular Wall ◽  
Critical Determinant

Ventricular wall stress (WS) is an important hemodynamic parameter to represent myocardial oxygen demand and ventricular workload. The normalization of WS is regarded as a physiological feedback signal that regulates the rate and extent of ventricular hypertrophy to maintain myocardial homeostasis. Although hypertrophy is an adaptive response to increased biomechanical stress, persistent hypertrophic stimulation forces the stressed myocardium into a progressive maladaptive process called ventricular remodeling, consisting of ventricular dilatation and dysfunction in conjunction with the development of myocyte hypertrophy, apoptosis, and fibrosis. The critical determinant of this pathological transition is not fully understood, but an energetic mismatch due to uncontrolled WS is thought to be a central mechanism. Despite extensive basic investigations conducted to understand the complex signaling pathways involved in this maladaptive process, clinical diagnostic studies that translate these molecular and cellular changes are relatively limited. Echocardiographic assessment with or without direct measurement of left ventricular pressure used to be a mainstay in estimating ventricular WS in clinical medicine, but in recent years more and more noninvasive applications with magnetic resonance imaging have been studied. In this review article, basic clinical applications of WS assessment are discussed to help understand the progression of ventricular remodeling.

Sex differences in noninvasive estimates of left ventricular pressure energetics but not myocardial oxygen demand in young adults

2014 ◽  
Vol 8 (4) ◽  
pp. 197 ◽  
Author(s):  
William E. Hughes ◽  
Nicole L. Spartano ◽  
Wesley K. Lefferts ◽  
Jaqueline A. Augustine ◽  
Kevin S. Heffernan
Keyword(s):  
Young Adults ◽  
Sex Differences ◽  
Oxygen Demand ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Myocardial Oxygen Demand

Amelioration of effects of hypertension and diabetes on myocardium by cardiac glycoside

1992 ◽  
Vol 262 (3) ◽  
pp. H734-H742
Author(s):  
J. M. Capasso ◽  
E. Puntillo ◽  
B. Halpryn ◽  
G. Olivetti ◽  
P. Li ◽  
...  
Keyword(s):  
Ventricular Remodeling ◽  
Diastolic Pressure ◽  
Renal Hypertension ◽  
Time Derivative ◽  
Left Ventricular Pressure ◽  
Wall Stress ◽  
Capillary Density ◽  
Left Ventricular ◽  
Numerical Density ◽  
Arterial Blood

To determine whether digoxin protects the myocardium during the initial phases of hypertension and diabetes combined, adult male Wistar rats with two-kidney, one-clip renal hypertension and streptozotocin-induced diabetes mellitus were treated with digoxin (500 micrograms.kg-1.day-1) by gavage for 10 wk immediately after the onset of hypertension and diabetes. Systemic arterial blood pressures, ventricular pressures, the first time derivative of left ventricular pressure, diastolic wall stress, and the quantitative analysis of the number and distribution of myocardial lesions and capillary density of the myocardium were measured. In comparison to untreated hypertensive-diabetic animals, digoxin-treated rats showed a lesser elevation in left ventricular end-diastolic pressure and diastolic and systolic wall stress despite comparable degrees of hypertension and blood glucose levels. In addition, chamber diameter was smaller and the diffusion distance for oxygen was within normal values in animals treated with this glycoside. However, the numerical density of the foci of replacement fibrosis was similar to that found in untreated hypertensive-diabetic animals. In conclusion, digoxin reduces the magnitude of ventricular remodeling and diastolic wall stress in this model of hypertension and diabetes.

scholarly journals Higher left ventricular mass–wall stress–heart rate product and outcome in aortic valve stenosis

Heart ◽  
2019 ◽  
Vol 105 (21) ◽  
pp. 1629-1633 ◽  
Author(s):  
Eva Gerdts ◽  
Sahrai Saeed ◽  
Helga Midtbø ◽  
Anne Rossebø ◽  
John Boyd Chambers ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cox Regression ◽  
Oxygen Demand ◽  
Wall Stress ◽  
Left Ventricular ◽  
Adverse Event Rate ◽  
Myocardial Oxygen Demand ◽  
Lv Mass ◽  
All Cause Mortality

ObjectiveWhether increased myocardial oxygen demand could help explain the association of left ventricular (LV) hypertrophy with higher adverse event rate in patients with aortic valve stenosis (AS) is unknown.MethodsData from 1522 patients with asymptomatic mostly moderate AS participating in the Simvastatin-Ezetimibe in AS study followed for a median of 4.3 years was used. High LV mass–wall stress–heart rate product was identified as >upper 95% CI limit in normal subjects. The association of higher LV mass–wall stress–heart rate product with major cardiovascular (CV) events, combined CV death and hospitalised heart failure and all-cause mortality was tested in Cox regression analyses, and reported as HR and 95% CI.ResultsHigh LV mass–wall stress–heart rate product was found in 19% at baseline, and associated with male sex, higher body mass index, hypertension, LV hypertrophy, more severe AS and lower LV ejection fraction (all p<0.01). Adjusting for these confounders in time-varying Cox regression analysis, 1 SD higher LV mass–wall stress–heart rate product was associated with higher HR of major CV events (HR 1.16(95% CI 1.06 to 1.29)), combined CV death and hospitalised heart failure (HR 1.29(95% CI 1.09 to 1.54)) and all-cause mortality (HR 1.34(95% CI 1.13 to 1.58), all p<0.01).ConclusionIn patients with initially mild–moderate AS, higher LV mass–wall stress–heart rate product was associated with higher mortality and heart failure hospitalisation. Our results suggest that higher myocardial oxygen demand is contributing to the higher adverse event rate reported in AS patients with LV hypertrophy.Trial registration numberNCT000092677;Post-results.

Cardiac mechanics

2020 ◽  
pp. 53-72
Author(s):  
Stephen Huang
Keyword(s):  
Left Ventricular Pressure ◽  
Wall Stress ◽  
Cardiac Mechanics ◽  
Left Ventricular ◽  
Physical Factors ◽  
Ventricular Wall ◽  
Ventricular Contractility ◽  
Intrinsic Properties ◽  
Extrinsic Factors ◽  
Cardiac Pump Function

Cardiac mechanics involves the study of the mechanical properties of the heart (ventricles) as a pump, and the physical factors that alter these properties. Neurohumoral factors aside, the function of the heart is determined by its intrinsic physical properties as well as extrinsic physical factors. The intrinsic properties include ventricular wall stress, elastance (stiffness) of the ventricle, contractility, and heart rate. The main extrinsic physical factors are blood volume, vessels properties, and extracardiac pressures. This chapter will review these intrinsic properties and how they interact with extrinsic factors to alter the cardiac (pump) function. Neurohumoral factors are excluded in this consideration. LaPlace’s law will be introduced to explain the idea of ventricular wall stress, hence the concepts of preload and afterload. The left ventricular pressure–volume relationship will be reviewed to explain how preload, afterload, and ventricular contractility interact and affect stroke volume. Finally, for completeness, the Frank–Starling relationship and Guyton’s venous return graph will be covered to explain steady state cardiac output.

scholarly journals P1514 Increased myocardial oxygen demand is associated with impaired left ventricular strain in patients with morbid obesity referred for bariatric surgery

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
L M Grymyr ◽  
S Nadirpour ◽  
E Gerdts ◽  
B G Nedreboe ◽  
J J Hjertaas ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Pulse Pressure ◽  
Systolic Function ◽  
Oxygen Demand ◽  
Wall Stress ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Lv Mass ◽  
Obese Subjects ◽  
Lv Systolic Function

Abstract Background Obesity predisposes for left ventricular (LV) hypertrophy and systolic dysfunction. Higher myocardial oxygen demand in LV hypertrophy is associated with higher risk for cardiovascular events, while the association with LV systolic function has been less explored. Purpose To assess the association of myocardial oxygen demand with LV systolic function in morbidly obese subjects without known heart disease. Methods Clinical and echocardiographic data from 110 obese subjects referred for gastric bypass surgery (mean age 42 ± 11 years, 74% women, mean body mass index [BMI] 41.9 ± 4.8 kg/m², 33% with hypertension, 15% with diabetes) in the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study was used. LV function was assessed by ejection fraction (EF) by Simpson"s biplane method and endocardial global longitudinal strain (GLS) by 2D vector velocity imaging using a 16-segment model (Image Arena 4.6, Tomtec, Unterschleissheim, Germany). Myocardial oxygen demand was estimated from LV mass - wall stress - heart rate product according to a previously validated formula. Results Myocardial oxygen demand was higher in men (1884 vs. 1579 x 10³ g x kdyne/cm² x bpm, p &lt; 0.05), and associated with higher BMI (r = 0.24) and pulse pressure (r = 0.28), and with lower EF (r = -0.22) and lower GLS (r = 0.26, all p &lt; 0.05). In multiple regression analysis, higher myocardial oxygen demand was associated with lower LV GLS (Beta = 0.21, p &lt; 0.05) independent of age, gender, BMI, pulse pressure, diabetes, and EF (Table). Conclusion In obese patients without known heart disease referred for bariatric surgery, higher myocardial oxygen demand was associated with lower LV systolic function measured by GLS independent of confounders. Covariates of lower GLS in multivariable Variable β correlation coefficient p LV mass - wall stress - heart rate product (g x kdyne/cm&sup2; x bpm x 10&sup3;) 0.21 0.04 Age (years) -0.12 0.22 Gender 0.34 &lt;0.01 BMI (kg/m&sup2;) 0.25 &lt;0.01 Pulse pressure (mmHg) -0.04 0.71 Diabetes -0.17 0.09 LV EF (%) -0.01 0.90

scholarly journals Left Ventricular Wall Stress Calculated from One-Plane Cineangiography

1970 ◽  
Vol 26 (1) ◽  
pp. 71-83 ◽  
Author(s):  
HERMAN L. FALSETTI ◽  
ROBERT E. MATES ◽  
COLIN GRANT ◽  
DAVID G. GREENE ◽  
IVAN L. BUNNELL
Keyword(s):  
Wall Stress ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall

scholarly journals Mechanically Unloading the Left Ventricle Before Coronary Reperfusion Reduces Left Ventricular Wall Stress and Myocardial Infarct Size

Circulation ◽  
2013 ◽  
Vol 128 (4) ◽  
pp. 328-336 ◽  
Author(s):  
Navin K. Kapur ◽  
Vikram Paruchuri ◽  
Jose Angel Urbano-Morales ◽  
Emily E. Mackey ◽  
Gerard H. Daly ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Wall Stress ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Myocardial Infarct Size ◽  
Ventricular Wall ◽  
Coronary Reperfusion

scholarly journals Levosimendan treatment of severe acute congestive heart failure refractory to dobutamine/milrinone in children

2011 ◽  
Vol 68 (11) ◽  
pp. 979-984
Author(s):  
Sergej Prijic ◽  
Sanja Rakic ◽  
Ljubica Nikolic ◽  
Bosiljka Jovicic ◽  
Mila Stajevic ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Myocardial Contractility ◽  
Severe Heart Failure ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Univentricular Heart ◽  
Dilatative Cardiomyopathy ◽  
Hemodynamic Improvement

Introduction. Levosimendan is a novel positive inotropic agent which, improves myocardial contractility through its calcium-sensitizing action, without causing an increase in myocardial oxygen demand. Also, by opening ATP-sensitive potassium channels, it causes vasodilatation with the reduction in both afterload and preload. Because of the long halflife, its effects last for up 7 to 9 days after 24-hour infusion. Case report. We presented three patients 2, 15 and 17 years old. All the patients had severe acute deterioration of the previously diagnosed chronic heart failure (dilatative cardiomyopathy; univentricular heart with bidirectional Glenn anastomosis and restrictive bulboventricular foramen; bacterial endocarditis on artificial aortic valve with severe stenosis and regurgitation). Signs and symptoms of severe heart failure, cardiomegaly (cardio-thoracic index 0.65) and left ventricular dilatation (end-diastolic diameter z-score 2.6; 4.1 and 4.0) were confirmed on admission. Also, myocardial contractility was poor with ejection fraction (EF - 27%, 25%, 35%), fractional shortening (FS - 13%, 11%, 15%) and stroke volume (SV - 40, 60, 72 mL/m2). The treatment with standard intravenous inotropic agents resulted in no improvement but in clinical deterioration. Thus, standard intravenous inotropic support was stopped and levosimendan treatment was introduced. All the patients received a continuous 24-h infusion 0.1 ?g/kg/min of levosimendan. In a single patient an initial loading dose of 11 ?g/kg over 10 min was administrated, too. Levosimendan treatment resulted in both clinical and echocardiography improvement with the improved EF (42%, 34%, 44%), FS (21%, 16%, 22%) and SV (59, 82, 93 mL/m2). Hemodynamic improvement was registered too, with the reduction in heart rate in all the treated patients from 134-138 bpm before, to less than 120 bpm after the treatment. These parameters were followed by the normalization of lactate levels. Nevertheless, left ventricular end-diastolic diameter did not change after the levosimendan treatment. Conclusion. Our initial experience demonstrates that administration of levosimendan in patients with severe chronic heart failure not responsive to standard intravenous inotropic treatment might result in a significant clinical and hemodynamic improvement and that, in selected patients, it might be life saving. According to our best knowledge patients presented are the first pediatric patients treated with levosimendan in our country.

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