scholarly journals Pressure and Volume Characteristics of the Left Ventriclе in Its Diastolic and Systolic Dysfunction

Kardiologiia ◽  
2019 ◽  
Vol 59 (4) ◽  
pp. 45-51
Author(s):  
A. A. Abramov ◽  
V. L. Lakomkin ◽  
A. V. Prosvirnin ◽  
V. I. Kapelko

The Aimof the study was a detailed investigation of pressure volume-loop (PV-loop) curves in the rat heart during development of doxorubicin cardiomyopathy.Materials and methods. Cardiomyopathy in rats has been developed after 4 weeks doxorubicin administration (2 mg / kg weekly).Results. Echocardiographic study of rats in 8 weeks from onset of doxorubicin administration showed preponderance of systolic dysfunction (67 %) with decrease of left ventricular (LV) ejection fraction (EF) by 30 %. Simultaneous registration of LV pressure and volume showed that diastolic LV volume was preserved in doxorubicin-treated rats due to considerable lengthening of the diastole, the heart rate was reduced by 22 %. These hearts also showed slowing of relaxation, reduced maximal rate of pressure development and stroke work, as well as significant reduction in peripheral arterial resistance. Diastolic dysfunction differed from the systolic one by normal systolic EF and preserved LV contractility index as well as lower diastolic LV pressure throughout the diastole.Conclusions. Based on these data, four compensatory mechanisms associated with cardiomyopathy were distinguished - 1) slowing of myocardial relaxation, prolonging myofibrillar active state, 2) reduction of peripheral arterial resistance for easier LV ejection, 3) heart rate reduction, prolonging diastolic pause and thus facilitating better LV filling and 4) increased pressure in the small circle, also contributing to the LV rapid filling.

Author(s):  
Alexandre Mebazaa ◽  
Mervyn Singer

Organ congestion upstream of the dysfunctional left and/or right ventricle, with preserved stroke volume, is the most frequkeywordent feature of myocardial failure.Clinical manifestations do not necessarily correlate with the degree of left ventricular systolic dysfunction (i.e. left ventricular ejection fraction).Systolic and/or diastolic dysfunction may be present, with systolic dysfunction usually predominating.Pulmonary oedema is related to left ventricular diastolic dysfunction. Compensatory mechanisms (within the heart and/or periphery) may prove paradoxically disadvantageous on ventricular stroke work and stroke volume.


2011 ◽  
pp. 7-17
Author(s):  
Hai Thuy Nguyen ◽  
Anh Vu Nguyen

Thyroid hormone increases the force of the contraction and the amount of the heart muscle oxygen demand. It also increases the heart rate. Due to these reasons, the work of the heart is greatly increased in hyperthyroidism. Hyperthyroidism increases the amount of nitric oxide in the intima, lead them to be dilated and become less stiff. Cardiac symptoms can be seen in anybody with hyperthyroidism, but can be particularly dangerous in whom have underlying heart diseases. Common symptoms include: tachycardia and palpitations. Occult hyperthyroidism is a common cause of an increased heart rate at rest and with mild exertion. Hyperthyroidism can also produce a host of other arrhythmias such as PVCs, ventricular tachycardia and especially atrial fibrillation. Left ventricular diastolic dysfunction and systolic dysfunction, Mitral regurgitation and mitral valve prolapsed are heart complications of hyperthyroism could be detected by echocardiography. The forceful cardiac contraction increases the systolic blood pressure despite the increased relaxation in the blood vessels reduces the diastolic blood pressure. Atrial fibrillation, atrial enlargement and congestive heart failure are important cardiac complications of hyperthyroidism. An increased risks of stroke is common in patients with atrial fibrillation. Graves disease is linked to autoimmune complications, such as cardiac valve involvement, pulmonary arterial hypertension and specific cardiomyopathy. Worsening angina: Patients with coronary artery disease often experience a marked worsening in symptoms with hyperthyroidism. These can include an increase in chest pain (angina) or even a heart attack.


1998 ◽  
Vol 274 (3) ◽  
pp. H937-H944 ◽  
Author(s):  
M. Miyamoto ◽  
D. E. McClure ◽  
E. R. Schertel ◽  
P. J. Andrews ◽  
G. A. Jones ◽  
...  

In previous studies, we observed left ventricular (LV) systolic and diastolic dysfunction in association with interstitial myocardial edema (IME) induced by either coronary venous hypertension (CVH) or lymphatic obstruction. In the present study, we examined the effects of myocardial edema induced by acute hypoproteinemia (HP) on LV systolic and diastolic function. We also combined the methods of HP and CVH (HP-CVH) to determine their combined effects on LV function and myocardial water content (MWC). We used a cell-saving device to lower plasma protein concentration in HP and HP-CVH groups. CVH was induced by inflating the balloon in the coronary sinus. Six control dogs were treated to sham HP. Conductance and micromanometer catheters were used to assess LV function. Contractility, as measured by preload recruitable stroke work, did not change in control or HP groups but declined significantly (14.5%) in the HP-CVH group. The time constant of isovolumic LV pressure decline (τ) increased significantly from baseline by 3 h in the HP (24.8%) and HP-CVH (27.1%) groups. The end-diastolic pressure-volume relationship (stiffness) also increased significantly from baseline by 3 h in the HP (78.6%) and HP-CVH (42.6%) groups. Total plasma protein concentration decreased from 5.2 ± 0.2 g/dl at baseline to 2.5 ± 0.0 g/dl by 3 h in the HP and HP-CVH groups. MWC of the HP (79.8 ± 0.25%) and HP-CVH groups (79.8 ±0.2%) were significantly greater than that of the control group (77.8 ± 0.3%) but not different from one another. In conclusion, hypoproteinemia-induced myocardial edema was associated with diastolic LV dysfunction but not systolic dysfunction. The edema caused by hypoproteinemia was more than twice that produced by our previous models, yet it was not associated with systolic dysfunction. CVH had a negative inotropic effect and no significant influence on MWC. IME may not have the inverse causal relationship with LV contractility that has been previously postulated but appears to have a direct causal association with diastolic stiffness as has been previously demonstrated.


Author(s):  
N. P. Mitkovskaya ◽  
E. M. Balysh ◽  
T. V. Statkevich ◽  
N. A. Ladygina ◽  
E. B. Petrova ◽  
...  

The aim of the study was to investigate the features of clinically suspected myocarditis complicated by the left ventricular systolic dysfunction development. 93 patients with clinically suspected myocarditis were examined. The average age was 36.63 ± 1.15 years. In 43.01 % of patients the disease was accompanied by a decrease in left ventricular systolic function. In the group of patients with left ventricular systolic dysfunction in comparison with those with preserved left ventricular ejection fraction, a significantly lower proportion of men (75 % versus 81 %, respectively, χ2 = 9.3, p < 0,01) and a higher average group age (40.7 ± 1.87 versus 33.6 ± 1.3 years, respectively, p <  0,01) were revealed. The course of the disease in patients with left ventricular systolic dysfunction was characterized by a more frequent development of rhythm disturbances (65 % versus 43.3 %, respectively, χ2  = 4.3, p  < 0,05) and a higher heart rate at admission (94.5 (75‒100) and 85 (70‒89) beats per minute, respectively, p = 0.006). The structural and functional state of the heart according to echocardiography in patients with a reduced left ventricular ejection fraction versus comparison group was characterized by larger heart chambers sizes, more pronounced violations of local left ventricular contractility, more frequent involvement of the right ventricle in the pathological process (56.3  % versus 22.2  %, respectively, χ2   =  6.4, p  < 0,05). The relationships between the left ventricular ejection fraction Весці Нацыянальнай акадэміі навук Беларусі. Серыя медыцынскіх навук. 2020. Т. 17, № 4. C. 452–460 453 and the patient’s age (r = ‒0.36), the value of the heart rate at admission (r = ‒0.32), the severity of heart failure at admission, the degree of impaired local contractility of the left ventricle, the degree of right ventricular function (TAPSE, r  =  0.58), the severity of myocardial fibrosis according to cardiovascular magnetic resonance imaging (r = ‒0.32) were revealed.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M A Losi ◽  
C Mancusi ◽  
E Gerdts ◽  
K Wachtell ◽  
S E Kjeldsen ◽  
...  

Abstract Background Myocardial energetic efficiency (MEE) per unit of left ventricular (LV) mass significantly predicts composite of cardiovascular (CV) events in treated hypertensive patients and specifically heart failure in an event-free population-based cohort with normal ejection fraction, independently of LV hypertrophy (LVH). Purpose To investigate whether MEEi changes over time in treated hypertensive patients, and whether different treatments have different effects. Methods From the Losartan Intervention For Endpoint study (LIFE Echo Sub-study) we selected 744 hypertensive patients (age 66±7 years; 45% women) with LVH at ECG, without atrial fibrillation, previous or incident myocardial infarction and with normal echocardiographic ejection fraction (>50%). MEE was estimated as the ratio of stroke work to the “double” product of heart rate times systolic blood pressure (BP), simplified as the ratio of stroke volume to heart rate, as previously reported. MEE was normalized for LVM (MEEi) and analyzed in quartiles at baseline and at the end treatment, according to an “intention-to-treat” protocol. Results Age and proportion of women were not significantly different from the highest to the lowest quartiles (from 65±7 to 66±7 years, p for trend=0.352; from 45% to 42%, p=0.946, respectively), whereas diastolic blood pressure (from 97±8 to 100±9 mmHg, p=0.006), prevalence of obesity (from 14 to 31%, p=0.001) and diabetes (from 4 to 14%, 0.004) progressively increased. Prevalence of concentric LV geometry and echocardiographic LVH also progressively increased from the highest to the lowest quartile (from 14 to 70%, and 61 to 90%, both p<0.0001). MEEi increased over time (p<0.007), independently of initial diastolic BP, diabetes and obesity, significantly more in patients treated with atenolol than with losartan (p<0.0001) (Figure), due to both increased stroke volume and decreased heart rate (both p<0.0001). Figure 1 Conclusions In a randomized clinical study, MEEi improves with anti-hypertensive therapy. Improvement is more evident in patients with atenolol than with losartan-based treatment, possibly providing pathophysiologic explanation of the comparable performance in prevention of ischemic heart disease previously reported in the LIFE study.


1997 ◽  
Vol 272 (2) ◽  
pp. H753-H759
Author(s):  
N. Sato ◽  
M. Uechi ◽  
K. Asai ◽  
T. Patrick ◽  
R. K. Kudej ◽  
...  

Traditional inotropic agents, e.g., those that increase myocardial contraction through enhanced cyclic AMP or those that increase contractility at a relatively high O2 cost are frequently not useful in the clinical setting. Accordingly, newer agents that operate through different mechanisms have been synthesized. The goal of the present study was to compare the effects of a new Ca2+ promotor, BAY y 5959, with more traditional inotropic agents, dobutamine and milrinone, in 11 conscious dogs chronically instrumented for measurement of left ventricular (LV) and arterial pressures, LV internal diameter, wall thickness, coronary blood flow, and arterial and coronary sinus O2 content. Equi-inotropic doses of BAY y 5959 (20 microg x kg(-1) x min(-1)), dobutamine (10 microg x kg(-1) x min(-1)), and milrinone (10 microg x kg(-1) x min(-1)) were selected, which increased the LV rate of pressure development in sinus rhythm by 71-78% from similar baselines. Heart rate rose with dobutamine (+24 +/- 4%) and milrinone (+23 +/- 2%) but fell with BAY y 5959 (-35 +/- 3%). Dobutamine increased myocardial O2 consumption (MV(O2)) by 88 +/- 10%. In contrast, MV(O2) increased less with BAY y 5959 (+9 +/- 3%) and milrinone (+16 +/- 5%; P < 0.05). Furthermore, mechanical efficiency was also calculated either with direct measurement of cardiac output or by pressure-volume loops. Dobutamine and milrinone did not change efficiency; however, BAY y 5959 increased efficiency by 19 +/- 5%. With the heart rate held constant, BAY y 5959 increased MV(O2) by 32 +/- 4% but still increased efficiency by 28 +/- 7%. Thus the Ca2+ promotor BAY y 5959 has unique features that might be desirable for clinical applications where inotropic support is indicated, but increased MV(O2) without enhanced mechanical efficiency is deleterious.


2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Xue-Ming Li ◽  
Li Jiang ◽  
Ying-Kun Guo ◽  
Yan Ren ◽  
Pei-Lun Han ◽  
...  

Abstract Background Type 2 diabetes mellitus (T2DM) increases the risks of heart failure and mortality in patients with hypertension, however the underlying mechanism is unclear. This study aims to investigate the impact of coexisting T2DM on left ventricular (LV) deformation and myocardial perfusion in hypertensive individuals. Materials and methods Seventy hypertensive patients without T2DM [HTN(T2DM−)], forty patients with T2DM [HTN(T2DM+)] and 37 age- and sex-matched controls underwent cardiac magnetic resonance examination. Left ventricular (LV) myocardial strains, including global radial (GRPS), circumferential (GCPS) and longitudinal peak strain (GLPS), and resting myocardial perfusion indices, including upslope, time to maximum signal intensity (TTM), and max signal intensity (MaxSI), were measured and compared among groups by analysis of covariance after adjusting for age, sex, body mass index (BMI) and heart rate followed by Bonferroni’s post hoc test. Backwards stepwise multivariable linear regression analyses were performed to determine the effects of T2DM on LV strains and myocardial perfusion indices in patients with hypertension. Results Both GRPS and GLPS deteriorated significantly from controls, through HTN(T2DM−), to HTN(T2DM+) group; GCPS in HTN(T2DM+) group was lower than those in both HTN(T2DM−) and control groups. Compared with controls, HTN(T2DM−) group showed higher myocardial perfusion, and HTN(T2DM+) group exhibited lower perfusion than HTN(T2DM−) group and controls. Multiple regression analyses considering covariates of systolic blood pressure, age, sex, BMI, heart rate, smoking, indexed LV mass and eGFR demonstrated that T2DM was independently associated with LV strains (GRPS: p = 0.002, model R2= 0.383; GCPS: p < 0.001, model R2= 0.472; and GLPS: p = 0.002, model R2= 0.424, respectively) and perfusion indices (upslope: p < 0.001, model R2= 0.293; TTM: p < 0.001, model R2= 0.299; and MaxSI: p < 0.001, model R2= 0.268, respectively) in hypertension. When both T2DM and perfusion indices were included in the regression analyses, both T2DM and TTM were independently associated with GRPS (p = 0.044 and 0.017, model R2= 0.390) and GCPS (p = 0.002 and 0.001, model R2= 0.424), and T2DM but not perfusion indices was independently associated with GLPS (p = 0.002, model R2= 0.424). Conclusion In patients with hypertension, T2DM had an additive deleterious effect on subclinical LV systolic dysfunction and myocardial perfusion, and impaired myocardial perfusion by coexisting T2DM was associated with deteriorated LV systolic dysfunction.


2003 ◽  
Vol 285 (6) ◽  
pp. H2630-H2638 ◽  
Author(s):  
Hirotsugu Yamada ◽  
David O. Martin ◽  
Kent A. Mowrey ◽  
Neil L. Greenberg ◽  
Don W. Wallick

Atrial tachycardia (AT) and fibrillation (AF) result in rapid ventricular rates that are detrimental to optimal cardiac function. The purpose of this study was to determine whether the application of a coupled pacing (CP) regimen would improve ventricular function by decreasing the ventricular rate of mechanical contractions (VRMCs). We simulated AT by pacing either atrium at a rate that resulted in a rapid but regular ventricular rate in seven anesthetized dogs. AF was induced by increasing the atrial pacing rate until atrial activation did not follow the pacing. After the induction of either AT or AF, we applied CP after each intrinsic ventricular activation. We measured the VRMCs and left ventricular (LV) pressures and volumes via a pressure-conductance catheter. The marked reductions in VRMCs during CP resulted in increases in LV end-diastolic volume. The CP resulted in virtually no mechanical contractions, whereas the strength of contractions from the normal electrical activation increased. The increases in the positive LV rate of pressure development over time and LV ejection fraction during CP were the result of postextrasystolic potentiation. The average stroke work (area of the pressure-volume loops) increased as a result of CP during both AT and AF. Despite the large increases in stroke volume (≅2×) during CP, the changes in cardiac output were moderate because the VRMCs markedly decreased (≅½). We conclude that CP therapy may be a viable therapy for slowing the heart rate and improving cardiac performance in patients with AT and AF.


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