Left ventricular diastolic function of remodeled myocardium in dogs with pacing-induced heart failure

1998 ◽  
Vol 274 (3) ◽  
pp. H945-H954 ◽  
Author(s):  
Steven B. Solomon ◽  
Srdjan D. Nikolic ◽  
Stanton A. Glantz ◽  
Edward L. Yellin
Keyword(s):  
Heart Failure ◽  
Elastic Properties ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Elastic Recoil ◽  
Systolic Volume ◽  
Left Ventricular Chamber ◽  
Volume Relation

In patients with heart failure, decreased contractility resulting in high end-diastolic pressures and a restrictive pattern of left ventricular filling produces a decrease in early diastolic filling, suggesting a stiff ventricle. This study investigated the elastic properties of the myocardium and left ventricular chamber and the ability of the heart to utilize elastic recoil to facilitate filling during pacing-induced heart failure in the anesthetized dog. Elastic properties of the myocardium were determined by analyzing the myocardial stress-strain relation. Left ventricular chamber properties were determined by analyzing the pressure-volume relation using a logarithmic approach. Elastic recoil was characterized using a computer-controlled mitral valve occluder to prevent transmitral flow during diastole. We conclude that, during heart failure, the high end-diastolic pressures suggestive of a stiff ventricle are due not to stiffer myocardium but to a ventricle whose chamber compliance characteristics are changed due to geometric remodeling of the myocardium. The restrictive filling pattern is a result of the ventricle being forced to operate on the stiff portion of the diastolic pressure-volume relation to maintain cardiac output. Slowed relaxation and decreased contractility result in an inability of the heart to contract to an end-systolic volume below its diastolic equilibrium volume. Thus the left ventricle cannot utilize elastic recoil to facilitate filling during heart failure.

Relationship between diastolic shape (eccentricity) and passive elastic properties in canine left ventricle

1990 ◽  
Vol 259 (2) ◽  
pp. H457-H463 ◽  
Author(s):  
S. D. Nikolic ◽  
E. L. Yellin ◽  
M. Dahm ◽  
O. Pajaro ◽  
R. W. Frater
Keyword(s):  
Regression Analysis ◽  
Linear Regression ◽  
Elastic Properties ◽  
Diastolic Pressure ◽  
Linear Regression Analysis ◽  
Left Ventricular ◽  
Elastic Recoil ◽  
Systolic Volume ◽  
End Systolic Volume ◽  
Lv Volume

This study was designed to investigate the relationship between left ventricular (LV) eccentricity, volume, and passive elastic properties. Eight open-chest fentanyl-anesthetized dogs were instrumented with an LV micromanometer, a remote-controlled mitral valve occluder, and two pairs of ultrasonic crystals to measure anterior-posterior and base-apex dimensions. We identified the presence of elastic recoil forces with negative LV diastolic pressure in nonfilling diastoles (end-systolic volume clamp). Using linear regression analysis we related midwall eccentricity to volume in nonfilling diastoles at the time of LVPmin and at end diastole, and in normal beats at end systole at LVPmin and at end-diastole. Intersection of the end-systolic and end-diastolic lines (transitional volume, Vt = 38.0 + 6.4 ml) divides cycles with and without the presence of elastic recoil forces. Vt is analogous to the equilibrium volume (V0), determined as the volume intercept of the logarithmic passive pressure-volume (P-V) relationship using LV volume estimated from LV weights (V0 nl = 37.6 + 4.4 ml), or the volume intercept of the linearized P-V relationship calculated from a prolate spheroidal model using measured minor and major diameters (V0 l = 44.5 + 3.5 ml). Linear regression analysis was also used to relate the square of peak mitral flow (MF2) with the corresponding atrioventricular pressure gradient (delta P); the slope represents a dissipative constant for the cycles without, P = 0.00058(MF)2 + 0.35 (n = 48, r = 0.73), and with elastic recoil P = 0.00035(MF)2 + 0.21 (n = 24, r = 0.81).(ABSTRACT TRUNCATED AT 250 WORDS)

Regional ischemia increases sensitivity of left ventricular relaxation to volume in pigs

1999 ◽  
Vol 276 (6) ◽  
pp. H1994-H2005 ◽  
Author(s):  
Steven B. Solomon ◽  
Stanton A. Glantz
Keyword(s):  
Diastolic Pressure ◽  
Contractile Function ◽  
Left Ventricular ◽  
Left Ventricular Filling ◽  
Diastolic Filling ◽  
Left Ventricular Relaxation ◽  
Ventricular Relaxation ◽  
Regional Ischemia ◽  
Volume Relation ◽  
Ventricular Filling

Regional ischemia impairs early diastolic filling due, in part, to changes in left ventricular relaxation. This study uses open-chest pigs instrumented with high-fidelity pressure transducers to investigate the effect of regional ischemia on the active component of relaxation independent of the passive effects of filling and the effect of left ventricular filling and stretch on the rate, duration, and extent of relaxation. During regional ischemia, active relaxation was impaired in the nonfilling ventricle, with a slower rate of relaxation. Stretching the myocardium as the ventricle fills slows the rate of relaxation more during regional ischemia than during normal perfusion, reflecting an increased sensitivity to stretch due to filling and an increased dependence of relaxation on volume. The duration of relaxation depends on the effect of regional ischemia on the end-diastolic pressure-volume relation. Stronger baseline contractile function results in an upward shift in the end-diastolic pressure-volume relation during regional ischemia and no net effect on the duration of relaxation. If this curve is shifted upward, the duration of relaxation shortens. All these effects combine to reduce the atrioventricular pressure gradient and left ventricular filling during regional ischemia.

Abstract 486: Increased Afterload In Sub-acute Phase Of Myocardial Infarction Exacerbates Heart Failure

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Kiyotake Ishikawa ◽  
Jaume Aguero ◽  
Kenneth Fish ◽  
Lauren Leonardson ◽  
Roger J Hajjar
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Phase ◽  
Diastolic Pressure ◽  
Interstitial Fibrosis ◽  
Myocardial Dysfunction ◽  
Resistance Index ◽  
Left Ventricular ◽  
Systolic Volume ◽  
Lv Remodeling

Background: Hypertension (HT) increases cardiac afterload and is one of the risk factors of poor prognosis after myocardial infarction (MI). However, there is little information on how HT impacts the healing processes during sub-acute phase MI. We investigated the role of an increased afterload on left ventricular (LV) performance and remodeling shortly after MI. Methods: Anterior MIs were created in 15 Yorkshire pigs via percutaneous access. To mimic HT condition, 7 pigs (Banding, n=7) underwent surgical banding of the ascending aorta 10 days after the MI, and were compared to the remaining pigs (Control, n=8). LV remodeling and function were assessed one month after MI using 3-D echocardiography and invasive hemodynamic measurements. Results: Echocardiographic assessment at day 10 revealed no significant differences in LV ejection fraction (EF) or LV volumes. One month after MI, aortic banding increased the systemic vascular resistance index, but was not statistically significant (1658±282 dyn/s/cm5/m 2 vs 1153±658 dyn/s/cm5/m 2 , P=0.08). Banding group presented with significantly impaired LVEF (Figure, P=0.002), larger end systolic volume (Figure, P=0.045), lower cardiac index (3.1±0.9 L/min/m 2 vs 4.4±0.6 L/min/m 2 , P=0.01), and elevated LV end diastolic pressure (22.4±5.0 mmHg vs 14.4±7.5 mmHg: P=0.04, Banding vs Control, respectively). Reduced EF was associated with remote myocardial dysfunction and histological analysis revealed increased interstitial fibrosis in this area. Conclusion: Increased afterload in sub-acute phase of MI induces more severely impaired cardiac function and LV remodeling, and was associated with worse heart failure status.

scholarly journals Levosimendan improves LV systolic and diastolic performance at rest and during exercise after heart failure

2005 ◽  
Vol 288 (2) ◽  
pp. H914-H922 ◽  
Author(s):  
Hideo Tachibana ◽  
Heng-Jie Cheng ◽  
Tomohiko Ukai ◽  
Akihiko Igawa ◽  
Zhu-Shan Zhang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Mechanical Efficiency ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Beneficial Effects ◽  
Total P ◽  
Contractile Performance

The new myofilament Ca2+ sensitizer levosimendan (LSM) is a positive inotropic and vasodilatory agent. Its beneficial effects have been demonstrated at rest in congestive heart failure (CHF). However, its effect during exercise (Ex) in CHF is unknown. We assessed the effects of LSM on left ventricular (LV) dynamics at rest and during Ex in eight conscious, instrumented dogs with pacing-induced CHF. After CHF, with dogs at rest, LSM decreased arterial elastance ( Ea) and increased LV contractile performance as assessed by the slope of LV pressure-volume (P-V) relation. LSM caused a >60% increase in the peak rate of mitral flow (dV/d tmax) due to decreases in minimal LV pressure and the time constant of LV relaxation (τ). LV arterial coupling, quantified as the ratio of end-systolic elastance ( Ees) to Ea, was increased from 0.47 to 0.85%. LV mechanical efficiency, determined as the ratio of stroke work to total P-V area, was improved from 0.54 ± 0.09 to 0.61 ± 0.07. These beneficial effects persisted during Ex after CHF. Compared with CHF Ex dogs, treatment with LSM prevented Ex-induced abnormal increases in mean left atrial pressure and end-diastolic pressure and decreased Ees/ Ea. With LSM treatment during CHF Ex, the early diastolic portion of the LV P-V loop was shifted downward with decreased minimal LV pressure and τ values and a further augmented dV/d tmax. Ees/ Ea improved, and mechanical efficiency further increased from 0.61 ± 0.07 to 0.67 ± 0.07, which was close to the value reached during normal Ex. After CHF, LSM produced arterial vasodilatation; improved LV relaxation and diastolic filling; increased contractility, LV arterial coupling, and mechanical efficiency; and normalized the response to Ex.

Influence of filling on left ventricular diastolic pressure-volume curve during pacing ischemia in dogs

1994 ◽  
Vol 266 (4) ◽  
pp. H1373-H1385 ◽  
Author(s):  
H. Shintani ◽  
S. A. Glantz
Keyword(s):  
Diastolic Pressure ◽  
Calcium Sensitivity ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Perfused Heart ◽  
Upward Shift ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Volume Relation

The reversible upward shift of the diastolic pressure-volume curve that occurs during pacing-induced ischemia has not been fully explained by increases in passive chamber stiffness or reductions in relaxation rate. We measured the fully relaxed pressure-volume relation defined by both filling and nonfilling beats and the isovolumic relaxation time constant in nonfilling beats before and during demand ischemia using our in situ left ventricular volume clamping technique in 10 dogs. Pacing-induced ischemia shifted the diastolic pressure-volume curves in filling beats upward compared with the end-diastolic pressure-volume relation of the normally perfused heart. In contrast, the end-diastolic points for nonfilling beats during pacing-induced ischemia fell on the fully relaxed pressure-volume relation defined by the normally perfused heart. Left ventricular filling per se was necessary for the upward shift of the diastolic pressure-volume curve observed during pacing-induced ischemia. We speculate that active force developed during diastole induced by stretch activation or, perhaps, length-dependent changes in calcium sensitivity of the myofilaments in the ischemic myocardium due to stretch of the myocardium during rapid diastolic filling may contribute to the upward shift of the diastolic pressure-volume curve observed during pacing-induced ischemia.

Abstract 12583: C-Type Natriuretic Peptide Improves Left Ventricular Systolic and Diastolic Functional Performance at Rest and During Exercise After Heart Failure

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Che Ping Cheng ◽  
Hiroshi Hasegawa ◽  
Atsushi Morimoto ◽  
Heng-Jie Cheng ◽  
William C Little
Keyword(s):  
Heart Failure ◽  
Natriuretic Peptide ◽  
Functional Performance ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Arterial Elastance ◽  
Beneficial Effects ◽  
Mitral Flow

Background: In heart failure (HF), the impaired left ventricular (LV) arterial coupling and diastolic dysfunction present at rest are exacerbated during exercise (Ex). C-type natriuretic peptide (CNP), the third member of the natriuretic peptide family produced by the vascular endothelium and heart is elevated in HF. However, its functional effects are unclear. We tested the hypotheses that CNP with vasodilating, natriuretic, and lusitropic actions may prevent this abnormal Ex response after HF. Methods: We assessed the effects of CNP on LV functional performance at rest and during submaximum Ex (3.5-5.5 mph for 6-8 min) in 10 instrumented dogs with pacing-induced HF. Since CNP mediated its biological actions via cGMP, we also measured plasma cGMP levels in response to CNP infusion at rest before and after HF. Results: CNP (2 μg/kg plus 0.4 μg/kg/min, iv, 20 min) caused a similar increase in cGMP levels before (7.2±3.8 to 24.7±4.9 pmol/ml) and after HF (20.2±4.4 to 71.6±5.0 pmol/ml). After HF, at rest, CNP reduced LV end-systolic pressure (P ES , CNP: 93 vs Baseline: 104 mmHg), arterial elastance (E A , 8.3 vs 11.7 mmHg/ml) and end-diastolic pressure (P ED , 37.2 vs 42.4 mmHg) (p<0.05). The peak mitral flow (dV/dt max , 201±51 vs 160±34ml/sec) was also increased due to decreased minimum LVP (LVP min , 17.1 vs 23.8 mmHg) and the time constant of LV relaxation (t, 40±4 vs 48±6 msec) (p<0.05). In addition, the slope of LV end-systolic pressure-volume relations (E ES ) was increased (5.6±0.7 vs 4.2±0.9 mmHg/ml). The LV-arterial coupling, quantified as E ES /E A , was improved (0.69±0.22 vs 0.48±0.16) (p<0.05). The beneficial effects persisted during Ex. At matched levels of Ex, treatment with CNP, Ex-induced significantly less increases in P ES (ΔP= 3.4±0.5 vs 7.4±0.8 mmHg), mean LAP (ΔP= -3.1±2.2 vs 3.6±2.9 mmHg), and LVP min (ΔP= -3.6±1.4 vs 1.4±1.2 mmHg) (p<0.05). With CNP, t was much shortened (Δ= -0.8±4.0 vs 2.8±3.2 ms), and the peak mitral flow was further augmented (ΔdV/dt max , 75±20 vs 43±12 ml/sec) (p<0.05). Conclusion: After HF, the generation of cGMP in response to CNP is not blunted. CNP produces arterial vasodilatation and augments LV contraction, relaxation, diastolic filling and LV arterial coupling, thus improving LV performance, both at rest and during Ex after HF.

scholarly journals Features of structural and geometric remodeling of the heart and changes in the diastolic filling of the heart in patients with chronic heart failure of ischemic genesis with preserved left ventricular ejection fraction

2021 ◽  
Vol 14 (1) ◽  
pp. 93-102
Author(s):  
V. A. Lysenko ◽  
M. S. Potapenko ◽  
V. V. Syvolap
Keyword(s):  
Heart Failure ◽  
Mitral Valve ◽  
Left Ventricle ◽  
Diastolic Function ◽  
Ventricular Dysfunction ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Lv Mass ◽  
Diastolic Left Ventricular Dysfunction

Chronic heart failure (CHF) is the most common cardiovascular disease worldwide, estimated at 23 million. With the increase in the growing of the elderly population, the prevalence of hypertension, atrial fibrillation, obesity, diabetes, as well as the improvement of ultrasound diagnostic methods, a further increase in the number of cases of CHF with preserved left ventricular EF. Despite the large number of studies dedicated to analyzing the features of structural and geometric remodeling of the heart, changes in the systolic and diastolic function of the ventricles in patients with CHF, this issue hasn’t been definitively resolved and needs further improvement. The aim of the work – to investigate changes in structural and geometric parameters and diastolic function of the heart in patients with CHF of ischemic origin with preserved LV EF. Materials and methods. The study was included 43 patients (men – n = 19; women – n = 24) for CHF of ischemic origin with preserved LV EF, with sinus rhythm, stage II AB, II-IV FC for NYHA (main group), and 90 patients on coronary heart disease without signs of CHF (men – n = 40 (44.5 %); women – n = 50 (55.5 %)), (comparison group). Groups of patients were comparable in age, sex, height, weight, body surface area. Doppler echocardiographic examination was performed on the device Esaote MyLab Eight (Italy). Results. In patients with CHF preserved LV EF, the indicators prevailed: the size of the LA by 25 % (P = 0.005), the long axis of the LA by 11 % (P = 0.001), the LV EDV index of the LV by 13 % (P = 0.042), the LV mass index by 16 % (P = 0.013) according to the Penn Convention and (P = 0.004) the ASE. Eccentric left ventricular hypertrophy was diagnosed in 56 % of patients. Diastolic left ventricular dysfunction was absent in 2 % of patients with CHF. In 72 % of cases, the type of “relaxation disorder” was established, and in 26 % – “pseudonormal” LV filling profile. In none of the cases was a “restrictive” LV filling profile recorded. The following indicators of left ventricular diastolic function were lower in patients with CHF: e’ of the medial fibrous ring of the mitral valve by 26 % (P = 0.0001) and e’ lateral by 21 % (P = 0.0001), and the A’ the medial fibrous ring of mitral valve by 9 % (P = 0.022), and greater ratios of velocities E/e’ medial by 41 % (P = 0.0001), and E/e’ lateral fibrous ring of the mitral valve by 28 % (P = 0.0001), mean E/e’ by 36 % (P = 0.0001), which indicates a significant increase in end-diastolic pressure in the left ventricle. Conclusions. Structural and geometric remodeling of the heart in patients with CHF with preserved LV EF was characterized by dilatation of the left atrium, a moderate increase in the LV EDV index by 13 % (P = 0.042), a 16 % increase (P = 0.013) in the LV mass index, with the formation eccentric (56 %) and concentric (18 %) LV hypertrophy. Diastolic left ventricular dysfunction was absent in 2 % of patients with CHF. Disorders of diastolic filling of the left ventricle (72 % “relaxation disorder” and 26 % “pseudonormal” type) were occurred due to an increase in end-diastolic pressure in the left ventricle (increase by 41 % (P = 0.0001) ratio E/e’ medial fibrous ring MK), in LA (increase of more than 2 times (P = 0.0001) pulmonary capillary wedge pressure), and was accompanied by the development of postcapillary pulmonary hypertension (increase by 34 % (P = 0.0001) systolic pressure in the pulmonary artery). Despite the preserved LV EF, patients with CHF had significantly lower left and right ventricular contractility (10 % MAPSE med (P = 0.031), 18 % S med (P = 0.001) and 19 % (P = 0.007) RV EF).

Acute Changes in Left Ventricular End Diastolic Pressure following the Transcatheter Closure of an Atrial Septal Defect in Adults

2016 ◽  
Vol 19 (3) ◽  
pp. 145 ◽  
Author(s):  
Young Hwa Kong ◽  
Jinyoung Song ◽  
Kyung Hee Kim ◽  
June Huh ◽  
I-Seok Kang
Keyword(s):  
Elderly Patients ◽  
Atrial Septal Defect ◽  
Septal Defect ◽  
Transcatheter Closure ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Device Closure ◽  
Acute Changes ◽  
Asd Closure

<strong>Background:</strong> Acute changes in left ventricular diastolic function shortly after ASD closure in elderly patients have not been well known. We aimed to investigate acute changes in left ventricular end diastolic pressure (LVEDP) in elderly patients following transcatheter closure of atrial septal defect (ASD). <br /><strong>Methods:</strong> All 19 adults with ASDs who underwent transcatheter closure between June 2013 and December 2014 were enrolled. LVEDP was measured prior to device closure and compared with that immediately following device closure and 15 minutes after device closure. <br /><strong>Results:</strong> The median age of the patients was 48 years old. The baseline E/e’ and LVEDP values were 8.3 ± 2.8 and 13 ± 3 mmHg. The LVEDP value immediately following closure was 19 ± 4 mmHg, and 15 minutes after closure was 16 ± 4 mmHg. The median increase in the LVEDP value immediately following closure was 6 mmHg, which significantly differed from that prior to closure. The LVEDP 15 minutes after closure decreased but remained significantly higher than the value observed immediately after closure. No significant changes were observed with regard to E/e’ at either 1 day or 3 months following closure. The LVEDP value <br />15 minutes after device closure was significantly correlated with those observed before closure and immediately following closure; however, no significant correlations were observed with regard to patient age, Qp/Qs, E/e’ before closure, or E/e’ 3 months after device closure.<br /><strong>Conclusion:</strong> LVEDP in adults with ASDs significantly increases following device closure. LVEDP before closure predicts LVEDP following device closure.

A Systematic Review and Meta-analysis : Safety and Efficacy of Mesenchymal stem Cells Therapy for Heart Failure

2020 ◽  
Vol 15 ◽  
Author(s):  
Tiantian Shen ◽  
Lin Xia ◽  
Wenliang Dong ◽  
Jiaxue Wang ◽  
Feng Su ◽  
...  
Keyword(s):  
Heart Failure ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Safety And Efficacy ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume

Background: Preclinical and clinical evidence suggests that mesenchymal stem cells (MSCs) may be beneficial in treating heart failure (HF). However, the effects of stem cell therapy in patients with heart failure is an ongoing debate and the safety and efficacy of MSCs therapy is not well-known. We conducted a systematic review of clinical trials that evaluated the safety and efficacy of MSCs for HF. This study aimed to assess the safety and efficacy of MSCs therapy compared to the placebo in heart failure patients. Methods: We searched PubMed, Embase, Cochrane library systematically, with no language restrictions. Randomized controlled trials(RCTs) assessing the influence of MSCs treatment function controlled with placebo in heart failure were included in this analysis. We included RCTs with data on safety and efficacy in patients with heart failure after mesenchymal stem cell transplantation. Two investigators independently searched the articles, extracted data, and assessed the quality of the included studies. Pooled data was performed using the fixed-effect model or random-effect model when it appropriate by use of Review Manager 5.3. The Cochrane risk of bias tool was used to assess bias of included studies. The primary outcome was safety assessed by death and rehospitalization and the secondary outcome was efficacy which was assessed by six-minute walk distance and left ventricular ejection fraction (LVEF)，left ventricular end-systolic volume（LVESV），left ventricular end-diastolic volume（LVEDV） and brain natriuretic peptide（BNP） Results: A total of twelve studies were included, involving 823 patients who underwent MSCs or placebo treatment. The overall rate of death showed a trend of reduction of 27% (RR [CI]=0.73 [0.49, 1.09], p=0.12) in the MSCs treatment group. The incidence of rehospitalization was reduced by 47% (RR [CI]=0.53[0.38, 0.75], p=0.0004). The patients in the MSCs treatment group realised an average of 117.01m (MD [95% CI]=117.01m [94.87, 139.14], p<0.00001) improvement in 6MWT.MSCs transplantation significantly improved left ventricular ejection fraction (LVEF) by 5.66 % (MD [95% CI]=5.66 [4.39, 6.92], p<0.00001), decreased left ventricular end-systolic volume (LVESV) by 14.75 ml (MD [95% CI]=-14.75 [-16.18, -12.83], p<0.00001 ) and left ventricular end-diastolic volume (LVEDV) by 5.78 ml (MD [95% CI]=-5.78[-12.00, 0.43], p=0.07 ) ,in the MSCs group , BNP was decreased by 133.51 pg/ml MD [95% CI]= -133.51 [-228.17,-38.85], p=0.54, I2= 0.0%) than did in the placebo group. Conclusions: Our results suggested that mesenchymal stem cells as a regenerative therapeutic approach for heart failure is safe and effective by virtue of their self-renewal potential, vast differentiation capacity and immune modulating properties. Allogenic MSCs have superior therapeutic effects and intracoronary injection is the optimum delivery approach. In the tissue origin, patients who received treatment with umbilical cord MSCs seem more effective than bone marrow MSCs. As to dosage injected, (1-10)*10^8 cells were of better effect.

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