scholarly journals Effects of Apelin on Left Ventricular-Arterial Coupling and Mechanical Efficiency in Rats with Ischemic Heart Failure

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Qiufang Ouyang ◽  
Tao You ◽  
Jinjian Guo ◽  
Rong Xu ◽  
Quehui Guo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Fibrosis ◽  
Diastolic Pressure ◽  
Systolic Function ◽  
Mechanical Efficiency ◽  
Left Ventricular ◽  
Mesenteric Arteries ◽  
Stroke Work ◽  
Reduced Ejection Fraction ◽  
Left Ventricular Arterial Coupling

Apelin plays important roles in cardiovascular homeostasis. However, its effects on the mechanoenergetics of heart failure (HF) are unavailable. We attempted to investigate the effects of apelin on the left ventricular-arterial coupling (VAC) and mechanical efficiency in rats with HF. HF was induced in rats by the ligation of the left coronary artery. The ischemic HF rats were treated with apelin or saline for 12 weeks. The sham-operated animals served as the control. The left ventricular (LV) afterload and the systolic and diastolic functions, as well as the mechanoenergetic indices were estimated from the pressure-volume loops. Myocardial fibrosis by Masson’s trichrome staining, myocardial apoptosis by TUNEL, and collagen content in the aorta as well as media area in the aorta and the mesenteric arteries were determined. Our data indicated that HF rats manifested an increased arterial load (Ea), a declined systolic function (reduced ejection fraction, +dP/dtmax, end-systolic elastance, and stroke work), an abnormal diastolic function (elevated end-diastolic pressure, τ, and declined −dP/dtmax), and decreased mechanical efficiency. Apelin treatment improved those indices. Concomitantly, increased fibrosis in the LV myocardium and the aorta and enhanced apoptosis in the LV were partially restored by apelin treatment. A declined wall-to-lumen ratio in the mesenteric arteries of the untreated HF rats was further reduced in the apelin-treated group. We concluded that the rats with ischemic HF were characterized by deteriorated LV mechanoenergetics. Apelin improved mechanical efficiency, at least in part, due to the inhibiting cardiac fibrosis and apoptosis in the LV myocardium, reducing collagen deposition in the aorta and dilating the resistant artery.

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.

Desflurane, Sevoflurane, and Isoflurane Impair Canine Left Ventricular-Arterial Coupling and Mechanical Efficiency

1996 ◽  
Vol 85 (2) ◽  
pp. 403-413 ◽  
Author(s):  
Douglas A. Hettrick ◽  
Paul S. Pagel ◽  
David C. Warltier
Keyword(s):  
Arterial Pressure ◽  
Myocardial Contractility ◽  
Minimum Alveolar Concentration ◽  
Systolic Pressure ◽  
Mechanical Efficiency ◽  
Left Ventricular ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Ventricular Afterload ◽  
Left Ventricular Arterial Coupling

Background The effects of desflurane, sevoflurane, and isoflurane on left ventricular-arterial coupling and mechanical efficiency were examined and compared in acutely instrumented dogs. Methods Twenty-four open-chest, barbiturate-anesthetized dogs were instrumented for measurement of aortic and left ventricular (LV) pressure (micromanometer-tipped catheter), dP/dtmax, and LV volume (conductance catheter). Myocardial contractility was assessed with the end-systolic pressure-volume relation (Ees) and preload recruitable stroke work (Msw) generated from a series of LV pressure-volume diagrams. Left ventricular-arterial coupling and mechanical efficiency were determined by the ratio of Ees to effective arterial elastance (Ea; the ratio of end-systolic arterial pressure to stroke volume) and the ratio of stroke work (SW) to pressure-volume area (PVA), respectively. Results Desflurane, sevoflurane, and isoflurane reduced heart rate, mean arterial pressure, and left ventricular systolic pressure. All three anesthetics caused similar decreases in myocardial contractility and left ventricular afterload, as indicated by reductions in Ees, Msw, and dP/dtmax and Ea, respectively. Despite causing simultaneous declines in Ees and Ea, desflurane decreased Ees/Ea (1.02 +/- 0.16 during control to 0.62 +/- 0.14 at 1.2 minimum alveolar concentration) and SW/PVA (0.51 +/- 0.04 during control to 0.43 +/- 0.05 at 1.2 minimum alveolar concentration). Similar results were observed with sevoflurane and isoflurane. Conclusions The present findings indicate that volatile anesthetics preserve optimum left ventricular-arterial coupling and efficiency at low anesthetic concentrations (< 0.9 minimum alveolar concentration); however, mechanical matching of energy transfer from the left ventricle to the arterial circulation degenerates at higher end-tidal concentrations. These detrimental alterations in left ventricular-arterial coupling produced by desflurane, sevoflurane, and isoflurane contribute to reductions in overall cardiac performance observed with these agents in vivo.

scholarly journals Retrospective evaluation of echocardiographic variables for prediction of heart failure hospitalization in heart failure with preserved versus reduced ejection fraction: A single center experience

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0244379
Author(s):  
Michael M. Hammond ◽  
Changyu Shen ◽  
Stephanie Li ◽  
Dhruv S. Kazi ◽  
Marwa A. Sabe ◽  
...  
Keyword(s):  
Heart Failure ◽  
Wall Thickness ◽  
Systolic Function ◽  
Medical Center ◽  
Left Ventricular ◽  
Single Center ◽  
Reduced Ejection Fraction ◽  
Medicare Claims ◽  
Structural Variables ◽  
Eccentric Hypertrophy

Background Limited data exist on the differential ability of variables on transthoracic echocardiogram (TTE) to predict heart failure (HF) readmission across the spectrum of left ventricular (LV) systolic function. Methods We linked 15 years of TTE report data (1/6/2003-5/3/2018) at Beth Israel Deaconess Medical Center to complete Medicare claims. In those with recent HF, we evaluated the relationship between variables on baseline TTE and HF readmission, stratified by LVEF. Results After excluding TTEs with uninterpretable diastology, 5,900 individuals (mean age: 76.9 years; 49.1% female) were included, of which 2545 individuals (41.6%) were admitted for HF. Diastolic variables augmented prediction compared to demographics, comorbidities, and echocardiographic structural variables (p < 0.001), though discrimination was modest (c-statistic = 0.63). LV dimensions and eccentric hypertrophy predicted HF in HF with reduced (HFrEF) but not preserved (HFpEF) systolic function, whereas LV wall thickness, NT-proBNP, pulmonary vein D- and Ar-wave velocities, and atrial dimensions predicted HF in HFpEF but not HFrEF (all interaction p < 0.10). Prediction of HF readmission was not different in HFpEF and HFrEF (p = 0.93). Conclusions In this single-center echocardiographic study linked to Medicare claims, left ventricular dimensions and eccentric hypertrophy predicted HF readmission in HFrEF but not HFpEF and left ventricular wall thickness predicted HF readmission in HFpEF but not HFrEF. Regardless of LVEF, diastolic variables augmented prediction of HF readmission compared to echocardiographic structural variables, demographics, and comorbidities alone. The additional role of medication adherence, readmission history, and functional status in differential prediction of HF readmission by LVEF category should be considered for future study.

Progressive myocardial dysfunction associated with increased vascular resistance

1980 ◽  
Vol 239 (4) ◽  
pp. H477-H477 ◽  
Author(s):  
Joseph A. Franciosa ◽  
Richard Heckel ◽  
Catherine Limas ◽  
Jay N. Cohn
Keyword(s):  
Heart Failure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Myocardial Dysfunction ◽  
Peripheral Circulation ◽  
Left Ventricular ◽  
Stroke Work ◽  
Low Cardiac Output

To study heart failure from a myocardial lesion, we injected glass beads into the circumflex coronary artery of 11 conscious dogs and followed hemodynamics for 10 mo. Heart rate remained unchanged. Control mean arterial pressure of 112.3 ± 3.0 (SE) mmHg was unchanged at 1 and 3 mo, but rose to 127.2 ± 8.5 to 84.0 ± 7.6 ml . kg-1 . min-1 at 10 mo (P < 0.02), but was unchanged at 1 and 3 mo. Left ventricular end-diastolic pressure (LVEDP) averaged 4.6 ± 0.8 mmHg at control and rose to 11.8 ± 1.4 mmHg at 1 mo and 14.9 ± 2.5 mmHg at 10 mo (both P < 0.01). Systemic vascular resistance rose significantly by 10 mo. The ratio of stroke work to LVEDP fell from 13.1 ± 0.1 at control to 3.8 ± 0.5 by 10 mo (P < 0.01). In this dog model, left ventricular dysfunction is manifest early by increased LVEDP and later by high systemic vascular resistance with low cardiac output, thus suggesting a role of the peripheral circulation in the progression of heart failure.

Impaired subendocardial function in tachycardia-induced cardiac failure

1995 ◽  
Vol 268 (5) ◽  
pp. H1788-H1794 ◽  
Author(s):  
I. J. LeGrice ◽  
Y. Takayama ◽  
J. W. Holmes ◽  
J. W. Covell
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Substantial Reduction ◽  
Median Sternotomy ◽  
Vena Cava ◽  
Oxygen Demand ◽  
Experimental Models ◽  
Left Ventricular ◽  
Miniature Swine ◽  
Reduced Ejection Fraction

Chronic rapid ventricular pacing (CRVP) in many experimental models induces ventricular dilatation, reduced ejection fraction, and symptomatic congestive heart failure. We have investigated transmural mechanical function in the left ventricular (LV) wall of five Hanford miniature swine before and after CRVP-induced failure. Three columns of radiopaque markers 1 mm in diameter were implanted in the anterior LV wall through a median sternotomy. A pair of LV pacing wires were sutured into the myocardium, a pneumatic cuff was placed around the inferior vena cava (IVC), and two fluid-filled Silastic catheters were implanted into the LV apex. Two weeks after surgery, the pigs were suspended awake in a sling, and markers were tracked with biplane cineradiography. The hearts were paced for 3 wk (225-240 beats/min), and the study was repeated with the pacemaker off. Saline infusion and IVC occlusion were used to vary LV end-diastolic pressure (EDP) so control-to-failure comparisons could be made at matched LV EDPs. End-systolic strains in the circumferential (E11), longitudinal (E22), and transmural (E33) directions were quantified using finite element methods. There was a significant reduction in E11 and E33 for the subendocardium: in E11, from -0.27 to -0.18; in E33, from 0.83 to 0.46. There were no significant changes in subendocardial E22 or in any of the outer wall normal strains. These results indicate that CRVP causes substantial reduction of subendocardial, but not subepicardial, function; taken together with previous data indicating subendocardial hypoperfusion, these results support the contention that an imbalance between blood flow and oxygen demand plays a role in the etiology of heart failure in this model.

Trabecular cutting: a novel surgical therapy to increase diastolic compliance

2019 ◽  
Vol 127 (2) ◽  
pp. 457-463
Author(s):  
Meagan Oglesby ◽  
Danny Escobedo ◽  
Gladys Patricia Escobar ◽  
Fatemeh Fatemifar ◽  
Edward Y. Sako ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Ex Vivo ◽  
Systolic Function ◽  
Wall Stress ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Before And After ◽  
Diastolic Compliance

Heart failure with preserved ejection fraction (HFpEF) is a common cause of hospital admission in patients over 65 yr old and has high mortality. HFpEF is characterized by left ventricular (LV) hypertrophy that reduces compliance. Current HFpEF therapies control symptoms, but no existing medications or therapies can sustainably increase LV compliance. LV trabeculae develop hypertrophy and fibrosis that contribute to reduced LV compliance. This study expands our previous results in ex vivo human hearts to show that severing LV trabeculae increases diastolic compliance in an ex vivo working rabbit heart model. Trabecular cutting was performed in ex vivo rabbit hearts set up in a working heart perfusion system perfused with oxygenated Krebs-Henseleit buffer. A hook was inserted in the LV to cut trabeculae. End-systolic and end-diastolic pressure-volume relationships during transient preload reduction were recorded using an admittance catheter in the following three groups: control (no cutting; n = 9), mild cutting (15 cuts; n = 5), and aggressive cutting (30 cuts; n = 5). In a second experiment, each heart served as its own control. Hemodynamic data were recorded before and after trabecular cutting ( n = 10) or sham cutting ( n = 5) within the same heart. In the first experiments, trabecular cutting did not affect systolic function ( P > 0.05) but significantly increased overall diastolic compliance ( P = 0.009). Greater compliance was seen as trabecular cutting increased ( P = 0.002, r2 = 0.435). In the second experiment, significant increases in systolic function ( P = 0.048) and diastolic compliance ( P = 0.002) were seen after trabecular cutting compared with baseline. In conclusion, trabecular cutting significantly increases diastolic compliance without reducing systolic function. NEW & NOTEWORTHY We postulate that, in mammalian hearts, free-running trabeculae carneae exist to provide tensile support to the left ventricle and minimize diastolic wall stress. Because of hypertrophy and fibrosis of trabeculae in patients with left ventricular hypertrophy, this supportive role can become pathologic, worsening diastolic compliance. We demonstrate a novel operation involving cutting trabeculae as a method to acutely increase diastolic compliance in patients presenting with heart failure and diastolic dysfunction to improve their left ventricle compliance.

scholarly journals Levosimendan restores the positive force-frequency relation in heart failure

2011 ◽  
Vol 301 (2) ◽  
pp. H488-H496 ◽  
Author(s):  
Satoshi Masutani ◽  
Heng-Jie Cheng ◽  
Hideo Tachibana ◽  
William C. Little ◽  
Che-Ping Cheng
Keyword(s):  
Heart Failure ◽  
Contractile Function ◽  
Mechanical Efficiency ◽  
Left Ventricular ◽  
Force Frequency ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Major Mechanism ◽  
Frequency Relation ◽  
Positive Force

Frequency potentiation of contractile function is a major mechanism of the increase in myocardial performance during exercise. In heart failure (HF), this positive force-frequency relation is impaired, and the abnormal left ventricular (LV)-arterial coupling is exacerbated by tachycardia. A myofilament Ca2+ sensitizer, levosimendan, has been shown to improve exercise tolerance in HF. This may be due to its beneficial actions on the force-frequency relation and LV-arterial coupling (end-systolic elastance/arterial elastance, EES/ EA). We assessed the effects of therapeutic doses of levosimendan on the force-frequency relation and EES/ EA in nine conscious dogs after pacing-induced HF using pressure-volume analysis. Before HF, pacing tachycardia increased EES, shortened τ, and did not impair EES/ EA and mechanical efficiency (stroke work/pressure-volume area, SW/PVA). In contrast, after HF, pacing at 140, 160, 180, and 200 beat/min (bpm) produced smaller a increase of EES or less shortening of τ, whereas EES/ EA (from 0.56 at baseline to 0.42 at 200 bpm) and SW/PVA (from 0.52 at baseline to 0.43 at 200 bpm) progressively decreased. With levosimendan, basal EES increased 27% (6.2 mmHg/ml), τ decreased 11% (40.8 ms), EES/ EA increased 34% (0.75), and SW/PVA improved by 15% (0.60). During tachycardia, EES further increased by 23%, 37%, 68%, and 89%; τ decreased by 9%, 12%, 15%, and 17%; and EES/ EA was augmented by 11%, 16%, 31%, and 33%, incrementally, with pacing rate. SW/PVA was improved (0.61 to 0.64). In conclusion, in HF, treatment with levosimendan restores the normal positive LV systolic and diastolic force-frequency relation and prevents tachycardia-induced adverse effect on LV-arterial coupling and mechanical efficiency.

scholarly journals Treatment of Heart Failure with Mid-Range Ejection Fraction: What Is the Evidence

2021 ◽  
Vol 10 (2) ◽  
pp. 203
Author(s):  
Eleni-Evangelia Koufou ◽  
Angelos Arfaras-Melainis ◽  
Sahil Rawal ◽  
Andreas P. Kalogeropoulos
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Current Knowledge ◽  
Systolic Function ◽  
Angiotensin Receptor Blockers ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Current Evidence ◽  
Converting Enzyme Inhibitors ◽  
Reduced Ejection Fraction

In this review, we briefly outline our current knowledge on the epidemiology, outcomes, and pathophysiology of heart failure (HF) with mid-range ejection fraction (HFmrEF), and discuss in more depth the evidence on current treatment options for this group of patients. In most studies, the clinical background of patients with HFmrEF is intermediate between that of patients with HF and reduced ejection fraction (HFrEF) and patients with HF and preserved ejection fraction (HFpEF) in terms of demographics and comorbid conditions. However, the current evidence, stemming from observational studies and post hoc analyses of randomized controlled trials, suggests that patients with HFmrEF benefit from medications that target the neurohormonal axes, a pathophysiological behavior that resembles that of HFrEF. Use of β-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, mineralocorticoid receptor antagonists, and sacubitril/valsartan is reasonable in patients with HFmrEF, whereas evidence is currently scarce for other therapies. In clinical practice, patients with HFmrEF are treated more like HFrEF patients, potentially because of history of systolic dysfunction that has partially recovered. Assessment of left ventricular systolic function with contemporary noninvasive modalities, e.g., echocardiographic strain imaging, is promising for the selection of patients with HFmrEF who will benefit from neurohormonal antagonists and other HFrEF-targeted therapies.

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