Abstract 13421: Ventricular and Arterial Elastance During Isometric Handgrip Exercise and Post-exercise Circulatory Arrest in Heart Failure With and Without Preserved Ejection Fraction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Naoki Fujimoto ◽  
Keishi Moriwaki ◽  
Issei Kameda ◽  
Masaki Ishiyama ◽  
Taku Omori ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Circulatory Arrest ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Isometric Handgrip ◽  
Arterial Elastance ◽  
Post Exercise

Introduction: Isometric handgrip (IHG) training at 30% maximal voluntary contraction (MVC) lowers blood pressure in hypertensive patients. Impacts of IHG exercise and post-exercise circulatory arrest (PECA), which isolates metaboreflex control, have been unclear in heart failure (HF). Purpose: To investigate the impacts of IHG exercise and PECA on ventricular-arterial stiffness and left ventricular (LV) relaxation in HF with preserved (HFpEF) and reduced ejection fraction (HFrEF). Methods: We invasively obtained LV pressure-volume (PV) loops in 20 patients (10 HFpEF, 10 HFrEF) using conductance catheter with microtip-manometer during 3 minutes of IHG at 30%MVC and 3 minutes of PECA. Hemodynamics and LV-arterial function including LV end-systolic elastance (Ees) by the single-beat method, effective arterial elastance (Ea), and time constant of LV relaxation (Tau) were evaluated every minute. Results: At rest, HFpEF had higher LV end-systolic pressure (ESP) and lower heart rate than HFrEF with similar LV end-diastolic pressure (EDP). The coupling ratio (Ees/Ea) was greater in HFpEF than HFrEF (1.0±0.3 vs. 0.6±0.3, p<0.01). IHG for 3minutes similarly increased heart rate in HFpEF (by 10±8 bpm) and HFrEF (by 14±6 bpm). IHG also increased end-diastolic and LVESP (134±21 vs. 158±30 mmHg and 113±25 vs. 139±25 mmHg) in both groups (groupхtime effect p≥0.25). In HFpEF, Ees, Ea and Ees/Ea (1.0±0.3 vs. 1.1±0.4) were unaffected during IHG. In HFrEF, IHG induced variable increases in Ea. LV end-systolic volume and the ESPV volume-axis intercept were larger, and Ees at IHG 3 rd min was greater (1.30±0.7 vs. 3.1±2.1 mmHg/ml, p<0.01) than baseline, resulting in unchanged Ees/Ea at IHG 3 rd min (0.6±0.3 vs. 0.8±0.4, p≥0.37). Tau was prolonged only in HFrEF during IHG and was returned to the baseline value during PECA. During the first 2 minutes of PECA, LVESP was lower than that at IHG 3 rd min only in HFpEF, suggesting less metaboreflex control of blood pressure in HFpEF during IHG. Conclusions: IHG exercise at 30%MVC induced modest increases in LV end-systolic and end-diastolic pressures in HFpEF and HFrEF. Although the prolongation of LV relaxation was observed only in HFrEF, the ventricular and arterial coupling was maintained throughout the IHG exercise in both groups.

Abstract 17249: Impacts of Isometric Handgrip Exercise and Post-Exercise Circulatory Arrest on Hemodynamics and Left Ventricular Function in Heart Failure With Preserved Ejection Fraction

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Keishi Moriwaki ◽  
Naoki Fujimoto ◽  
So Miyahara ◽  
Shusuke Fukuoka ◽  
Masaki Ishiyama ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Diastolic Pressure ◽  
Circulatory Arrest ◽  
Left Ventricular ◽  
Voluntary Contraction ◽  
Lv Function ◽  
Preserved Ejection Fraction ◽  
Isometric Handgrip ◽  
Post Exercise

Introduction: Isometric handgrip (IHG) training at 30% maximal voluntary contraction (MVC) lowers blood pressure (BP) in patients with hypertension and healthy individuals. However, impacts of IHG and post-exercise circulatory arrest (PECA), which isolates the metaboreflex control, on left ventricular (LV) function and hemodynamics have been unclear in patients with heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). Methods: Sixteen patients with HF (age 63±13 years, 5M:11F, 10HFpEF:6HFrEF) underwent invasive LV pressure-volume assessments using conductance catheter with microtip-manometer during 3min of IHG exercise at 30% MVC, followed by 3 min of PECA. Impacts of IHG and PECA on LV function and hemodynamics were evaluated and compared between HFpEF and HFrEF. Results: During 3 min of IHG at 30% MCV, heart rate increased by 10±8 bpm in HFpEF and by 14±6 bpm in HFrEF. IHG elevated LV end-systolic BP in both HFpEF (134±21 vs. 158±30 mmHg, p<0.01) and HFrEF (119±30 vs. 142±31 mmHg, p<0.01) with no change in stroke volume. There was a trend towards an increase in LV end-diastolic pressure in both groups (HFpEF:14±5 vs. 19±10 mmHg, HFrEF: 15±12 vs. 23±11 mmHg). Time constant of LV relaxation was unchanged by 3 min of IHG in HFpEF (52±14 vs. 54±15 ms), while it was prolonged in HFrEF (48±7 vs. 60±9 ms, p<0.01, groupхtime interaction effect p=0.08). During PECA, LV end-systolic BP decreased in both groups and was maintained higher than baseline throughout PECA only in HFpEF. Conclusions: Although IHG exercise at 30% MVC for 3 min would elevate LV end-systolic and end-diastolic pressures, this IHG exercise has no detrimental effect on LV systolic and diastolic function, especially in HFpEF patients. Chronic effect of IHG training on BP and hemodynamics will need to be evaluated in HFpEF patients who often suffer from arterial hypertension.

scholarly journals Ventricular-arterial coupling parameters and its prognostic value in patients with decompensated heart failure

2020 ◽  
Vol 25 (1) ◽  
pp. 39-45
Author(s):  
Z. D. Kobalava ◽  
O. I. Lukina ◽  
I. Meray ◽  
S. V. Villevalde
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Prognostic Value ◽  
Systolic Pressure ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Pulmonary Artery Systolic Pressure ◽  
Arterial Elastance ◽  
Increased Risk ◽  
All Cause Mortality

Aim. To assess ventricular-arterial coupling (VAC) parameters and their prognostic value in patients with decompensated heart failure (HF).Material and methods. VAC parameters were evaluated upon admission using two-dimensional echocardiography in 355 patients hospitalized with decompensated HF. VAC was expressed as the ratio between arterial elastance (Ea) and end-systolic LV elastance (Ees). The optimal VAC range was considered 0,6-1,2. Parameters of left ventricular (LV) efficacy were calculated using the appropriate formulas. Differences were considered significant at p<0,05.Results. The median values of Ea, Ees and VAC were 2,2 (1,7;2,9) mmHg/ml, 1,8 (1,0;3,0) mmHg/ml and 1,32 (0,75;2,21) respectively. In 63% of patients, VAC disorders were detected: 55% of patients had VAC >1,2 (predominantly patients with HF with reduced ejection fraction (HFrEF)-79%), 8% of patients had VAC <0,6 (all patients with HF with preserved ejection fraction (HFpEF)). Normal VAC was observed in 78%, 42%, and 1% of patients with HFpEF, HF with mid-range EF and HFrEF, respectively. There was significant correlation between Ea/Ees ratio and levels of NTproBNP (R=0,35), hematocrit (R=-0,29), hemoglobin (R=-0,26), pulmonary artery systolic pressure (PAPs) (R=0,18), dimensions of left atrium (R=0,32) and right ventricle (RV) (R=0,32). After 6 months, rehospitalization with decompensated HF was recorded in 72 (20,3%) patients, 42 (11,8%) patients died. Ea decrease <2,2 mmHg/ml and PAPs increase >45 mmHg increased the risk of rehospitalization with decompensated HF and all-cause mortality 2,5 and 3,7 times, respectively.Conclusion. Impaired VAC was diagnosed in 63% of patients with decompensated HF. However, the increased risk of all-cause mortality and rehospitalization with decompensated HF over the 6 months was associated with Ea decrease <2,2 mmHg/ml and PAPs increase >45 mmHg.

scholarly journals A Comparative Study of Bisoprolol with Carvedilol on LV Systolic Function in Patients with Chronic Heart Failure

2018 ◽  
Vol 14 (1) ◽  
pp. 3-8
Author(s):  
Mohammad Ashraf Hossain ◽  
Khurshed Ahmed ◽  
Md Faisal Ibn Kabir ◽  
Md Fakhrul Islam Khaled ◽  
Rakibul H Rashed ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
Group I ◽  
End Systolic Volume ◽  
Group Ii

Background: Chronic heart failure (CHF) is the most common and prognostically unfavorable outcome of many diseases of the cardiovascular system. Recent data suggest that beta-blockers are beneficial in patients with CHF. Among β-blocker class of drugs, bisoprolol is a highly selective β1-adrenergic receptor blocker whereas Carvedilol is non-selective. Many large-scale trials have confirmed that both these β-blockers are superior to placebo and other β-blockers. This study was designed to compare the effects of carvedilol and bisoprolol in patients with chronic HF in a single center.Methods: It was a quasi experimental study. A total of 288 cases of heart failure were selected by purposive sampling, from January 2017 to June 2017. Each patient was allocated into either of the two groups, and was continued receiving treatment with either bisoprolol (Group-I) or carvedilol (Group-II). Each patient was evaluated clinically and echocardiographically at the beginning of treatment (baseline) and at the end of 3rd month. Echocardiography was performed to find out change in left ventricular systolic function.Result: After 3 months of treatment, ejection fraction was found higher in the bisoprolol group (42.6 ± 6.5 versus 38.3 ± 4.6%; P < 0.05). Ejection fraction (EF) changes were 8.4% in bisoprolol group and 4.1% in carvedilol group. A significant reduction in left ventricular end-systolic volume (21.9±2.5 in group I versus 14.9±5.7 in group II; P < 0.05) and left ventricular systolic diameter (3.2±0.1 in group I versus 2.3±0.5 in group II; P<0.05) occurred after 3 months of treatment. But no significant differences were observed in left ventricular end-diastolic volume (10.1±3.2 versus 6.1±6.4; P=0.101) and left ventricular diastolic diameter (1.7±0.8 versus 1.3±0.8; P=0.081) between groups. Three months after treatment, heart rate was reduced in the bisoprolol group from 87.7±9 to 74.5±8.1 and carvedilol group from 88.8±9.1 to 80.1±8.7. Differences in heart rate responses between 2 groups were not statistically significant (P=0.113). Assessment of blood pressure three months later of treatment shows, systolic blood pressure (SBP) and diastolic blood pressure (DBP) were improved in both group but difference between two groups were statistically non significant (p>0.05).Conclusion: In this study, bisoprolol was superior to carvedilol in increasing left-ventricular ejection fraction, improving left ventricular end systolic volume and left ventricular end systolic diameter but no significant difference was observed in LV end diastolic volume, LV end diastolic diameter, heart rate and blood pressure.University Heart Journal Vol. 14, No. 1, Jan 2018; 3-8

scholarly journals Muscle metaboreflex-induced increases in effective arterial elastance: effect of heart failure

2020 ◽  
Vol 319 (1) ◽  
pp. R1-R10 ◽  
Author(s):  
Joseph Mannozzi ◽  
Jasdeep Kaur ◽  
Marty D. Spranger ◽  
Mohamed-Hussein Al-Hassan ◽  
Beruk Lessanework ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Dynamic Exercise ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Muscle Metaboreflex ◽  
Effective Arterial Elastance

Dynamic exercise elicits robust increases in sympathetic activity in part due to muscle metaboreflex activation (MMA), a pressor response triggered by activation of skeletal muscle afferents. MMA during dynamic exercise increases arterial pressure by increasing cardiac output via increases in heart rate, ventricular contractility, and central blood volume mobilization. In heart failure, ventricular function is compromised, and MMA elicits peripheral vasoconstriction. Ventricular-vascular coupling reflects the efficiency of energy transfer from the left ventricle to the systemic circulation and is calculated as the ratio of effective arterial elastance ( Ea) to left ventricular maximal elastance ( Emax). The effect of MMA on Ea in normal subjects is unknown. Furthermore, whether muscle metaboreflex control of Ea is altered in heart failure has not been investigated. We utilized two previously published methods of evaluating Ea [end-systolic pressure/stroke volume ( EaPV)] and [heart rate × vascular resistance ( EaZ)] during rest, mild treadmill exercise, and MMA (induced via partial reductions in hindlimb blood flow imposed during exercise) in chronically instrumented conscious canines before and after induction of heart failure via rapid ventricular pacing. In healthy animals, MMA elicits significant increases in effective arterial elastance and stroke work that likely maintains ventricular-vascular coupling. In heart failure, Ea is high, and MMA-induced increases are exaggerated, which further exacerbates the already uncoupled ventricular-vascular relationship, which likely contributes to the impaired ability to raise stroke work and cardiac output during exercise in heart failure.

scholarly journals Acute Hemodynamic Effects and Tolerability of Phosphodiesterase-1 Inhibition With ITI-214 in Human Systolic Heart Failure

2021 ◽  
Author(s):  
Nisha A. Gilotra ◽  
Adam D. DeVore ◽  
Thomas J. Povsic ◽  
Allison G. Hays ◽  
Virginia S. Hahn ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Single Dose ◽  
Adverse Events ◽  
Ejection Fraction ◽  
Systolic Heart Failure ◽  
Left Ventricular ◽  
Guanosine Monophosphate ◽  
Reduced Ejection Fraction

Background: PDE1 (phosphodiesterase type 1) hydrolyzes cyclic adenosine and guanosine monophosphate. ITI-214 is a highly selective PDE1 inhibitor that induces arterial vasodilation and positive inotropy in larger mammals. Here, we assessed pharmacokinetics, hemodynamics, and tolerability of single-dose ITI-214 in humans with stable heart failure with reduced ejection fraction. Methods: Patients with heart failure with reduced ejection fraction were randomized 3:1 to 10, 30, or 90 mg ITI-214 single oral dose or placebo (n=9/group). Vital signs and electrocardiography were monitored predose to 5 hours postdose and transthoracic echoDoppler cardiography predose and 2-hours postdose. Results: Patient age averaged 54 years; 42% female, and 60% Black. Mean systolic blood pressure decreased 3 to 8 mm Hg ( P <0.001) and heart rate increased 5 to 9 bpm ( P ≤0.001 for 10, 30 mg doses, RM-ANCOVA). After 4 hours, neither blood pressure or heart rate significantly differed among cohorts (supine or standing). ITI-214 increased mean left ventricular power index, a relatively load-insensitive inotropic index, by 0.143 Watts/mL 2 ·10 4 ( P =0.03, a +41% rise; 5–71 CI) and cardiac output by 0.83 L/min ( P =0.002, +31%, 13–49 CI) both at the 30 mg dose. Systemic vascular resistance declined with 30 mg (–564 dynes·s/cm– 5 , P <0.001) and 90 mg (–370, P =0.016). Diastolic changes were minimal, and no parameters were significantly altered with placebo. ITI-214 was well-tolerated. Five patients had mild-moderate hypotension or orthostatic hypotension recorded adverse events. There were no significant changes in arrhythmia outcome and no serious adverse events. Conclusions: Single-dose ITI-214 is well-tolerated and confers inodilator effects in humans with heart failure with reduced ejection fraction. Further investigations of its therapeutic utility are warranted. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03387215.

Abstract 13027: Differential Direct Effects of Equal Hypotensive Natriuretic Peptides (NPs) of ANP, BNP and CNP on Left Ventricular Contractile Performance in Heart Failure: Assessment by Left Ventricular Pressure-Volume Analysis

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Che Cheng ◽  
Zhi Zhang ◽  
Tiankai Li ◽  
Xiaowei Zhang ◽  
Xiaoqiang Sun ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Natriuretic Peptides ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Lv Function ◽  
Arterial Elastance ◽  
Inotropic Effects ◽  
Cardiac Effects

Background: Natriuretic peptides (NPs) play a crucial role in maintaining cardiovascular homeostasis. NPs stimulate the production and release of cGMP, leading to the vasodilating and natriuretic actions. In heart failure (HF), circulating and cardiac ANP, BNP, and CNP are increased and exhibit a range of actions. However, although they serve as therapeutic agents, their direct cardiac effects in HF are uncertain due to the confounding influence of NPs-produced changes in loading condition on conventional measures of LV function. We test the hypothesis that equal hypotensive 3 NPs may have different inotropic effects on LV contractility and relaxation in HF. Methods: We assessed the cardiac effects of intravenous infusion (20 min) of ANP (2 μg/kg plus 0.5 μg/kg/min), BNP (2 μg/kg plus 0.04 μg/kg/min) and CNP (2 μg/kg plus 0.4 μg/kg/min) on different days in 6 instrumented conscious dogs with pacing-induced HF by using pressure (P)-volume (V) analysis, a load-independent measure of LV contractility. Results: Versus baselines, 3 NPs produced arterial vasodilation with similar and significant decreases in LV end-systolic pressure (10 to 12 mmHg) with relatively unchanged heart rate. ANP caused significant reductions (13%) of E ES (4.2 vs 4.8 mmHg/ml) and M SW (54.6 vs 62.8 mmHg). The time constant of LV relaxation (τ, 45.1 vs 37.6 ms) was lengthened. The LV-arterial coupling, E ES / E A (arterial elastance) (0.57 vs 0.58) was unaltered. The peak mitral flow, dV/dt max was only increased by 7% (178 vs 166 ml/s). With BNP, there were no significant changes in E ES (5.1 vs 4.9 mmHg/ml) and M SW, but E ES /E A was improved 30% (0.74 vs 0.57) due to decreased E A . τ (33.4 vs 37.9 ms) was significantly shortened and dV/dt max increased 15% (189 vs 165 ml/s). In contrast, CNP produced significant increases (~30%) in E ES (6.3 vs 4.8 mmHg/ml) and M SW (80.5 vs 62.4 mmHg) with enhanced increase in E ES /E A (50%, 0.87vs 0.58), but decrease in τ (25%, 28.4 vs 38.1 ms) and significantly greater augmented dV/dt max (25%, 205 vs 164 ml/s). Similar observations of NPs were made at constant heart rate, or after autonomic blockade. Conclusion: In conscious dogs with HF, equal hypotensive ANP, BNP and CNP have negative, no effect, and positive inotropic effects on LV contractility and relaxation, respectively.

scholarly journals Heart Rate–Induced Myocardial Ca 2+ Retention and Left Ventricular Volume Loss in Patients With Heart Failure With Preserved Ejection Fraction

2020 ◽  
Vol 9 (17) ◽  
Author(s):  
Daniel N. Silverman ◽  
Mehdi Rambod ◽  
Daniel L. Lustgarten ◽  
Robert Lobel ◽  
Martin M. LeWinter ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Sinus Rhythm ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Preserved Ejection Fraction ◽  
Volume Loss ◽  
Heart Rates ◽  
Patients With Heart Failure

Background Increases in heart rate are thought to result in incomplete left ventricular (LV) relaxation and elevated filling pressures in patients with heart failure with preserved ejection fraction (HFpEF). Experimental studies in isolated human myocardium have suggested that incomplete relaxation is a result of cellular Ca 2+ overload caused by increased myocardial Na + levels. We tested these heart rate paradigms in patients with HFpEF and referent controls without hypertension. Methods and Results In 22 fully sedated and instrumented patients (12 controls and 10 patients with HFpEF) in sinus rhythm with a preserved ejection fraction (≥50%) we assessed left‐sided filling pressures and volumes in sinus rhythm and with atrial pacing (95 beats per minute and 125 beats per minute) before atrial fibrillation ablation. Coronary sinus blood samples and flow measurements were also obtained. Seven women and 15 men were studied (aged 59±10 years, ejection fraction 61%±4%). Patients with HFpEF had a history of hypertension, dyspnea on exertion, concentric LV remodeling and a dilated left atrium, whereas controls did not. Pacing at 125 beats per minute lowered the mean LV end‐diastolic pressure in both groups (controls −4.3±4.1 mm Hg versus patients with HFpEF −8.5±6.0 mm Hg, P =0.08). Pacing also reduced LV end‐diastolic volumes. The volume loss was about twice as much in the HFpEF group (controls −15%±14% versus patients with HFpEF −32%±11%, P =0.009). Coronary venous [Ca 2+ ] increased after pacing at 125 beats per minute in patients with HFpEF but not in controls. [Na + ] did not change. Conclusions Higher resting heart rates are associated with lower filling pressures in patients with and without HFpEF. Incomplete relaxation and LV filling at high heart rates lead to a reduction in LV volumes that is more pronounced in patients with HFpEF and may be associated with myocardial Ca 2+ retention.

First clinical trial with etomoxir in patients with chronic congestive heart failure

2000 ◽  
Vol 99 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Stephan SCHMIDT-SCHWEDA ◽  
Christian HOLUBARSCH
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Sarcoplasmic Reticulum ◽  
Left Ventricular Ejection Fraction ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Left Ventricular ◽  
Ventricular Ejection ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

In the failing human myocardium, both impaired calcium homoeostasis and alterations in the levels of contractile proteins have been observed, which may be responsible for reduced contractility as well as diastolic dysfunction. In addition, levels of a key protein in calcium cycling, i.e. the sarcoplasmic reticulum Ca2+-ATPase, and of the α-myosin heavy chain have been shown to be enhanced by treatment with etomoxir, a carnitine palmitoyltransferase inhibitor, in normal and pressure-overloaded rat myocardium. We therefore studied, for the first time, the influence of long-term oral application of etomoxir on cardiac function in patients with chronic heart failure. A dose of 80 mg of etomoxir was given once daily to 10 patients suffering from heart failure (NYHA functional class II–III; mean age 55±4 years; one patient with ischaemic heart disease and nine patients with dilated idiopathic cardiomyopathy; all male), in addition to standard therapy. The left ventricular ejection fraction was measured echocardiographically before and after a 3-month period of treatment. Central haemodynamics at rest and exercise (supine position bicycle) were defined by means of a pulmonary artery catheter and thermodilution. All 10 patients improved clinically; no patient had to stop taking the study medication because of side effects; and no patient died during the 3-month period. Maximum cardiac output during exercise increased from 9.72±1.25 l/min before to 13.44±1.50 l/min after treatment (P < 0.01); this increase was mainly due to an increased stroke volume [84±7 ml before and 109±9 ml after treatment (P < 0.01)]. Resting heart rate was slightly reduced (not statistically significant). During exercise, for any given heart rate, stroke volume was significantly enhanced (P < 0.05). The left ventricular ejection fraction increased significantly from 21.5±2.6% to 27.0±2.3% (P < 0.01). In acute studies, etomoxir showed neither a positive inotropic effect nor vasodilatory properties. Thus, although the results of this small pilot study are not placebo-controlled, all patients seem to have benefitted from etomoxir treatment. Etomoxir, which has no acute inotropic or vasodilatory properties and is thought to increase gene expression of the sarcoplasmic reticulum Ca2+-ATPase and the α-myosin heavy chain, improved clinical status, central haemodynamics at rest and during exercise, and left ventricular ejection fraction.

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