scholarly journals Impaired myocardial function does not explain reduced left ventricular filling and stroke volume at rest or during exercise at high altitude

2015 ◽  
Vol 119 (10) ◽  
pp. 1219-1227 ◽  
Author(s):  
Mike Stembridge ◽  
Philip N. Ainslie ◽  
Michael G. Hughes ◽  
Eric J. Stöhr ◽  
James D. Cotter ◽  
...  
Keyword(s):  
Stroke Volume ◽  
High Altitude ◽  
Systolic Function ◽  
Left Ventricular ◽  
Limiting Factor ◽  
End Diastolic Volume ◽  
Apical Rotation ◽  
Diastolic Relaxation ◽  
Ventricular Filling

Impaired myocardial systolic contraction and diastolic relaxation have been suggested as possible mechanisms contributing to the decreased stroke volume (SV) observed at high altitude (HA). To determine whether intrinsic myocardial performance is a limiting factor in the generation of SV at HA, we assessed left ventricular (LV) systolic and diastolic mechanics and volumes in 10 healthy participants (aged 32 ± 7; mean ± SD) at rest and during exercise at sea level (SL; 344 m) and after 10 days at 5,050 m. In contrast to SL, LV end-diastolic volume was ∼19% lower at rest ( P = 0.004) and did not increase during exercise despite a greater untwisting velocity. Furthermore, resting SV was lower at HA (∼17%; 60 ± 10 vs. 70 ± 8 ml) despite higher LV twist (43%), apical rotation (115%), and circumferential strain (17%). With exercise at HA, the increase in SV was limited (12 vs. 22 ml at SL), and LV apical rotation failed to augment. For the first time, we have demonstrated that EDV does not increase upon exercise at high altitude despite enhanced in vivo diastolic relaxation. The increase in LV mechanics at rest may represent a mechanism by which SV is defended in the presence of a reduced EDV. However, likely because of the higher LV mechanics at rest, no further increase was observed up to 50% peak power. Consequently, although hypoxia does not suppress systolic function per se, the capacity to increase SV through greater deformation during submaximal exercise at HA is restricted.

scholarly journals Female hormones prevent sepsis-induced cardiac dysfunction: an experimental randomized study

2021 ◽  
Author(s):  
Alexandre Xerri ◽  
Frédéric Gallardo ◽  
Frank Kober ◽  
Calypso Mathieu ◽  
Natacha Fourny ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Stroke Volume ◽  
Cardiac Dysfunction ◽  
Randomized Study ◽  
Calcium Signalling ◽  
Left Ventricular ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
End Diastolic Volume

Abstract Introduction: Although epidemiologic research has demonstrated significant differences in incidence and outcomes of sepsis according to gender, their underlying biological mechanisms are poorly understood. Here, we studied the influence of hormonal status by comparing in vivo cardiac performances measured by MRI in non-ovariectomized and ovariectomized septic female rats.Methods: Control and ovariectomized rats were randomly allocated to the following groups: sham, sepsis and sepsis plus landiolol. Sepsis was induced by caecum ligation and punction (CLP). Cardiac MRI was carried out 18 hours after induction of sepsis to assess in vivo cardiac function. Capillary permeability was evaluated by Evans Blue administration and measurement of its tissue extravasation. Variation in myocardial gene expression was also assessed by qPCR in the left ventricular tissue.Results: Sepsis reduced indexed stroke volume, cardiac index and indexed end-diastolic volume compared to sham group in ovariectomized females whereas it had no effect in control females. Landiolol increased the indexed stroke volume by reversing the indexed end-diastolic volume reduction after sepsis in ovariectomized females, while it decreased indexed stroke volume and cardiac index in control. Major differences in the left ventricular expression of genes coding for calcium signalling and contractile proteins were observed in ovariectomized females compared to control after sepsis, partially restored by landiolol. Moreover, in control females, increase of apoptotic genes by sepsis was maintained after landiolol infusion.Conclusions: Sepsis decreased in vivo cardiac performances in ovariectomized females but not in control females, presumably associated with apoptosis and calcium protein-related contractility defects. Administration of landiolol prevents this cardiac dysfunction in ovariectomized females, while it has deleterious effects in control females.

Impaired left ventricular filling due to right-to-left ventricular interaction in patients with pulmonary arterial hypertension

2006 ◽  
Vol 290 (4) ◽  
pp. H1528-H1533 ◽  
Author(s):  
C. Tji-Joong Gan ◽  
Jan-Willem Lankhaar ◽  
J. Tim Marcus ◽  
Nico Westerhof ◽  
Koen M. Marques ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Left Atrial ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Left Ventricular Filling ◽  
Filling Rate ◽  
End Diastolic Volume ◽  
Ventricular Interaction ◽  
Pulmonary Arterial ◽  
Ventricular Filling

The aim of this study was to investigate the contribution of direct right-to-left ventricular interaction to left ventricular filling and stroke volume in 46 patients with pulmonary arterial hypertension (PAH) and 18 control subjects. Stroke volume, right and left ventricular volumes, left ventricular filling rate, and interventricular septum curvature were measured by magnetic resonance imaging and left atrial filling by transesophageal echocardiography. Stroke volume, left ventricular end-diastolic volume, and left ventricular peak filling rate were decreased in PAH patients compared with control subjects: 28 ± 13 vs. 41 ± 10 ml/m2( P < 0.001), 46 ± 14 vs. 61 ± 14 ml/m2( P < 0.001), and 216 ± 90 vs. 541 ± 248 ml/s ( P < 0.001), respectively. Among PAH patients, stroke volume did not correlate to right ventricular end-diastolic volume or mean pulmonary arterial pressure but did correlate to left ventricular end-diastolic volume ( r = 0.62, P < 0.001). Leftward interventricular septum curvature was correlated to left ventricular filling rate ( r = 0.64, P < 0.001) and left ventricular end-diastolic volume ( r = 0.65, P < 0.001). In contrast, left atrial filling was normal and not correlated to left ventricular end-diastolic volume. In PAH patients, ventricular interaction mediated by the interventricular septum impairs left ventricular filling, contributing to decreased stroke volume.

P4465Acute Cardio-Selective Functional Modulation via a Small-Molecule Direct Myosin-Attenuator (MYK-581) Preserves Diaphragmatic Function in vivo: Comparison versus Disopyramide

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C L Del Rio ◽  
S Roof ◽  
A R Anto ◽  
R L Anderson
Keyword(s):  
Exercise Capacity ◽  
Small Molecule ◽  
Systolic Function ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Mechanically Ventilated ◽  
Diaphragmatic Function ◽  
Sprague Dawley Rats ◽  
Ventricular Filling

Abstract Background Hypertrophic cardiomyopathy (HCM) is a heritable cardiac disease characterized by hyper-contractility, hindered relaxation, and impaired exercise capacity. Conventional negative inotropes can alleviate enhanced inotropy in HCM, but do not improve ventricular filling and have the potential to further decrease exercise capacity due to their off/on-target systemic effects. Recently, a novel small molecule cardiac-myosin attenuator, Mavacamten, has been shown to normalize hyper-contractility in the setting of HCM. This study evaluated and compared the in vivo functional selectivity of MYK-581, a mavacamten analog, with those of disopyramide (DISO), a commonly-used negative inotrope. Methods In vivo, the acute cardiac (left ventricular pressures) and neuro-muscular (force of diaphragmatic and skeletal muscle contractions) responses to MYK-581 (up to 0.5 mg/kg IV) and DISO (up to 10 mg/kg IV) were simultaneously evaluated using anesthetized and mechanically-ventilated Sprague-Dawley rats; diaphragmatic (both intrinsic and phrenic nerve stimulated) and skeletal contractions (stimulated quadriceps) were measured via strain gauges. Results MYK-581 decreased indices of systolic function (dP/dtmax: −32±2% and vmax: −14±2%, P<0.05 vs. pre-dose) and increased LV EDV (+9±2%, P<0.05), while preserving EDP (6±1 to 6±1 mmHg), suggesting improved ventricular distensibility. Despite these marked cardiac effects, MYK-581 preserved both diaphragmatic (23.7±2.0 to 23.3±2.2 g) and skeletal in situ function (14.9±1.4 to 13.9±0.8 g). In contrast, DISO at matched levels of negative inotropy (dP/dtmax: −25±2% and vmax: −19±2%, P<0.05 vs. pre-dose) depressed diaphragmatic force (−16±3%, 23.8±1.9 to 19.8±1.2 g, P<0.05). Finally, the cardiac selectivity of MYK-581 was confirmed in kinetic experiments evaluating the Ca2+-activated ATPase activity of both cardiac and diaphragmatic myofibrils. Conclusions Direct myosin modulation with MYK-581, a mavacamten analog, is characterized in vivo by reductions in systolic function with preserved filling pressures and improved LV compliance. Moreover, this cardiovascular profile was devoid in vivo of diaphragmatic/skeletal off-target effects that could further hinder exercise capacity in patients with HCM.

scholarly journals Prognostic value of NT-proBNP for myocardial recovery in peripartum cardiomyopathy (PPCM)

2021 ◽  
Author(s):  
J. Hoevelmann ◽  
E. Muller ◽  
F. Azibani ◽  
S. Kraus ◽  
J. Cirota ◽  
...  
Keyword(s):  
Prognostic Value ◽  
Systolic Function ◽  
Point Of Care ◽  
Diagnostic Value ◽  
Left Ventricular ◽  
Peripartum Cardiomyopathy ◽  
Lv Function ◽  
Myocardial Recovery ◽  
End Diastolic Volume

Abstract Introduction Peripartum cardiomyopathy (PPCM) is an important cause of pregnancy-associated heart failure worldwide. Although a significant number of women recover their left ventricular (LV) function within 12 months, some remain with persistently reduced systolic function. Methods Knowledge gaps exist on predictors of myocardial recovery in PPCM. N-terminal pro-brain natriuretic peptide (NT-proBNP) is the only clinically established biomarker with diagnostic value in PPCM. We aimed to establish whether NT-proBNP could serve as a predictor of LV recovery in PPCM, as measured by LV end-diastolic volume (LVEDD) and LV ejection fraction (LVEF). Results This study of 35 women with PPCM (mean age 30.0 ± 5.9 years) had a median NT-proBNP of 834.7 pg/ml (IQR 571.2–1840.5) at baseline. Within the first year of follow-up, 51.4% of the cohort recovered their LV dimensions (LVEDD < 55 mm) and systolic function (LVEF > 50%). Women without LV recovery presented with higher NT-proBNP at baseline. Multivariable regression analyses demonstrated that NT-proBNP of ≥ 900 pg/ml at the time of diagnosis was predictive of failure to recover LVEDD (OR 0.22, 95% CI 0.05–0.95, P = 0.043) or LVEF (OR 0.20 [95% CI 0.04–0.89], p = 0.035) at follow-up. Conclusions We have demonstrated that NT-proBNP has a prognostic value in predicting LV recovery of patients with PPCM. Patients with NT-proBNP of ≥ 900 pg/ml were less likely to show any improvement in LVEF or LVEDD. Our findings have implications for clinical practice as patients with higher NT-proBNP might require more aggressive therapy and more intensive follow-up. Point-of-care NT-proBNP for diagnosis and risk stratification warrants further investigation.

Resizable Ventricular Patch Plasty in the Porcine Left Ventricle a Pilot Study

2010 ◽  
Vol 5 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Willemijn H. F. Huijgen ◽  
Paul F. Gründeman ◽  
Tycho van der Spoel ◽  
Maarten-Jan Cramer ◽  
Paul Steendijk ◽  
...  
Keyword(s):  
Pilot Study ◽  
Animal Experiments ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Left Ventricular Aneurysm ◽  
Patch Shape ◽  
End Diastolic Volume ◽  
Patch Plasty

Objective Endoventricular circular patch plasty is a method used to reconstruct the ventricular cavity in patients with (post) ischemic left ventricular aneurysm or global dilatation. However, late redilatation with mitral regurgitation has been reported, in which postoperative apex shape seems to play an important role. We studied the feasibility of ventricular volume downsizing with a variably shaped patch in porcine hearts. Methods In five in vitro and two acute animal experiments, a dyskinetic aneurysm was simulated with a pericardial insert. Reducing patch surface by changing patch shape diminished end-diastolic volume. In vitro, static end-diastolic volume was determined for each patch shape using volumetry and echocardiography. In the acute animal experiments, preliminary observations of patch behavior in live material were made, and pressure/time relationship, dPdTmax, was registered. Results In vitro, bringing the convex patch into a flat plane reduced LV volume from 66 ± 7 mL (aneurysm) to 49 ± 5 mL. Four of 5 patch shapes further reduced volume to a mean of 38 ± 7 mL (P = 0.03). The in vitro echocardiographic measurements correlated with volumetry findings (r = 0.81). In the acute animal experiments, dPdTmax varied with patch shape, independent of volume changes. Conclusions In this pilot study, in vitro shape configuration of the resizable ventricular patch resulted in a calibrated end-diastolic volume reduction. The data of the two in vivo pilot experiments clearly indicate that change in patch configuration in the situation of more or less unchanged end-diastolic volume had impact on cardiac performance. Future studies must substantiate the results of this observation.

P613Cardiac magnetic resonance imaging derived left ventricular mechanical function in patients with atrial fibrillation and left atrial low voltage zones

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Ulbrich ◽  
R S Schoenbauer ◽  
B Kirstein ◽  
J Tomala ◽  
Y Huo ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Atrial Fibrillation ◽  
Magnetic Resonance ◽  
Stroke Volume ◽  
Left Atrial ◽  
Low Voltage ◽  
Left Ventricular ◽  
Left Ventricular Stroke Volume ◽  
Resonance Imaging ◽  
Ventricular Filling

Abstract Background The relation of left atrial low voltage zones (LVZ) to left ventricular function in patients undergoing pulmonary vein isolation (PVI) is not known. Objective To explore the relationship of left atrial low voltage zones (LVZ) on left ventricular function in patients with atrial fibrillation. Methods From June to Nov. 2018, 107 (mean age 67y, 70 men, 73 persistent AF) consecutive patients with symptomatic AF underwent a PVI with LVZ mapping. Before PVI the left ventricular ejection fraction (EF) and stroke volume (SV) were measured by cardiac magnetic resonance imaging (CMR). From feature-tracking of CMR-cine images left ventricular global, systolic and diastolic longitudinal strains (GLS), circumferential strains (GCS) and radial strains (GRS) were calculated. Results Of 59 patients CMR scanning in sinus rhythm was performed, LVZ were present in 24 patients. LVEF was significantly lower in patients with left atrial LVZ (62±9% vs. 55±15%) (p=0,03). Left ventricular stroke volume was significantly decreased by the extent of LVZ (94±23 vs. 72±21ml), (p=0,03). The left ventricular diastolic strains during ventricular filling (caused by atrial contraction) of GLS (r=−0,52), GCS (r=−0,65) and GRS (r=−0,65) were highly signifcantly correlated to the occurence and extent of LVZ (each p<0,001 respectively). The only systolic ventricular strain was GLS, which decreased (r=−0,3, p=0,03) by the occurance of atrial low voltage. Conclusion The active, atrial part of diastolic left ventricular filling properties is impaired by the occurrence and extent of left atrial LVZ. In patients with left atrial LVZ the left ventricular stroke volume and ejection fraction is decreased already in sinus rhythm. It seems possible that atrial mechanical dysfunction and presence of atrial low voltage maybe predicted by LV diastolic strain analysis.

Use of the Frank-Starling mechanism during submaximal versus maximal upright exercise

1986 ◽  
Vol 251 (6) ◽  
pp. H1101-H1105 ◽  
Author(s):  
G. D. Plotnick ◽  
L. C. Becker ◽  
M. L. Fisher ◽  
G. Gerstenblith ◽  
D. G. Renlund ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Blood Pool ◽  
Left Ventricular ◽  
Peak Exercise ◽  
Vigorous Exercise ◽  
Systolic Volume ◽  
Early Exercise ◽  
End Diastolic Volume ◽  
Blood Pool Scintigraphy ◽  
End Systolic Volume

To evaluate the extent to which the Frank-Starling mechanism is utilized during successive stages of vigorous upright exercise, absolute left ventricular end-diastolic volume and ejection fraction were determined by gated blood pool scintigraphy at rest and during multilevel maximal upright bicycle exercise in 30 normal males aged 26-50 yr, who were able to exercise to 125 W or greater. Left ventricular end-systolic volume, stroke volume, and cardiac output were calculated at rest and during each successive 3-min stage of exercise [25, 50, 75, 100, and 125–225 W (peak)]. During early exercise (25 W), end-diastolic and stroke volumes increased (+17 +/- 1 and +31 +/- 4%, respectively), with no change in end-systolic volume. With further exercise (50–75 W) end-diastolic volume remained unchanged as end-systolic volume decreased (-12 +/- 4 and -24 + 5%, respectively). At peak exercise end-diastolic volume decreased to resting level, stroke volume remained at a plateau, and end-systolic volume further decreased (-48 +/- 7%). Thus the Frank-Starling mechanism is used early in exercise, perhaps because of a delay in sympathetic mobilization, and does not appear to play a role in the later stages of vigorous exercise.

Increased ventricular stiffness and decreased cardiac function in Atlantic cod (Gadus morhua) at high temperatures

2013 ◽  
Vol 305 (8) ◽  
pp. R864-R876 ◽  
Author(s):  
Douglas A. Syme ◽  
A. Kurt Gamperl ◽  
Gordon W. Nash ◽  
Kenneth J. Rodnick
Keyword(s):  
Stroke Volume ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Isometric Force ◽  
Full Range ◽  
Large Strains ◽  
High Heart Rate ◽  
Ventricular Filling ◽  
Ventricular Trabeculae

We employed the work loop method to study the ability of ventricular and atrial trabeculae from Atlantic cod to sustain power production during repeated contractions at acclimation temperatures (10°C) and when acutely warmed (20°C). Oxygen tension (Po2) was lowered from 450 to 34% air saturation to augment the thermal stress. Preparations worked under conditions simulating either a large stroke volume (35 contractions/min rate, 8–12% muscle strain) or a high heart rate (70 contractions/min, 2–4% strain), with power initially equal under both conditions. The effect of declining Po2 on power was similar under both conditions but was temperature and tissue dependent. In ventricular trabeculae at 10°C (and atria at 20°C), shortening power declined across the full range of Po2 studied, whereas the power required to lengthen the muscle was unaffected. Conversely, in ventricular trabeculae at 20°C, there was no decline in shortening power but an increase in lengthening power when Po2 fell below 100% air saturation. Finally, when ventricular trabeculae were paced at rates of up to 115 contractions/min at 20°C (vs. the maximum of 70 contractions/min in vivo), they showed marked increases in both shortening and lengthening power. Our results suggest that although elevated heart rates may not impair ventricular power as they commonly do isometric force, limited atrial power and the increased work required to expand the ventricle during diastole may compromise ventricular filling and hence, stroke volume in Atlantic cod at warm temperatures. Neither large strains nor high contraction rates convey an apparent advantage in circumventing this.

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