Morbidity and Mortality After Traumatic Pneumonectomy: The Effect of Compromised Oxygenation and Cardiac Function

1995 ◽  
Vol 10 (4) ◽  
pp. 193-199 ◽  
Author(s):  
Wendell A. Goins
Keyword(s):  
Cardiac Function ◽  
Air Embolism ◽  
Gunshot Wounds ◽  
Left Ventricular ◽  
Stroke Work ◽  
Hemodynamic Changes ◽  
Contralateral Lung ◽  
Level 1 ◽  
The Right ◽  
And Control

I describe the pathophysiological and hemodynamic events that occur after an emergency pneumonectomy for trauma and how they impact on subsequent mortality. Four patients were identified as requiring an emergency right pneumonectomy for trauma at a level 1 Urban Trauma Center within a 39-month period. A retrospective review of their hospital course served as the basis for our analysis. Three patients sustained gunshot wounds and one patient was a victim of blunt trauma. Hemodynamic data were available for three patients who survived more than 24 hours. All patients presented in shock and required massive transfusion. One patient died in the operating room due to air embolism and shock. After pneumonectomy, there was an increase in pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) more than 2 times normal, which coincided with a decrease in stroke volume, cardiac output, and right and left ventricular stroke work (RVSW/LVSW). The RVSW gradually increased to above normal levels by postoperative day 5, whereas the LVSWI remained below normal. Adult respiratory distress syndrome (ARDS) developed in all patients early in the postoperative period. There was evidence of oxygen delivery (DO2) dependent of oxygen consumption (VO2) and the DO2 remained below normal despite inotrope administration. The remaining three patients died 7 to 13 days after surgery due to various combinations of ARDS, cardiac failure, and sepsis. Until we have better methods to decrease PAP selectively, traumatic pneumonectomy should be avoided if possible, especially when it involves the right side or is associated with a contralateral lung injury. Early operative intervention and control of the pulmonary hilum may lessen the severity of shock. The hemodynamic changes that occur after pneumonectomy for trauma becomes additive in the presence of ARDS. This combination results in inadequate cardiac function, oxygen transport, and, ultimately, death.

Abstract 3292: Cardiac Dysfunction Induced By Chronic Restrain Stress Is Mediated By Opioid Receptors

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Jinping Gao ◽  
Chu C Chua ◽  
Deling Yin ◽  
Hong Wang ◽  
Ronald C Hamdy ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Chronic Stress ◽  
Opioid Receptors ◽  
Cardiac Dysfunction ◽  
Left Ventricular ◽  
Opioid Antagonist ◽  
Stroke Work ◽  
Ventricular Performance ◽  
Major Health Problem ◽  
Stressed Group

Psychological and physical stressors are a major health problem in our society. The effect of chronic stress on myocardial function has not been assessed. Our hypothesis is that chronic stress induces cardiac dysfunction and that its effect is mediated by activation of opioid receptors (OPR). Six week-old male ICR mice were restrained for 12 h with no food and water. This was followed by 12 h of rest with food and water provided ad labium. Unstressed (control) mice were kept in the original cage and were not given food and water during the stress period of the experimental group. Left ventricular performance was analyzed in mice anesthetized with 2% isoflurane using an ARIA pressure-volume conductance system (Millar Instruments). Our studies demonstrated for the first time that cardiac function was significantly depressed in restrained mice, as evidenced by a significant decrease in body weight (9%), heart rate (21%), stroke volume (38%), cardiac output (52%), ejection fraction (27%) and preload recruitable stroke work (43%). Systolic function (control vs. stressed group) (P<0.05), was 88 ± 2.2 vs. 68 ± 2.8 mmHg for end-systolic pressure, 6.1 ± 0.15 vs. 7.6 ± 0.15 μl for end-systolic volume, and 11,471 ± 913 vs. 5,860 ± 761 mmHg/s for +dP/dt. Diastolic function (control vs. stressed group) (P<0.05), was 2.9 ± 0.3 vs. 5.0 ± 0.5 mmHg for end-diastolic pressure, 17.1 ± 0.4 vs. 14.4 ± 0.5 μl for end-diastolic volume, 7,678 ± 419 vs. 4,195 ± 358 mmHg/s for -dP/dt, and 7.1 ± 0.5 vs. 10.8 ± 1.1 ms for tau (time constant of isovolumic relaxation). Peripheral vascular resistance (Ea) increased from 7.7 ± 0.2 in the control group to 9.8 ± 0.7 mmHg/μ l in the stressed group (P<0.05). Administration of an opioid antagonist naltrexone (8 mg/kg, i.p.) during each cycle of stress completely restored the cardiac function of stressed mice. Naltrexone alone had no effect on cardiac function in unstressed mice. These intriguing data suggest that opioid receptors are involved in the chronic stress-induced cardiac dysfunction and that treatment with an opioid antagonist can prevent this cardiac dysfunction.

scholarly journals Environmentally persistent free radicals decrease cardiac function and increase pulmonary artery pressure

2012 ◽  
Vol 303 (9) ◽  
pp. H1135-H1142 ◽  
Author(s):  
Sarah Mahne ◽  
Gin C. Chuang ◽  
Edward Pankey ◽  
Lucy Kiruri ◽  
Philip J. Kadowitz ◽  
...  
Keyword(s):  
Free Radicals ◽  
Left Ventricle ◽  
Cardiac Function ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Diastolic Pressure ◽  
Silica Particles ◽  
Left Ventricular ◽  
Heme Oxygenase 1 ◽  
Stroke Work

Epidemiological studies have consistently linked inhalation of particulate matter (PM) to increased cardiac morbidity and mortality, especially in at risk populations. However, few studies have examined the effect of PM on baseline cardiac function in otherwise healthy individuals. In addition, airborne PM contain environmentally persistent free radicals (EPFR) capable of redox cycling in biological systems. The purpose of this study was to determine whether nose-only inhalation of EPFRs (20 min/day for 7 days) could decrease baseline left ventricular function in healthy male Sprague-Dawley rats. The model EPFR tested was 1,2-dichlorobenzene chemisorbed to 0.2-μm-diameter silica/CuO particles at 230°C (DCB230). Inhalation of vehicle or silica particles served as controls. Twenty-four hours after the last exposure, rats were anesthetized (isoflurane) and ventilated (3 l/min), and left ventricular function was assessed using pressure-volume catheters. Compared with controls, inhalation of DCB230 significantly decreased baseline stroke volume, cardiac output, and stroke work. End-diastolic volume and end-diastolic pressure were also significantly reduced; however, ventricular contractility and relaxation were not changed. DCB230 also significantly increased pulmonary arterial pressure and produced hyperplasia in small pulmonary arteries. Plasma levels of C-reactive protein were significantly increased by exposure to DCB230, as were levels of heme oxygenase-1 and SOD2 in the left ventricle. Together, these data show that inhalation of EPFRs, but not silica particles, decreases baseline cardiac function in healthy rats by decreasing cardiac filling, secondary to increased pulmonary resistance. These EPFRs also produced systemic inflammation and increased oxidative stress markers in the left ventricle.

Immersion before dry simulated dive reduces cardiomyocyte function and increases mortality after decompression

2010 ◽  
Vol 109 (3) ◽  
pp. 752-757 ◽  
Author(s):  
Svein Erik Gaustad ◽  
Alf O. Brubakk ◽  
Morten Høydal ◽  
Daniele Catalucci ◽  
Gianluigi Condorelli ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Survival Time ◽  
Left Ventricular ◽  
Endoplasmic Reticulum Calcium ◽  
Protein Levels ◽  
Left Ventricular Tissue ◽  
Bubble Detection ◽  
Ventricular Tissue ◽  
The Right ◽  
Phospholamban Phosphorylation

Diving and decompression performed under immersed conditions have been shown to reduce cardiac function. The mechanisms for these changes are not known. The effect of immersion before a simulated hyperbaric dive on cardiomyocyte function was studied. Twenty-three rats were assigned to four groups: control, 1 h thermoneutral immersion, dry dive, and 1 h thermoneutral immersion before a dive (preimmersion dive). Rats exposed to a dive were compressed to 700 kPa, maintained for 45 min breathing air, and decompressed linearly to the surface at a rate of 50 kPa/min. Postdive, the animals were anesthetized and the right ventricle insonated for bubble detection using ultrasound. Isolation of cardiomyocytes from the left ventricle was performed and studied using an inverted fluorescence microscope with video-based sarcomere spacing. Compared with a dry dive, preimmersion dive significantly increased bubble production and decreased the survival time (bubble grade 1 vs. 5, and survival time 60 vs. 17 min, respectively). Preimmersion dive lead to 18% decreased cardiomyocyte shortening, 20% slower diastolic relengthening, and 22% higher calcium amplitudes compared with controls. The protein levels of the sarco-endoplasmic reticulum calcium ATPase (SERCA2a), Na+/Ca2+ exchanger (NCX), and phospholamban phosphorylation in the left ventricular tissue were significantly reduced after both dry and preimmersion dive compared with control and immersed animals. The data suggest that immersion before a dive results in impaired cardiomyocyte and Ca2+ handling and may be a cellular explanation to reduced cardiac function observed in humans after a dive.

scholarly journals A case report of unexpected right-to-left shunt under mechanical support for post-infarction ventricular septal defect: evaluation with haemodynamic simulator

2021 ◽  
Vol 5 (8) ◽  
Author(s):  
Arudo Hiraoka ◽  
Keita Saku ◽  
Takuya Nishikawa ◽  
Kenji Sunagawa
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Septal Defect ◽  
Cardiac Function ◽  
Septal Defect ◽  
Left Ventricular ◽  
Haemodynamic Instability ◽  
Shunt Flow ◽  
Oxygenation Level ◽  
The Right

Abstract Background Post-myocardial infarction ventricular septal defect (PIVSD) is a complication of acute myocardial infarction with high mortality. A percutaneous left ventricular assist device, Impella, is currently used in maintaining haemodynamic stability in PIVSD. Case summary A 65-year-old man was transferred to our hospital for treatment of acute myocardial infarction of the proximal right coronary artery. Percutaneous intervention was performed but haemodynamic instability continued. At 10 days after onset, the patient was diagnosed with PIVSD by echocardiogram. To stabilize haemodynamics, we initiated venoarterial extracorporeal membrane oxygenation (ECMO). Three days after ECMO initiation, pulmonary congestion increased and an echocardiogram revealed closed aortic valve and spontaneous echo contrast at the aortic root. After an Impella 2.5 was inserted for unloading of the left ventricle, the oxygenation level and cardiac function rapidly declined. Unexpectedly, an echocardiogram showed a right-to-left shunt (to-and-fro pattern) via PIVSD. By increasing the ECMO and decreasing Impella flow, the shunt flow changed to left-to-right, and oxygenation level and cardiac function improved. Ten days after ECMO was started, elective surgical repair was successfully performed. Conclusion ECPELLA (ECMO + Impella) can offset the adverse effects of isolated ECMO support and reduce the PIVSD shunt flow. However, the risk of right-to-left shunt has not been reported, and ECPELLA caused a right-to-left shunt with deoxygenated systemic perfusion in the present case. A simulation study indicated that the right ventricular failure in PIVSD may pose a risk for right-to-left PIVSD shunt under Impella support.

Effect of vasopressin on left ventricular performance

1993 ◽  
Vol 264 (1) ◽  
pp. H53-H60
Author(s):  
C. P. Cheng ◽  
Y. Igarashi ◽  
H. S. Klopfenstein ◽  
R. J. Applegate ◽  
Z. Shihabi ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Ventricular Performance ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
The Right

We assessed the effect of arginine vasopressin (AVP) on left ventricular (LV) performance in eight conscious dogs. Five minutes after AVP infusion (6 microns.kg-1 x min-1 for 2 min) the plasma AVP was elevated from 3.9 +/- 0.9 to 14.7 +/- 4.6 pg/ml (P < 0.05). With all reflexes intact, AVP caused significant increases in LV end-systolic pressure (P) (112 +/- 8 vs. 122 +/- 7 mmHg, P < 0.05) end-systolic volume (V) (30 +/- 5.8 vs. 38 +/- 7.7 ml, P < 0.05), total systemic resistance (6.2 +/- 1.8 vs. 10.6 +/- 4.0 mmHg.dl-1 x min, P < 0.01) and arterial elastance (Ea) (6.8 +/- 3.0 vs. 8.6 +/- 3.9 mmHg/ml, P < 0.05), while the heart rate (110 +/- 6 vs. 82 +/- 10 beats/min, P < 0.05) and stroke volume (16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml, P < 0.05) were decreased. There was no significant change in the coronary sinus blood flow (82 +/- 19 vs. 78 +/- 22 ml/min, P = not significant). AVP decreased the slopes of LV end-systolic P-V relation (10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml, P < 0.05), the maximal first derivative of LV pressure (dP/dtmax)-end-diastolic volume (VED) relation (135.2 +/- 18.7 vs. 63.1 +/- 7.7 mmHg.s-1 x ml-1, P < 0.05), and the stroke work-VED relation (81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg, P < 0.05) and shifted the relations to the right, indicating a depression of LV performance. A similar increase in Ea produced by methoxamine did not depress LV performance.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Endotoxin impairs cardiac hemodynamics by affecting loading conditions but not by reducing cardiac inotropism

2010 ◽  
Vol 299 (2) ◽  
pp. H492-H501 ◽  
Author(s):  
Li Jianhui ◽  
Nathalie Rosenblatt-Velin ◽  
Noureddine Loukili ◽  
Pal Pacher ◽  
François Feihl ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Myocardial Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Laboratory Animals ◽  
Lv Function ◽  
Stroke Work ◽  
Loading Conditions ◽  
Arterial Elastance ◽  
End Diastolic Volume

Acute myocardial dysfunction is a typical manifestation of septic shock. Experimentally, the administration of endotoxin [lipopolysacharride (LPS)] to laboratory animals is frequently used to study such dysfunction. However, a majority of studies used load-dependent indexes of cardiac function [including ejection fraction (EF) and maximal systolic pressure increment (dP/d tmax)], which do not directly explore cardiac inotropism. Therefore, we evaluated the direct effects of LPS on myocardial contractility, using left ventricular (LV) pressure-volume catheters in mice. Male BALB/c mice received an intraperitoneal injection of E. coli LPS (1, 5, 10, or 20 mg/kg). After 2, 6, or 20 h, cardiac function was analyzed in anesthetized, mechanically ventilated mice. All doses of LPS induced a significant drop in LV stroke volume and a trend toward reduced cardiac output after 6 h. Concomitantly, there was a significant decrease of LV preload (LV end-diastolic volume), with no apparent change in LV afterload (evaluated by effective arterial elastance and systemic vascular resistance). Load-dependent indexes of LV function were markedly reduced at 6 h, including EF, stroke work, and dP/d tmax. In contrast, there was no reduction of load-independent indexes of LV contractility, including end-systolic elastance (ejection phase measure of contractility) and the ratio dP/d tmax/end-diastolic volume (isovolumic phase measure of contractility), the latter showing instead a significant increase after 6 h. All changes were transient, returning to baseline values after 20 h. Therefore, the alterations of cardiac function induced by LPS are entirely due to altered loading conditions, but not to reduced contractility, which may instead be slightly increased.

scholarly journals Levosimendan versus dobutamine for sepsis-induced cardiac dysfunction: a systematic review and meta-analysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dong-Hua Liu ◽  
Yi-Le Ning ◽  
Yan-Yan Lei ◽  
Jing Chen ◽  
Yan-Yan Liu ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Blood Lactate ◽  
Random Effects ◽  
Myocardial Dysfunction ◽  
Length Of Hospital Stay ◽  
Left Ventricular ◽  
Cochrane Library ◽  
Stroke Work ◽  
Cardiovascular Failure ◽  
Significant Difference

AbstractLevosimendan and dobutamine are extensively used to treat sepsis-associated cardiovascular failure in ICU. Nevertheless, the role and mechanism of levosimendan in patients with sepsis-induced cardiomyopathy remains unclear. Moreover, previous studies on whether levosimendan is superior to dobutamine are still controversial. More importantly, these studies did not take changes (before-after comparison to the baseline) in quantitative parameters such as ejection fraction into account with the baseline level. Here, we aimed to determine the pros and cons of the two medicines by assessing the changes in cardiac function and blood lactate, mortality, with the standardized mean difference used as a summary statistic. Relevant studies were obtained by a thorough and disciplined literature search in several notable academic databases, including Google Scholar, PubMed, Cochrane Library and Embase until November 2020. Outcomes included changes in cardiac function, lactic acid, mortality and length of hospital stay. A total of 6 randomized controlled trials were included in this study, including 192 patients. Compared with dobutamine, patients treated with levosimendan had a greater improvement of cardiac index (ΔCI) (random effects, SMD = 0.90 [0.20,1.60]; I2 = 76%, P < 0.01) and left ventricular stroke work index (ΔLVSWI) (random effects, SMD = 1.56 [0.90,2.21]; I2 = 65%, P = 0.04), a significant decrease of blood lactate (Δblood lactate) (random effects, MD =  − 0.79 [− 1.33, − 0.25]; I2 = 68%, P < 0.01) at 24-h after drug intervention, respectively. There was no significant difference between levosimendan and dobutamine on all-cause mortality in ICU (fixed effect, OR = 0.72 [0.39,1.33]; I2 = 0%, P = 0.99). We combine effect sizes related to different measurement parameters to evaluate cardiac function, which implied that septic patients with myocardial dysfunction might have a better improvement of cardiac function by levosimendan than dobutamine (random effects, SMD = 1.05 [0.69,1.41]; I2 = 67%, P < 0.01). This study suggested a significant improvement of CI, LVSWI, and decrease of blood lactate in septic patients with myocardial dysfunction in ICU after 24-h administration of levosimendan than dobutamine. However, the administration of levosimendan has neither an impact on mortality nor LVEF. Septic patients with myocardial dysfunction may partly benefit from levosimendan than dobutamine, mainly embodied in cardiac function improvement.

Abstract 176: Saxagliptin and Tadalafil Differentially Alter Global and Cellular Cardiac Function in a Translational Miniature Swine Model of Left Ventricle Hypertrophy

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Jessica A Hiemstra ◽  
Anne K Gibson ◽  
Jan R Ivey ◽  
Melissa S Cobb ◽  
Christopher P Baines ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Pde5 Inhibitor ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Lv Function ◽  
Swine Model ◽  
Stroke Work ◽  
Wall Stiffness ◽  
Cgmp Signaling ◽  
Whole Heart

Left ventricular (LV) hypertrophy is a common characteristic of heart failure with preserved ejection fraction (HFpEF). Our lab recently characterized a mini-swine model of LV hypertrophy induced by aortic banding (AB) that displays clinical features associated with HFpEF including LV hypertrophy, diastolic dysfunction, and depressed contractile reserve. Disrupted cGMP signaling, a result of impaired production or enhanced catabolism, may play a role in development of HFpEF. We hypothesized preservation of cGMP signaling would attenuate pathological remodeling and improve cardiac function. The purpose of this study was to promote cGMP signaling via two mechanisms: 1) the DPP4 inhibitor saxagliptin; and 2) the PDE5 inhibitor tadalafil. We assessed whole heart and individual cardiomyocyte function 6 months post-AB in: control non-banded (CON; n=6), AB-control (AB; n=7), AB saxagliptin-treated (AB-SAX; n=7), and AB tadalafil-treated (AB-TAD; n=8) swine. Heart weight:body weight ratio increased to a similar extent in all AB groups. However, changes in cardiomyocyte morphology were variable. Cardiomyocyte length was increased only in the AB-TAD group, while cell width increased in both AB and AB-TAD animals. Cardiomyocyte length:width ratio decreased in the AB and AB-TAD groups, commensurate with decreased LV end diastolic (ED) and end systolic (ES) volumes. These changes were prevented in AB-SAX animals, as LV volumes and cell morphology were similar to CON. Pressure-volume analysis showed resting LV wall stiffness (ED pressure volume relationship [EDPVR] slope) was increased similarly in all AB groups. Increased resting LV contractility (ESPVR and preload recruitable stroke work) was observed in AB and AB-TAD animals. Interestingly, cardiomyocyte shortening was reduced in the AB-TAD group contrasting findings observed at the whole heart level. Saxaglitpin attenuated hypercontractile LV function at rest and preserved normal cardiomyocyte shortening. In conclusion, LV and cardiomyocyte function was distinctly altered in response to separate methods of pharmacological cGMP regulation. Our data suggest different pharmacological approaches to augment cGMP signaling promote distinct LV functional adaptations to developing HF.

scholarly journals TLR2 ligands attenuate cardiac dysfunction in polymicrobial sepsis via a phosphoinositide 3-kinase-dependent mechanism

2010 ◽  
Vol 298 (3) ◽  
pp. H984-H991 ◽  
Author(s):  
Tuanzhu Ha ◽  
Chen Lu ◽  
Li Liu ◽  
Fang Hua ◽  
Yulong Hu ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Cardiac Dysfunction ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Stroke Work ◽  
Therapeutic Treatment ◽  
Phosphoinositide 3 Kinase ◽  
Dependent Mechanism ◽  
Tlr2 Ligands

Myocardial dysfunction is a major consequence of septic shock and contributes to the high mortality of sepsis. In the present study, we examined the effect of Toll-like receptor 2 (TLR2) ligands, peptidoglycan (PGN), and Pam3CSK4 (Pam3) on cardiac function in cecal ligation and puncture (CLP)-induced sepsis in mice. We also investigated whether the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is involved in the effect of TLR2 ligands on cardiac function in CLP mice. PGN was administered to C57B6/L mice 1 h before the induction of CLP. Sham surgically operated mice served as a control. Cardiac function indexes (rate of change in left ventricular pressure, stroke work, cardiac output, and ejection fraction) were examined by a microconductance pressure catheter. Cardiac function was significantly decreased 6 h after CLP-induced sepsis compared with sham-operated control. In contrast, PGN administration attenuated CLP-induced cardiac dysfunction. Importantly, the therapeutic treatment with Pam3 1 h after CLP also significantly attenuated cardiac dysfunction in CLP mice. However, the beneficial effect of TLR2 ligands on cardiac dysfunction in CLP-mice was abolished in TLR2-deficient mice. PGN administration significantly increased the levels of phospho-Akt and phospho-GSK-3β in the myocardium compared with the levels in untreated CLP mice. PI3K inhibition abolished the PGN-induced attenuation of cardiac dysfunction in CLP mice. In conclusion, these data demonstrate that the administration of TLR2 ligands, PGN, or Pam3 attenuates cardiac dysfunction in septic mice via a TLR2/PI3K-dependent mechanism. More significantly, Pam3 therapeutic treatment will have a potential clinical relevance.

scholarly journals Synergy in the heart: RV systolic function plays a key role in optimizing LV performance during exercise

2020 ◽  
Vol 319 (3) ◽  
pp. H642-H650
Author(s):  
B. Ruijsink ◽  
M. N. Velasco Forte ◽  
P. Duong ◽  
L. Asner ◽  
K. Pushparajah ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Right Ventricle ◽  
Cardiac Function ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Systolic Function ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Exact Role ◽  
The Right

The right ventricle appears to have an important impact on maintaining systemic cardiac function and delivering stroke volume. However, its exact role in supporting left ventricular function has so far been unclear. This study demonstrates a new mechanism of ventricular interaction that provides mechanistic understanding of the key importance of the right ventricle in driving cardiac performance.

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