Right Ventricular Cardiac Output Research Articles

Comparative Study of Cardiovascular Effects of Selected Pulmonary Vasodilators in Canine Models of Mitral Valve Disease.

Previous reports have shown that various oral pulmonary vasodilators are effective against canine pulmonary hypertension (PH). However, no studies have compared their hemodynamic effects. We aimed to compare the hemodynamic effects of 15 µg/kg beraprost sodium, 1.0 mg/kg sildenafil, and their combination, in dogs with experimentally induced mitral regurgitation. This experimental crossover study evaluated the hemodynamic and functional effects of oral pulmonary vasodilators by application of right-sided heart catheterization and echocardiography. Beraprost significantly decreased pulmonary and systemic vascular resistance. Additionally, beraprost increased right-ventricular stroke volume and left-ventricular cardiac output without worsening left-heart size and left-atrial pressure. The pulmonary vasodilatory effects of sildenafil were stronger, and its systemic vasodilatory effects were weaker than those of beraprost. However, sildenafil significantly increased the left-ventricular volume, left-atrial pressure indicator, and right-ventricular cardiac output. Combination therapy resulted in the strongest pulmonary and systemic vasodilating effects without worsening the left-heart size and left-atrial pressure indicators. Both beraprost and sildenafil were effective against canine PH; however, sildenafil was associated with the risk of worsening left-heart loading. Combination therapy with beraprost and sildenafil synergistically dilated pulmonary and systemic vessels, indicating a more potent treatment option for severe PH cases.

The alterations of cardiac function during venovenous artificial placenta support in fetal goats.

Venovenous artificial placenta (VVAP) may mimic the intrauterine environment for maintaining fetal circulation. However, changes in ventricular function in fetal goats undergoing VVAP support remain unclear. Pump-assisted VVAPs were established in five fetal goats for 9 h. The myocardial performance index (Tei index), cardiac output (CO), and blood biochemical parameters were measured during VVAP support. An increasing trend of the right ventricular (RV) Tei index was seen during VVAP support (p for trend < 0.01). The right ventricular cardiac output (RVCO) increased after the initiation of VVAP, while a significant trend of reduction was observed after 3 h (p for trend = 0.03). During VVAP support, we observed remarkable elevations of plasma cTnI and arterial lactic acid, which were positively correlated with the RV Tei index, but not the left ventricular (LV) Tei index, LVCO, and RVCO. The RVCO increases initially while a tendency of decrease could be observed during VVAP support. Special attention should be paid to right ventricular dysfunction during VVAP support.

Effects of empagliflozin on right ventricular adaptation to pressure overload.

Right ventricular (RV) failure is the prime cause of death in patients with pulmonary arterial hypertension. Novel treatment strategies that protect the RV are needed. Empagliflozin, a sodium-glucose co-transporter-2 inhibitor, shows cardioprotective effects on the left ventricle in clinical and preclinical studies, but its direct effects on RV remain elusive. We investigated the effects of empagliflozin on RV dysfunction induced by pulmonary trunk banding (PTB). Male Wistar rats (116 ± 10 g) were randomized to PTB or sham surgery. One week after surgery, PTB animals received empagliflozin mixed into the chow (300 mg empagliflozin/kg chow; PTB-empa, n = 10) or standard chow (PTB-control, n = 10). Sham rats (Sham, n = 6) received standard chow. After five weeks, RV function was evaluated by echocardiography, cardiac MRI, and invasive pressure-volume measurements. PTB caused RV failure evident by decreased cardiac output compared with sham. PTB-empa rats had a 49% increase in water intake compared with PTB-control yet no differences in hematocrit or blood glucose. Treatment with empagliflozin decreased RV end-systolic pressures without any changes in RV cardiac output or ventricular-arterial coupling (Ees/Ea). The decrease in RV end-systolic pressure was complemented by a slight reduction in RV cross sectional area as a sign of reduced hypertrophy. Load-independent measures of RV systolic and diastolic function were not affected in PTB-empa rats compared with PTB-control. Empagliflozin treatment reduced RV end-systolic pressure in RV failure induced by pressure overload. Further studies are needed to elucidate whether this simply relates to a diuretic effect and/or additional independent beneficial RV effects.

Reference Values for Fetal Cardiac Dimensions, Volumes, Ventricular Function and Left Ventricular Longitudinal Strain Using Doppler Ultrasound Gated Cardiac Magnetic Resonance Imaging in Healthy Third Trimester Fetuses.

Recent advances in hardware and software permit the use of cardiac MRI of late gestation fetuses, however there is a paucity of MRI-based reference values. To provide initial data on fetal cardiac MRI-derived cardiac dimensions, volumes, ventricular function, and left ventricular longitudinal strain in healthy developing fetuses >30 weeks gestational age. Prospective. Twenty-five third trimester (34 ± 1 weeks, range of 32-37 weeks gestation) women with healthy developing fetuses. Studies were performed at 1.5 T and 3 T. Cardiac synchronization was achieved with a Doppler ultrasound device. The protocol included T2 single shot turbo spin echo stacks for fetal weight and ultrasound probe positioning, and multiplanar multi-slice cine balanced steady state free precession gradient echo sequences. Primary analyses were performed by a single observer. Weight indexed right ventricular (RV) and left ventricular (LV) volumes and function were calculated from short axis (SAX) stacks. Cardiac dimensions were calculated from the four-chamber and SAX stacks. Single plane LV longitudinal strain was calculated from the four-chamber stack. Interobserver variability was assessed in 10 participants. Cardiac MRI values were compared against available published normative fetal echocardiogram data using z-scores. Mean and SDs were calculated for baseline maternal/fetal demographics, cardiac dimensions, volumes, ventricular function, and left ventricular longitudinal strain. Bland-Altman and intraclass correlation coefficient analysis was performed to test interobserver variability. The mean gestational age was 34 ± 1.4 weeks. The mean RV and LV end diastolic volumes were 3.1 ± 0.6 mL/kg and 2.4 ± 0.5 mL/kg respectively. The mean RV cardiac output was 198 ± 49 mL/min/kg while the mean LV cardiac output was 173 ± 43 mL/min/kg. This paper reports initial reference values obtained by cardiac MRI in healthy developing third trimester fetuses. MRI generally resulted in slightly larger indexed values (by z-score) compared to reports in literature using fetal echocardiography. 1 TECHNICAL EFFICACY: Stage 2.

Cardiac structural and functional remodeling in the fetuses associated with maternal hypothyroidism during pregnancy

Objectives We sought to investigate the effect of maternal hypothyroidism during pregnancy on fetal cardiac structural and functional remodeling using fetal echocardiography. Methods A total of 59 pregnant women with history of hypothyroidism were prospectively enrolled as the study group, and 74 normal fetuses as the control group. Fetal echocardiography was performed on each subject. Demographic, clinical, and fetal echocardiographic variables were measured, including left ventricular (LV) and right ventricular (RV) free wall and ventricular septal thickness, fractional shortening (FS), stroke volume (SV), cardiac output (CO), combined cardiac output (CCO), cardiac index (CI), combined cardiac index (CCI), aortic and pulmonary artery velocity, ductus venosus (DV) and pulmonary vein (PV) spectral Doppler, and Tei index. Results The incidence of echogenic intracardiac foci (EIF) was higher in the study group than that in the control group (18.6% vs. 6.8%, p = .036). The thickness of LV free wall and interventricular septum was reduced, the pulmonary velocities and CCI, RV FS, CO, and CI were lower, the S, D, S/A, and pulsatility index (PI) of DV were higher, and LV Tei index was higher in the study group compared with the control group. There was no significant difference in other variables between the two groups. Conclusions There is cardiac remodeling, and systolic, diastolic functional alterations in fetuses with maternal hypothyroidism. Further investigation is warranted to develop strategies to optimize the outcome of these fetuses.

L-Carnitine therapy improves right heart dysfunction throughCpt1-dependent fatty acid oxidation.

Pulmonary arterial hypertension (PAH) is a fatal vasculopathy that ultimately leads to elevated pulmonary pressure and death by right ventricular (RV) failure, which occurs in part due to decreased fatty acid oxidation and cytotoxic lipid accumulation. In this study, we tested the hypothesis that decreased fatty acid oxidation and increased lipid accumulation in the failing RV is driven, in part, by a relative carnitine deficiency. We then tested whether supplementation of l‐carnitine can reverse lipotoxic RV failure through augmentation of fatty acid oxidation. In vivo in transgenic mice harboring a human BMPR2 mutation, l‐carnitine supplementation reversed RV failure by increasing RV cardiac output, improving RV ejection fraction, and decreasing RV lipid accumulation through increased PPARγ expression and augmented fatty acid oxidation of long chain fatty acids. These findings were confirmed in a second model of pulmonary artery banding‐induced RV dysfunction. In vitro, l‐carnitine supplementation selectively increased fatty acid oxidation in mitochondria and decreased lipid accumulation through a Cpt1‐dependent pathway. l‐Carnitine supplementation improves right ventricular contractility in the stressed RV through augmentation of fatty acid oxidation and decreases lipid accumulation. Correction of carnitine deficiency through l‐carnitine supplementation in PAH may reverse RV failure.

Mitral valve Doppler for cardiac output assessment in preterm neonates.

Cardiac output (CO) assessment in neonates is commonly done by echocardiography. It is unclear which is the best site to measure the left ventricular (LV) outflow tract for CO assessment (the aortic valve [AV] aortic sinus [AS] or the sinotubular junction [STJ]). In the normal heart, the blood flow entering the LV equals the blood ejected from it. Therefore, measuring the blood flow into the LV through the mitral valve (MV) is an alternative way to measure CO. In stable preterm infants the MV CO was compared with the right ventricular (RV) CO and the three ways to measure LV CO, in 30 stable preterm neonates. Interobserver variability for MV CO was established. In the 30 neonates studied, MV CO was best correlated and had a minimal bias to the RV CO and LV CO measured at the STJ. Left ventricular CO measured at the AV and AS had significant bias relative to RV CO and MV CO. MV CO inter-observer variability was similar to other echocardiographic CO assessment methods. MV CO may be used as an alternative way to assess CO. The STJ may be the optimal site to measure LV outflow tract.

End-Systolic Eccentricity Index Obtained by Enhanced Computed Tomography Is a Predictor of Pulmonary Vascular Resistance in Patients with Chronic Thromboembolic Pulmonary Hypertension.

The usefulness of the parameters of biventricular function simultaneously measured using enhanced multi-detector computed tomography (MDCT) pulmonary angiography in patients with chronic thromboembolic pulmonary hypertension (CTEPH) has not been clarified. This study aimed to verify the correlation between left and right ventricular (RV) parameters and pulmonary vascular resistance (PVR). Patients who underwent enhanced MDCT before diagnostic right heart catheterization at Nagoya University Hospital between October 2014 and April 2021 were enrolled. The correlation of biventricular function and volume parameters with PVR was assessed. Eighty patients were retrospectively analyzed. Patients’ mean age was 65 ± 13 years, mean PVR was 9.1 (range, 6.1–11.3) Wood units, and mean end-systolic eccentricity index (esEI) was 1.76 ± 0.50. RV end-systolic volume (ESV) (p = 0.007), RV cardiac output (CO) (p < 0.001), RV ejection fraction (p < 0.001), LV end-diastolic volume (EDV) (p < 0.001), left ventricular (LV) ESV (p = 0.006), LVCO (p < 0.001), end-diastolic EI (p < 0.001), and esEI (p < 0.001) were significantly correlated with PVR. The LVEDV (p = 0.001) and esEI (p < 0.009) were independent predictors of PVR. Systolic pulmonary arterial pressure (PAP) (p < 0.001), diastolic PAP (p < 0.001), mean PAP (p < 0.001), right atrial pressure (p < 0.023), and PVR (p < 0.001) were significantly higher in the high esEI group than in the low esEI group. The esEI was a simple predictor of CTEPH severity.

Abstract 13104: L-carnitine Supplementation Improves Right Ventricular Function in Two Models of Right Ventricular Failure

Introduction: Previous studies have shown that right ventricular (RV) failure in pulmonary arterial hypertension is characterized by diminished fatty acid oxidation and ultimate lipotoxicity due to accumulation of toxic lipid intermediates. Whether or not augmenting fatty acid oxidation can reverse lipotoxic RV failure in PAH is not known. Hypothesis: In this study, we tested the hypothesis that augmentation of fatty acid oxidation through L-carnitine supplementation reverses RV failure in two models of RV failure. Methods: BMPR2 (R899X) mice were allowed to develop PAH for 10 weeks prior to supplementation of L-carnitine or control in their water for 8 weeks. In a second model, wild type C57/BL6 mice underwent pulmonary artery banding and were treated with L-carnitine or control 2 weeks after banding surgery. Finally, L-carnitine supplementation was also tested on H9C2 cardiomyocyte-like cells transfected with mutant BMPR2. Lipid accumulation was measured by Oil Red O or BODIPY stain. Fatty acid-mediated mitochondrial respiration was measured by Oroboros Oxygraph or Seahorse analysis. Results: In vivo , L-carnitine in BMPR2 mice and pulmonary artery banded mice increased RV cardiac output, RV ejection fraction, and mitochondrial respiration of long-chain fatty acids. Hemodynamic improvement in RV cardiac output was confirmed in pulmonary artery banded mice. In vitro , L-carnitine reduced lipid accumulation and increased fatty acid oxidation in BMPR2 mutant H9C2 cells through a Cpt1-dependent mechanism. Conclusions: In summary, augmentation of fatty acid oxidation in right ventricular failure through L-carnitine supplementation improves RV function, increases fatty acid oxidation, and decreases lipid accumulation.

CHANGES IN MUSCLE-SPECIFIC MICRORNAS ACCOMPANY TERMINAL STAGES OF MONOCROTALINE-INDUCED PULMONARY HYPERTENSION IN RAT

Objective: Importance of muscle-specific microRNAs (miR-1/miR-133a/miR-208/miR-499) has been identified in various cardiovascular pathologies, including their potential of being biomarkers in these diseases. Pulmonary arterial hypertension (PAH) is an incurable disease progressing into right ventricular (RV) failure as the leading cause of death. Here, we hypothesised that muscle-specific microRNAs influence RV damage in PAH and their plasma levels might be used also as indicators of disease severity. Design and method: 12-weeks old male Wistar rats were administered either monocrotaline (MCT group) or vehicle (CON group) and the animals were sacrificed 4 weeks after this treatment. Certain animals from MCT group, in which the condition of pulmonary hypertension (PH) developed more severely, were terminated prematurely (ptMCT group), since they displayed signs of serious clinical worsening and so represented the terminal stage of PH. Additionally, plasma samples of patients diagnosed with PAH were obtained from a PAH referral centre. Expression of microRNAs, both in rats and humans, was determined by RT-qPCR. Results: Fulton index of MCT and ptMCT animals was gradually increased by 47% (p &lt; 0.05 vs CON) and by 110% (p &lt; 0.05 vs CON and MCT) respectively. Expression of muscle-specific microRNAs in RV was not significantly altered in MCT group, but we noted decrease in ptMCT group (-52% for miR-1, -61% for miR-133a, -64% for miR-208, -57% for miR-499 vs CON, all p &lt; 0.05). In human plasma samples, only miR-1 and miR-133a expressions were reliably determinable by RT-qPCR, nevertheless, we noted no significant correlations with mean pulmonary arterial pressure, pulmonary vascular resistance, RV cardiac output or NT-proBNP levels. Conclusions: The decrease of muscle-specific microRNAs in ptMCT group suggests that they might not be responsible for RV modifications in earlier stages of developed PH, but their downregulation in RV tissue mirrors the severity of terminal stages of this experimental model. On the other hand, based on our results, the use of muscle-specific microRNAs as clinical biomarkers of PAH remains elusive and the attention should be directed to other miRNA candidates.

Noninvasive Assessment of Right Ventricle Function and Pulmonary Artery Pressure Using Transthoracic Echocardiography in Women With Pre-Eclampsia: An Exploratory Study.

Background and objectivePre-eclampsia (PEC) is associated with the release of anti-angiogenic factors that are incriminated in raising systemic and pulmonary vascular resistance (PVR). Compared to the left heart and systemic circulation, much less attention has been paid to the right heart and pulmonary circulation in patients with PEC. We used transthoracic echocardiography (TTE) to estimate pulmonary artery (PA) pressure and right ventricular (RV) function in women with PEC.Materials and methodsWe conducted a case-control study at a tertiary care academic center. Ten early PEC (<34-week gestation) and nine late PEC (≥34-week gestation) patients with 11 early and 10 late gestational age-matched controls were enrolled. Two-dimensional TTE was performed on all patients. The estimated mean PA pressure (eMPAP) was calculated based on PA acceleration time (PAAT). PVR was estimated from eMPAP and RV cardiac output (RV CO). RV myocardial performance index (RV MPI), tricuspid annular plane systolic excursion (TAPSE), tissue tricuspid annular displacement (TTAD), and lateral tricuspid annular tissue peak systolic velocity (S’) were measured.ResultsCompared to early controls, in early PEC, the eMPAP and estimated PVR (ePVR) were elevated, PAAT was reduced, RV MPI was increased, TTAD was reduced, and TAPSE and TV S’ were unchanged. Compared to late controls, in late PEC, the eMPAP and ePVR were elevated, PAAT was reduced, and RV MPI was increased, while TAPSE, TTAD, and TV S’ were unchanged.ConclusionsIn a sample of women with PEC, early PEC was found to be associated with increased eMPAP and ePVR and subclinical decrement of RV function as assessed by TTE. TTE may be a useful noninvasive screening tool for early detection of pulmonary hypertension and RV dysfunction in PEC. An adequately powered longitudinal study is needed to determine the implications of these findings on long-term outcomes.

Clinical Outcomes of Myocarditis after Moderate-Dose Steroid Therapy in Systemic Sclerosis: A Pilot Study.

Background Myocarditis is reported in systemic sclerosis (SSc); however, treatment options and outcomes are limited. Our objective was to define cardiac outcomes after moderate-dose steroid therapy in SSc patients with myocarditis. Method An open-label study was conducted among SSc patients with myocarditis—as defined by cardiovascular magnetic resonance (CMR), disease onset <5 years, and a NYHA functional class ≥II. All enrolled patients received prednisolone (30 mg/d) which would be tapered off by week 24, and CMR was followed up at the end of treatment. Results A total of 20 SSc patients were enrolled which 12 patients completed the study. At week 24, 8 of the 12 cases experienced improvement of myocarditis. Compared to those with no improvement, these 8 patients had significantly longer disease duration (p = 0.03), higher heart rate at baseline (p = 0.049) and week 24 (p = 0.04), lower left ventricular (LV) and right ventricular (RV) stroke volume at baseline (p = 0.002 and p = 0.01) and week 24 (p = 0.01 and p = 0.02), and lower LV and RV cardiac output at week 24 (p = 0.01 and p = 0.01). Four cases died during follow-up (3 due to cardiac complications, 1 due to renal crisis). The two who died from heart failure had very high NT-prohormone-brain natriuretic peptide (NT-proBNP) and impaired LV ejection fraction (LVEF), and the one who died from arrhythmia had very high sensitivity of cardiac Troponin-T (hs-cTnT). Conclusions Moderate-dose steroid therapy may improve myocarditis in SSc. A proportion of patients died due to cardiac complications during treatment, particularly those with high hs-cTnT, high NT-proBNP, and impaired LVEF. This trial is registered with NCT03607071.

Z Score Reference Ranges of Fetal Cardiac Output From 12 to 40 Weeks of Pregnancy.

To develop the Z score reference ranges of fetal cardiac output (CO) in healthy fetuses from 12 to 40 weeks of pregnancy. A cross-sectional descriptive study was undertaken among low-risk singleton pregnancies with healthy fetuses between 12 and 40 weeks. The right ventricular cardiac output (RCO), left ventricular cardiac output (LCO), and combined cardiac output (CCO) were measured by 2-dimensional ultrasound with the Doppler velocity of the aorta and pulmonary arteries. The pregnancies were followed until delivery RESULTS: The RCO, LCO, and CCO were determined in 700 fetuses. The predictive models of the CO as a function of gestational age (GA) and biparietal diameter were identified, and the Z score reference ranges were constructed. The means and standard deviations of CO on both sides were increased with GA and biparietal diameter as power models. Nomograms for the LCO, RCO, and CCO were established (ie, RCO = 0.000148 × GA4.283034 ; SD = 0.000131 × GA4.026209 ; LCO = 0.000514 × GA3.790944 ; SD = 0.000169 × GA3.815546 ). The RCO was much more increased than the LCO with advancing GA. The Z score reference ranges and percentile charts of fetal CO were constructed throughout gestation with a large sample size. This may be helpful in detection of cardiac disorders, especially cardiomyopathy, cardiac anomalies, fetal anemia, and fetal growth restriction.

Role of Doppler echocardiography for assessing right ventricular cardiac output in patients with atrial septal defect.

Although Doppler echocardiography is routinely used to assess left ventricle cardiac output, there are limited data about the feasibility of Doppler echocardiography for right ventricular (RV) cardiac output assessment in patients with left-to-right shunt. The purpose of the study was to determine the correlation between Doppler-derived and Fick-derived RV cardiac index (CI), and the interobserver correlation in Doppler-derived RV CI assessment. Retrospective study of patients (age ≥18years) with unrepaired atrial septal defect who underwent cardiac catheterization and echocardiography (within 3days), 2004-2017. RV CI was calculated using the hydraulic orifice formula: [.785×(right ventricle outflow tract diameter)2 ×right ventricular outflow tract (RVOT) time velocity integral×heart rate]/body surface area. A total of 128 patients (age 52±17years; female 88 [69%]) met the inclusion criteria. There was a modest correlation between Doppler-derived and Fick-derived RV CI (r=.57, P<.001), and the mean difference between Doppler-derived and Fick-derived RV CI was -.3 (95% confidence interval of agreement, -.8 to +.9) L/min/m2 . There was also a modest correlation between Doppler-derived RV CI from observer #1 and observer #2 (r=.62, P<.001), and the mean difference between Doppler-derived RV CI from observer #1 and observer #2 was -.2 (95% confidence interval of agreement, -.9 to +.6). The current study demonstrated a modest correlation between Doppler-derived and Fick-derived RV cardiac output, and a modest interobserver correlation in Doppler-derived RV cardiac output assessment. Further studies are required to validate these results and to explore other potential applications such as in patients with chronic pulmonary regurgitation.

Cardio-pulmonary MRI for detection of treatment response after a single BPA treatment session in CTEPH patients

Chronic thromboembolic pulmonary hypertension (CTEPH) can be treated with balloon pulmonary angioplasty (BPA) in inoperable patients. Sensitive non-invasive imaging methods are missing to detect treatment response after a single BPA treatment session. Therefore, the aim of this study was to measure treatment response after a single BPA session using cardio-pulmonary MRI. Overall, 29 patients with CTEPH were examined with cardio-pulmonary MRI before and 62 days after their initial BPA session. Pulmonary blood flow (PBF), first-pass bolus kinetic parameters, and biventricular mass and function were determined. Multiple linear regression analysis was implemented to estimate the relationship of PBF change in the treated lobe with treatment change of full width at half maximum (FWHM), cardiac output (CO), ventricular mass index (VMI), pulmonary transit time (PTT) and PBF change in the non-treated lobes. Paired Wilcoxon rank sum test and Spearman rho correlation were used. After BPA regional PBF increased in the treated lobe (p < 0.0001) as well as in non-treated lobes (p = 0.015). PBF treatment changes in the treated lobe were significantly larger compared with the non-treated lobes (p = 0.0049). Change in NT proBNP, MRI-derived mean pulmonary artery pressure (mPAP), PTT, FWHM, right ventricular (RV) ejection fraction, RV stroke volume, CO, VMI and PBF in the non-treated lobes correlated with PBF change in the treated lobe (p < 0.05). PBF changes in the treated lobe were independently predicted by PTT as well as PBF change in the non-treated lobes. Cardio-pulmonary MRI detects and quantifies treatment response after a single BPA treatment session. • Two months after BPA regional parenchymal pulmonary perfusion (PBF) increased in the total lung parenchyma (p = 0.005), the treated lobes (p < 0.0001) and non-treated lobes (p = 0.015). • The PBF treatment changes in the treated lobe were significantly larger than in the non-treated lobes (p = 0.0049). • Change in NT proBNP, MRI-derived mean pulmonary artery pressure, pulmonary transit time, full width at half maximum, right ventricular (RV) ejection fraction, RV stroke volume, cardiac output, ventricular mass index and PBF in the non-treated lobes correlated with PBF change in the treated lobe (p < 0.05).

Dobutamine stress-induced ischemic right ventricular dysfunction in patients with three-vessel coronary artery disease.

BackgroundDobutamine stress echocardiography (DSE) is a non-invasive technique to detect coronary artery diseases (CAD). There are limited studies on evaluation of the right ventricular function by stress echocardiography. The appropriate evaluation of RV function and early diagnosis of its failure can help to improve outcomes for the patients undergoing cardiac surgery.ObjectiveTo determine right ventricular dysfunction in patients with three-vessel CAD by using DSE.MethodsThis cross-sectional study was among 13 patients who were candidates for coronary artery bypass grafting (CABG) referred to Ghaem Hospital, Mashhad, Iran; from September 2015 to May 2016. After a physical examination and initial measures, DSE was performed and echocardiographic parameters were recorded by a cardiologist. Paired-samples t-test was performed using SPSS Software v.16.0 for data analysis.ResultsThe study included 13 patients (9 males) with a mean age of 65.4±7.6 years. The mean of TAPS was 16.9±4.5 mm and 15.7±2.9 mm before and after stress echocardiography, respectively (p=0.69). Systolic right ventricular (SRV) peak increased from before DSE compared with after DSE (8.0±2.2 vs. 13.7±4.2 mm/s, p<0.001). In addition, after dobutamine injection, right ventricular (RV) cardiac output decreased in 7 patients and one patient was affected by post-ejection shortening.ConclusionIt seems that TAPS and RV cardiac output after injection of dobutamine, can be used as markers for the recognition of ischemic RV dysfunction.

Study of the changing of right atrial volume and phasic function and its clinical value in patients with pulmonary hypertension

Objective To evaluate the right atrial(RA) volume and phasic function using three-dimensional echocardiography(3DE), and to examine the clinical relevance in pulmonary hypertension(PH). Methods Fifty PH patients and 20 control subjects were studied.RA volume, including maximum RA volume (Vmax), minimum RA volume (Vmin) and the volume before active systolic (Vpre-A) were evaluated by 3DE. RA maximum volume index (VmaxI), total emptying volume index (TotEVI), passive emptying volume index (PassEVI) and active ejection fraction (ActEF) were calculated. The correlation between RAVmaxI and the parameters of RV structure, function, pulmonary hemodynamics were analyzed. Results Maximum RA volume index (RAVmaxI) was higher in WHO functional class (WHO-FC) Ⅲ, Ⅳ of PH patients than in controls (all P<0.01). TotEVI was significantly higher in PH patients than in controls (P<0.001), but PassEVI was lower in PH patients than in controls (P=0.011). ActEF was similar when comparing PH patients of WHO-FC Ⅱ with controls.ActEF increased in PH patients with WHO-FC Ⅲ as compared with controls (P=0.008) but reduced in advanced with WHO-FC Ⅳ patients (P<0.001). RAVmaxI correlated with the indices of right ventricular (RV) structure, function and RV cardiac output index (all P<0.05). Conclusions PH is associated with increased RA size, increased TotEVI, and decreased PassEVI. ActEF increases in PH patients with WHO-FC Ⅲ but decreases in patients with WHO-FCⅣ.RA systolic function plays an important role in compensating RV dysfunction. Key words: Echocardiography, three-dimensional; Hypertension, pulmonary; Atrial function, right

Abstract P104: Oxygen Drastically Increases Cardiac Output Without Changing Mean Pulmonary Arterial Pressure in a Patient With Severe, Progressive Pulmonary Hypertension

Background: The diagnosis of PH requires a high degree of clinical suspicion and is defined as a mean pulmonary artery (mPAP) greater than or equal to 25 mmHg. Systolic pulmonary artery pressure (sPAP) can be estimated by transthoracic echocardiolography (TTE) and mPAP directly measured by right heart catheterization (RHC). The hemodynamic data obtained from RHC provide diagnostic, therapeutic, and prognostic information important for the complete assessment of PH. We present a case of severe, progressive PH evidenced by serial TTE over a 6-year period. RHC confirmed severe mPAP elevation and showed a marked increase in cardiac output (CO) after giving 100% oxygen, observed with no significant change in mPAP, but decrease in heart rate (HR) and therefore increased right ventricular (RV) stroke volume (SV) in response to oxygen-induced decrease in pulmonary vascular resistance (PVR). Method A 68 year old female presented with exertional dyspnea, severe PH, but class 1 exercise capacity. Data was retrieved from serial TTE and RHC performed at rest on room air and after giving 100% oxygen. Results: Serial TTE conducted over a 6-year period showed a steady progression of sPAP at a rate of 10% annually, reaching 67 mmHg at the time of the RHC, which recorded mPAP at 51 mmHg on room air (RA) and 47 mmHg with 100% oxygen. CO was at 5.84 L/min on RA and increased by 33% to 7.79 L/min with oxygen. HR was at 99 bpm on RA and at 88 with oxygen meanwhile stroke volume (SV) showed a 50% increase from 59 ml to 88 ml. Discussion/Conclusion: Our patient had no significant change in mPAP facing oxygen-induced decrease in PVR. Instead, there was a marked increase in RV CO explainable only by an increase in RV SV facing decreased RV afterload, as HR decreased with oxygen. These findings are consistent with the patient’s class 1 exercise capacity despite having severe PH, indicating an ability to increase CO with activity and suggesting a positive response to medications and better prognosis. Our case shows the importance of assessing hemodynamic data in the workup and management of PH. We propose using TTE assessment of CO coupled with 100% oxygen administration in addition to sPAP estimation as a noninvasive, readily available means of obtaining this critical and underutilized information.

Evaluation of right ventricular function in fetal hypoplastic left heart syndrome using spatio-temporal image correlation (STIC).

BackgroundPostnatal outcome of fetuses with hypoplastic left heart syndrome (HLHS) is mainly determined by right ventricular function. In the present study we used spatio-temporal image correlation (STIC) to assess right ventricular function of fetuses with HLHS.MethodsThree-dimensional ultrasound with STIC technique was used to acquire heart images from fetuses that had HLHS and the normal controls, between 24+0 and 37+6 weeks of gestation. Right ventricular end-diastolic volume (RVEDV) and right ventricular end-systolic volume (RVESV) were determined using the virtual organ computer-aided analysis software, and the parameters of right ventricular function were calculated.ResultsBoth RVEDV and RVESV were found to be significantly higher in fetuses with HLHS as compared to that in normal controls (P < 0.001). There were no significant differences in the parameters between fetuses with and without a visible left ventricular cavity (P > 0.05). Compared to fetuses with HLHS plus mild tricuspid regurgitation (TR), fetuses with HLHS plus severe TR exhibited lower right ventricular stroke volume (RVSV), right ventricular cardiac output (RVCO) and standardized RVCO (P < 0.05). The right ventricular ejection fraction (RVEF) was significantly lower in HLHS fetuses that had severe TR (P < 0.001).ConclusionAs the right ventricle is solely responsible for maintenance of circulation, the right ventricular systolic function undergoes compensatory enhancement in fetuses with HLHS and mild TR, compared to that in normal controls. Size of the left ventricle does not significantly affect the right ventricular function in HLHS. However, right ventricular systolic function may be impaired prenatally in HLHS fetuses that have severe TR.

Acute response of right ventricular function to iloprost inhalations in patients with pulmonary arterial hypertension: preliminary evaluation with cardiac magnetic resonance imaging

背景与目的肺动脉高压（pulmonary arterial hypertension, PAH）是以肺循环压力异常增高为特征的进展性疾病，可引起右心室（right ventricle, RV）功能进行性衰竭，最终导致死亡。因此RV功能的评估在PAH的诊断、随访中起着重要作用。心脏磁共振成像（cardiac magnetic resonance imaging, CMRI）成为无创评价心室功能的参照标准，尤其是RV功能。本研究通过CMRI评估吸入伊洛前列素对PAH患者RV功能影响的即刻效应。方法2012年3月-2014年3月PAH患者48例，吸入单剂量20 μg的伊洛前列素溶液前、后立即进行CMRI检查，测量RV的舒张末期容积（end-diastolic volume, EDV）、收缩末期容积（end-systolic volume, ESV）、每搏输出量（stroke volume, SV）、射血分数（ejection fraction, EF）、心输出量（cardiac output, CO）、舒张末期面积（end-diastolic area, EDA）及收缩末期面积（end-systolic area, ESA）。RV面积变化百分比（percentage of RV area change, %RVAC）由公式[%RVAC=（EDA-ESA）/EDA×100%]计算获得。采用Wilcoxon符号秩和检验或配对t检验分析吸入伊洛前列素前、后RV功能参数变化。P＜0.05为差异有统计学意义。结果吸入伊洛前列素后，患者的RV功能改善，RV EDV、RV ESV显著下降（P=0.007, P＜0.001），RV SV、RV EF及%RVAC增加（P=0.014, P=0.009, P=0.006），RV CO无变化（P=0.851）。结论吸入伊洛前列素能立即明显改善PAH患者的RV功能，CMRI能准确、无创地评估该即刻效应。