Significant Increase In Cardiac Index Research Articles

Cardiogenic Shock Intravascular Cooling Trial (CHILL-SHOCK)

Cardiogenic shock (CS) is complicated by high mortality rates. Targeted temperature control (TTC) has been proposed as an adjunct therapy in CS. This study aims to examine the safety of TTC in patients presenting with CS. In this open-label, randomized controlled pilot trial, 20 patients with hemodynamic criteria for CS were assigned to standard of care plus TTC vs standard of care alone. The primary outcome was a composite safety outcome, including well-described complications of TTC. Secondary outcomes included mortality at 90 days, invasive hemodynamic and echocardiographic parameters, electrocardiographic measurements, and inotrope dosing. There were no significant differences in the composite analysis of prespecified safety outcomes (3 events in the TTC group vs 0 events in the control group; P = 0.24). Patients randomized to TTC demonstrated a statistically significant increase in cardiac index and cardiac power index compared to the control group at 48-96 hours after randomization (3.6 [3.1, 3.9] L/min/m2 vs 2.6 [2.5, 3.15] L/min/m2; P = 0.029 and 0.61 [0.55, 0.7] W/m2 vs 0.53 [0.435, 0.565] W/m2; P = 0.029, respectively). TTC may be a safe adjunct therapy for patients presenting with CS and may yield improvement in specific hemodynamic parameters.

The increase in cardiac output induced by a decrease in positive end-expiratory pressure reliably detects volume responsiveness: the PEEP-test study

BackgroundIn patients on mechanical ventilation, positive end-expiratory pressure (PEEP) can decrease cardiac output through a decrease in cardiac preload and/or an increase in right ventricular afterload. Increase in central blood volume by fluid administration or passive leg raising (PLR) may reverse these phenomena through an increase in cardiac preload and/or a reopening of closed lung microvessels. We hypothesized that a transient decrease in PEEP (PEEP-test) may be used as a test to detect volume responsiveness.MethodsMechanically ventilated patients with PEEP ≥ 10 cmH2O (“high level”) and without spontaneous breathing were prospectively included. Volume responsiveness was assessed by a positive PLR-test, defined as an increase in pulse-contour-derived cardiac index (CI) during PLR ≥ 10%. The PEEP-test consisted in reducing PEEP from the high level to 5 cmH2O for one minute. Pulse-contour-derived CI (PiCCO2) was monitored during PLR and the PEEP-test.ResultsWe enrolled 64 patients among whom 31 were volume responsive. The median increase in CI during PLR was 14% (11–16%). The median PEEP at baseline was 12 (10–15) cmH2O and the PEEP-test resulted in a median decrease in PEEP of 7 (5–10) cmH2O, without difference between volume responsive and unresponsive patients. Among volume responsive patients, the PEEP-test induced a significant increase in CI of 16% (12–20%) (from 2.4 ± 0.7 to 2.9 ± 0.9 L/min/m2, p < 0.0001) in comparison with volume unresponsive patients. In volume unresponsive patients, PLR and the PEEP-test increased CI by 2% (1–5%) and 6% (3–8%), respectively. Volume responsiveness was predicted by an increase in CI > 8.6% during the PEEP-test with a sensitivity of 96.8% (95% confidence interval (95%CI): 83.3–99.9%) and a specificity of 84.9% (95%CI 68.1–94.9%). The area under the receiver operating characteristic curve of the PEEP-test for detecting volume responsiveness was 0.94 (95%CI 0.85–0.98) (p < 0.0001 vs. 0.5). Spearman’s correlation coefficient between the changes in CI induced by PLR and the PEEP-test was 0.76 (95%CI 0.63–0.85, p < 0.0001).ConclusionsA CI increase > 8.6% during a PEEP-test, which consists in reducing PEEP to 5 cmH2O, reliably detects volume responsiveness in mechanically ventilated patients with a PEEP ≥ 10 cmH2O.Trial registration ClinicalTrial.gov (NCT 04,023,786). Registered July 18, 2019. Ethics Committee approval CPP Est III (N° 2018-A01599-46).

Secukinumab and Black Garlic Downregulate OPG/RANK/RANKL Axis and Devitalize Myocardial Interstitial Fibrosis Induced by Sunitinib in Experimental Rats.

Sunitinib has been associated with several cardiotoxic effects such as cardiac fibrosis. The present study was designed to explore the role of interleukin (IL)-17 in sunitinib-induced myocardial fibrosis (MF) in rats and whether its neutralization and/or administration of black garlic (BG), a form of fermented raw garlic (Allium sativum L.), could extenuate this adverse effect. Male Wistar albino rats received sunitinib (25 mg/kg three times a week, orally) and were co-treated with secukinumab (3 mg/kg, subcutaneously, three times total) and/or BG (300 mg/kg/day, orally) for four weeks. Administration of sunitinib induced significant increase in cardiac index, cardiac inflammatory markers, and cardiac dysfunction that were ameliorated by both secukinumab and BG, and to a preferable extent, with the combined treatment. Histological examination revealed disruption in the myocardial architecture and interstitial fibrosis in cardiac sections of the sunitinib group, which were reversed by both secukinumab and BG treatments. Both drugs and their co-administration restored normal cardiac functions, downregulated cardiac inflammatory cytokines, mainly IL-17 and NF-κB, along with increasing the MMP1/TIMP1 ratio. Additionally, they attenuated sunitinib-induced upregulation of the OPG/RANK/RANKL axis. These findings highlight another new mechanism through which sunitinib can induce interstitial MF. The current results propose that neutralizing IL-17 by secukinumab and/or supplementation with BG can be a promising therapeutic approach for ameliorating sunitinib-induced MF.

Abstract 14498: Cardiogenic Shock Intravascular Cooling Trial (CHILL-SHOCK)

Introduction: Despite advances in revascularization and mechanical support, cardiogenic shock (CS) remains a highly morbid clinical state with 30-day mortality approaching 50%. Therapeutic hypothermia (TH) has been demonstrated to improve hemodynamics and reduce inflammation in small studies, but prospective randomized data is limited. We aimed to assess the safety and hemodynamic effects of TH (33 °C for 24 hours) in patients with CS. Methods: A total of 20 patients in CS were randomized to either TH plus standard therapy or standard therapy alone in this pilot study. Patients randomized to TH were cooled and rewarmed via intravenous cooling catheter. The primary safety endpoint was a composite of bradycardia requiring treatment, bleeding requiring transfusion as a result of catheter placement or secondary to resulting coagulopathy, shivering, hyperglycemia requiring insulin for non-diabetic patients, electrolyte derangement unexplained by other therapies, and complications from cooling catheter insertion. Secondary endpoints included hemodynamic parameters (cardiac output, pulmonary artery pressure, systemic vascular resistance, and cardiac power index). Results: There were no statistically significant differences in the composite analysis of prespecified safety outcomes (3 events in TH group vs 0 events in control group, p = 0.24). Patients randomized to TH demonstrated a statistically significant increase in cardiac index (3.6 [3.1, 3.9] L/min/m 2 vs 2.6 [2.5, 3.2] L/min/m 2 , p = 0.03) and cardiac power index (0.61 [0.55, 0.70] W/m 2 vs 0.53 [0.44, 0.57] W/m 2 , p = 0.03) compared to the control group at 48-96 hours after randomization. There were no statistically significant differences between the two groups for other collected hemodynamic variables. Conclusions: TH is a safe adjunct therapy for patients presenting with CS and may yield improvement in specific hemodynamic parameters. Larger studies are necessary to better understand the clinical benefits of TH in patients presenting with CS.

Abstract 8870: Hemodynamic Impact of Atrial Pacing in Patients with Fontan Physiology and Junctional Rhythm: A Cardiac Catheterization Study

Introduction: Sinus node dysfunction is a common problem and can adversely impact patients who have undergone the Fontan operation (FO). In FO patients with an adequate junctional escape rhythm (JR), the benefit of atrial pacing to restore atrioventricular synchrony remains unclear. We studied the impact of atrial pacing on hemodynamics in patients with FO and JR undergoing cardiac catheterization. Methods: Data was collected retrospectively on all FO patients with JR who underwent atrial pacing during cardiac catheterization. Hemodynamics (pulmonary artery pressure, left atrial pressure, and cardiac index) were obtained at baseline and after atrial pacing for 5-10 minutes. Results: Six patients, with a mean age of 11 years (range 3-21) met inclusion criteria. The type of FO was extracardiac in 5 and a lateral tunnel in one. A pacing catheter was placed through the Fontan fenestration in 4, via the IVC recess behind the right atrium in 1, and via the left pulmonary artery in 1. Patients were paced 10 bpm faster than their JR rate (100 bpm in 3, 88 bpm in 1 and 70 bpm in 2. With pacing, there was a significant decrease in left atrial pressure from (mean ±SEM) 9.4 ± 1.1 mmHg to 5.8 ± 1.4 mmHg (p=0.02), a significant increase in cardiac index from 2.7 ± 0.4 L/min/m 2 to 3.5 ± 0.5 L/min/m 2 (p=0.03) and no significant change in pulmonary artery pressure, from 13mmHg ± 1.4 to 12.2mmHg ± 2.2 (p=0.1) Conclusion: In FO patients with JR, atrial pacing acutely decreased the left atrial pressure, increased the cardiac output and did not result in a significant change in the pulmonary artery pressure. Our study supports further investigation into the utility of prophylactic atrial pacemaker implantation in Fontan patients with significant durations of JR on ambulatory monitoring.

Hemodynamic Impact of Atrial Pacing in Patients with Fontan Physiology and Junctional Rhythm: A Cardiac Catheterization Study.

Sinus node dysfunction is a common problem and adversely impacts patients who have undergone the Fontan operation. In Fontan patients with an adequate junctional escape rhythm, the benefit of atrial pacing to restore atrioventricular synchrony remains unclear. Data were collected retrospectively on all Fontan patients with junctional rhythm who underwent atrial pacing during cardiac catheterization. Hemodynamics were obtained at baseline and after atrial pacing for 5-10min. Seven patients, mean age 10years (3-21) were studied. The type of Fontan was extracardiac in 6 and lateral tunnel in one. Patients were paced at 10bpm faster than their junctional rate. With pacing, there was a significant decrease in left atrial pressure from (mean ± SEM) 8.8 ± 2.6 to 5.5 ± 2.9mmHg (p = 0.02), a significant increase in cardiac index from 2.7 ± 0.8 to 3.5 ± 1 L/min/m2 (p = 0.01) and pulmonary blood flow from 2.1 ± 0.6 to 2.7 ± 0.7 L/min/m2 (p = 0.001), and no significant change in pulmonary artery pressure, from 13.4 ± 2.8 to 12.4mmHg ± 3.6 (p = 0.06) or pulmonary vascular resistance from 2.1 ± 0.86 to 3.25 ± 1.9 WU × M2 (p = 0.1). In Fontan patients with junctional rhythm, atrial pacing decreased the left atrial pressure, increased cardiac output and did not significantly change the pulmonary artery pressure. Our study supports further investigation into the utility of prophylactic atrial pacemaker implantation in Fontan patients with significant durations of JR on ambulatory monitoring.

Effects of Prone Positioning on Venous Return in Patients With Acute Respiratory Distress Syndrome.

To examine the effects of prone positioning on venous return and its determinants such as mean systemic pressure and venous return resistance in patients with acute respiratory distress syndrome. Prospective monocentric study. A 25-bed medical ICU. About 22 patients with mild-to-severe acute respiratory distress syndrome in whom prone positioning was decided. We obtained cardiac index, mean systemic pressure, and venous return resistance (the latter two estimated through the heart-lung interactions method) before and during prone positioning. Preload responsiveness was assessed at baseline using an end-expiratory occlusion test. Prone positioning significantly increased mean systemic pressure (from 24 mm Hg [19-34 mm Hg] to 35 mm Hg [32-46 mm Hg]). This was partly due to the trunk lowering performed before prone positioning. In seven patients, prone positioning increased cardiac index greater than or equal to 15%. All were preload responsive. In these patients, prone positioning increased mean systemic pressure by 82% (76-95%), central venous pressure by 33% (21-59%), (mean systemic pressure - central venous pressure) gradient by 144% (83-215)%, while it increased venous return resistance by 71% (60-154%). In 15 patients, prone positioning did not increase cardiac index greater than or equal to 15%. In these patients, prone positioning increased mean systemic pressure by 28% (18-56%) (p < 0.05 vs. patients with significant increase in cardiac index), central venous pressure by 21% (7-54%), (mean systemic pressure - central venous pressure) gradient by 28% (23-86%), and venous return resistance by 37% (17-77%). Eleven of these 15 patients were preload unresponsive. Prone positioning increased mean systemic pressure in all patients. The resulting change in cardiac index depended on the extent of increase in (mean systemic pressure - central venous pressure) gradient, of preload responsiveness, and of the increase in venous return resistance. Cardiac index increased only in preload-responsive patients if the increase in venous return resistance was lower than the increase in the (mean systemic pressure -central venous pressure) gradient.

Assessment of hemodynamic responses to exercise in aortic coarctation using MRI-ergometry in combination with computational fluid dynamics

In patients with aortic coarctation it would be desirable to assess pressure gradients as well as information about blood flow profiles at rest and during exercise. We aimed to assess the hemodynamic responses to physical exercise by combining MRI-ergometry with computational fluid dynamics (CFD). MRI was performed on 20 patients with aortic coarctation (13 men, 7 women, mean age 21.5 ± 13.7 years) at rest and during ergometry. Peak systolic pressure gradients, wall shear stress (WSS), secondary flow degree (SFD) and normalized flow displacement (NFD) were calculated using CFD. Stroke volume was determined based on MRI. On average, the pressure gradient was 18.0 ± 16.6 mmHg at rest and increased to 28.5 ± 22.6 mmHg (p < 0.001) during exercise. A significant increase in cardiac index was observed (p < 0.001), which was mainly driven by an increase in heart rate (p < 0.001). WSS significantly increased during exercise (p = 0.006), whereas SFD and NFD remained unchanged. The combination of MRI-ergometry with CFD allows assessing pressure gradients as well as flow profiles during physical exercise. This concept has the potential to serve as an alternative to cardiac catheterization with pharmacological stress testing and provides hemodynamic information valuable for studying the pathophysiology of aortic coarctation.

Hemodynamic Changes During Surgical Decompression in Traumatic Brain Injury Patients

To understand the hemodynamic changes that occur with surgical decompression of lesions caused by traumatic brain injury. In this prospective, observational study, patients with traumatic brain injury requiring craniotomy within 48 hours of injury were recruited. Cardiac index (CI), stroke volume index, stroke volume variation, systemic vascular resistance index (SVRI), heart rate, and mean arterial pressure were monitored throughout surgery using a FloTrac transducer. Standard anesthetic and surgical regimens were followed. Hemodynamic data in 107 patients were compared before skin incision and after hematoma decompression (comparable anesthetic state). There was a significant increase in CI and stroke volume index and a decrease in SVRI and mean arterial pressure following surgical decompression. On subgroup analysis based on preincision CI, the changes were similar in patients with low and normal CI, whereas in patients with high CI, SVRI did not decrease significantly. High preincision CI with no change in SVRI with decompression was associated with poor neurologic outcome at discharge. In patients with TBI, surgical decompression leads to an increase in CI and a decrease in mean arterial pressure owing to a decrease in SVRI in patients with preincision low or normal cardiac output. These changes were not seen in patients with preincision high CI, and such patients had a poor neurologic outcome.

P1856Percutaneous mitral edge-to-edge valvuloplasty in end-stage heart failure as a bridge to heart transplant: a case series from a single tertiary referral center

Abstract Background Improved outcomes after percutaneous edge-to-edge mitral valvuloplasthy with MitraClip implantation were recently observed in patients with heart failure (HF) and functional severe mitral regurgitation (MR). Nonetheless, its efficacy in end-stage heart failure (HF) are lacking. Purpose Our aim was to investigate feasibility, preliminary efficacy on hemodynamics and follow-up of MitraClip implantation in a cohort of patients with very advanced HF. Methods Patients were retrospectively included in the present analysis if already in HT list, unsuitable for HT despite optimal medical and device therapy, or if implantation was a “bridge-to-candidacy”. Results Baseline and procedural characteristics are listed in Table 1; MR etiology was predominantly functional (n=7). No major complications were observed in the peri-operative period. At 6-month follow-up, invasive hemodynamics was available for 8 patients. A significant increase in cardiac index was observed (Least Square Mean Difference, LSMD = +0.47 L/min/m2; p=0.03; Figure 1), in conjunction with a numerical reduction in pulmonary vascular resistance (LSMD = −1.02 WU; p=0.3), a trend towards lower mean pulmonary arterial pressure (LSMD = −6.5 mmHg; p=0.053) and lower ejection fraction (LSMD = −6.5%; p=0.053). At a median follow-up of 772 days (IQR 156–1,578), all three patients unsuitable for HT at baseline could be eligible to HT list and one of them received LVAD. Moreover, two patients were transplanted, four experienced unplanned rehospitalization for HF, and one died of non-cardiac cause. Table 1. Baseline clinical evaluation (n=10) Age (y) 53.67±8.43 HF Etiology – post ischemic 4 (40) Male sex 6 (60) HF Etiology – no CAD 4 (40) Body Surface Area (m2) 1.76±0.22 HF Etiology – other 2 (20) Chronic Resynchronization Therapy 5 (50) Euroscore II 6.00±2.74 Baseline MR grade (+) 4 (40) STS mortality 1.71±2.65 Residual MR grade (+) 1.71±0.49 Clips implanted (number) 1.78±0.67 Data are expressed as mean ± SD or count (valid %). MR scored on a scale from 0+ to 4+. STS, Society of Thoracic Surgeons. Figure 1 Conclusions Percutaneous edge-to-edge mitral valvuloplasty with MitraClip appears safe and effective in end-stage patients, impacts on clinical decision-making and therefore might be considered as a “bridge” towards a more definite strategy. Acknowledgement/Funding None

Hemodynamic Changes Following High-Velocity Circuit Resistance or Treadmill Training in Adults with Cardiometabolic Risk Factors

Cardiometabolic syndrome (CMS) is classified as a combination of maladaptive cardiovascular and metabolic abnormalities that includes hypertension, dyslipidemia, and blood vessel dysfunction. These outcomes can negatively influence hemodynamics (HDYN) via a decrease in myocardial efficiency due to increased afterload and/or decreased vascular elasticity. Studies have reported changes in HDYN during and following acute exercise in clinical populations. However, there is a paucity of information on how high-velocity circuit resistance training (CRT) compared to continuous treadmill exercise (TM) affects these parameters at rest. PURPOSE: To compare the effects of CRT, TM and no exercise (CONT) on HDYN variables at rest in older adults with multiple CMS risk factors. METHODS: Eleven women (66.4 ± 6.4 years) participated in 12-weeks of CRT or TM. Stroke volume (SV), cardiac index (CI), systemic vascular resistance (SVR), end-diastolic volume (EDV), ejection fraction (EF), and oxygen consumption (rV02) were measured by impedance electrocardiography and indirect calorimetry before and after training. RESULTS: A within-group analysis revealed significant increases in CI (MD= 0.257, SE= .092, p=.023) and EDV (MD= 31.10, SE= 11.96, p=.032), a trend towards an increase in SV (MD=8.63, SE=4.28 p=.07) and a decrease in SVR (MD=−154.15, SE=71.07, p=.06) for CRT. TM resulted in significant increases in CI (MD=.218, SE=.080, p=.026) and EDV (MD=26.16, SE=10.36, p=.035); however, increases were not comparative to those seen with CRT. The CONT group showed a significant decrease in rVO2 (MD=−1.60, SE=.64, p=.03). No significant differences were observed for EF. At post-testing CONT resulted in a decrease in rVO2 approaching significance compared to TM (MD=−3.10, SE=1.12, p=.07). CRT demonstrated more favorable changes in SV, CI, SVR and EDV than TM or CONT. However, these changes did not reach statistical significance. CONCLUSION: These preliminary results indicate that CRT and TM lead to significant favorable changes in CI and EDV, however, CRT showed greater improvements in each and a trend towards improvements in HDYN when compared to TM and CONT. It is expected that completion of testing on existing subjects will further strengthen our results.

Phosphodiesterase type 5 inhibitor to riociguat transition is associated with hemodynamic and symptomatic improvement in pulmonary hypertension.

Riociguat is a soluble guanylate cyclase stimulator approved for the treatment of pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension. We studied the clinical and hemodynamics effects of transitioning 12 pulmonary hypertension patients from Phosphodiesterase type 5 inhibitor (PDE5i) to riociguat, and demonstrated a significant increase in cardiac index, fall in pulmonary vascular resistance, and improvement in functional class with this switch. Switch from PDE5i to riociguat appeared to be safe and fairly well tolerated in most patients.

359 - Hemodynamic and Renal Effects of a New Percutaneous Support System in NYHA III-IV Patients

Purpose: To investigate the haemodynamic and renal effects of a percutaneous circulatory support device (Reitan Catheter Pump [RCP]) in patients (NYHA III-IV) with acutely decompensated heart failure (ADHF) in need of inotropic or mechanical support. Methods and Results: The RCP is a percutaneous 14 French circulatory support system with a foldable propeller/cage inserted via the femoral artery. Once positioned in the descending aorta (10–15 cm below the left subclavian artery) the propeller, 15 mm in diameter, is deployed inside the foldable cage. The rotating propeller (8–13000 revolutions per minute) creates an afterload of the left ventricle and an increased pressure to the lower part of the body. After use the pump can be closed to the original size and removed through the introducer. The system was tested in a prospective observational study of 20 patients presenting with ADHF, with the following inclusion criteria: left ventricular ejection fraction (LVEF) < 30%, and a cardiac index (CI) < 2.1 L/min/m2. According to the ethically approved protocol, the system could be utilised up to 24 hours. The patients underwent RCP support for a mean of 18.3 (+/−6.3) hours. The RCP increased CI by 31% from 1.84 L/min/m2 (+/−0.27), to 2.41 L/min/m2 (+/−0.45, P = .04) at 24 hours. The RCP brought about a significant diuresis, starting at a mean of 71 ml / hr (+/−65), and increased to 227 ml / hr (+/−179) at 12 hours (P = .006). The system also led to a reduction in serum creatinine from a mean of 188 µmol/L (+/− 87.) to 161 µmol /L (+/−78) at 24 hours (P = .0007), and an associated improvement in the estimated glomerular filtration rate (eGFR) from 37.9 ml/min/1.73 m2 (+/−17) to 45.7 ml/min/1.73 m2 (+/−19.5, P = .002) at 24 hours using the Modification of Diet in Renal Disease Formula (MDRD formula). After haemodynamic and renal improvement 3 patients could undergo successful heart transplantation. There were no significant haemolysis, vascular injury, or thrombo-embolic complications. In the trial, a 14 F device was utilised, since then a 10 F device has been developed and will soon be available. Conclusions: The RCP resulted in a significant increase in cardiac index, with improved diuresis and renal function as measured by serum creatinine and eGFR in acutely decompensated heart failure patients. This was achieved without significant haemolysis, bleeding, or vascular complications.

Global myocardial oedema in advanced decompensated heart failure.

To use cardiac magnetic resonance (CMR) imaging with quantitative T2 mapping as surrogate for myocardial water content in patients with advanced decompensated heart failure (ADHF), compare these values with T2-values observed in chronic heart failure, and evaluate the change with decongestive therapy. Volumetric CMR measurements and quantitative T2 mapping were performed in 18 consecutive ADHF patients with clinical signs of volume overload. Eleven patients with stable heart failure were used as controls. Vasodilator therapy and diuretics were administered to achieve a pulmonary arterial wedge pressure (PAWP) of <18 mmHg and central venous pressure (CVP) of <12 mmHg, after which CMR was repeated. ADHF patients (62 ± 12 years; 89% male; left ventricular ejection fraction 23 ± 8%) presented with low cardiac index (2.08 ± 0.59 L/min/m2), high PAWP (25 ± 7 mmHg), and high CVP (14 ± 5 mmHg). After decongestion, the patients had a significant increase in cardiac index (+0.41 ± 0.53 L/min/m2; P = 0.005) and decreases in both PAWP (-9 ± 6 mmHg; P < 0.001) and CVP (-6 ± 5 mmHg; P < 0.001). At baseline, global left ventricular T2-values were higher in ADHF patients compared with controls (59.5 ± 4.6 vs. 54.7 ± 2.2 ms, respectively; P = 0.001). After decongestion, T2-values fell significantly to 55.9 ± 5.1 ms (P = 0.001), comparable with controls (P = 0.580). In contrast, psoas muscle T2-values were similar at baseline (38.6 ± 4.4 ms) vs. after decongestion (37.8 ± 4.8 ms; P = 0.397). Each 1 ms decrease in global left ventricular T2-value during decongestion was associated with a 1.14 ± 0.40 mmHg decrease in PAWP (P = 0.013), after correction for age and gender. Patients presenting with ADHF and volume overload have increased global left ventricular-but not psoas muscle-T2-values, which decrease with successful decongestion. Relief of myocardial oedema correlates with haemodynamic unloading.

Pulmonary Arterial Hypertension-Specific Drug Therapy in COPD Patients with Severe Pulmonary Hypertension and Mild-to-Moderate Airflow Limitation

Background: Patients with severe pulmonary hypertension (PH) associated with chronic obstructive pulmonary disease (COPD) present a poor outcome. Specific PH treatment could improve the clinical and hemodynamic status of these patients but may worsen arterial blood gases. Objectives: Our study retrospectively included 28 patients with severe precapillary PH (mean pulmonary arterial pressure >35 mm Hg) associated with mild-to-moderate COPD [forced expiratory volume in 1 s (FEV₁) >50% predicted]. All patients underwent specific pulmonary arterial hypertension (PAH) treatment as mono-, bi- or triple therapy. Methods: Our single-center study was conducted based on retrospective data of 537 right heart catheterizations (RHCs) performed on patients with COPD from January 2004 to June 2014. An echocardiography, comprehensive blood tests, pulmonary function tests, and a high-resolution computed tomography were performed before the RHCs. All patients underwent RHC with a Swan-Ganz catheter. Results: Compared to baseline, patients treated with specific PAH drugs showed a significant increase in cardiac index at long term (2.5 ± 0.7 liters/min/m² at baseline vs. 3.2 ± 0.6 liters/min/m² at 6/12 months; p = 0.003) as well as a decrease in pulmonary vascular resistance in the long term (8.4 ± 4.2 Wood units at baseline vs. 5 ± 1.7 Wood units at 6/12 months; p = 0.008). There was a slight decrease in arterial oxygen tension (Pa<smlcap>O</smlcap>₂) after 3 months of treatment (-2.4 ± 7.21 mm Hg; p = 0.066). During a median follow-up of 3 years, 12 patients (42.8%) died (including all causes of death). Conclusions: This preliminary report suggests that the use of specific PH therapy in severe PH associated with mild-to-moderate COPD can improve pulmonary hemodynamic parameters, with worsening of Pa<smlcap>O</smlcap>₂, which had no clinical significance and did not lead to specific PAH therapy withdrawal in any patient.

Cardiac dysfunction in patients with cirrhosis: is the systolic component its main feature?

To investigate the subclinical cardiac morphological and functional modifications in cirrhotic patients according to the stage of liver disease. One hundred and thirteen cirrhotic patients underwent standard Doppler echocardiography and were compared with healthy individuals. Left ventricular (LV) geometry, systolic/diastolic function, and the main hemodynamic parameters were assessed according to current guidelines. Cirrhotic patients showed a reduction in the peripheral vascular resistance (PVR), a compensatory hyperdynamic syndrome, and a significant increase in cardiac index (CI), cardiac output (CO), and cardiac work, with a consequent increase in the prevalence of LV hypertrophy and associated diastolic dysfunction (DD). Age (P=0.005) and LV mass index (P=0.03) were the strongest predictors of DD. Even though all the systolic parameters assessed were similar between patients and controls, in patients with refractory ascites, the reduction of the PVR and mean blood pressure was not balanced by a further increase in cardiac work and therefore the CI and CO were supported only by the increase in heart rate. In cirrhotic patients, DD is strongly related to the increase in LV mass, not related to the stage of the liver disease, and can be correctly detectable only by the use of tissue Doppler imaging. For systolic dysfunction, along with the development and worsening of ascites, CO and CI do not increase further to compensate the continuous reduction of PVR and mean blood pressure, and their maintenance becomes critically dependent on the heart rate, thus suggesting a possible detrimental effect of β-blockers in these patients.

The effects of propofol and dexmedetomidine infusion on fluid responsiveness in critically ill patients

BackgroundWe studied the effects of propofol or dexmedetomidine on preload dependency and fluid responsiveness in critically ill patients. MethodsIn the study, we included 91 patients with acute circulatory failure (70 ± 15 y) who received propofol (n = 45 patients, PROP group) or dexmedetomidine (n = 46 patients, DEX group). An initial passive leg-raising (PLR 1) test was performed in all patients to evaluate preload dependency at baseline. Propofol and dexmedetomidine were infused and titrated according to the Richmond Agitation Sedation Scale; the results ranged from −2 to −1, and the bispectral index values ranged from 60–75. A second PLR test (PLR 2) was performed before administration of a 250-mL normal saline fluid challenge over a 5-min period. We obtained central venous pressure and cardiac index (CI) measurements before and after the two PLR tests and volume expansion. An increase of ≥10% in CI during PLR was considered to be a positive test finding that was indicative of preload dependency, whereas an increase of <10% in CI during PLR was considered to be a negative test finding. ResultsAt baseline, 22 of 45 patients had negative PLR 1 in the PROP group, whereas 20 of 46 patients had negative PLR 1 in the DEX group. After propofol or dexmedetomidine sedation, there were significant decreases in CI (−9.5% [±6.6%] versus −16.4% [±8.5%], P < 0.001) in the PROP and DEX groups, respectively. In the PROP group, there were significant increases in CI (+18.4% [±9.5%] versus +10.7% [±12.3%], P < 0.05) induced by PLR 2 compared with that induced by PLR 1. In the DEX group, there were no significant increases in CI (+13.2% [±14.9%] versus +12.8% [±17.7%]) induced by PLR 2 compared with that induced by PLR 1. Although the mean arterial pressure values increased comparably with the volume expansion observed in both groups, the volume expansion resulted in a significantly higher increase in CI compared with the baseline values in the PROP group (3.2 ± 0.8 versus 3.2 ± 0.7 L/min/m2) but not in the DEX group (2.9 ± 0.7 versus 3.1 ± 0.8 L/min/m2, P < 0.05). ConclusionsWe observed that propofol infusion, but not dexmedetomidine infusion, can increase preload dependency and fluid responsiveness in patients with circulatory failure.

Effect of ephedrine and phenylephrine on cardiopulmonary parameters in horses undergoing elective surgery

ObjectiveTo assess the cardiopulmonary effects of ephedrine and phenylephrine for management of isoflurane‐induced hypotension in horses. Study designProspective randomized clinical study. AnimalsFourteen isoflurane‐anesthetized horses undergoing digital palmar neurectomy. MethodsEphedrine (EPH group; 0.02 mg kg−1 minute−1; n = 7) or phenylephrine (PHE group; 0.002 mg kg−1 minute−1; n = 7) was administered to all horses when mean arterial pressure (MAP) was <60 mmHg. The infusions were ended when the target MAP was achieved, corresponding to a 50% increase over the pre‐infusion MAP (baseline). The horses were instrumented with an arterial catheter to measure blood pressure and allow the collection of blood for pH and blood‐gas analysis and a Swan‐Ganz catheter for measurement of cardiac output using thermodilution. Cardiopulmonary parameters were recorded at baseline and at 5, 30, 60 and 90 minutes after achieving the target MAP. ResultsIn both groups, the MAP and systemic vascular resistance (SVR) increased significantly at 5, 30, 60 and 90 minutes post infusion compared to baseline (p < 0.05). The EPH group had a significant increase in cardiac index (CI) and systemic oxygen delivery index at 5, 30, 60 and 90 minutes post infusion compared to baseline (p < 0.05) and compared to the PHE group (p < 0.05). The PHE group had significantly higher SVR and no decrease in oxygen extraction compared with the EPH group at 30, 60 and 90 minutes post infusion (p < 0.05). No significant differences in ventilatory parameters were observed between groups after the infusion. ConclusionsEphedrine increased the MAP by increasing CI and SVR. Phenylephrine increased MAP by increasing SVR but cardiac index decreased. Ephedrine resulted in better tissue oxygenation than phenylephrine. Clinical relevanceEphedrine would be preferable to phenylephrine to treat isoflurane‐induced hypotension in horses since it increases blood flow and pressure.

Haemodynamic effects, safety, and pharmacokinetics of human stresscopin in heart failure with reduced ejection fraction†

Human stresscopin is a corticotropin-releasing factor (CRF) type 2 receptor (CRFR2) selective agonist and a member of the CRF peptide family. Stimulation of CRFR2 improves cardiac output and left ventricular ejection fraction (LVEF) in patients with stable heart failure (HF) with reduced LVEF. We examined the safety, pharmacokinetics, and effects on haemodynamics and serum biomarkers of intravenous human stresscopin acetate (JNJ-39588146) in patients with stable HF with LVEF ≤ 35% and cardiac index (CI) ≤ 2.5 L/min/m(2). Sixty-two patients with HF and LVEF ≤ 35% were instrumented with a pulmonary artery catheter and randomly assigned (ratio 3:1) to receive an intravenous infusion of JNJ-39588146 or placebo. The main study was an ascending dose study of three doses (5, 15, and 30 ng/kg/min) of study drug or placebo administered in sequential 1 h intervals (3 h total). Statistically significant increases in CI and reduction in systemic vascular resistance (SVR) were observed with both the 15 ng/kg/min (2 h time point) and 30 ng/kg/min (3 h time point) doses of JNJ-39588146 without significant changes in heart rate (HR) or systolic blood pressure (SBP). No statistically significant reductions in pulmonary capillary wedge pressure (PCWP) were seen with any dose tested in the primary analysis, although a trend towards reduction was seen. In HF patients with reduced LVEF and CI, ascending doses of JNJ-39588146 were associated with progressive increases in CI and reductions in SVR without significant effects on PCWP, HR, or SBP. NCT01120210.

A comparison of hemodynamic effects of levosimendan and dobutamine in patients undergoing mitral valve repair / replacement for severe mitral stenosis

We aimed to compare the hemodynamic effects of levosimendan and dobutamine in patients undergoing mitral valve surgery on cardiopulmonary bypass (CPB). Sixty patients were divided into 2 groups of 30 each. Group-L patients received levosimendan 0.1 μg/kg/min and Group-D patients received dobutamine 5 μg/kg/min while weaning off CPB. Additional inotrope and/or vasoconstrictor were started based on hemodynamic parameters. Hemodynamic data were collected at the end and at 30 minutes after CPB, thereafter at 6, 12, 24, and 36 hours post-CPB. Mean arterial pressure (MAP), central venous pressure (CVP), heart rate (HR), cardiac index (CI), systemic vascular resistance index (SVRI), and lactate levels were measured. Group-L showed increased requirement of inotropes and vasoconstrictors. The SVRI, CVP, and MAP were reduced more in Group-L. The CI was low in Group-L in the initial period when compared to Group-D. Later Group-L patients showed a statistically significant increase in CI even after 12 hrs of discontinuation of levosimendan infusion. The HR was increased more in Group-D. Lactate levels, intensive care unit stay, and duration of ventilation were similar in both groups. Levosimendan 0.1 μg/kg/min compared to dobutamine 5 μg/kg/min showed more vasodilation and lesser inotropic activity in patients undergoing mitral valve surgery for mitral stenosis. Levosimendan compared to dobutamine showed a statistically significant increase in CI even after 12 hrs of discontinuation. The requirement of another inotrope or vasopressor was frequent in levosimendan group.