Increase In Pulmonary Capillary Wedge Pressure Research Articles

Temporary balloon occlusion test can overestimate the risk of acute pulmonary edema after transcatheter atrial septal defect closure.

Atrial septal defect (ASD) closure can cause acute pulmonary edema. Before transcatheter closure is performed, temporary balloon occlusion test (BOT) is recommended in patients with left ventricular dysfunction to predict the risk of pulmonary edema. However, the accuracy of BOT has not been verified. This study aimed to compare hemodynamic differences between BOT and transcatheter closure. A total of 42 patients with a single ASD over age 18 years who underwent BOT before transcatheter ASD closure between October 2010 and May 2020 were analyzed. Pulmonary capillary wedge pressure (PCWP) was measured using a Swan-Ganz catheter placed in the pulmonary artery at baseline, after 10 min of BOT, and after transcatheter closure. Amplatzer septal occluder was used for all transcatheter closures. Mean patient age was 64 ± 18 years (range, 18-78). Mean ASD diameter and pulmonary to systemic flow ratio were 18 ± 5and 2.8 ± 1.0 mm, respectively. Mean PCWP at baseline, during BOT, and after transcatheter closure was 8.9 ± 2.9, 13.5 ± 4.2, and 9.5 ± 2.6 mmHg, respectively. The difference between BOT and after transcatheter closure values was significant (p < 0.001). During BOT, PCWP increased ≥18 mmHg in 7patients, whereas after ASD closure, PCWP was <18 mmHg in all 7and none developed acute pulmonary edema. Temporary balloon occlusion of an ASD and transcatheter ASD closure result in different hemodynamic change. BOT overestimates increase of PCWP after transcatheter ASD closure and requires careful interpretation. Well-designed, larger studies in higher-risk patients are warranted to verify the clinical implications of BOT in more detail.

Hemodynamic changes during aortic valve surgery among patients with aortic stenosis

Introduction. Patients with severe aortic stenosis (AS) undergoing surgery are at increased risk of hypotension and hypoperfusion. Although treatable with inotropic agents or fluid, little is known about how these therapies affect central hemodynamics in AS patients under general anesthesia. We measured changes in central hemodynamics after dobutamine infusion and fluid bolus among patients with severe AS and associated these changes with preoperative echocardiography. Methods. We included 33 patients with severe AS undergoing surgical AVR. After induction of general anesthesia, hemodynamic measurements were obtained with a pulmonary artery catheter, including Cardiac index (CI), stroke volume index (SVi) and pulmonary capillary wedge pressure (PCWP). Measurements were repeated during dobutamine infusion, after fluid bolus and lastly after sternotomy. Results. General anesthesia resulted in a decrease in CI and SVi compared to preoperative values. During dobutamine infusion CI increased but mean SVi did not (38 ± 12 vs 37 ± 13 ml/m2, p = .90). Higher EF and SVi before surgery and a larger decrease in SVi after induction of general anesthesia were associated with an increase in SVi during dobutamine infusion. After fluid bolus both CI, SVi (48 ± 12 vs 37 ± 13 ml/min/m2, p < .0001) and PCWP increased. PCWP increased mostly among patients with a larger LA volume index. Conclusion. In patients with AS, CI can be increased with both dobutamine and fluid during surgery. Dobutamine’s effect on SVI was highly variable and associated with baseline LVEF, and an increase in CI was mostly driven by an increase in heart rate. Fluid increased SVi at the cost of an increase in PCWP.

Autologous red blood cell transfusion does not result in a more profound increase in pulmonary capillary wedge pressure compared to saline in critically ill patients: A randomized crossover trial.

Background and ObjectivesTransfusion‐associated circulatory overload (TACO) is a major cause of severe transfusion‐related morbidity. Transfusion of red blood cells (RBCs) has been shown to induce hydrostatic pressure overload. It is unclear which product‐specific factors contribute. We set out to determine the effect of autologous RBC transfusion versus saline on pulmonary capillary wedge pressure (PCWP) change.Materials and MethodsIn a randomized crossover trial, patients who had undergone coronary bypass surgery were allocated to treatment post‐operatively in the intensive care unit with either an initial 300 ml autologous RBC transfusion (salvaged during surgery) or 300 ml saline infusion first, followed by the other. Primary outcome was the difference in PCWP change. Secondary outcome measures were the difference in extra‐vascular lung water index (EVLWI) and pulmonary vascular permeability index (PVPI).ResultsChange in PCWP was not higher after autologous RBC transfusion compared to saline (ΔPCWP 0.3 ± 0.4 vs. 0.1 ± 0.4 mmHg). ΔEVLWI and ΔPVPI were significantly decreased after autologous RBC transfusion compared to saline (ΔEVLWI −1.6 ± 0.6 vs. 0.2 ± 0.4, p = 0.02; ΔPVPI −0.3 ± 0.1 vs. 0.0 ± 0.1, p = 0.01). Haemodynamic variables and colloid osmotic pressure were not different for autologous RBC transfusion versus saline.ConclusionTransfusion of autologous RBCs did not result in a more profound increase in PCWP compared to saline. RBC transfusion resulted in a decrease of EVLWI and PVPI compared to saline. Our data suggest that transfusing autologous RBCs may lead to less pulmonary oedema compared to saline. Future studies with allogeneic RBCs are needed to investigate other factors that may mediate the increase of PCWP, resulting in TACO.

Invasive exercise hemodynamics predict survival in patients with clinical heart failure irrespective of left ventricular systolic function

Abstract Funding Acknowledgements Type of funding sources: None. Introduction When aiming to stratify heart failure patients for mortality risk, exercise stress testing has proven to be relevant in specific populations of heart failure patients, but is not universally applied. Analysis of left ventricular systolic function (LVEF) remains the cornerstone for stratifying heart failure patients for prognosis and clinical treatment. The aim of the present study is to investigate the prognostic capabilities of invasive exercise testing in a real-world cohort of suspected heart failure patients in whom non-cardiac causes of dyspnea were excluded. Methods We retrospectively analyzed survival of patients who underwent right heart catheterization at rest and during exercise between 2007 to 2017 for dyspnea and expected heart failure. Pulmonary capillary wedge pressure (PCWP) at rest and the PCWP response to exercise, expressed as the ratio of PCWP at peak exercise to workload normalized to body weight [PCWL (mmHg/W/kg)], were determined. Mortality data was deducted from the official German death registry. Results A total of 682 patients [aged 64.1 ± 12 years, 269 (39.2%) women] were included. Based on LVEF, 515 patients (76.4%) had sustained LVEF ≥50%, 71 patients (10.5%) had heart failure with mildly-impaired LVEF (40-49%) and 88 patients (13.1%) had heart failure with reduced LVEF (≤40%). Absolute LVEF was not associated with all-cause mortality (HR 0.995; 95% CI 0.99-1.00; p=0.231). While increases in PCWP at rest an PCWL during exercise were both associated with death, the discriminative properties of pressure measurements derived during exercise were superior in ROC-analysis (AUC 0.637 for PCWP and AUC 0.728 for PCWL, p&amp;lt;0.001) Exercise hemodynamics and systolic function were next used to re-classify patients in four groups based on normal vs. impaired LVEF (≥/&amp;lt; 50%) and response to exercise (PCWL≥/&amp;lt;25.5 mmHg/W/kg for normal LVEF and PCWL≥/&amp;lt;34.7 mmHg/W/kg for impaired LVEF). In multivariate models adjusted for pertinent baseline parameters, patients with pathological response to exercise carried a 2.0-fold (with sustained LVEF, 95% CI 1.17-3.52, p=0.011) to 3.2-fold (with impaired LVEF, 95% CI 1.83-5.91, p&amp;lt;0.001) increased risk for death. Patients with impaired LVEF but featuring a normal response to exercise did not carry an increased risk for death (HR 1.117, 95% CI 0.453-2.757, p=0.810). Discussion: In patients with clinical heart failure, invasive exercise testing improves the prediction of mortality. Subjects with a normal response to exercise have a relatively low mortality irrespective of systolic function.

332 Clinical and prognostic significance of junctional late gadolinium enhancement in patients with non-ischaemic cardiomyopathy

Abstract Aims Pulmonary hypertension (PH) carries a poor prognosis in patients with non-ischaemic dilated cardiomyopathy (NIDC). Cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) evaluation can identify myocardial abnormalities. In particular, junctional LGE is already an established marker of adverse right ventricular (RV) remodelling in patients with pre-capillary PH. This study sought to assess the prevalence of junctional LGE by CMR in NIDC, its relationship with hemodynamic parameters and, moreover, its prognostic significance. Methods and results Patients with NIDC who underwent right heart catheterization (RHC) and CMR within 3 months in a tertiary hospital were enrolled. Patients with acute heart failure were excluded. Among others, RV and left ventricular (LV) volumes, junctional LGE at CMR, pulmonary artery pressure (PAP) and pulmonary capillary wedge pressure (PCWP) at RHC were tabulated. Pulmonary hypertension was defined accordingly to current Guidelines (median PAP at RHC ≥ 25 mmHg). The primary endpoint consisted of heart failure (HF) hospitalization during follow-up. A total of 188 patients [median age 49 (SD 15), 71% males] were evaluated. At morpho-functional CMR evaluation, most subjects (76%) had important systolic dysfunction (LV EF ≤ 35%). Junctional LGE was observed in 83 (44%) patients. Among patients with junctional LGE, 21 had LGE confined only to the junctional region, while 61 had also mid-wall interventricular septal stria and 21 a mid-wall stria in the lateral free LV wall. Patients with junctional LGE had lower RV EF (49% vs. 56%, P &amp;lt; 0.001) and LV EF (27% vs. 30%, P = 0.012) when compared to those without junctional LGE although no differences in LV and RV dimensions were found. RHC showed PH in 83 patients (44%). Patients with junctional LGE showed a worse hemodynamic profile in terms of PH (55% vs. 36%; P = 0.011) and increase in PCWP (PCWP &amp;gt; 15 mmHg in 60% vs. 42%; P = 0.015) compared to subjects without junctional LGE. Among 79 patients with PH and PCWP &amp;gt; 15 mmHg, 75 (95%) had a combined post capillary and pre-capillary PH (diastolic pressure gradient ≥7 mmHg). Univariate analysis showed that junctional LGE was associated with a worse hemodynamic profile; on multivariable model, RV EF was significantly associated with the presence of junctional LGE (OR: 0.91; 95% CI: 0.87–0.96, P &amp;lt; 0.001). During a median follow-up of 58 months, 33 patients (18%) died or underwent heart transplantation/ventricular assist device implantation, 17% in the junctional LGE group vs. 18% among those without junctional LGE. Thirty-eight patients (20%) had at least one episode of HF, 22 among junctional LGE group and 16 in control group (27% vs. 15%, P = 0.056). When adjusted for age, junctional LGE resulted a significant determinant of HF hospitalization (OR: 2.13, 95% CI: 1.02–4.44, P = 0.044). Conclusions Junctional LGE is detectable in almost half of NIDC patients and it is related to a worse haemodynamic profile, characterized by PH and elevated PCWP. Moreover, after adjustment for age, it was a significant determinant of HF hospitalization during follow-up in our population. Junctional LGE can therefore represent a useful prognostic tool, as marker of adverse ventricular remodelling likely related to ventricular interdependence.

Abstract 9925: Impaired Cardiac Output and Peripheral Reserve Predict Morbidity and Mortality in Heart Failure and Preserved Ejection Fraction

Introduction: Reduced peak oxygen consumption (VO 2 ) is common and associated with adverse outcomes in patients with heart failure (HF) and preserved ejection fraction (HFpEF). According to the Fick principle, VO 2 is equal to the product of cardiac output (CO) and arterial-venous O 2 difference (AVO 2 diff). Patients with HFpEF display abnormalities each component, but no study has yet evaluated their prognostic impacts. Methods: Patients with HFpEF (n=501) and controls without HF (n=207) underwent invasive hemodynamic exercise testing with expired gas analysis and clinical follow up for the composite event of HF hospitalization or death. Results: Compared to controls, patients with HFpEF displayed slightly lower CO at rest with higher pulmonary capillary wedge pressure (PCWP). On exercise, subjects with HFpEF displayed blunted increases in CO and greater increase in PCWP (Figure A). As compared with controls, the slope of the increase in CO relative to VO 2 was lower in HFpEF (6.4 ± 3.3 vs 5.4 ± 3.2 L/L; P =0.0004), while augmentation in AVO 2 diff relative to VO 2 was greater in HFpEF (7.7 ± 5.4 vs 10.0 ± 5.6 min/dL; P &lt;0.0001). Over a median 2.8 (1.1-4.6) years of follow up, 101 patients experienced the composite event. Patients with CO reserve below the median and increases in AVO 2 diff below median displayed higher risk of the composite endpoint (Figure B-C). After adjustments for age, sex, BMI, atrial fibrillation, LV mass, and EF, CO reserve remained strongly associated with the primary outcome (HR [95%CI] = 0.51 [0.38-0.68]; P &lt;0.0001, per 1 SD increase) and the change of AVO 2 diff remained significant, but was less predictive (HR [95%CI] = 0.74 [0.60-0.92]; P =0.007, per 1 SD increase) in patients with HFpEF. Conclusions: Impaired ability to augment CO and peripheral O 2 delivery are associated with increasing risk of adverse events in HFpEF. Further study is required to identify therapeutic interventions targeting these hemodynamic perturbations to improve outcomes in HFpEF.

Hemodynamic changes during transcatheter atrial septal defect closure predict midterm heart failure deterioration in adults.

To investigate whether hemodynamic changes during balloon occlusion test (BOT) predict future heart failure (HF) deterioration after transcatheter atrial septal defect closure (tASD-closure). Midterm HF deterioration can sometimes occur after tASD-closure in adults. Whether hemodynamic changes during tASD-closure can help identify patients at risk is unknown. This prospective observational study enrolled 86 consecutive adult patients who underwent tASD-closure. Hemodynamic parameters, including pulmonary capillary wedge pressure (PCWP), were measured at baseline, during BOT, and after tASD-closure. The changes in PCWP during BOT and after tASD-closure were defined as ΔPCWP (Occ-Pre) and ΔPCWP (Post-Pre), respectively. Clinical parameters were evaluated before tASD-closure and during the 3-month follow-up. We assessed the occurrence of HF deterioration (HF requiring hospitalization or additional diuretics) during a 2-year follow-up period and categorized patients into HF (+) and HF (-) groups accordingly. The aforementioned parameters were compared between groups. Midterm HF deterioration occurred in 12 patients (13.9%). Compared to the HF (-) group, the HF (+) group presented a significantly higher ΔPCWP (Occ-Pre) (9.5 ± 4.4 mmHg vs. 3.0 ± 3.3 mmHg; p < 0.001) and ΔPCWP (Post-Pre) (4.0 ± 2.8 mmHg vs. 0.6 ± 1.8 mmHg; p=0.004). Receiver operating characteristic curve analysis showed that the ΔPCWP (Occ-Pre) cutoff value of 5.5 mmHg had excellent ability to predict HF deterioration (Area under the curve 0.886 [0.779-0.993], p < 0.001; sensitivity 0.917, specificity 0.824). Increases in PCWP during BOT predict midterm HF deterioration after tASD-closure. Close surveillance may be needed in patients with a ΔPCWP (Occ-Pre) >5 mmHg.

Iloprost and exercise haemodynamics in heart failure with preserved ejection fraction—the ILO‐HOPE randomised controlled trial

AimsA dramatic increase in pulmonary capillary wedge pressure (PCWP) during exercise is observed in patients with heart failure with preserved ejection fraction (HFpEF). This study was designed to determine whether iloprost inhalation could improve exercise haemodynamics and cardiac reserve in patients with HFpEF.MethodsThirty‐four HFpEF patients were enrolled in this double‐blind, randomized, placebo‐controlled, parallel‐group trial. Patients received both cardiac catheterization and underwent expired gas analysis at rest, during exercise, and before and 10 minutes after treatment with either inhaled iloprost or placebo. The primary endpoint was decrease in exercise PCWP.ResultsAt baseline, enrolled patients showed an increase in PCWP during exercise (from 16 [range, 14–23] mmHg to 27 [21–36] mmHg; P &lt; .0001). After iloprost inhalation, exercise PCWP was significantly reduced compared to placebo (adjusted mean: 20 [16–29] mmHg vs 23 [17–32] mmHg; P = .002). There was no difference for cardiac output reserve with exercise in the 2 groups (0.2 [−1.3–1.2] L/min vs –0.7 [−1.9–0.1] L/min; P = .099). Iloprost improved the pulmonary artery pressure flow relationships in HFpEF with exercise compared to placebo.ConclusionIloprost inhalation improved haemodynamic deficits during exercise in patients with HFpEF. Prospective trials testing long‐term iloprost therapy in this population are warranted.

1406Inhaled iloprost, exercise hemodynamics, and ventricular performance in heart failure with preserved ejection fraction

Abstract Background A dramatic increase in pulmonary capillary wedge pressure (PCWP) during exercise is observed in patients with heart failure with preserved ejection fraction (HFpEF). The prostacyclin pathway is involved in pulmonary hypertension and iloprost is a prostacyclin analogue. The acute onset vasodilator effect of inhaled iloprost makes it a good candidate to decrease exercise-induced PCWP. This study determined whether iloprost inhalation could improve exercise hemodynamics and cardiac reserve in HFpEF. Methods Thirty-four HFpEF subjects were enrolled in this double-blind, randomized, placebo-controlled, parallel-group trial. Subjects received invasive cardiac catheterization and underwent expired gas analysis at rest and during exercise, before and 15 minutes after treatment with either inhaled iloprost or placebo. Results At baseline, enrolled subjects showed an increase in PCWP during exercise (PCWP = 16 (14–23) mmHg to 27 (21–36) mmHg; p&lt;0.0001). After drug inhalation treatment, the primary endpoint was achieved whereby exercise PCWP was significantly reduced by iloprost compared to placebo (adjusted mean: 20 (16–29) mmHg vs. 23 (17–32) mmHg; p=0.002). Iloprost showed a trend for better cardiac output reserve with exercise (0.2 (−1.3 to 1.2) L/min vs. −0.7 (−1.9 to 0.1) L/min; p=0.099) and normalized the increase in cardiac output relative to oxygen consumption. Iloprost improved the pulmonary artery pressure flow relationships in HFpEF and showed a trend for increased left ventricular stroke work with exercise compared to placebo, indicating an improvement in ventricular performance with stress. Table shows exercise baseline-corrected values (exercise values after receiving study drug minus exercise values prior to study drug) Placebo (n=17) Iloprost (n=17) p Value PA systolic, mmHg 0 (−4 to 6) −11 (−23 to −5) &lt;0.0001 PCWP, mmHg −2 (−3 to 2) −7 (−12 to −5) &lt;0.0001 PVR, mmHg/l/min 0 (−0.5 to 0.3) −0.1 (−0.5 to 0.4) 0.9 SVR, DSC 102 (16 to 188) 5 (−162 to 108) 0.057 LVSW, g/beat −3 (−30 to 6) 7 (−13 to 20) 0.079 CO, l/min −0.7 (−1.9 to 0.1) 0.2 (−1.3 to 1.2) 0.099 Stroke volume, ml −8 (−24 to 1) 0 (−19 to 10) 0.3 Values are median (interquartile range). Conclusions Iloprost inhalation improved hemodynamic deficit during exercise in patients with HFpEF. Prospective trials testing long-term iloprost therapy in this population are warranted.

Hemodynamic Response to Rapid Saline Infusion Compared with Exercise in Healthy Participants Aged 20–80 Years

Background and ObjectiveRapid saline infusion and exercise has been proposed as methods to unmask cardiovascular disease. However, the normal hemodynamic response to rapid saline infusion has not been compared to exercise nor is it known whether the responses are age-dependent.We assessed the hemodynamic response to rapid saline infusion in healthy participants over a wide age-range and compared it to exercise in the same participants. Methods and resultsFifty healthy participants (young <40 years, n = 16, middle-aged 40–59 years, n = 15, elderly 60–80 years, n = 19) underwent right heart catheterization at rest, during semisupine ergometer exercise at three exercise levels (25%, 50%, and 75% of peak VO2) and after rapid saline infusion (10 ml/kg at a rate of 150 ml/min). Rapid saline infusion significantly increased pulmonary capillary wedge pressure (PCWP) similarly across all age groups (∆PCWP 6 ± 2; 7 ± 2; 6 ± 4 mmHg for the young, middle-aged and elderly respectively) with no correlation between age and ∆PCWP (r = 0.05; p = 0.74). However, there was a negative correlation between age and ∆stroke volume (SV) as elderly participants had a lower increase in SV following rapid saline infusion (r = 0.44; p = 0.002). On the contrary, exercise-induced significantly larger and age-dependent increases in PCWP (r = 0.58; p < 0.0001). Exercise also caused a larger increase in SV compared with rapid fluid loading (p = 0.0003) ConclusionUnlike exercise, rapid saline infusion caused an age-independent increase in PCWP in healthy adults. Suggesting that age-related impairments beyond passive stiffness have a greater impact on exercise-induced increase in PCWP. Clinical trial registrationhttps://clinicaltrials.gov/ct2/show/NCT01974557

Poor Left Ventricular Unloading is Associated with Increased Mortality after Continuous Flow Left Ventricular Assist Device Implantation

Purpose The role of routine right heart catheterization (RHC) to evaluate for left ventricular (LV) unloading remains unclear in patients with continuous flow left ventricular assist devices (CF-LVAD). We hypothesized that persistently elevated pulmonary capillary wedge pressure (PCWP) would be associated with increased mortality on CF-LVAD support. Methods A single center continuous flow LVAD cohort (n=451) was queried for patients with follow-up RHC data at 6 months +/- 3 months (n=179). To determine the relationship between follow-up PCWP and mortality, a multivariable cox regression analysis was performed. Results The mean age of the study cohort was 57±13 years. 79% (141/179) were males, 56% (101/179) had ischemic cardiomyopathy and 74% (133/179) were designated bridge to transplant (BTT). The median follow-up time on LVAD support after RHC was 4.4 years. The only pre-implant variables that were associated with elevated PCWP in the multivariate analysis were renal function and BMI (each 2.5 unit increase in BMI was associated with an adjusted 0.6 mmHg increase in follow-up PCWP, 95% CI 0.2-0.9 mmHg, p=0.004; each 0.5 mg/dL increase in creatinine was associated with a 1.2 mmHg increase in follow-up PCWP, 95% CI 0.4-2.1, p=0.003). In the final multivariate models, each 5 mmHg increase in PCWP at the time of RHC was associated with a 22% increase in the hazards rate of death during follow-up (adjusted HR 1.2, 95% CI 1.01-1.47, p=0.039). All models were adjusted for age, sex, INTERMACS profile, body mass index, bridge to transplant status and renal function. Conclusion Incomplete LV unloading following CF-LVAD implantation is associated with increased all-cause mortality. Our results emphasize the importance of invasive hemodynamic optimization in this patient population. Further studies are warranted to determine the optimal filling pressures in patients with CF-LVAD.

Clinical Hemodynamic and Echocardiography Data Analysis for Patients with Mitral Stenosis Before and After PTMC Procedure at Rajaie Cardiovascular Center Between 2015 and 2016

Background: Mitral stenosis is a common and important type of valvular heart disease. This study was performed to determine and compare the hemodynamic, echocardiographic and clinical data before and after percutaneous transvenous mitral commissurotomy (PTMC). Methods: In this prospective cohort, the data for 171 consecutive patients with PTMC at a university referral heart hospital have been collected and analyzed from March 2015 till September 2016. Due to the missing data reported on the medical charts, 20 cases were further dismissed. Therefore, clinical study on hemodynamic monitoring and echocardiography have been observed and compared on the remaining 151 consecutive cases. In this study, demographic data, clinical symptoms and medication before the procedure and systolic pulmonary arterial pressure (SPAP), pulmonary capillary wedge pressure (PCWP), trans mitral valve gradient and mitral valve area (MVA) before and after PTMC have been measured. Results: The results showed that according to Wilcoxon test there was a significant increase in PCWP, significant decrease in mean gradient of mitral valve and significant reduction in SPAP after PTMC (P = 0.0001). In this study, post-procedure mitral regurgitation (MR) values after echocardiography and angiography have been compared and it was stated that about 90.4% (138 cases) are diagnosed with mild MR (no MR and mild MR) in angiography while 10.6% (16 cases) have trivial and mild MR in echocardiography (P < 0.0001). Conclusions: Totally it may be concluded that there is significant difference between the hemodynamic and echocardiographic data after PTMC. Echocardiography estimates the MR complications after PTMC to be higher than angiography.

Usefulness of Diastolic Strain Measurements in Predicting Elevated Left Ventricular Filling Pressure and Risk of Rejection or Coronary Artery Vasculopathy in Pediatric Heart Transplant Recipients

In pediatric heart transplant recipients, elevated pulmonary capillary wedge pressure (PCWP) is associated with rejection and coronary artery vasculopathy. This study aimed to evaluate which echocardiographic parameters track changes in PCWP and predict adverse outcomes (rejection or coronary artery vasculopathy). This prospective single-center study enrolled 49 patients (median 11.4 years old, interquartile range 7.4 to 16.5) at time of cardiac catheterization and echocardiography. Median follow-up was 2.4 years (range 1.2 to 3.1 years), with serial testing per clinical protocol. Ratio of early mitral inflow to annular velocity (E/E'), left atrial (LA) distensibility, peak LA systolic strain, E/left ventricular (LV) diastolic strain, and E/LV diastolic strain rate were measured from echocardiograms. Increase in PCWP ≥3 mm Hg was associated with changes in LA distensibility, E/E', and E/LV diastolic strain, with highest area under the receiver operating characteristic curve for E/LV diastolic strain (0.76). In 9 patients who subsequently developed rejection or coronary artery vasculopathy, E/LV diastolic strain rate at baseline differed from patients without events (median 57.0 vs 43.6, p = 0.02). On serial studies, only change in LV ejection fraction differed in patients with events (median -10% vs -1%, p = 0.01); decrease in LV ejection fraction of -19% had a specificity of 100% and sensitivity of 44%. In conclusion, LV diastolic strain and strain rate measurements can track changes in PCWP and identify patients at risk for subsequent rejection or coronary artery vasculopathy. Further studies are necessary to confirm these data in a larger cohort.

Sodium Nitrite Improves Exercise Hemodynamics and Ventricular Performance in Heart Failure With Preserved Ejection Fraction

BackgroundThere is no effective medical treatment for heart failure with preserved ejection fraction (HFpEF). Increases in pulmonary capillary wedge pressure (PCWP) develop in patients with HFpEF during exercise coupled with impaired nitric oxide (NO) signaling. Nitrite can be reduced to bioactive NO in vivo, particularly under conditions of tissue hypoxia, as with exercise. ObjectivesThis study sought to determine whether acute nitrite administration improves exercise hemodynamics and cardiac reserve in HFpEF. MethodsIn a double-blind, randomized, placebo-controlled, parallel-group trial, subjects with HFpEF (N = 28) underwent invasive cardiac catheterization with simultaneous expired gas analysis at rest and during exercise, before and 15 min after treatment with either sodium nitrite or matching placebo. ResultsBefore the study drug infusion, HFpEF subjects displayed an increase in PCWP with exercise from 16 ± 5 mm Hg to 30 ± 7 mm Hg (p < 0.0001). After study drug infusion, the primary endpoint of exercise PCWP was substantially improved by nitrite compared with placebo (adjusted mean: 19 ± 5 mm Hg vs. 28 ± 6 mm Hg; p = 0.0003). Nitrite-enhanced cardiac output reserve improved with exercise (+0.5 ± 0.7 l/min vs. −0.4 ± 0.7 l/min; p = 0.002) and normalized the increase in cardiac output relative to oxygen consumption. Nitrite improved pulmonary artery pressure-flow relationships in HFpEF and increased left ventricular stroke work with exercise versus placebo, indicating an improvement in ventricular performance with stress. ConclusionsAcute sodium nitrite infusion favorably attenuates hemodynamic derangements of cardiac failure that develop during exercise in individuals with HFpEF. Prospective trials testing long-term nitrite therapy in this population are warranted. (Acute Effects of Inorganic Nitrite on Cardiovascular Hemodynamics in Heart Failure With Preserved Ejection Fraction; NCT01932606)

Exercise-Induced Pulmonary Hypertension in Scleroderma Patients: A Common Finding but with Elusive Pathophysiology

The etiology of exercise-induced pulmonary hypertension (exPH) in systemic sclerosis (SSc) remains a complex task, as both left ventricle (LV) diastolic dysfunction and pulmonary vascular disease can contribute to its development. We determined the incidence of exPH in SSc and examined the association between pulmonary artery systolic pressure (PASP) and tissue Doppler-derived indexes of pulmonary capillary wedge pressure (PCWP). Thirty-eight patients with SSc were studied, using a cycloergometer protocol; 10 were excluded due to resting PH or absence of tricuspid regurgitation (TR); TR and mitral E-wave velocities, LV outflow tract time-velocity integral and LV septal E'-wave were measured before and in peak exercise to calculate cardiac output (CO), PCWP and pulmonary vascular resistance (PVR). Mean age of diagnosis was 57.9 ± 8.9 years. At a mean workload of 64 ± 29 Watts, 48% of patients increased PASP ≥ 50 mmHg. PCWP, assessed by the E/e' ratio, did not change significantly during exercise (10.2 ± 3.1-10.0 ± 5.1; P = NS). Only 3 patients had elevations of the E/e' ratio ≥ 13 during exercise; 2 of them had an exercise PASP ≥ 50 mmHg, yielding a proportion of exPH due to elevated LV filling pressures of 2/11 (18%). Patients with exPH had lower DLCO and had more frequently the diffuse SSc. The elevation of PASP during exercise in most patients of this cohort seems to be related to a reduced pulmonary vascular reserve, and not to an increase in PCWP. Further studies are warranted to determine the therapeutic, as well as prognostic implications of these findings.

Deep Pericardial Traction Suture versus Vacuum-Assisted Apical Suction to Expose the Posterior Wall of the Heart in Off-Pump Coronary Artery Bypass: A Prospective, Randomized Study

Displacement of the heart to expose the posterior vessels during off-pump coronary artery bypass (OPCAB) may cause hemodynamic instability. Deep pericardial traction suture (DPTS) and vacuum-assisted apical suction (VAS) with the Starfish positioning device help to provide good exposure without relevant hemodynamic changes. Our aim was to compare these two methods in patients undergoing multivessel OPCAB. We prospectively randomized 20 patients undergoing multivessel OPCAB to the use of VAS or DPTS. The Octopus device was used in both groups to stabilize the target vessel. Hemodynamic parameters, including venous oxygen content (SvO(2)), cardiac index (CI), central venous pressure (CVP), mean arterial pressure (MAP), pulmonary artery pressure (PAP), and pulmonary capillary wedge pressure (PCWP), were measured before grafting (baseline), after heart positioning, and during performance of peripheral anastomoses. Perioperative data for the two groups were similar. During exposure of the lateral wall, there were fewer hemodynamic changes in the DPTS group (increase in CVP) than in the VAS group (increases in CVP, PAP, and PCWP); the CVP was significantly higher in the DPTS group (P < .05). During exposure of the posterior wall, significant hemodynamic changes occurred only in the DPTS group (increase in PCWP). Values for all other parameters were similar, including anastomosis time, graft flow, postoperative myocardial enzymes, and inotropic support. Heart positioning during OPCAB with either VAS or DPTS is a safe and effective maneuver for exposure of coronary arteries. In our study, the use of the VAS device produced less hemodynamic impairment during exposure of the lateral and posterior walls.

A histamine H2 receptor blocker ameliorates development of heart failure in dogs independently of β-adrenergic receptor blockade

Histamine has a positive inotropic effect on ventricular myocardium and stimulation of histamine H₂ receptors increases the intracellular cAMP level via Gs protein, as dose stimulation of β-adrenergic receptors, and worsens heart failure. To test whether a histamine H₂ receptor blocker had a beneficial effect in addition to β-adrenergic receptor blockade, we investigated the cardioprotective effect of famotidine, a histamine H₂ receptor blocker, in dogs receiving a β-blocker. We induced heart failure in dogs by rapid ventricular pacing (230 beats/min). Animals received no drugs (control group), famotidine (1 mg/kg daily), carvedilol (0.1 mg/kg daily), or carvedilol plus famotidine. Both cardiac catheterization and echocardiography were performed before and 4 weeks after the initiation of pacing. Immunohistochemical studies showed the appearance of mast cells and histamine in the myocardium after 4 weeks of pacing. In the control group, the left ventricular ejection fraction (LVEF) was decreased after 4 weeks compared with before pacing (71 ± 2 vs. 27 ± 2%, p < 0.05) and mean pulmonary capillary wedge pressure (PCWP) was increased (8 ± 1 vs. 19 ± 3 mmHg). Famotidine ameliorated the decrease of LVEF and increase of PCWP, while the combination of carvedilol plus famotidine further improved both parameters compared with the carvedilol groups. These beneficial effects of famotidine were associated with a decrease of the myocardial cAMP level. Histamine H₂ receptor blockade preserves cardiac systolic function in dogs with pacing-induced heart failure, even in the presence of β-adrenergic receptor blockade. This finding strengthens the rationale for using histamine H₂ blockers in the treatment of heart failure.

One Year of Endurance Exercise Training Does Not Improve Left Ventricular Relaxation in Sedentary Seniors

BACKGROUND: Life-long endurance exercise training may attenuate the age-related changes in left ventricular (LV) relaxation. However, it is unclear whether endurance exercise training started later in life can improve LV relaxation in previously sedentary healthy seniors. PURPOSE: To determine the effect of one year of endurance exercise training on LV relaxation in sedentary healthy seniors. METHODS: Nine well-screened sedentary healthy seniors (71±3 years) who were not taking any cardiovascular medications and had no provocable ischemia during exercise were enrolled into the study. Pulmonary capillary wedge pressure (PCWP) and echocardiographic LV diastolic variables were measured at supine rest. Global LV diastolic function was assessed by the ratio of early-to-late mitral inflow velocity (E/A ratio), while LV relaxation was assessed by tissue Doppler velocities of the septal and lateral mitral annulus (Em), isovolumic relaxation time (IVRT) and color M-mode propagation velocity (Vp). LV filling pressure was assessed by PCWP. All subjects completed the one year of training, which increased maximal aerobic power (VO2 max) by ∼19% (22.8±3.4 vs. 27.2±4.3 ml/kg/min, p<0.001). Measurements were repeated after one year of exercise training. RESULTS: Heart rate was decreased (59±8 vs. 55±11 beats/min, p=0.003), while systolic (p=0.30) and diastolic blood pressure (p=0.57) were unaffected by exercise training The E/A ratio was increased after training (0.81±0.16 vs. 0.99±0.25, p=0.022). Em was decreased (9.8±1.8 vs. 8.3 ±1.0 cm/s, p=0.006), while Vp was unaffected by training (34.3±8.3 vs. 33.5±9.3, p=0.75). In contrast, IVRT was shortened after training (145±17 vs.114±11 ms, p=0.012). There was a small training-related increase in PCWP (11.4±1.7 vs. 12.5±2.8 mmHg, p=0.26). CONCLUSIONS: These results suggest that one year of exercise training does not improve LV relaxation assessed by Em or Vp in previously sedentary seniors. The effect of training on IVRT likely reflects the small increase in left atrial pressure as measured from PCWP. Based on Em and Vp, the increased E/A ratio after exercise training is more likely due to changes in driving pressure, but not likely due to improved LV relaxation.

The Relationship of Right- and Left-Sided Filling Pressures in Patients With Heart Failure and a Preserved Ejection Fraction

Although right-sided filling pressures often mirror left-sided filling pressures in systolic heart failure, it is not known whether a similar relationship exists in heart failure with preserved ejection fraction. Eleven subjects with heart failure with preserved ejection fraction underwent right heart catheterization at rest and under loading conditions manipulated by lower body negative pressure and saline infusion. Right atrial pressure (RAP) was classified as elevated when >or=10 mm Hg and pulmonary capillary wedge pressure (PCWP) when >or=22 mm Hg. If both the RAP and the PCWP were elevated or both not elevated, they were classified as concordant; otherwise, they were classified as discordant. Correlation of RAP and PCWP was determined by a repeated measures model. Among 66 paired measurements of RAP and PCWP, 44 (67%) had a low RAP and PCWP and 8 (12%) a high RAP and PCWP, yielding a concordance rate of 79%. In a sensitivity analysis performed by varying the definition of elevated RAP (from 8 to 12 mm Hg) and PCWP (from 15 to 25 mm Hg), the mean+/-SD concordance of RAP and PCWP was 76+/-10%. The correlation coefficient of RAP and PCWP for the overall cohort was r=0.86 (P<0.0001). Right-sided filling pressures often reflect left-sided filling pressures in heart failure with preserved ejection fraction, supporting the role of estimation of jugular venous pressure to assess volume status in this condition.

Cardiac Dysfunction during Exercise in Uncomplicated Type 2 Diabetes

Type 2 diabetes mellitus (T2DM) has been associated with reduced peak exercise capacity (VO(2peak)). The causes of this impairment are not clearly established, but evidence suggests that abnormalities in cardiac function play a significant role. We hypothesized that exercise would be associated with impaired cardiac function and hemodynamics in recently diagnosed T2DM, even in the absence of clinically evident cardiovascular complications. After baseline normal echocardiography screening, 10 premenopausal women with uncomplicated T2DM (average duration of diagnosed T2DM, 3.6 yr) and 10 healthy nondiabetic women of similar age, weight, and activity levels performed a peak cardiopulmonary exercise test while instrumented with an indwelling pulmonary artery catheter for assessing cardiac function. On separate days, technetium-99m sestamibi (cardolite) imaging was performed to assess myocardial perfusion at rest and peak exercise in seven T2DM and seven control patients. Resting measures of cardiac hemodynamics were similar in T2DM and control subjects. Absolute VO(2peak) (mL x min(-1)) and peak cardiac output (L x min(-1)) tended to be lower in T2DM than in control subjects but did not reach statistical significance. However, pulmonary capillary wedge pressure (PCWP) rose significantly more during exercise in T2DM than in controls (148% vs 109% increase at peak exercise, P < 0.01). Normalized myocardial perfusion index was lower in persons with diabetes than in controls (11.0 +/- 3.5 x e(-9) vs 17.5 +/- 8.1 x e(-9), respectively, P < 0.05) and inversely related to peak exercise PCWP (R = -0.56, P < 0.05). Cardiac hemodynamics during graded exercise are altered in women with recently diagnosed T2DM as demonstrated by the disproportionate increase in PCWP at peak exercise compared with controls subjects. Cardiac abnormalities observed are potentially early signs of subclinical cardiac dysfunction associated with T2DM, which may precede the more greatly impaired cardiac function at rest and with exercise observed in longer established T2DM.