Low Mixed Venous Oxygen Saturation Research Articles

The Impact of Diabetes on Haemodynamic and Cardiometabolic Responses in Heart Failure With Preserved Ejection Fraction

Heart failure with preserved ejection (HFpEF) and diabetes mellitus (DM) commonly co-exist. However, it is unclear if DM modifies the haemodynamic and cardiometabolic phenotype in patients with HFpEF. We aimed to interrogate the haemodynamic and cardiometabolic effects of DM in HFpEF. We compared the haemodynamic and metabolic profiles of non-DM patients and patients with DM-HFpEF at rest and during exercise using right heart catheterisation and mixed venous blood gas analysis. Of 181 patients with HFpEF, 37 (20%) had DM. Patients with DM displayed a more adverse exercise haemodynamic response vs HFpEF alone (mean pulmonary arterial pressure: 47 mmHg [interquartile range {IQR} 42-55] vs 42 [38-47], p<0.001; workload indexed pulmonary capillary wedge pressure indexed: 0.80 mmHg/W [0.44-1.23] vs 0.57 [0.43-1.01], p=0.047). HFpEF-DM patients had a lower mixed venous oxygen saturation at rest (70% [IQR 66-73] vs 72 [69-75], p=0.003) and were unable to enhance O2 extraction to the same extent (Δ-28% [-33 to -15] vs -29 [-36 to -21], p=0.029), this occurred at a 22% lower median workload. Resting mixed venous lactate levels were higher in those with DM (1.5 mmol/L [IQR 1.1-1.9] vs 1 [0.9-1.3], p<0.001), and during exercise indexed to workload (0.09 mmol/L/W [0.06-0.13] vs 0.08 [0.05-0.11], p=0.018). Concurrent diabetes and HFpEF was associated with greater metabolic responses at rest, with enhanced wedge driven pulmonary hypertension and relative lactataemia during exercise without appropriate augmentation of oxygen consumption.

Unresponsive Low Mixed Venous Oxygen Saturation During Early Intensive Care Unit Stay is Associated With Increased Risk of Organ Dysfunction After Cardiac Surgery: A Single-Center Retrospective Study

The aim of the study was to determine if unresponsive mixed venous oxygen saturation (SvO2) values during early postoperative hours are associated with postoperative organ dysfunction. A single-center retrospective observational study. A university hospital. A total of 6,282 adult patients requiring cardiac surgery who underwent surgery in a University Hospital from 2007 to 2020. A pulmonary artery catheter was used to gather SvO2 samples after surgery at admission to the intensive care unit (ICU) and 4 hours later. For the analysis, patients were divided into 4 groups according to their SvO2 values. The rate of organ dysfunctions categorized according to the SOFA score was then studied among these subgroups. The crude mortality rate for the cohort at 1 year was 4.3%. Multiple organ dysfunction syndrome (MODS) was present in 33.0% of patients in the early postoperative phase. During the 4-hour initial treatment period, 43% of the 931 patients with low SvO2 on admission responded to goal-directed therapy to increase SvO2 >60%; whereas, in 57% of the 931 patients, the low SvO2 was sustained. According to the adjusted logistic regression analyses, the odds ratio for MODS (4.23 [95% CI 3.41-5.25]), renal- replacement therapy (4.97 [95% CI 3.28-7.52]), time on a ventilator (2.34 [95% CI 2.17-2.52]), and vasoactive-inotropic score >30 (3.62 [95% CI 2.96-4.43]) were the highest in the group with sustained low SvO2. Patients with SvO2 <60% at ICU admission and 4 hours later had the greatest risk of postoperative MODS. Responsiveness to a goal-directed therapy protocol targeting maintaining or increasing SvO2 ≥60% at and after ICU admission may be beneficial.

Epidemiology and outcome of an acute kidney injuries in the polytrauma victims admitted at the apex trauma center in Dubai.

Polytrauma from road accidents is a common cause of hospital admissions and deaths, frequently leading to acute kidney injury (AKI) and impacting patient outcomes. This retrospective, single-center study included polytrauma victims with an Injury Severity Score (ISS) >25 at a tertiary healthcare center in Dubai. The incidence of AKI in polytrauma victims is 30.5%, associated with higher Carlson comorbidity index (P=0.021) and ISS (P=0.001). Logistic regression shows a significant relationship between ISS and AKI (odds ratio [OR], 1.191; 95% confidence interval [CI], 1.150-1.233; P<0.05). The main causes of trauma-induced AKI are hemorrhagic shock (P=0.001), need for massive transfusion (P<0.001), rhabdomyolysis (P=0.001), and abdominal compartment syndrome (ACS; P<0.001). On multivariate logistic regression AKI can be predicated by higher ISS (OR, 1.08; 95% CI, 1.00-1.17; P=0.05) and low mixed venous oxygen saturation (OR, 1.13; 95% CI, 1.05-1.22; P<0.001). The development of AKI after polytrauma increases length of stay (LOS)-hospital (P=0.006), LOS-intensive care unit (ICU; P=0.003), need for mechanical ventilation (MV) (P<0.001), ventilator days (P=0.001), and mortality (P<0.001). After polytrauma, the occurrence of AKI leads to prolonged hospital and ICU stays, increased need for mechanical ventilation, more ventilator days, and a higher mortality rate. AKI could significantly impact their prognosis.

111 POST-OPERATIVE OUTCOME OF ADULT PATIENTS WITH PRE-TRICUSPID SHUNT UNDERGOING DEFECT CLOSURE

Abstract Background patients with pulmonary arterial hypertension (PAH) associated with corrected congenital heart disease (CHD) have a worse prognosis than other 3 groups of patients with PAH associated with CHD (Eisenmenger, small defect, prevalent systemic-to-pulmonary shunt). For this reason, in CHD the indication and timing of defect repair should be evaluated carefully. Current recommendations rely essentially on pulmonary vascular resistance (PVR) when deciding about defect closure, but this may be insufficient as PAH may develop even in cases of normal pre-operative PVR. In particular, patients with PVR below 3 WU are usually deemed operable and patients between 3 and 5 WU (gray zone) are deemed operable in case of significant persistence of left-to-right shunt. Detecting preoperative characteristics of patients who developed PAH after pre-tricuspid shunt repair can be helpful when deciding about CHD correction. Methods we enrolled adult patients referred to our centre for the suspicious of PAH after pre-tricuspid shunt correction from 2006 to 2021. We evaluated clinical, echocardiographic and hemodynamic parameters before and after defect repair (a post-correction hemodynamic evaluation was performed only in case of non-invasive signs of PAH) and PAH after defect closure was defined by the concomitant occurrence of a mean pulmonary artery pressure (mPAP) &amp;gt;25 mmHg and PVR &amp;gt;3 WU. Continuous variables were summarized using mean and standard deviation and Student's t-test was used for comparisons. Results sixty patients were included in the final analysis. After shunt repair, 10 patients (16.6%) were diagnosed with PAH during the long-term follow-up, with no differences given by the type of defect or type of correction. As expected, these patients already had an abnormal baseline hemodynamic profile: 7 had a clear PAH diagnosis before the correction [mPAP &amp;gt;25 mmHg with PVR between 3 and 5 WU and with a pulmonary/systemic cardiac output ratio of at least 1.5] while 3 had pulmonary hypertension related to high pulmonary blood flow (mPAP &amp;gt;25 mmHg and PVR &amp;lt;3 WU). At the baseline hemodynamic evaluation, patients with PAH after shunt repair had higher mPAP (39±6 vs 24±10 mmHg, p &amp;lt;0.001) and PVR (3.7±1.2 vs 1.5±0.9, p &amp;lt;0.001) and lower mixed venous oxygen saturation (81±3 vs 87±3, p &amp;lt;0.001). At the baseline echocardiographic evaluation, patients with PAH after shunt repair had a greater right ventricular hypertrophy (RV wall thickness 0.7±0.1 vs 0.5±0.2 cm, p= 0.011), tricuspid regurgitation jet velocity (424±63 vs 319±62 cm/s, p &amp;lt;0.001) and a significant lower RV fractional area change (34±8 vs 43±9%, p= 0.009). Conclusions currently there are no established evidence-based algorithms to predict the development of PAH after defect correction. Our study shows that this condition may persist or develop even when PVR values are lower than 5 WU despite a significant left-to-right shunt before defect closure. Patients with grey zone PVR values require a global clinical, instrumental and hemodynamic assessment that takes into account more than bare calculated PVR that, especially in patients with a high pulmonary blood flow, can be less reliable.

Influence of Iron Deficiency on Clinical and Haemodynamic Parameters in Pulmonary Arterial Hypertension Cohorts.

Iron deficiency (Fedef) has been shown to be common in patients with group 1 or pulmonary arterial hypertension (PAH). Several studies have shown a negative impact of Fedef on clinical and haemodynamic parameters of the disease, but data from individual studies have not been strong enough to lead to incorporation of the finding of Fedef into prognostic or therapeutic algorithms. The goal of this meta-analysis was to combine data from available studies to better define any associations between Fedef and established variables of prognostic importance in PAH. A literature search identified nine studies with extractable data relevant to the study questions. The impact of Fedef upon the following parameters was evaluated: 6-minute walk distance (6MWD), WHO-functional class, N-terminal pro-brain natriuretic peptide (NT-proBNP) levels, echocardiography, and findings from right heart catheterisation (RHC). Pooled results were reported as mean difference or risk difference with 95% confidence intervals utilising a random effects modeling approach. Fedef in the PAH population was common (47% of cases) and was associated with cardiovascular dysfunction (lower tricuspid annular plane systolic excursion [TAPSE], elevated NT-proBNP, and lower mixed venous oxygen saturation) and with reduction in functional capacity (lower 6MWD and higher functional class). This meta-analysis strengthens the relationships between Fedef and several markers of poor outcome in PAH. Fedef in patients with PAH warrants further scrutiny and merits consideration as a cause of clinical deterioration. Even though causation and longitudinal relationships between Fedef and PAH could not be identified, effect of Fedef on factors that affect disease prognosis is noteworthy and worthy of more focussed studies.

Prognostic role of comorbidities in patients with pulmonary arterial hypertension

Abstract Background Epidemiology of pulmonary arterial hypertension (PAH) is changing and the age at diagnosis and the prevalence of comorbidities are increasing but their prognostic relevance is substantially undefined. Purpose To evaluate the prognostic value of comorbidities in patients with PAH and in the different clinical subgroups. Methods All patients with PAH referred to a single centre underwent baseline right heart catheterization, brain natriuretic peptide (BNP) plasma levels, 6-min walking distance (6MWD), WHO functional class and anamnestic comorbidities evaluation. Cox regression model was used for analysis (p-value &amp;lt;0.1 was considered for inclusion in multivariate analysis). Results 1311 patients were included [age 51 years; aetiology: 522 idiopathic/heritable/drug-induced (I/H/D)-PAH, 258 connective tissue disease (CTD)-associated PAH, 242 congenital heart disease (CHD)-associated PAH, 196 portal hypertension/HIV (PoHIV)-associated PAH and 93 pulmonary veno-occlusive disease (PVOD)]. 5% of patients have no comorbidities. At multivariate analysis comorbidities independently associated with prognosis are: systemic hypertension in I/H/D [HR 0.616, p=0.030], mean systemic blood pressure in CTD [HR 0.980, p=0.002] and PVOD [HR 0.962, p=0.006], dyslipidemia in CTD [HR 0.447, p=0.001] and PoHIV [HR 0.201, p=0.026], estimated glomerular filtration rate in PoHIV [HR 1.000, p&amp;lt;0.001] and body mass index (BMI) [HR 0.966, p=0.069] in CTD. In CHD comorbidities are not independent determinants of prognosis. Other variables independently predictive of a worse prognosis are: advanced age in all PAH subgroups except PVOD; male gender in I/H/D; reduced 6MWD in I/H/D, CTD and PVOD; high BNP in I/H/D, CHD and PVOD; low cardiac index in CTD, high right atrial pressure in I/H/D and low mixed venous oxygen saturation in CHD. Conclusion The age at PAH diagnosis and the prevalence of comorbidities are increasing but their prognostic role seems of poor relevance as we found a protective role of these variables: high systemic blood pressure (maybe indicative of a better haemodynamic stability) in I/H/D, CTD and PVOD; dyslipidemia and high BMI (maybe indicative of a better nutritional status and a less severe autoimmune disease) in CTD; dyslipidemia and a high glomerular filtration rate (both indicative of a less severe liver disease) in PoHIV. Funding Acknowledgement Type of funding source: None

Association between splenectomy and portal hypertension in the development of pulmonary hypertension.

Both portal hypertension and splenectomy are risk factors for pulmonary hypertension. However, the interactions between portal hypertension and splenectomy in the development of pulmonary hypertension remain unclear. Twelve newly diagnosed pulmonary hypertension patients with a previous history of splenectomy induced by portal hypertension were recruited between November 2008 and May 2017. We compared their clinical features, hemodynamics, and prognosis with idiopathic pulmonary arterial hypertension patients, who were matched by cardiac index, mean pulmonary arterial pressure, and pulmonary vascular resistance. We also compared the clinical characteristics of portal hypertension-post-splenectomy-pulmonary hypertension patients with eight portopulmonary hypertension patients. Compared with the matched idiopathic pulmonary arterial hypertension patients, the portal hypertension-post-splenectomy-pulmonary hypertension patients showed significantly wider red blood cell distribution width (16.7 ± 2.8% versus 13.3 ± 1.7%, p = 0.004), higher total bilirubin concentration (31.0 ± 13.8 µmol/l versus 18.9 ± 10.0 µmol/l, p = 0.010), and higher lactate dehydrogenase concentration (321.5 ± 41.2 IU/l versus 229.2 ± 69.4 IU/l, p = 0.001). Kaplan-Meier survival analyses showed that the portal hypertension-post-splenectomy-pulmonary hypertension patients tended to have poorer prognosis than the matched idiopathic pulmonary arterial hypertension patients (log-rank test: p = 0.010). Compared with the portal hypertension-post-splenectomy-pulmonary hypertension patients, the portopulmonary hypertension cohort appeared to exhibit poorer clinical conditions, including significantly lower mixed venous oxygen saturation (62.9 ± 8.0% versus 73.9 ± 6.5%, p = 0.004) and a significantly higher proportion of pericardial effusion (75.0% versus 8.3%, p = 0.004), even though the two cohorts showed similar hemodynamics. The mean intervals from diagnosis of portal hypertension to pulmonary hypertension in portopulmonary hypertension patients were significantly shorter than the intervals from splenectomy to diagnosis of pulmonary hypertension in portal hypertension-post-splenectomy-pulmonary hypertension patients (5.5 ± 5.2 years versus 13.1 ± 5.9 years, p = 0.008). Splenectomy might be involved in the initiation and development of pulmonary hypertension in patients with portal hypertension, although the precise mechanisms involved remain unknown. Portal hypertension-post-splenectomy-pulmonary hypertension patients might have poorer prognosis even with mild hemodynamics.

Right Ventricular Function is Associated With Quality of Life in Patients With Systemic Lupus Erythematosus Associated Pulmonary Arterial Hypertension

Right ventricular (RV) function has been identified as an important determinant of outcome in patients with pulmonary hypertension. We aimed to investigate the relationship between echocardiographic-derived RV function and health-related quality of life (HRQOL) in patients with systemic lupus erythematosus associated pulmonary arterial hypertension (SLE-APAH), and to identify the best echocardiographic parameter for evaluating RV function in these patients. Sixty (60) consecutive patients with SLE-APAH (all female, mean age 33.6±8.2years) were recruited from May 2013 to November 2014. Echocardiograph, right heart catheterisation, SLE disease activity index (SLEDAI), and functional status and SF-36 generic questionnaire were assessed. Echocardiograph-derived RV systolic function was significantly correlated with haemodynamics (p<0.05), with tricuspid annular plane systolic excursion (TAPSE) showing the strongest correlation with pulmonary vascular resistance (R2=0.278, p<0.001) and cardiac index (R2=0.215, p<0.001). Patients with a TAPSE<17mm had a shorter 6-minute-walk-distance (6MWD), lower mixed venous oxygen saturation, and higher plasma N-terminal pro-brain natriuretic peptide (p<0.05). Patients with TAPSE <17mm had lower physical component summary (PCS) and mental component summary (MCS) scores than those with TAPSE ≥17mm (35.5±13.2 vs. 55.0±15.5; 46.3±15.3 vs. 64.8±18.8, respectively, all p<0.05). On multiple regression analysis, a TAPSE <17mm was independently related to lower PCS (β -15.797, 95% confidence interval [CI] -24.746 to -6.848, p=0.001) and lower MCS (β -12.887, 95% CI -24.018 to -1.755, p=0.024). TAPSE is a useful index for RV function assessment, and is associated with HRQOL in patients with SLE-APAH.

Plasma Growth Differentiation Factor-15 is a Potential Biomarker for Pediatric Pulmonary Arterial Hypertension Associated with Congenital Heart Disease.

We aimed to investigate plasma growth differentiation factor-15 (GDF-15) levels in pediatric pulmonary arterial hypertension secondary to congenital heart disease (PAH-CHD), and assess the association with hemodynamic parameters. Plasma GDF-15 levels were measured in children with PAH-CHD (n=46) and compared to children with CHD without PAH (n=39). Normal individuals (n=30) served as health control group. Plasma GDF-15 levels were significantly elevated in patients with PAH-CHD compared with those with CHD without PAH (median 1415ng/L, interquartile range [IQR] 926.7-2111.7ng/L vs. 890.6ng/L, IQR 394.7-1094.3ng/L, p<0.01). Elevated plasma GDF-15 levels were positively related to Functional Class, uric acid, N-terminal pro-B-type natriuretic peptide (NT-proBNP), pulmonary artery systolic pressure, mean pulmonary artery pressure, pulmonary blood flow/systemic blood flow and pulmonary vascular resistance, and a lower mixed venous oxygen saturation (Svo2). The area under the curve (AUC) for adding GDF-15 to NT-proBNP was not superior to the AUC of NT-pro BNP alone (AUC difference 0.0295, p=0.324) (NT-proBNP, AUC 0.823, 95% CI 0.725-0.897; GDF-15 plus NT-proBNP, AUC 0.852, 95% CI 0.759-0.92), whereas it revealed a slightly greater specificity and positive predictive value. The diagnostic power of NT-pro BNP was not inferior to GDF-15 (AUC difference 0.0443, p=0.43). Plasma GDF-15 levels might be a surrogate marker for pediatric PAH-CHD.

Persistent hypoxemia on ECMO

Extracorporeal membrane oxygenation (ECMO) is used to support patients with hypoxemia due to severe respiratory failure. Hypoxemia can persist during ECMO as a result of reduction in mechanical ventilatory support as part of a lung protective strategy, following which gas exchange provided by the native lungs is reduced or absent. If tissue oxygen delivery is maintained, mild to moderate hypoxemia will be well tolerated, but if tissue hypoxia develops, then the cause of hypoxemia must be addressed and corrected. Patterns of hypoxemia are dependent on the mode of ECMO support. During veno-venous support for respiratory failure, hypoxemia is global, with all tissues receiving hypoxemic blood. When femoral veno-arterial support is used in the presence of respiratory failure, then differential hypoxemia can result, with hypoxemia limited to the upper part of the body. The approach to hypoxemia is dependent on whether veno-venous (VV) or veno-arterial (VA) ECMO is used. Adequate oxygen saturation on VV ECMO requires adequate hemoglobin, a membrane lung operating below its rated flow, low recirculation, and extracorporeal circuit flow that captures most of the cardiac output. The approach to hypoxemia during VV ECMO includes addressing each of these. Identifying and limiting recirculation will improve effective extracorporeal flow. Anemia has two detrimental effects. First, it limits oxygen transfer through the membrane lung. Second, it increases oxygen extraction resulting in low mixed venous oxygen saturation that increases the effective venous admixture with circuit blood. Transfusion to near normal levels will help improve oxygen saturation. Increasing effective extracorporeal flow to capture at least 60% of the cardiac output is necessary.1 If the extracorporeal flow fraction is less than 60% due to an increased cardiac output, then reducing cardiac output through reducing exogenous catecholamines, use of beta blockade,2 or hypothermia3 will help improve the extracorporeal flow fraction. Hypothermia has the added benefit of reducing oxygen consumption and therefore improving mixed venous saturation. A final option is to leverage the native lungs, such as through prone positioning, as long as lung protective strategies can be maintained.4 Oxygen saturation on femoral VA ECMO is typically normal (>90%). The upper part of the body is provided with blood from the left ventricle that has been saturated by normally functioning lungs. The lower part of the body is provided with fully saturated blood from the extracorporeal circuit. The two circulations meet at some point in the aorta that depends on the relative magnitude of flow rate in these two circulations. If there is pulmonary dysfunction, then the blood ejected by the left ventricle will be hypoxemic, and tissues perfused proximal to the mixing point will be perfused with hypoxemic blood, while the lower body will have a normal saturation. Management of this differential hypoxemia is through improvement of pulmonary gas exchange if possible, increasing extracorporeal flow to decrease pulmonary blood flow, or conversion of VA ECMO to VVA (hybrid veno-arterial and veno-venous).

Preoperative Stabilization of Infants With Hypoplastic Left Heart Syndrome Before Stage I Palliation.

Hypoplastic left heart syndrome is a severe form of congenital heart disease that results in single-ventricle physiology. Although surgical palliation in infants with this syndrome is widely agreed on in practice, variation occurs in both surgical and medical management. Perinatal factors that affect preoperative management include the subtype of the syndrome and the patient's birth weight, gestational age, and genetic abnormalities. The general aspects of perioperative stabilization and management are monitoring, use of vasoactive infusions, ventilatory support, and nutrition. Management strategies for balancing single-ventricle physiology are aimed at addressing the 3 major causes of desaturation: diminished pulmonary blood flow, low mixed venous oxygen saturation, and pulmonary venous desaturation.

Sedation and Anesthesia in Pediatric and Congenital Cardiac Catheterization: A Prospective Multicenter Experience

Sedation/anesthesia is critical to cardiac catheterization in the pediatric/congenital heart patient. We sought to identify current sedation/anesthesia practices, the serious adverse event rate related to airway, sedation, or anesthesia, and the rate of intra-procedural conversion from procedural sedation to the use of assisted ventilation or an artificial airway. Data from 13,611 patients who underwent catheterization at eight institutions were prospectively collected from 2007 to 2010. Ninety-four (0.69 %) serious sedation/airway-related adverse events occurred; events were more likely to occur in smaller patients (<4 kg, OR 4.4, 95 % CI 2.3-8.2, p < 0.001), patients with non-cardiac comorbidities (OR 1.7, 95 % CI 1.1-26, p < 0.01), and patients with low mixed venous oxygen saturation (OR 2.3, 95 % CI 1.4-3.6, p < 0.001). Nine thousand three hundred and seventy-nine (69 %) patients were initially managed with general endotracheal anesthesia, LMA, or tracheostomy, whereas 4232 (31 %) were managed with procedural sedation without an artificial airway, of which 75 (1.77 %) patients were converted to assisted ventilation/general anesthesia. Young age (<12 months, OR 5.2, 95 % CI 2.3-11.4, p < 0.001), higher-risk procedure (category 4, OR 10.1, 95 % CI 6.5-15.6, p < 0.001), and continuous pressor/inotrope requirement (OR 11.0, 95 % CI 8.6-14.0, p < 0.001) were independently associated with conversion. Cardiac catheterization in pediatric/congenital patients was associated with a low rate of serious sedation/airway-related adverse events. Smaller patients with non-cardiac comorbidities or low mixed venous oxygen saturation may be at higher risk. Patients under 1 year of age, undergoing high-risk procedures, or requiring continuous pressor/inotrope support may be at higher risk of requiring conversion from procedural sedation to assisted ventilation/general anesthesia.

LGE Patterns in Pulmonary Hypertension Do Not Impact Overall Mortality

ObjectivesThe goal of this study was to determine the prognostic value of late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) features in patients with pulmonary hypertension. BackgroundThe prognostic significance of LGE in the clinical assessment of patients with pulmonary hypertension remains uncertain. MethodsConsecutive patients with suspected pulmonary hypertension seen at a specialist pulmonary hypertension referral center who underwent right heart catheterization and CMR with LGE imaging within 48 h were identified. Short-axis late-enhancement imaging was performed using a 3-dimensional gradient spoiled echocardiography sequence on a 1.5-T scanner. Three groups were identified: 1) no late enhancement of the myocardium; 2) late enhancement at the right ventricular insertion points (LGE-IP); and 3) late enhancement involving the right ventricular insertion points and the interventricular septum (LGE-S). ResultsOf 194 patients, 162 had pulmonary hypertension. LGE was identified in 135 of 162 (83%) patients with pulmonary hypertension, and 47 (29%) of patients demonstrated LGE-S. Patients with LGE-S had significantly higher right ventricular end-diastolic volume index (p = 0.013) and lower mixed venous oxygen saturation (p = 0.045) than patients with LGE-IP alone. The presence of LGE-S (p = 0.022), but not LGE-IP alone, right ventricular end-systolic volume (p = 0.045), right ventricular ejection fraction (p = 0.034), mixed venous oxygen saturation (p = 0.021), mean right atrial pressure (0.027), and male sex (p = 0.002) predicted mortality. At multivariate analysis, male sex was the only significant predictor of mortality independent of covariate predictors (p = 0.027). ConclusionsThe presence of LGE at the right ventricular insertion points is suggestive of the presence of pulmonary hypertension. LGE may also be more extensive, involving the septum; however, after multivariable analysis including other factors associated with pulmonary hypertension, septal LGE was not associated with an increase in overall mortality.

Connective tissue disease-associated pulmonary arterial hypertension in Chinese patients

We sought to investigate the characteristics, survival and risk factors for mortality in Chinese patients with connective tissue disease (CTD)-associated pulmonary arterial hypertension (APAH) in modern therapy era. 129 consecutive adult patients who visited one of three referral centres in China with a diagnosis of CTD-APAH confirmed by right heart catheterisation during the previous 5 years were enrolled. The end-point was all-cause death or data censoring. Systemic lupus erythematosus was the most common underlying CTD (49%) and systemic sclerosis just accounted for 6% in this cohort. The overall survival at 1 and 3 years was 92% and 80%, respectively. Pericardial effusion, a shorter 6-min walk distance, lower mixed venous oxygen saturation, higher pulmonary vascular resistance (PVR) and alkaline phosphatase (ALP), and lower total cholesterol levels were all associated with a higher risk of death among the study population. Higher PVR and ALP were independent predictors of mortality. In conclusion, unlike in western patients, systemic lupus erythematosus is the most common underlying disease in Chinese patients with CTD-APAH. The survival of Chinese patients with CTD-APAH in the modern treatment era is similar to that in western countries. Elevated PVR and ALP are independent risk factors for poor outcomes.

Impact of Sildenafil on Survival of Patients With Idiopathic Pulmonary Arterial Hypertension

It has been reported that short-term sildenafil therapy is safe and effective for patients with pulmonary arterial hypertension. However, data regarding the impact of sildenafil on the survival of patients with idiopathic pulmonary arterial hypertension remain limited. The study was conducted on 77 patients with newly diagnosed idiopathic pulmonary arterial hypertension at Fu Wai Hospital between September 2005 and September 2009. Patients were divided into 2 groups: the sildenafil group and the conventional group. Nine patients treated with sildenafil were re-evaluated by right heart catheterization after 3 months. Our data demonstrated that the 6-minute walk distance, World Health Organization functional class, mixed venous oxygen saturation, and hemodynamics significantly improved after 3 months of sildenafil therapy (P < .05). The baseline characteristics of the sildenafil group were similar to those of the conventional group. The 1-, 2-, and 3-year survival rates in the sildenafil group were 88%, 72%, and 68% compared with 61%, 36%, and 27% in the conventional group (P < .001). The absence of sildenafil therapy, lower body mass index, and lower mixed venous oxygen saturation were found to be independent predictors of mortality. In conclusion, sildenafil therapy was found to be associated with improved survival in patients with idiopathic pulmonary arterial hypertension.

Elevated Serum Cobalamin (B12) Levels Identify a Sicker Population of Patients With Advanced Heart Failure

IntroductionElevated serum cobalamin (B12) has been associated with advanced liver dysfunction and malignancy. Little is know about serum B12 in advanced heart failure.MethodsWe examined 115 consecutive patients with advanced heart failure undergoing considerations for advanced therapies including hemodynamic evaluation. Patients receiving B12 injections were excluded. Serum B12 >900pg/mL values are considered as elevated levels.ResultsMean and median serum B12 levels were 843± 362 pg/mL, and 795 pg/mL (IQR 551-1046), respectively. Patients with elevated values (37% of population) were more likely to be older, with wider red cell distribution width (RDW), higher total bilirubin (albeit similar blood urea nitrogen), and lower mixed-venous oxygen saturation (all p≤0.05). At 2 years follow-up, patients with serum B12 >900pg/mL had reduced survival compared to those with ≤900pg/mL (51% versus 80%, respectively; p=0.006). Serum B12 was found to be an independent predictor for all-cause mortality after adjusting above-mentioned covariates (Hazard ratio 1.02, p=0.04). See Figure 1 for adjusted survival analysis.Conclusions IntroductionElevated serum cobalamin (B12) has been associated with advanced liver dysfunction and malignancy. Little is know about serum B12 in advanced heart failure. Elevated serum cobalamin (B12) has been associated with advanced liver dysfunction and malignancy. Little is know about serum B12 in advanced heart failure. MethodsWe examined 115 consecutive patients with advanced heart failure undergoing considerations for advanced therapies including hemodynamic evaluation. Patients receiving B12 injections were excluded. Serum B12 >900pg/mL values are considered as elevated levels. We examined 115 consecutive patients with advanced heart failure undergoing considerations for advanced therapies including hemodynamic evaluation. Patients receiving B12 injections were excluded. Serum B12 >900pg/mL values are considered as elevated levels. ResultsMean and median serum B12 levels were 843± 362 pg/mL, and 795 pg/mL (IQR 551-1046), respectively. Patients with elevated values (37% of population) were more likely to be older, with wider red cell distribution width (RDW), higher total bilirubin (albeit similar blood urea nitrogen), and lower mixed-venous oxygen saturation (all p≤0.05). At 2 years follow-up, patients with serum B12 >900pg/mL had reduced survival compared to those with ≤900pg/mL (51% versus 80%, respectively; p=0.006). Serum B12 was found to be an independent predictor for all-cause mortality after adjusting above-mentioned covariates (Hazard ratio 1.02, p=0.04). See Figure 1 for adjusted survival analysis. Mean and median serum B12 levels were 843± 362 pg/mL, and 795 pg/mL (IQR 551-1046), respectively. Patients with elevated values (37% of population) were more likely to be older, with wider red cell distribution width (RDW), higher total bilirubin (albeit similar blood urea nitrogen), and lower mixed-venous oxygen saturation (all p≤0.05). At 2 years follow-up, patients with serum B12 >900pg/mL had reduced survival compared to those with ≤900pg/mL (51% versus 80%, respectively; p=0.006). Serum B12 was found to be an independent predictor for all-cause mortality after adjusting above-mentioned covariates (Hazard ratio 1.02, p=0.04). See Figure 1 for adjusted survival analysis. Conclusions

Exercise testing in the clinical management of patients affected by pulmonary arterial hypertension

Patients affected by pulmonary arterial hypertension (PAH) show a reduced exercise tolerance with early occurrence of dyspnoea and fatigue. The origin of functional capacity limitation is multifactorial and several mechanisms have been proposed, including right heart failure, which leads to a limited increase in cardiac output during exercise, and hyperventilation with a reduced perfusion of properly ventilated alveoli. In addition, abnormalities in arterial blood gases are observed, with the occurrence of hypoxemia and hypocapnia, related to an abnormal ventilation/perfusion match, gas diffusion abnormalities, low mixed venous oxygen saturation and to the development of intra- and extra-pulmonary right-to-left shunts. At present, the 6-minute walking test is the most used method to assess exercise tolerance in PAH; it is also useful to monitor the response to therapy and provides prognostic information. However, the assessment of functional capacity by cardiopulmonary exercise test (CPET) seems to be more complete, because CPET allows for discrimination between the metabolic, cardiovascular and pulmonary components of exercise limitation. Moreover, CPET estimates the severity of disease and assesses patients' prognosis and response to therapy. In PAH, a typical CPET-response is observed, characterized by a severe reduction in peak VO2, work rate, O2 pulse and anaerobic threshold and by a marked increase in VE/VCO2 slope and in the dead space to tidal volume ratio. However, the use of CPET should be limited to experienced centres. This review will focus on resting lung function and exercise tolerance tests, showing that CPET can provide the physiological explanation of functional limitation in PAH.

Benefits and risks of red blood cell transfusion in pediatric patients undergoing cardiac surgery

As the number of neonates and young infants undergoing cardiac surgery requiring cardiopulmonary bypass (CPB) increases, red blood cell (RBC) transfusion will continue to be an integral part of the practice of pediatric cardiac anesthesiology. The decision of when to transfuse RBCs to these patients is complex and influenced by multiple factors such as size, presence of cyanotic heart disease, complexity of the surgical procedure, and the hemostatic alterations induced by CPB. The known benefits of RBC transfusion include an increase in the oxygen-carrying capacity of blood, improved tissue oxygenation, and improved hemostasis. Unfortunately, there is no minimum hemoglobin level that serves as a transfusion trigger for all pediatric patients undergoing cardiac surgery. Physiologic signs such as tachycardia, hypotension, low mixed venous oxygen saturation and increased oxygen extraction ratios can provide objective evidence of the need to augment a given hemoglobin level. Nevertheless, the benefits of RBC transfusion must be balanced against its risks and, in recent years, RBC transfusion has been subjected to intense scrutiny. The adverse consequences of RBC transfusion include the transmission of infectious diseases and immune-mediated and nonimmune-mediated complications. Advances in donor selection, infectious disease testing of donated blood, use of leukocyte reduction and irradiation of blood in defined situations have improved the safety of the blood supply in terms of infection transmission. However, a growing number of prospective randomized clinical trials are finding an association between RBC transfusion and an increased risk of morbidity and mortality even with the use of leuko-reduced blood. Thus, it is becoming increasingly important that the decision to transfuse RBCs be made with a thorough understanding of the benefit-to-risk ratio. This review addresses the benefits and risks of RBC transfusion, pertinent data acquired in the setting of congenital cardiac surgery and techniques designed to minimize the need for RBC transfusion.

Association of physical examination with pulmonary artery catheter parameters in acute lung injury*

To correlate physical examination findings, central venous pressure, fluid output, and central venous oxygen saturation with pulmonary artery catheter parameters. Retrospective study. Data from the multicenter Fluid and Catheter Treatment Trial of the National Institutes of Health Acute Respiratory Distress Syndrome Network. Five hundred thirteen patients with acute lung injury randomized to treatment with a pulmonary artery catheter. Correlation of physical examination findings (capillary refill time >2 secs, knee mottling, or cool extremities), central venous pressure, fluid output, and central venous oxygen saturation with parameters from a pulmonary artery catheter. We determined association of baseline physical examination findings and on-study parameters of central venous pressure and central venous oxygen saturation with cardiac index <2.5 L/min/m2 and mixed venous oxygen saturation <60%. We determined correlation of baseline central venous oxygen saturation and mixed venous oxygen saturation and predictive value of a low central venous oxygen saturation for a low mixed venous oxygen saturation. Prevalence of cardiac index <2.5 and mixed venous oxygen saturation <60% was 8.1% and 15.5%, respectively. Baseline presence of all three physical examination findings had low sensitivity (12% and 8%), high specificity (98% and 99%), low positive predictive value (40% and 56%), but high negative predictive value (93% and 86%) for cardiac index <2.5 and mixed venous oxygen saturation <60%, respectively. Central venous oxygen saturation <70% predicted a mixed venous oxygen saturation <60% with a sensitivity 84%,specificity 70%, positive predictive value 31%, and negative predictive value of 96%. Low cardiac index correlated with cool extremities, high central venous pressure, and low 24-hr fluid output; and low mixed venous oxygen saturation correlated with knee mottling and high central venous pressure, but these correlations were not found to be clinically useful. In this subset of patients with acute lung injury, there is a high prior probability that cardiac index and mixed venous oxygen saturation are normal and physical examination findings of ineffective circulation are not useful for predicting low cardiac index or mixed venous oxygen saturation. Central venous oxygen saturation <70% does not accurately predict mixed venous oxygen saturation <60%, but a central venous oxygen saturation >or=70% may be useful to exclude mixed venous oxygen saturation <60%.

Long-term outcome with intravenous iloprost in pulmonary arterial hypertension

There is limited data on the long-term efficacy of intravenous iloprost in patients with pulmonary arterial hypertension (PAH). This retrospective multicentre analysis evaluated the clinical course of patients with PAH treated with i.v. iloprost, in most cases after having received inhaled iloprost as first-line therapy. Between 1997 and 2001, 79 PAH patients were treated with i.v. iloprost and followed until 2007. These patients had advanced and progressive disease as indicated by a mean pulmonary vascular resistance of 1,533 dyn x s x cm(-5) at the time of diagnosis and of 1,858 dyn x s x cm(-5) at the onset of i.v. iloprost therapy. Introduction of i.v. iloprost therapy resulted in initial haemodynamic and clinical improvement. At the end of the observation period, however, 50 (61%) patients had died and 21 (26%) required lung transplantation. Transplantation-free survival rates at 1, 3, and 5 yrs were 86%, 59% and 45%, respectively, after the diagnosis of PAH, and 54%, 31% and 15%, respectively, after the introduction of i.v. iloprost therapy. Predictors of an adverse outcome at baseline were a low 6-min walk distance and a low mixed venous oxygen saturation. In conclusion, despite initial haemodynamic and clinical improvement, overall long-term survival with i.v. iloprost therapy was limited.