Right Ventricular Dilatation Research Articles

Right ventricular failure in septic shock: characterization, incidence and impact on fluid responsiveness

ObjectiveIncidence of right ventricular (RV) failure in septic shock patients is not well known, and tricuspid annular plane systolic excursion (TAPSE) could be of limited value. We report the incidence of RV failure in patients with septic shock, its potential impact on the response to fluids, as well as TAPSE values.DesignAncillary study of the HEMOPRED prospective multicenter study includes patients under mechanical ventilation with circulatory failure.SettingThis is a multicenter intensive care unit studyPatientsTwo hundred and eighty-two patients with septic shock were analyzed. Patients were classified in three groups based on central venous pressure (CVP) and RV size (RV/LV end-diastolic area, EDA). In group 1, patients had no RV dilatation (RV/LVEDA < 0.6). In group 2, patients had RV dilatation (RV/LVEDA ≥ 0.6) with a CVP < 8 mmHg (no venous congestion). RV failure was defined in group 3 by RV dilatation and a CVP ≥ 8 mmHg. Pulse pressure variation (PPV) was systematically recorded.InterventionsNone.Measurements and main resultsIn total, 41% of patients were in group 1, 17% in group 2 and 42% in group 3. A correlation between RV size and CVP was only observed in group 3. Higher RV size was associated with a lower response to passive leg raising for a given PPV. A large overlap of TAPSE values was observed between the 3 groups. 63.5% of patients with RV failure had a normal TAPSE.ConclusionsRV failure, defined by critical care echocardiography (RV dilatation) and a surrogate of venous congestion (CVP ≥ 8 mmHg), was frequently observed in septic shock patients and negatively associated with response to a fluid challenge despite significant PPV. TAPSE was unable to discriminate patients with or without RV failure.

Echocardiography and cardiac magnetic resonance in children with repaired tetralogy of fallot and their correlations with exercise capacity

Abstract Background Severe pulmonary regurgitation (PR) and progressive right ventricular (RV) dilation and disfunction are common in patients with repaired Tetralogy of Fallot (r-TOF) and should be carefully monitored during the follow up of these patients. In this contest, Echocardiography and Cardiac Magnetic Resonance (CMR) have a complementary diagnostic role. Purpose To correlate Echo and CMR parameters in children (&amp;lt;18 years) with r-TOF with at least moderate PR assessed by Echocardiography and to analyse which parameter was associated with peak oxygen consumption (Vo2). Methods Paediatric patients with r- TOF with at least moderate PR at the echo evaluation who underwent a CMR study within six months were included by using hospital databases. All patients underwent standard echo-Doppler study including RV end-diastolic area (RVEDA), end-systolic area (RVESA), fractional area change (FAC) and TAPSE; PR was assessed by Color Doppler, continuous-wave (CW) Doppler and derived parameters such as pressure half time (PHT), PR index, ratio of diastolic and systolic time-velocity integrals (DSTVI) of the main pulmonary artery. By speckle tracking we measured also RV global longitudinal strain (RVGLS) and right atrial strain (RAS). All the patients underwent CMR to assess PR and right ventricular volumes and ejection fraction (EF). Of these, 36 patients underwent cardiopulmonary exercise test (CPET). Results Fourty-six children (aged 13.7±3.0 years) were included. Echo derived RV areas correlated significantly with CMR RV volumes (r=0.72, p&amp;lt;0.0001). RVEDA &amp;gt;21.9 cm2/m2 had a good sensitivity (83.3%) and specificity (73.5%) to identify a RV end-diastolic volume (RVEDV) ≥150 ml/m2. No correlation was found among TAPSE, FAC, RVGLS and RVEF calculated by CMR nor between PHT, PR index and DSTVI and PR-RF. Only A' wave velocity showed a significant but modest correlation with CMR RF (r=0.57, p&amp;lt;0.0001). Flow reversal in pulmonary branches showed a sensitivity of 95.8% and a specificity of 59.1% to identify PR RF ≥35%. RVEF by CMR was preserved in all patients, while TAPSE was reduced in 78.2% and RVGLS in 60.8%. None of the CMR parameters correlated with peak Vo2. At the multivariate analysis RAS was the best independent predictor of peak Vo2 (p&amp;lt;0.0001). Conclusion In children, flow reversal in pulmonary branches identifies hemodynamically significant PR at CMR. RV area by echocardiogram is a valid first-line parameter to screen RV dilation. Our study suggests that, also for the RV, there is longitudinal systolic dysfunction in presence of preserved RV EF. RAS is the best predictor of peak Vo2 and should be added in the follow up of these patients. Funding Acknowledgement Type of funding source: None

The truly forgotten chamber: prognostic value of right atrial dilation in patients with sinus rhythm and significant functional tricuspid regurgitation

Abstract Background Functional tricuspid regurgitation (FTR) can be caused by right ventricular (RV) and/or right atrial (RA) dilation, and it leads in turn to further RV and RA remodeling. While it is known that in these patients RV dilation is associated with worse prognosis, there are no data on the prognostic value of RA enlargement. Purpose To assess the prognostic impact of RA dilation in patients with significant (≥ moderate) FTR taking into account the presence of atrial fibrillation (AF). Methods 1382 patients (mean age: 69±13 year; 50% male) with moderate or severe FTR were included. Patients with congenital heart disease were excluded. Significant RA enlargement was identified by the value of RA area associated with excess of mortality according to spline curve analysis in the overall population (30 cm2 – Figure: Left Panel). The prognostic value of RA enlargement was investigated separately in patients with sinus rhythm (SR) and AF. The primary endpoint was all-cause mortality. Results A total of 987 (71%) patients were in SR while the remaining 395 (29%) had AF at the time of significant FTR diagnosis. Patients in SR with RA enlargement were more likely to present with RV failure symptoms and to receive diuretics compared with patients in SR with non-enlarged RA, whereas these differences were not detected in patients with AF. During a median follow-up of 53 (interquartile range, 20–89) months, 698 (51%) patients died. The survival rates of patients in SR with RA enlargement were significantly worse compared to the ones of patients in SR with normal RA size (Figure: Right Panel). In contrast, RA enlargement did not affect the prognosis of patients in AF (Log-rank χ2: 0.41; P=0.522). RA enlargement was associated with 33% increase risk of all-cause mortality in patients with SR and this association was retained on a multivariable Cox regression analysis (HR 1.27; 95% CI 1.04–1.56; P=0.022) together with older age, coronary artery disease, diabetes, severe renal impairment, reduced left ventricular or RV systolic function, and increased pulmonary artery pressures. Conclusion RA enlargement has an independent prognostic value for all-cause mortality in patients with FTR and SR, and therefore its evaluation might be useful to further improve their risk stratification. Funding Acknowledgement Type of funding source: None

Carcinoid heart disease: the role of echocardiography in predicting post-surgical outcomes

Abstract Background Carcinoid heart disease (CHD) often complicates neuroendocrine tumours (NET). The prognosis of CHD without intervention is poor; 3 year survival is estimated at 31%. Surgical valve replacement is the only treatment for CHD, but is associated with high 30-day mortality (10–15%). Purpose The aim is to identify pre-operative transthoracic echocardiogram (PTTE) findings that could determine which patients have a high likelihood of post-surgical mortality at 1 year. Methods This retrospective observational cohort study recruited 88 patients with a confirmed diagnosis of CHD between 2005–19 at University Hospital Birmingham; 49 (56%) of these were treated surgically. Indications for surgery: stable NET, symptomatic severe valvular dysfunction, progressive RV dilatation or RV dysfunction, no significant comorbidities. All patients underwent a standard PTTE. PTTE parameters assessed: right ventricular (RV) size, RV function (qualitative), TAPSE, RV fractional area change, RV S wave velocity, left ventricular (LV) size, LV ejection fraction and valve velocities. Surgery was performed by a single surgical team with bioprosthetic valve replacements. Results Patients were followed up for a median of 15 months (IQR: 6–59) after surgery, during which time there were 33 deaths, giving a median survival time of 30 months (IQR: 7–85). Increasingly severe RV dilatation was significantly associated with shorter survival (p=0.032). The estimated survival rate at three years was 67% in those with normal RV size, compared to 24% in the severe RV group (Figure 1). RV basal diameter was assessed used ROC curve analysis for the outcome of one year survival and returned an area under the curve of 0.66 (SE=0.10). Youden's index identified RV diameter &amp;gt;4.8cm to be the optimal cut-off for identifying high-risk patients. One year mortality rates were 26% (7/27) vs. 75% (9/12) in those with RV basal diameter of ≤4.8 vs. &amp;gt;4.8cm (p=0.006). Conclusion A pre-operative right ventricular basal diameter &amp;gt;4.8cm is associated with a near three-fold increase in post-operative mortality at one year. These findings highlight the importance of regular imaging in order to optimise the timing of surgery in patients with CHD. Figure 1. Kaplan-Meier curve of post-op survival Funding Acknowledgement Type of funding source: None

Characterization of arrhythmic presentation in patients with arrhythmogenic cardiomyopathy

Abstract Background/Introduction Arrhythmogenic cardiomyopathy (ACM) is one of the most arrhythmogenic conditions known to man. ACM is caused by desmosomal mutations in most cases, resulting in progressive replacement of the myocardium by adipose and fibrous tissue. It comes as no surprise that ACM is one of the leading causes of sudden cardiac death (SCD). Nonetheless, the characteristics of arrhythmic manifestations have not dissected after the release of most recent criteria. Purpose This study investigates different types of ventricular tachyarrhythmias which had occurred at first arrhythmic event in patients with ACM. Methods We investigated 91 consecutive patients with documented evidence of sustained ventricular tachyarrhythmias from 291 ACM patients followed at our center up to this date. Diagnosis of ACM was made using 2010 Task Force Criteria, and patients were defined as having an advanced disease if they had more than 4 TFC points at diagnosis. Presenting ventricular tachyarrhythmias were divided into (1) life-threatening arrhythmic event (LAE; ventricular fibrillation or hemodynamically unstable polymorphic ventricular tachycardia) and (2) hemodynamically stable monomorphic ventricular tachycardia (MMVT). Right ventricular (RV) involvement was defined as a presence of RV wall motion abnormalities and RV dilation at transthoracic echocardiography or cardiac magnetic resonance. Results Our study population was constituted of a predictably higher number of males (n=68; 75%), with an average age at the first arrhythmic event of 38±15 years of age. At first documented arrhythmia, majority of patients studied experienced a stable MMVT (n=53; 58%), while 38 patients experienced an LAE (n=38; 42%). The patients suffering an LAE as first arrhythmic event were slightly younger than the patients who experienced a stable MMVT (35±14 years vs. 40±15 years; p=0.076) but there were no statistically significant gender differences (28/38 males with LAE vs. 40/53 males with stable MMVT; p= n.s.). Interestingly, patients who presented with stable MMVT were more likely to have an advanced disease at diagnosis (OR=6.52; 95% CI 2.02–20.99; p=0.002). This is supported by the fact that RV involvement was significantly more common in patients presenting with stable MMVT (OR=4.38; 95% CI 1.26–15.26; p=0.021). Additionally, patients with stable MMVT were more commonly carriers of variants on PKP2 gene (OR=3.6; 95% CI 1.1–11.91; p=0.021). Conclusions Our data suggest that two types of arrhythmia reflect the two different stages of the disease. The early stage of the ACM is characterized by LAE in absence of RV structural involvement; while, stable MMVT is typical of PKP2 carriers and advanced stage of ACM with RV involvement. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): The Italian Ministry of Research and University Dipartimenti di Eccellenza 2018–2022 grant to the Molecular Medicine Department (University of Pavia)

A matter of proportions: a novel framework to classify functional tricuspid regurgitation

Abstract Background Current approaches for the assessment of tricuspid regurgitation (TR) severity do not correct for right ventricular (RV) size. Similarly to what recently proposed for the left heart, we hypothesized that TR severity can be proportional or disproportional to RV dilation. Purpose To characterize the clinical features and the prognosis of patients with disproportionate vs proportionate functional TR (FTR). Methods A total of 345 patients (mean age: 70±12 years; 40% male) with significant (≥ moderate) FTR, preserved left ventricular systolic function and who did not undergo tricuspid valvular repair during follow-up were included. Proportional and disproportional FTR were defined according to the ratio between TR severity (vena contracta [VC] width) and RV size (tricuspid annulus [TA] diameter). A prognostic relevant cut-off for VC/TA was identified with spline curve analysis. The primary end-point was all-cause mortality and the event rates were compared between patients with proportionate and disproportionate FTR. Results The cut-off for disproportionate FTR associated with an increase in all-cause mortality was identified at 0.24 (Figure 1: left panel). According to this cut-off, 172 (50%) patients showed disproportionate FTR, while the remaining had proportionate FTR. Patients with disproportionate FTR were more frequently symptomatic, had smaller RV basal diameter, higher TR severity, greater left atrial volume, higher prevalence of mitral regurgitation, and higher pulmonary artery pressures compared to those with proportionate FTR. During a median follow-up of 61 (interquartile range, 28–101) months, 135 (39%) patients died. The cumulative 5-year survival rate was significantly worse in patients with disproportionate FTR (57% vs 74%, P=0.001; Figure 1: right panel) and on multivariable Cox regression analysis disproportionate FTR was independently associated with poor outcome (HR 1.56; 95% CI 1.06–2.29; P=0.023) together with age, coronary artery disease, renal impairment, reduced RV systolic function, and increased pulmonary artery pressures. Importantly, this novel framework outperformed the TR grading system recommended by current guidelines, which in this population was not able to effectively stratify the prognosis (HR for severe FTR vs moderate FTR 1.09; 95% CI 0.72–1.64; P=0.694). Conclusions In patients with significant FTR, characterization of TR severity in relation to RV size significantly improves risk-stratification since disproportionate FTR if left untreated is associated with worse prognosis compared with proportionate FTR. Figure 1 Funding Acknowledgement Type of funding source: None

The effect of pulmonary arterial hypertension specific treatment on the left ventricle in patients with pulmonary arterial hypertension

Abstract Background Pulmonary arterial hypertension (PAH) is characterized by right ventricular (RV) pressure overload, leading to RV dilation, failure and death. In the course of the disease, the left ventricle (LV) is often impaired, due to interventricular interaction. Although the impact of PAH treatment on the RV has been well described, less is known on the LV. Purpose To examine effects of advanced PAH treatments on the volumes, function and strain of the left atrium and ventricle. Methods This is a retrospective study. All patients underwent CMR and right heart catheterization, both at diagnosis and at 12-months follow up. Ventricular volumes and LV filling rate were calculated from the stack of short axis cine images using Simpsons method while left atrial (LA) volumes from the 4-chamber cine images using the area-length method. Tissue tracking was used for the evaluation of myocardial deformation. The LV endocardial and epicardial borders were manually delineated in all analysed sections with the initial contour set at end-diastole. All analyses were performed offline using dedicated software. Results In total, 66 patients (mean age 56.3±17.9 years, 67%women, 77%idiopathic and heritable PAH, 23% connective tissue disease associated PAH) and 29 normal controls were included. The improvement in metrics of right and left heart size and function after the initiation of advanced PAH treatment, are presented in panel A. Of note, LV stroke volume was markedly increased (54.6±19.6ml at baseline vs 70.8±21.7ml at follow up, p&amp;lt;0.0001) to reach controls. LV filling was markedly increased in latter two-thirds of the diastolic phase (panel B), especially at atrial kick point (arrow). Change in LA max volume was associated with changes in diastolic filling (r=0.354, p=0.004), LV end-diastolic and end-systolic volumes and stroke volume. These correlations were more robust in patients that increased LV filling compared to those that failed to increase LV filling (panels C-E). No association between changes in LV circumferential strain and LV volume load was observed. A weak correlation of change of LV peak longitudinal strain with stroke volume (r=−0.345, p=0.006), LV end diastolic volume (r=−0.284, p=0.027), LV ejection fraction (r=−0.337, p=0.008) and LA maximum area (r=−0.447, p&amp;lt;0.0001) was observed. The changes of LV strain showed no correlation with the changes in patients' haemodynamics. Conclusion Improvement in stroke volume after the initiation of advanced PAH treatment is associated with an increase in LA size, LV end diastolic volume and normalisation of strain. This reflects the improved filling state of the left ventricle and the potential of the left atrium to monitor treatment effects. Changes after PAH treatment Funding Acknowledgement Type of funding source: None

Pacemaker lead-induced progression of primary vs. secondary tricuspid regurgitation

Abstract Background Currently no data are available whether the implantation of right ventricular (RV) pacemaker (PM) lead worsens preexisting primary or secondary (functional due to RV dilatation, RVD) tricuspid regurgitation (TR). Purpose The aim of the present retrospective analysis was to assess TR after PM implantation with a RV lead. Methods Patients with PM implantation (n=990) were enrolled if they had routine echocardiography including assessment of TR before first implantation and immediately after. RVD and severity of TR were characterized visually. Based on RVD in baseline echocardiography, patients were divided into 2 groups: with primary TR (without preexisting RVD, n=743) or secondary TR (with preexisting RVD, n=243). Results Lead-induced worsening of TR was present in both groups (Table 1). Progression from mild/moderate to severe TR was observed in 6.7% of patients with primary TR, compared to 25.6% of patients with secondary TR (P=0.001). Using an ordinal regression model, the probability to progress to severe TR with primary TR was 14.8% (95% CI 11.0%-19.7%), compared to 41.6% (95% CI 40.3%-42.8%) with secondary TR (P&amp;lt;0.001). Conclusion Preexisting secondary TR was associated with higher rates of lead-induced progression to severe TR compared to primary TR. Leadless pacing or tricuspid valve clipping post-PM implantation could be an option for patients with preexisting secondary TR and indication for a PM. Table 1. Patient characteristics. Funding Acknowledgement Type of funding source: Public grant(s) – EU funding. Main funding source(s): This study was supported by the European Union's Horizon 2020 Future and Emerging Technologies Programme [Grant number 732170].

Prevalence and prognostic value of right ventricular dysfunction in hypertrophic cardiomyopathy

Abstract Introduction Hypertrophic cardiomyopathy (HCM) is the main cause of sudden cardiac death in the young and a cause of heart failure and death at any age. Nevertheless, adverse long-term outcomes are not easy to predict. Objectives To assess the prevalence, predictors and prognostic value of right ventricular (RV) dysfunction in patients (pts) with HCM. Methods Retrospective single-center study of consecutive pts with HCM evaluated in a specialized medical appointment. Selected those submitted to cardiac magnetic resonance imaging (MRI) as the gold-standard for RV function assessment. The primary endpoint was a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, ventricular arrhythmias with hemodynamic instability and unplanned heart failure admission. Results Were included 112 pts (mean age at first appointment 57±15 years, 63% male). Septal asymmetric phenotype was the most frequent (75%), with a mean septal wall thickness of 18±4 mm. Late gadolinium enhancement was observed in 82%, mostly intramyocardial (67%) and in joint points (47%). RV dysfunction was detected in 6 pts (5.4%) and RV free wall hypertrophy in 3 pts (2.7%); no patient presented RV dilation. Factors associated with RV dysfunction were left atria area (HR 1.07/unit, 95% CI 1.01–1.12, p=0.02), left ventricular ejection fraction (HR 0.91/unit, 95% CI 0.86–0.97, p=0.02) and the presence of left ventricle wall motion abnormalities (HR 7, 95% CI 1.3–38, p=0.03) in cardiac MRI. During a mean follow-up of 60±31 months, the combined primary endpoint occurred in 15 pts (13%), significantly more in pts with RV dysfunction (HR 5.1, 95% CI 1.1–24, p=0.038) (graphic 1). Patients with RV dysfunction also presented more atrial fibrillation / flutter episodes during follow-up (HR 6.4, 95% CI 2.1–20, p=0.001). Conclusions Although not common, right ventricular dysfunction was associated with a higher rate of cardiovascular events. These results support a potential role of right ventricular function in the risk stratification of patients with hypertrophic cardiomyopathy. Figure 1 Funding Acknowledgement Type of funding source: None

Three-dimensional echocardiography to identify right ventricular dilatation in patients with corrected Fallot anomaly or pulmonary stenosis.

Background3‐Dimensional Echocardiography allows measuring volumes and parameters of myocardial deformation (strain). Myocardial strain has been suggested to be superior to conventional echo parameters in the assessment of right ventricular (RV) function. Myocardial strain can be assessed by cardiac magnetic resonance (CMR) or two‐ and three‐dimensional echocardiography (2D and 3DEcho). We performed a comprehensive assessment of the RV based on 3DEcho and compared the results with those based on CMR and 2DEcho.Methods36 patients with corrected heart defects underwent CMR and 3DEcho to assess RV volume, strain and cardio pulmonary exercise testing with peak VO2 measurement. 2DEcho was used for reference.ResultsThere was a moderate correlation between 3DEcho and CMR for measuring RV end‐diastolic and end‐systolic volumes (r = .82 and .72). 3DEcho tended to underestimate the RV volumes, mean difference EDV 8.5 ± 33 ml (CI −2.8; 19.7 ml) and ESV 13.2 ± 29 ml (CI 3.3; 23 ml). According to method‐specific reference values for RVEDV, 34/35 (3DEcho) and 29/36 (CMR) were dilated. Among those dilated according to CMR, all were identified by 3DEcho. The coefficient of correlation between RV atrioventricular plane displacement measured by CMR and tricuspid annular plane systolic excursion measured by 3D and 2DEcho was r = .6 for both. 2DEcho measured lower LV volumes than CMR. LVEF and GLS were similar in 2DEcho, 3DEcho and CMR. Patients with CMR‐determined RV free wall strain ≤ −14% tended to have lower peak VO2.ConclusionsAlthough 3DEcho underestimated RV volumes, it successfully identified all patients with RV dilatation based on method‐specific reference values.

Echocardiographic features of patients with COVID-19 infection: a cross-sectional study.

COVID-19 patients with cardiac involvement have a high mortality rate. The aim of this study was to investigate the echocardiographic features in COVID-19 patients between severe and non-severe groups. For this single-center study, data from patients who were treated for COVID-19 between March 25, 2020 and April 15, 2020 were collected. Two-dimensional echocardiography (2DE) images were obtained for all patients. Patients were divided into two groups based on the severity of their COVID-19 infections. 2DE parameters indicating right ventricular (RV) and left ventricular (LV) functions were compared between the two groups. A total of 90 patients hospitalized for COVID-19 were included in this study. The mean age of the severe group (n = 44) was 63.3 ± 15.7 years, and 54% were male. The mean age of non-severe group (n = 46) was 49.7 ± 21.4 years, and 47% were male. In the severe group, RV and LV diameters were larger (RV, 36.6 ± 5.9 mm vs. 33.1 ± 4.8 mm, p = 0.003; LV 47.3 ± 5.8 mm vs. 44.9 ± 3.8 mm, p = 0.023), the LE ejection fraction (LVEF) and the RV fractional area change (RV-FAC) were lower (LVEF, 54.0 ± 9.8% vs. 61.9 ± 4.8%, p < 0.001; RV-FAC, 41.4 ± 4.1% vs. 45.5 ± 4.5%, p < 0.001), and pericardial effusions were more frequent (23% vs. 0%) compared to patients in the non-severe group. A multiple linear regression analysis determined that LVEF, right atrial diameter, high-sensitivity troponin I, d-dimer, and systolic pulmonary artery pressure, were independent predictors of RV dilatation. The results demonstrate that both right and left ventricular functions decreased due to COVID-19 infection in the severe group. 2DE is a valuable bedside tool and may yield valuable information about the clinical status of patients and their prognoses.

Prognostic Utility of Right Ventricular Remodeling Over Conventional Risk Stratification in Patients With COVID-19

BackgroundCoronavirus disease 2019 (COVID-19) is a growing pandemic that confers augmented risk for right ventricular (RV) dysfunction and dilation; the prognostic utility of adverse RV remodeling in COVID-19 patients is uncertain. ObjectivesThe purpose of this study was to test whether adverse RV remodeling (dysfunction/dilation) predicts COVID-19 prognosis independent of clinical and biomarker risk stratification. MethodsConsecutive COVID-19 inpatients undergoing clinical transthoracic echocardiography at 3 New York City hospitals were studied; images were analyzed by a central core laboratory blinded to clinical and biomarker data. ResultsIn total, 510 patients (age 64 ± 14 years, 66% men) were studied; RV dilation and dysfunction were present in 35% and 15%, respectively. RV dysfunction increased stepwise in relation to RV chamber size (p = 0.007). During inpatient follow-up (median 20 days), 77% of patients had a study-related endpoint (death 32%, discharge 45%). RV dysfunction (hazard ratio [HR]: 2.57; 95% confidence interval [CI]: 1.49 to 4.43; p = 0.001) and dilation (HR: 1.43; 95% CI: 1.05 to 1.96; p = 0.02) each independently conferred mortality risk. Patients without adverse RV remodeling were more likely to survive to hospital discharge (HR: 1.39; 95% CI: 1.01 to 1.90; p = 0.041). RV indices provided additional risk stratification beyond biomarker strata; risk for death was greatest among patients with adverse RV remodeling and positive biomarkers and was lesser among patients with isolated biomarker elevations (p ≤ 0.001). In multivariate analysis, adverse RV remodeling conferred a >2-fold increase in mortality risk, which remained significant (p < 0.01) when controlling for age and biomarker elevations; the predictive value of adverse RV remodeling was similar irrespective of whether analyses were performed using troponin, D-dimer, or ferritin. ConclusionsAdverse RV remodeling predicts mortality in COVID-19 independent of standard clinical and biomarker-based assessment.

IMPORTANCE OF POINT-OF-CARE ULTRASONOGRAPHY IN THE EVALUATION OF UNDIFFERENTIATED SHOCK

SESSION TITLE: Fellows Critical Care Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Acute pulmonary embolism (PE) affects at least one in every 1000 individuals. Diagnosing PE accurately and in a timely manner can be challenging as the clinical presentation of PE is variable. In fact, up to two-thirds of clinically significant PE are undiagnosed until autopsy. Point-of-care ultrasonography (POCUS) has developed into a vital tool that can assist clinicians in appropriately diagnosing PE and elucidating etiology of undifferentiated shock. CASE PRESENTATION: A 71-year-old female with a history of reactive airway disease and minimal change nephropathy presented with two days of progressive dyspnea and wheezing. Vital signs on arrival were notable for tachycardia of 180 beats per minutes, hypotension of 86/50, and hypoxia which required four liters of supplemental oxygen to correct. Electrocardiogram showed new-onset atrial fibrillation (AF) with rapid ventricular response. Laboratory analysis was remarkable for a neutrophil predominant leukocytosis of 18.2 x 10^3/mcL, a serum bicarbonate of 14 mmol/L, blood urea nitrogen 36 mg/dL, creatinine 2.2 mg/dL, and a lactic acid greater than 12 mmol/L. A chest radiograph revealed no significant parenchymal infiltrates (Figure 1). Her condition quickly deteriorated requiring escalating doses of vasopressors and ventilatory support. POCUS cardiac exam identified right ventricular (RV) dilatation and McConnell’s sign (RV free wall hypokinesis with hyperdynamic apex) (Figure 2A-B). Furthermore, ultrasound evaluation of her lower extremities confirmed the presence of multiple deep vein thrombi. Given the high suspicion for massive PE, systemic intravenous tissue plasminogen activator was administered. Subsequently, hemodynamics started improving with a rapid decrease in vasopressor requirements. Unfortunately, the hospital course was complicated by acute renal failure prompting transition to comfort care measure per the patient’s wishes rather than pursing hemodialysis. DISCUSSION: Shock can be categorized into cardiogenic, hypovolemic, distributive/vasoplegic, and obstructive. Obstructive shock is caused by resistance to blood flow through the circulatory system. This can result from PE, cardiac tamponade, or pneumothorax. POCUS has been validated as a reliable tool to identify obstructive shock. Hallmark findings on POCUS for PE include, RV dilatation, septal flattening, paradoxical septal wall motion, and McConell’s sign. Additionally, the presence of new-onset AF in undifferentiated shock should prompt evaluation for PE, as those diagnosed with PE who present with AF have an increased mortality. CONCLUSIONS: Obstructive shock secondary to PE should always be considered in cases of undifferentiated shock. Moreover, all clinicians should become familiar with the role of POCUS in the evaluation of undifferentiated shock, as it can oftentimes provide rapid, reliable, and clinically actionable information. Reference #1: McLean A. S. (2016). Echocardiography in shock management. Critical care (London, England), 20, 275. https://doi.org/10.1186/s13054-016-1401-7 Reference #2: Walley, P. E., Walley, K. R., Goodgame, B., Punjabi, V., & Sirounis, D. (2014). A practical approach to goal-directed echocardiography in the critical care setting. Critical care (London, England), 18(6), 681. https://doi.org/10.1186/s13054-014-0681-z Reference #3: Matthews, J. C., & McLaughlin, V. (2008). Acute right ventricular failure in the setting of acute pulmonary embolism or chronic pulmonary hypertension: a detailed review of the pathophysiology, diagnosis, and management. Current cardiology reviews, 4(1), 49–59. https://doi.org/10.2174/157340308783565384 DISCLOSURES: No relevant relationships by Ethan Karle, source=Web Response No relevant relationships by Armin Krvavac, source=Web Response No relevant relationships by Tarang Patel, source=Web Response No relevant relationships by Rodger Wilhite, source=Web Response

PREDICTIVE FACTORS FOR THE DEVELOPMENT OF PULMONARY ARTERY ANEURYSMS AMONG PATIENTS WITH PULMONARY ARTERIAL HYPERTENSION

SESSION TITLE: Pulmonary Vascular Disease Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: October 18-21, 2020 PURPOSE: Pulmonary artery aneurysm (PAA) is defined as a main pulmonary artery (PA) diameter greater than 40 mm. It is seen in up to 20% of patients with Pulmonary Arterial Hypertension (PAH). Uncertainty remains regarding the predictive factors for the development of PAA in PAH patients as well as the characteristics of this subgroup of patients. We describe a retrospective cohort of patients to help address these knowledge gaps. METHODS: Data collection of patients in the Pulmonary Hypertension clinic at Keck Medical Center from January 2010 to January 2020 was conducted. Patient demographics and PAH etiology information was collected from clinical documentation. Additional data regarding functional status and hemodynamics was also collected. Patients were described as having Pulmonary Artery Aneurysms if their CT report described a main PA size greater than or equal to 40 mm. Univariate analysis was performed to identify variables correlating with the presence of PAA. RESULTS: A total of 473 patients were identified in the cohort of patients being treated in the PH clinic. Of these patients, 331 had a CT chest completed throughout their course. 68 patients were noted to have PAA during their follow-up period. Congenital heart disease (CHD) was the etiology of PAH most strongly associated with PAA (OR 3.61) while PAH secondary to connective tissue disease (CTD) was found to be negatively associated with the development of PAA (OR 0.29). Other etiologies of PAH were not found to significantly affect the prevalence of PAA. Patients with moderate and severe right ventricular (RV) dysfunction were more likely to have PAA (OR 2.10 and 2.16 respectively). The same was observed for severe RV dilation (OR 2.66). Higher values of mean pulmonary artery pressure (mPAP) as well as higher pulmonary vascular resistance (PVR) on initial testing were associated with the development of PAA (OR 1.05 and 1.15 respectively). CONCLUSIONS: PAA development in PAH has been previously associated with the duration of the disease. This might explain the positive association between PAA and PAH secondary to CHD, since these patients tend to have a more prolonged course of their disease, often from a young age. It was also noted that CTD was associated with lower rates of development of PAA. This may indicate that structural changes to the pulmonary artery wall caused by CTD protect against the development of PAA. The positive association between worse hemodynamic and echocardiographic parameters and the development of PAA suggests long standing increased stress on the pulmonary artery wall may contribute to the development of PAA. CLINICAL IMPLICATIONS: Understanding the factors that may contribute to the development of PAA may allow for early identification of PAH patients at risk of developing PAA and subsequent PAA-related complications. DISCLOSURES: No relevant relationships by Tiffany Chang, source=Web Response No relevant relationships by Lucas Cruz, source=Web Response No relevant relationships by Jared Geibig, source=Web Response No relevant relationships by Moses Koo, source=Web Response No relevant relationships by Ashil Panchal, source=Web Response Speaker/Speaker's Bureau relationship with Actelion, United therapeutic, and Bayer Please note: $20001 - $100000 Added 05/30/2020 by Bassam Yaghmour, source=Web Response, value=Honoraria

Journey of the Right Heart Following Left Ventricular Assist Device Implantation

Introduction Right heart function impacts outcomes in left ventricular assist devices (LVADs) but a comprehensive exploration of changes in right heart function over time and its effects on outcomes has not been fully elucidated. We sought to characterize changes in right heart function according to hemodynamic, imaging, and laboratory data at multiple time points and evaluate how pre-implant function compares to postoperative function in predicting heart failure (HF) outcomes. We hypothesized that postoperative (pre-discharge) right ventricular (RV) systolic function would be more predictive of HF readmissions compared to preoperative RV function. Methods In this single-center study, we included consecutive patients (n=298) who received primary LVADs between May 2008 and December 2018. Invasive hemodynamics, echocardiography (ECHO), and laboratory data were collected preoperatively, postoperatively, and at 3, 6, and 12 months following LVAD implantation. Post-implant readmission data were also collected up to 12 months post hospital discharge. Results Compared to pre-implant values, significant and persistent improvements in right atrial pressure (RAP), pulmonary artery (PA) pressures, pulmonary capillary wedge pressure (PCWP), pulmonary vascular resistance (PVR), and RAP/PCWP occurred at 3, 6, and 12 months post-implant respectively (figure 1a). On the other hand, PA pulsatility index (PAPi) fluctuated over time and RV stroke work index (RVSWI) decreased over time (figure 1a). In addition, the proportion of patients with moderate-severe/severe RV dilation, tricuspid regurgitation (TR), and RV systolic function reduction eventually decreased on average by 12 months post-implant (figure 1b). Significant improvements in BNP and bilirubin levels occurred (figure 1c). Finally, we found that postoperative (pre-discharge) RV systolic function by ECHO was significantly predictive of readmissions due to HF (p=.03) whereas preoperative RV systolic function was not (p=0.81). Conclusions Right heart function metrics generally improve and persist at various time points post-implant compared to preoperative values. However, normalization of right heart function is rarely achieved, highlighting the need to redefine “normal” in LVAD patients. Additionally, the superior predictive value of postoperative RV function on HF readmissions underscores the importance of re-assessing right heart function post-implant for improved risk stratification.

Respect The Notch: Under-appreciated Pulmonary Vascular Disease and Hemodynamic Collapse Post Left Ventricular Assist Device Placement

Introduction Right ventricular (RV) failure occurs in 15-20% of patients post Left ventricular Assist Device (LVAD) implantation and has been associated with increased mortality. Herein we describe a case of severe RV failure post LVAD implantation and how proper identification of the etiology led to a positive outcome. Case description A 58-year-old male with non-ischemic cardiomyopathy is admitted with decompensated heart failure. Right heart catheterization (RHC) showed right atrial pressure (RAP) 5 mmHg, Pulmonary artery pressure (PAP): 45/25, wedge pressure (PCWP) 24 mm Hg, pulmonary vascular resistance (PVR) of 1.4 woods units and cardiac index of 1.7 on inotropes. The patient underwent HMIII LVAD implantation. Immediately postop the patient developed shock. TTE showed an akinetic and dilated RV. He was placed on VA ECMO emergently and then transitioned to a percutaneous right ventricular assist device (RVAD). The patient eventually required dialysis. Decision-making Multiple mechanisms lead to RV failure after LVAD implantation. These include increased RV preload (from increased cardiac output and venous return or blood/fluid administration perioperatively), decreased contractility (LV decompression resulting in intraventricular septal left shift and decreased septal contribution to RV contractility), RV infarct, ventricular arrhythmias, and increased RV afterload (unmasking of pulmonary hypertension or pulmonary embolism). On review of the patient's echocardiogram post RVAD placement, there was RVAD flow dependent notching of the RV outflow tract (RVOT) pulse wave doppler (Figure 1A,B). RVOT notching is a validated sign of high PVR and prompted further review of patient's pre LVAD RHCs and TTEs. Excluding the RHC and TTE immediately pre LVAD implantation, prior RHCs showed RAP:PCWP ratio of 0.7, PAP of 70s/30s and PVR as high as 5.4 with concordant RVOT notching on TTE. The narrower pulmonary pulse pressure on the RHC immediately preceding LVAD implantation suggested a failing RV and was discordant with the lower RAP:PCWP (0.25) and lower PVR. Under-occlusion of the PCWP most likely led to a falsely elevated PCWP and falsely reduced PVR. With aggressive pulmonary vasodilator therapy, hemodynamics improved, the RVAD was explanted and dialysis was successfully discontinued. Figure 1C shows improvement of RVOT notching with this treatment. Conclusion Severe RV failure post LVAD implantation has a significant impact on morbidity/mortality. The echocardiogram provides valuable pathophysiological insights and is an important asset to interpreting invasive hemodynamics, especially pertaining to RV failure.

Tricuspid Valve Anterior Leaflet Strains in Ovine Functional Tricuspid Regurgitation

Functional tricuspid regurgitation (FTR) is thought to arise due to annular dilation and alteration of right ventricular (RV) geometry in the presence of normal leaflets, yet mitral leaflets have been shown to remodel significantly in functional mitral regurgitation. We set out to evaluate tricuspid valve anterior leaflet deformations in ovine FTR. Eleven animals (FTR group) underwent implantation of a pacemaker with high rate pacing to induce biventricular dysfunction and at least moderate TR. Subsequently, both FTR (n = 11) and Control (n = 12) animals underwent implantation of 6 sonomicrometry crystals around the tricuspid annulus, 4 on the anterior leaflet, and 14 on RV epicardium. Tricuspid valve geometry and anterior leaflet strains were calculated from crystal coordinates. Left ventricular ejection fraction and RV fractional area change were significantly lower in FTR animals versus Control. Tricuspid annular area, septo-lateral diameter, RV pressures were all significantly greater in the FTR group. Mean TR grade (+0-3) was 0.7 ± 0.5 in Control and 2.4 ± 0.5 in FTR (P = < 0.001). The anterior leaflet area and length increased significantly. Global radial leaflet strain was significantly lower in FTR mostly driven by decreased free edge leaflet strain. Global circumferential anterior leaflet strain was also significantly lower in FTR with more remarkable reduction in the belly region. Rapid ventricular pacing in sheep resulted in a clinically pertinent model of RV and annular dilation with FTR and leaflet enlargement. Both circumferential and radial anterior leaflet strains were significantly reduced with FTR. Functional TR may be associated with alteration of leaflet mechanical properties.

Transthoracic echocardiographic findings in patients admitted with SARS-CoV-2 infection.

IntroductionSevere acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2)–infected patients commonly have elevated troponin and D‐dimer levels, but limited imaging exists to support most likely etiologies in efforts to avoid staff exposure. The purpose of this study was to report transthoracic echocardiographic (TTE) findings in SARS‐CoV‐2 patients with correlating troponin and D‐dimer levels.MethodsWe identified 66 SARS‐CoV‐2 patients (mean age 60 ± 15.7 years) admitted within a large, eight‐hospital healthcare system over a 6‐week period with a TTE performed. TTE readers were blinded to laboratory data with intra‐observer and inter‐observer analysis assessed.ResultsSixty‐six of 1780 SARS‐CoV‐2 patients were included and represented a high‐risk population as 38 (57.6%) were ICU‐admitted, 47 (71.2%) had elevated D‐dimer, 41 (62.1%) had elevated troponin, and 25 (37.9%) died. Right ventricular (RV) dilation was present in 49 (74.2%) patients. The incidence and average D‐dimer elevation was similar between moderate/severe vs. mild/no RV dilation (69.6% vs 67.6%, P = 1.0; 3736 ± 2986 vs 4141 ± 3351 ng/mL, P = .679). Increased left ventricular (LV) wall thickness was present in 46 (69.7%) with similar incidence of elevated troponin and average troponin levels compared to normal wall thickness (66.7% vs 52.4%, P = .231; 0.88 ± 1.9 vs 1.36 ± 2.4 ng/mL, P = .772). LV dilation was rare (n = 6, 9.1%), as was newly reduced LV ejection fraction (n = 2, 3.0%).ConclusionTTE in SARS‐CoV‐2 patients is scarce, technically difficult, and reserved for high‐risk patients. RV dilation is common in SARS‐CoV‐2 but does not correlate with elevated D‐dimer levels. Increased LV wall thickness is common, while newly reduced LV ejection fraction is rare, and neither correlates with troponin levels.

Acute effects of intravenous pimobendan administration in dog models of chronic precapillary pulmonary hypertension

IntroductionPulmonary hypertension (PH) is a progressive and potentially life-threatening disease. Several drugs are used for the treatment of dogs with precapillary PH. Pimobendan is an inotropic drug with phosphodiesterase 3 inhibitory and calcium-sensitizing effects. Pimobendan administration improved right ventricular (RV) function and lowered pulmonary arterial pressure in some human patients with precapillary PH. However, the efficacy of pimobendan in dogs with precapillary PH is unknown. Animals, material, and methodsAn implantable port device was percutaneously placed in the cranial vena cava of five laboratory beagles. Chronic embolic precapillary PH was induced via the repeated injection of microspheres every 1–2 days. Microsphere injection was continued until systolic pulmonary arterial pressure reached 50 mmHg. Right heart catheterization and echocardiography were performed at baseline and after injections of placebo and pimobendan (0.15 mg/kg). ResultsRepeated injections of microspheres caused an increase in pulmonary vascular resistance, a decrease in stroke volume, RV dilation, left ventricular (LV) and RV dysfunction, and RV dyssynchrony as assessed using echocardiography. Compared with placebo, pimobendan improved LV and RV function based on the LV Tei index from 0.48 to 0.38 (p=0.002) and the RV Tei index from 0.76 to 0.61 (p=0.008), as well as the stroke volume index from 29.4 to 36.7 ml/m2 (p=0.012), respectively. ConclusionsIn dog models of chronic PH, intravenous pimobendan effectively improved RV and LV function and increased stroke volume. However, pimobendan administration did not decrease pulmonary arterial pressure or produce hypotension.

Right bundle branch block ventricular tachycardia in arrhythmogenic right ventricular cardiomyopathy more commonly originates from the right ventricle: Criteria for identifying chamber of origin

Right bundle branch block (RBBB) ventricular tachycardia (VT) morphology is a criterion for left ventricular (LV) involvement in arrhythmogenic right ventricular cardiomyopathy (ARVC). The purpose of this study was to determine the frequency and chamber of origin of RBBB VT in patients with ARVC and VT. We studied 110 consecutive patients with VT who met the diagnostic International Task Force criteria for ARVC and underwent VT mapping/ablation. Patients with ≥1 RBBB VT were identified. Right ventricular (RV) origin of the RBBB VT was determined based on standard mapping criteria and elimination with ablation. Nineteen patients (17%) had 26 RBBB VTs. Eleven of these 19 patients (58%) had 16 RBBB VTs from the RV, and 9 patients (47%) had 10 RBBB VTs originating from the LV, with 1 patient demonstrating both. RBBB VT from RV most commonly (13/16 RBBB VTs) had an early precordial QRS transition (V2 or V3), with superiorly and typically leftward directed frontal plane axis, consistent with exit from dilated RV adjacent to inferior LV septum, whereas all 10 VTs from LV had RBBB morphology with positive R waves to V5 or V6 and rightward axis in 6 VTs characteristic of basal lateral origin. In patients with ARVC and VT presenting for VT ablation, RBBB VT occurs in 17% of cases, with most RBBB VTs (62%) originating from the RV and not indicative of LV origin. Precordial R-wave transition and frontal plane axis can be used to identify the anticipated chamber of origin of RBBB VT.