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Pulmonary hypertension associated with left heart disease (PH-LHD) remains the most common cause of pulmonary hypertension globally. Etiologies include heart failure with reduced and preserved ejection fraction and left-sided valvular heart diseases. Despite the increasing prevalence of PH-LHD, there remains a paucity of knowledge about the hemodynamic definition, diagnosis, treatment modalities, and prognosis among clinicians. Moreover, clinical trials have produced mixed results on the usefulness of pulmonary vasodilator therapies for PH-LHD. In this expert review, we have outlined the critical role of meticulous hemodynamic evaluation and provocative testing for cases of diagnostic uncertainty. Therapeutic strategies—pharmacologic, device-based, and surgical therapies used for managing PH-LHD—are also outlined. PH-LHD in advanced heart failure, and the role of mechanical circulatory support in PH-LHD is briefly explored. An in-depth understanding of PH-LHD by all clinicians is needed for improved recognition and outcomes among patients with PH-LHD.

Durable left ventricular assist devices (VADs) improve survival in eligible patients, but allocation has been associated with patient race in addition to presumed heart failure (HF) severity.

Background: Black patients with peripartum cardiomyopathy (PPCM) have disproportionately worse outcomes than White patients, possibly related to variable involvement of cardiovascular specialists in their clinical care. We sought to determine whether race was associated with cardiology involvement in clinical care during inpatient admission and whether cardiology involvement in care was associated with higher claims of guideline-directed medical therapy (GDMT) a week after hospital discharge. Methods: Using Optum’s de-identified Clinformatics® Data Mart (CDM), we included Black and White patients’ first hospital admission for PPCM from 2008 to 2021. Cardiology involvement in clinical care was defined as the receipt of attending care from a cardiovascular specialist during admission. GDMT included beta-blockers (BB) for all patients and triple therapy (BB, angiotensin-responsive medications, and mineralocorticoid receptor antagonists) for non-pregnant patients. Logistic regression was used to determine the associations between cardiology involvement in clinical care during admission and (1) patient race and (2) GDMT prescription, adjusting for age and comorbidities. Results: Among 668 patients (32.6% Black, 67.4% White, 93.3% commercially insured), there was no significant difference in the odds of cardiology involvement in clinical care by race (aOR: 1.41; 95%CI: 0.87–2.33, P=0.17). Inpatient cardiology care was associated with 2.75 times increased odds of having a prescription claim for GDMT (BB) for White patients (aOR: 2.75; 95%CI 1.50–5.06, P=0.001), and the estimated effect size was similar but not statistically significant for Black patients (aOR: 2.20, 95% CI, 0.84–5.71, P=0.11). The interaction between race and cardiology involvement in clinical care was not statistically significant for the receipt of BB prescription. Among 274 non-pregnant patients with PPCM (37.2% Black, 62.8% White), 5.8% received triple GDMT. Of these, none of the Black patients lacking cardiology care had triple GDMT. However, cardiology involvement in care was not significantly associated with triple GDMT for either race. Conclusions: Among a commercially insured population within PPCM, race was not associated with cardiology involvement in clinical care during hospitalization. However, cardiology involvement in care was associated with significantly higher odds of prescription claims for BB for only White patients. Additional strategies are needed to support equitable GDMT prescription.

This review highlights the current evidence on racial, ethnic, and socioeconomic disparities in cardiac arrest outcomes within the United States. Several studies demonstrate that patients from Black, Hispanic, or lower socioeconomic status backgrounds suffer the most from disparities at multiple levels of the resuscitation pathway, including in the provision of bystander cardiopulmonary resuscitation, defibrillator usage, and postresuscitation therapies. These gaps in care may altogether lead to lower survival rates and worse neurological outcomes for these patients. A multisystem, culturally sensitive approach to improving cardiac arrest outcomes is suggested in this article.

Cardiac resynchronization therapy (CRT) response is complex, and better approaches are required to predict survival and need for advanced therapies.

Patients with heart failure (HF) are heterogeneous with various intrapersonal and interpersonal characteristics contributing to clinical outcomes. Bias, structural racism, and social determinants of health have been implicated in unequal treatment of patients with HF. Through several methodologies, artificial intelligence (AI) can provide models in HF prediction, prognostication, and provision of care, which may help prevent unequal outcomes. This review highlights AI as a strategy to address racial inequalities in HF; discusses key AI definitions within a health equity context; describes the current uses of AI in HF, strengths and harms in using AI; and offers recommendations for future directions.

Placement of an interatrial shunt device reduces pulmonary capillary wedge pressure during exercise in patients with heart failure and preserved or mildly reduced ejection fraction. We aimed to investigate whether an interatrial shunt can reduce heart failure events or improve health status in these patients.

Sleep apnea is highly prevalent in patients with atrial fibrillation (AF). Obstructive sleep apnea (OSA) is the most common type, and best studied in the context of AF. However, recent investigations have indicated that central sleep apnea (CSA) may be a risk factor for incident AF. We evaluated the burden of CSA events in patients referred for diagnostic polysomnography (PSG) and whether AF is associated with CSA. We identified patients with and without a history of AF who underwent clinically indicated PSG in a matched manner. OSA was defined as obstructive apnea‐hypopnea index (AHI) ≥15/h, and CSA was defined as central apnea index (CAI) ≥5/h. The association between AF and CSA was evaluated using multivariable logistic regression. Among 465 patients included, mean AHI was 25.5/h, and mean CAI was 1.7/h. OSA prevalence was 53.3%, while CSA prevalence was 8.4%. The prevalence of OSA in the AF and non‐AF groups (54.7% vs 52.0%, P= .56) was similar. CSA was more common in the AF group (12.3% vs 4.4%, P= .002). In multivariable analysis, AF (OR: 2.19 [1.02, 5.03], P= .05), male gender (OR: 2.5 [1.17, 5.84], P= .02), and older age (OR: 2.44, [1.16, 5.46], P= .02) were associated with CSA. Though CSA is much less common than OSA in patients with AF, the presence of AF is independently associated with CSA. In this study, we analyzed the central sleep apnea burden of patients with and without atrial fibrillation undergoing diagnostic polysomnography. We found that central sleep apnea, though uncommon, was independently associated with atrial fibrillation.

This study sought to determine whether the likelihood of receiving primary intensive care unit (ICU) care by a cardiologist versus a noncardiologist was greater for Caucasians than for African Americans admitted to an ICU for heart failure (HF). The authors further evaluated whether primary ICU care by a cardiologist is associated with higher in-hospital survival, irrespective of race.

A 64-year-old man developed sudden airway compromise after extubation following an elective mandibular debridement, requiring reintubation. Cardiogenic shock and hypoxemic respiratory failure ensued. Subsequent evaluation revealed acute pulmonary edema, severe left ventricular (LV) systolic dysfunction sparing the basal segments, and elevated cardiac biomarkers. Coronary angiogram was unremarkable. The patient's condition, along with his LV function, gradually improved and he was discharged. This case highlights the potential risk of acute upper airway obstruction causing negative pressure pulmonary edema, along with the possibility of stress- induced cardiomyopathy. [ABSTRACT FROM AUTHOR]

Minoritized racial and ethnic groups have the highest incidence, prevalence, and hospitalization rate for heart failure. Despite improvement in medical therapies and overall survival, the morbidity and mortality of these groups remain elevated. The reasons for this disparity are multifactorial, including social determinant of health (SDOH) such as access to care, bias, and structural racism. These same factors contributed to higher rates of COVID-19 infection among minoritized racial and ethnic groups. In this review, we aim to explore the lessons learned from the COVID-19 pandemic and its interconnection between heart failure and SDOH. The pandemic presents a window of opportunity for achieving greater equity in the health care of all vulnerable populations.

Introduction:Patients with cardiac resynchronization therapy (CRT) upgrades with right ventricular pacing (RVP) dependence may have a different prognosis after CRT and require a distinct implementation strategy.Hypothesis:Left ventricular (LV) size/function, optimal AHA segments for LV pacing, and survival post-CRT is different for patients with RV pacing undergoing CRT upgrade procedures.Methods:Cardiac magnetic resonance (CMR) with cine imaging, DENSE strain mechanical activation mapping, and scar imaging was performed prior to implants of CRT systems that were "de novo" (Group 1) or upgraded from pre-existing pacemakers or ICDs with RVP (Group 2) and without RVP (Group 3). Optimal LV pacing sites were identified based on latest activation. Patients were followed for clinical outcomes.Results:In 92 patients (23.5% female, 65.8 ± 10.7 years old), the baseline LVEDVI by CMR was significantly smaller in RVP upgrade (Group 2) patients (101.8 +/- 34.3 cc/m2) compared with de novo (Group 1; 140.5 +/- 38.2 cc/m2); p=0.001) and non-RVP upgrade patients (Group 3; 153.6 +/- 46.4 cc/m2; p=0.001) (Figure 1). RVP upgrade patients also had the widest baseline QRS (178.2 +/- 26.6 ms v. 159.7 +/- 18.5 ms in Group 1 v. 154.5 +/- 20.1 ms in Group 3; p = 0.001) and were more likely to have latest mechanical activation in an anterior LV segment (50%) versus Group 1 (10%) and Group 3 (35%) patients (p = 0.0007). As shown in Figure 2, RVP upgrade patients had the worst survival (p = 0.007).Conclusion:Patients with RVP dependence undergoing CRT upgrades are more likely to have smaller baseline LV volumes by CMR, greater QRS durations, optimal pacing sites in anterior segments, and unfavorable survival.

Introduction:Central sleep apnea (CSA) is common in patients with heart failure and is associated with a poor prognosis. A number of studies have linked the P2Y12 inhibitor, ticagrelor, with CSA. We aimed to evaluate CSA prevalence in patients with coronary heart disease (CHD) and whether ticagrelor use is associated with CSA in this population.Methods:We reviewed consecutive patients with CHD data who underwent a clinically indicated polysomnography (PSG) test over a 5-year period from three academic sleep centers. We sampled patients who were on ticagrelor or clopidogrel during their PSG test at a 1:4 ticagrelor:clopidogrel ratio. Patients with an active opioid prescription at time of PSG test were excluded. Age, left ventricle (LV) dysfunction (ejection fraction <45%), and P2Y12 inhibitor use were included in a multivariate logistic regression.Results:A total of 141 patients (age 63.7 ± 11.4, 33% female) were included with 30 on ticagrelor and 111 on clopidogrel. 106 (75.2%) patients had undergone percutaneous coronary intervention for ACS. 33 (23.4%) patients had LV dysfunction. The mean apnea hypopnea index (AHI) was 29 (/hr). High CSA burden (central apnea index [CAI] ≥5/h) and strict CSA (AHI ≥5/h and CAI >50% of AHI) were present in 16 (11.3%) and 5 (3.5%) patients, respectively. High CSA burden and strict CSA were more common in patients on ticagrelor than in those on clopidogrel (7 [23.3%] vs. 9 [8.1%] and 3 [10.0%] vs. 2 [1.8%]). In multivariable analysis ticagrelor use was associated with high CSA burden adjusting for LV dysfunction and age (OR 3.27, 95% CI 0.99-10.7, p=0.048). No variables were associated with strict CSA.Conclusions:Ticagrelor use was associated with high CSA burden in patients with coronary heart disease. Future studies should verify these results in a larger cohort and explore their clinical significance.

Introduction:Both LV dysfunction and AS lead to an increase in LVEDP, a decrease in oxygen delivery to cardiac muscle, and ultimately a decrease in the EVR.Hypothesis:We hypothesized that patients with low EVR would have less significant recovery of LV function after TAVR.Methods:Patients with LVEF <40% and severe AS undergoing TAVR at the University of Virginia (UVA) between 2012 and 2019 were retrospectively reviewed. EVR was calculated by dividing the diastolic pressure time index (DPTI) [(Diastolic blood pressure – LVEDP) x (60seconds/ heart rate – 0.2 seconds)] by the tension time index (TTI) [systolic pressure x 0.2 seconds] using catheter-derived hemodynamics prior to TAVR. LVEF and mAG values were obtained from TTE measurements done for procedural planning and at, or closest to, 1-year follow-up. The patients were divided into cohorts based on EVR above or below 0.7, a value indicative of subendocardial ischemia. Mean change in LVEF was evaluated between these two groups (Figure [1] and Table [1]) and multivariable regression was performed using pre-procedural LVEF, EVR, and change in mean aortic gradient as shown in Table [2].Results:128 patients that underwent TAVR had a LVEF <40%. 85 patients (32.5% female) had complete invasive hemodynamic and echocardiographic data. The mean change in post-TAVR LVEF in the lower subgroup was <5% with a standard deviation of 12.5. In patients with EVR >0.7 there was improvement of LVEF of >10% with a standard deviation of 10.8. Two-tailed t-testing was performed with a corresponding p-value of 0.0181. Multivariable regression on pre-procedural LVEF, pre-procedural EVR, and change in mean AG were all statistically significant.Conclusion:EVR >0.7 is associated with greater improvement in LV function in advanced heart failure patients after TAVR.

Introduction:Ventriculo-arterial coupling dynamics influence outcomes in heart failure (HF). Arterial stiffness (AS) is a key determinant of vascular load on the heart. We hypothesized that estimated pulse wave velocity (ePWV) would be associated with mortality.Methods:We analyzed the Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training (HF-ACTION) database for the association of ePWV with survival. ePWV was calculated using mean blood pressure (MBP) and Age using the equation: 9.587 – 0.402 х age + 4.560 х 10–3 х age2 – 2.621 х 10–5 х age2 х MBP + 3.176 х 10–3 х age х MBP – 1.832 х 10–2 х MBP. MBP was calculated as diastolic BP (DBP) + 0.4(SBP – DBP). Kaplan-Meier survival curves and Cox proportional hazards regression were used for analysis.Results:Among 768 patients (age 58.0 +/- 12.8 years, 31.8 % female), the median ePWV was 8.5 (IQR 7.2 to 10.2). There was a moderate correlation between ePWV and peak VO2 (r=-0.20, p<0.0001) and between ePWV and the six-minute walk duration (r=-0.20, p<0.0001). The unadjusted HR for ePWV and all-cause mortality was 1.15 per unit increase (95% CI 1.05-125). The unadjusted HRs for ePWV component covariates of age and MBP with all-cause mortality were 1.03 per year (95% CI 1.02-1.05, p < 0.0001) and 0.985 per mm Hg (95% CI 0.971-1.000, p=0.053), respectively. With adjustment by peak VO2 above or below the median in a multivariable model, increasing ePWV was still associated with a greater probability of all-cause mortality (HR 1.11 per unit increase, 95% CI 1.01-1.21, p=0.02). In the model with adjustment by the six-minute walk duration, risk associated with ePWV was similar (HR 1.09, 95% CI 0.998-1.120, p=0.056). Kaplan-Meier curves also demonstrated an increased risk for ePWV greater than the median value of 8.5 (Figure).Conclusion:ePWV is associated with all-cause mortality in stable HF patients. More studies are needed to assess the utility of ePWV as a therapeutic target in HF.

Introduction:Myocardial perfusion relative to left-ventricular workload may be estimated by the sub-endocardial viability index (SVI). This can be calculated myocardial oxygen supply-demand balance, which is the ratio of diastolic to systolic pressure-time indices, i.e. [(DBP - PAWP) x (60sec/heart rate - 0.2sec)] / (SBP x 0.2sec), assuming fixed 0.2sec for systole. Low SVI indicates reduced sub-endocardial perfusion and was hypothesized to associate with negative outcomes in HFrEF patients.Methods:HF-ACTION was a randomized trial evaluating the efficacy of aerobic exercise training and usual care versus usual care in chronic HFrEF patients. SVI was calculated in HF-ACTION trial patients with complete hemodynamic data. PAWP was calculated using the Nagueh formula from echocardiographic-derived measurements ([PAWP=1.24*(E/e’) +1.9] with e’ = [(e’lateral + e’septal)/2]). The association of SVI with the combined endpoint of death or hospitalization, as well as all-cause death, was assessed.Results:Of 2331 patients in HF-ACTION, 807 had complete data. The mean SVI was 1.59 ± 0.47. The Cox proportional hazards model for the combined endpoint and all-cause death had HR of 0.66 per unit increase in SVI (p<0.00001, 95% CI 0.55-0.79) and 0.67 (p=0.04, 95% CI 0.46-0.98), respectively. Survival during 4 year follow-up was worse below the mean SVI (p=0.0073) (Figure 1). In 26 patients below the critical sub-endocardial ischemia SVI of 0.7, survival was worse (p=0.0013) (Figure 2).Conclusion:Reduced SVI, a metric of the adequacy of sub-endocardial perfusion, is associated with negative outcomes in HFrEF patients.Figure 1.Figure 2.

Introduction:Ventricular-arterial coupling (VAC) dynamics reflect the interaction between myocardial and vascular functions and are known to influence cardiac outcomes. Systemic arterial pulsatility index (SAPi = [systemic systolic pressure-systemic diastolic pressure]/pulmonary capillary wedge pressure) is a metric of VAC, incorporating pulse pressure and left ventricular filling pressure. We hypothesized that SAPi would be associated with adverse outcomes in patients undergoing surgical aortic valve replacement (SAVR) and or concomitant coronary artery bypass graft surgery (CABG).Methods:This was a retrospective analysis of patients who underwent SAVR +/- CABG at a tertiary academic center from 2008 to 2016. SAPi was calculated using right heart catheterization hemodynamics prior to surgery. Logistic regression model was used to evaluate the relationship between SAPi and mortality.Results:Among 133 patients (mean age 73.4, 43% female) who underwent SAVR, 37 (28%) underwent concomitant CABG. The median SAPi was 4.3 (IQR 2.76-6.40). Patients with SAPi > 4.3 had a lower risk of mortality during the mean follow up of 6.9 years (OR 0.39 95% CI 0.18-0.85). Increasing SAPi was associated with a lower risk of mortality (OR 0.88 per unit increase in SAPi, 95% CI 0.76-0.99). A receiver operator characteristic curve is shown in Figure 1 with SAPI as a continuous variable adjusted for age. Area under the curve was 0.64 (95% CI 0.533-0.743).Conclusions:SAPi, a hemodynamic marker of VAC, was associated with mortality in patients undergoing SAVR +/- CABG. SAPi may have potential utility in pre-operative risk stratification of patients undergoing SAVR +/- CABG.

Background:The use of cardiac point-of-care ultrasound (c-POCUS) for patient care has been on the rise in many non-cardiology specialties. Perspectives on c-POCUS by cardiologists, the predominant user of comprehensive echocardiograms, have not been explored.Methods:A 19-item online survey was developed to evaluate respondents’ echocardiography experience as well as their current practices and perspectives on various aspects of c-POCUS. The survey was distributed to attending cardiologists at quaternary academic medical centers.Results:A total of 96 survey responses were collected from participants at 13 institutions. Majority of the respondents worked in an inpatient setting (97.9%) and formally practiced echocardiography (72.6%). C-POCUS use was common, with 37.9% of cardiologists using it more than twice per inpatient week. Cardiologists that practiced echocardiography used c-POCUS at higher frequency (43% vs. 23%, p=0.07). About half of respondents (47.9%) agreed that c-POCUS changed their clinical management. However, more than half agreed that c-POCUS should be further incorporated in practice (68.1%) and in formal fellowship education (71.3%). Few expressed time and labor intensiveness or impact on volume of comprehensive echocardiograms as major concerns. Major barriers to c-POCUS implementation included device availability, image documentation infrastructure, and reimbursement.Conclusion:This study demonstrates that the rising enthusiasm for c-POCUS also extends to cardiology. However, several barriers remain to more thorough utilization of this rapidly adopted diagnostic tool by cardiologists. Interventions to overcome these barriers would likely encourage further integration of c-POCUS use in clinical practice and fellowship training.

Introduction:The six-minute walk test (6MWT) is frequently performed in patients with pulmonary hypertension (PH) to assess exercise capacity. Systolic blood pressure (SBP) values and variation during 6MWT may hold prognostic significance, but technologic limitations have precluded routine measurement. We used a novel device for continuous SBP monitoring during 6MWT and analyzed the relationship with PH severity.Methods:Caretaker®, an FDA-approved wireless continuous noninvasive BP device that uses pulse decomposition analysis was worn during 6MWT in patients with and without PH. We compared SBP values before, during, and after 6MWT. A repeated-measures ANOVA was used to compare SBP between groups.Results:Of the 80 patients tested, fifty patients (62.5%) demonstrated adequate signal quality for SBP monitoring. SBP varied significantly with the 6MWT in the PH group (N = 26; before vs. during vs. after; 129.1 [18.7] vs. 126.7 [18.6] vs. 140.3 [23.5] mmHg, p = 0.0006), but not in the non-PH group (N = 24; 136.1 [17.6] vs. 137.8 [17.9] vs. 143.1 [20.0] mmHg, p = 0.16). In the PH group, SBP variation while walking was inversely correlated with baseline pulmonary artery systolic pressure (PASP) (R = -0.47, p = 0.039, Figure 1).Conclusions:Continuous, clinic based SBP monitoring was feasible in nearly two-thirds of patients undergoing 6MWT. SBP response during walking differed between patients with and without PH and may provide clinically relevant insight into a patients exercise response. In patients with PH, change in SBP during 6MWT was inversely correlated with baseline PASP, suggesting dysregulated exertional hemodynamic response in patients with severe PH.

Introduction:Systemic Arterial Pulsatility Index, (SAPi), [systemic pulse pressure/left ventricular end diastolic pressure (LVEDP)] has emerged as a useful prognostic tool in many cardiac diseases. We aimed to compare this hemodynamically derived index of pulsatility with directly measured pulsatility on gated CT imaging (SAPi-CT) in pre-TAVR patients, as well as with SAPi calculated from pre-TAVR transthoracic echocardiography (SAPi-TTE). We also evaluated the correlation of each of these measurements with the patients’ pre-TAVR 5-meter walk times (5MWT).Methods:The three SAPi were calculated as; SAPi-Cath using invasive hemodynamics, SAPi-TTE using the Nagueh formula (PCWP = 1.24 X (E/e’) +1.9) as surrogate for LVEDP, and SAPi-CT by calculating the difference in aortic cross-sectional area during systole and diastole on gated CT imaging at the level of the ascending aorta (the level of right pulmonary artery). Correlational comparisons of these methods with each other and with pre-TAVR 5MWT were made using R software.Results:Among 110 patients studied (mean age 77.3, 56% female), the mean SAPi-Cath, SAPi-TTE, and cross-sectional area on CT were 3.15, 3.03, and 53.83mm2respectively. There was a significant positive correlation between SAPi-Cath and SAPi-CT [(r=0.275, p=0.0073); shown in Figure 1a], but not between SAPi-Cath and SAPi-TTE (r=0.163, p=0.1852). SAPI-Cath was significantly associated 5MWT (r=0.287, p=0.0064); shown in Figure 1b. Using a linear regression, the relationship between SAPi-Cath and the 5MWT is estimated to be: 5MWT=4+SAPI. SAPi-CT did not correlate with 5MWT (r=0.021, p=0.8478).Conclusions:SAPi-Cath and SAPi-CT showed a significant positive correlation. Only SAPi-Cath showed a significant correlation with 5MWT. Given the known prognostic value of SAPi-Cath, future studies utilizing imaging variables should be performed to enhance prognostication with multi-modal data.

Introduction:Cardiac resynchronization therapy (CRT) response rates in unselected cohorts are suboptimal. Cardiac magnetic resonance (CMR) provides high-quality imaging of strain and scar, and post-CRT CMR offers reliable assessment of left ventricular (LV) reverse remodeling.Hypothesis:Cardiac magnetic resonance (CMR) guidance for CRT will increase CRT response rates, particularly in nonischemic cardiomyopathy (NICM).Methods:Patients were randomized 1:1 to standard CRT or CMR guidance for CRT using circumferential strain from Displacement Encoding with Stimulated Echoes (DENSE) and scar (late gadolinium enhancement [LGE]) by CMR. The primary endpoint is the percent change in LV end-systolic volume (LVESV) calculated from CMRs before CRT and 6 months after CRT. A pre-specified interim analysis by cardiomyopathy type was performed after completion of enrollment of 45 of the projected 90 patients needed for adequate power.Results:Of 45 patients enrolled (age 65.9 +/- 10.3 years, 29% female), two patients did not undergo a CRT procedure, and the LV lead could not be placed in one patient. Of the remaining 42 patients, 26/42 had NICM and 21/42 were randomized to CMR guidance. In a linear regression model for the primary endpoint adjusted for baseline QRS duration (p=0.04) and cardiomyopathy type (p=0.01), a favorable trend for the intervention on response was noted (p=0.06). Box plots demonstrate a significant difference in the primary endpoint among NICM patients (p=0.03) and a favorable trend for QRS shortening (0.07) in NICM patients (Figure). In all patients (including ICM patients), the overall p-value for the intervention relative to the primary endpoint was 0.08.Conclusion:An interim analysis in CRT patients with NICM demonstrated a favorable effect of CMR guidance on LV reverse remodeling after CRT, as assessed with post-CRT CMRs. Enrollment is continuing to evaluate the effect of the intervention on the entire cohort and other endpoints.

Introduction:Myocardial oxygen supply is an important determinant of cardiac function. The Endocardial Viability Ratio (EVR), a measure of myocardial oxygen supply-demand balance, is calculated as a ratio of the diastolic pressure time index [(diastolic blood pressure - left ventricular end diastolic pressure) x (60 sec/heart rate - 0.2 sec)] and tension time index [systolic pressure x 0.2 sec]. We hypothesized that low EVR would be associated with adverse events in patients with heart failure (HF).Methods:EVR was calculated in the invasive arm of the ESCAPE trial in patients with available discharge blood pressure, pulmonary arterial wedge pressure, and heart rate as the ratio of the diastolic pressure time index (a measure of coronary blood supply) and tension time index (a measure of myocardial oxygen demand). Kaplan-Meier analysis and Cox proportional hazards regression was used to assess associations with EVR and a composite death endpoint including cardiac transplantation and left ventricular assist device implantation.Results:Among 143 patients (56.9 ± 13.3 years, 30.1% female), the median EVR was 1.168 (IQR 0.923-1.398). Survival during 180 days of follow-up was worse in patients with EVR below the median (p=0.0004) (Figure panel 1A). Among the 10 patients with EVR < 0.7, considered to represent subendocardial ischemia, 50% reached this endpoint within 100 days (p=0.01 versus remaining patients) (Figure 1B). An increase of 0.1 in EVR was associated with an 18% relative risk reduction for this endpoint (HR 0.82, 95% CI 0.74-0.91, p=0.0002), while an increase of 0.5 in EVR was associated with a 62% relative risk reduction (HR 0.38, 95% CI 0.22-0.64, p=0.002).Conclusion:Decreased EVR, a marker of myocardial oxygen supply, is associated with adverse events in advanced HF patients. Further studies on the prognostic utility of EVR in HF are needed.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare, morbid, potentially curable subtype of pulmonary hypertension that negatively impacts health-related quality of life (HRQoL). Little is known about differences in HRQoL and hospitalization between CTEPH patients and idiopathic pulmonary arterial hypertension (IPAH) patients. Using multivariable linear regression and mixed effects models, we examined differences in HRQoL assessed by emPHasis-10 (E10) and SF-12 between CTEPH and IPAH patients in the Pulmonary Hypertension Association Registry, a prospective multicenter cohort of patients newly evaluated at a Pulmonary Hypertension Care Center. Multivariable negative binomial regression models were used to estimate incidence rate ratios (IRR) for hospitalization amongst the two groups. We included 461 IPAH patients and 169 CTEPH patients. Twenty-one percent of CTEPH patients underwent pulmonary thromboendarterectomy (PTE) before the end of follow-up. At baseline, patients with CTEPH had significantly worse HRQoL (higher E10 scores) (ß 2.83, SE 1.11, p = 0.01); however, differences did not persist over time. CTEPH patients had higher rates of hospitalization (excluding the hospitalization for PTE) compared to IPAH patients after adjusting for age, sex, body mass index, WHO functional class and six-minute walk distance (IRR 1.66, 95%CI 1.04–2.65, p = 0.03). CTEPH patients who underwent PTE had improved HRQoL as compared to those who were medically managed, but patients who underwent PTE were younger, had higher cardiac outputs and greater six-minute walk distances. In this large, prospective, multicenter cohort, CTEPH patients had significantly worse baseline HRQoL and higher rates of hospitalizations than those with IPAH. CTEPH patients who underwent PTE had significant improvements in HRQoL.

Compared to idiopathic pulmonary arterial hypertension (IPAH), patients with portopulmonary hypertension (POPH) have worse survival. Health disparities may contribute to these differences but have not been studied. We sought to compare socioeconomic factors in patients with POPH and IPAH and to determine whether socioeconomic status and/or POPH diagnosis were associated with treatment and health-care utilization. We performed a cross-sectional study of adults enrolled in the Pulmonary Hypertension Association Registry. Patients with IPAH (n = 344) and POPH (n = 57) were compared. Compared with IPAH, patients with POPH were less likely to be college graduates (19.6% vs. 34.9%, p = 0.02) and more likely to be unemployed (54.7% vs. 30.5%, p < 0.001) and have an annual household income below poverty level (45.7% vs. 19.0%, p < 0.001). Patients with POPH had similar functional class, quality of life, 6-min walk distance, and mean pulmonary arterial pressure with a higher cardiac index. Compared with IPAH, patients with POPH were less likely to receive combination therapy (46.4% vs. 62.2%, p = 0.03) and endothelin receptor antagonists (28.6% vs. 55.1%, p < 0.001) at enrollment with similar treatment at follow-up. Patients with POPH had more emergency department visits (1.7 ± 2.1 vs. 0.9 ± 1.2, p = 0.009) and hospitalizations in the six months preceding enrollment (1.5 ± 2.1 vs. 0.8 ± 1.1, p = 0.02). Both POPH diagnosis and lower education level were independently associated with a higher number of emergency department visits. Compared to IPAH, patients with POPH have lower socioeconomic status, are less likely to receive initial combination therapy and endothelin receptor antagonists but have similar treatment at follow-up, and have increased health-care utilization.

Background WHO Group 1 pulmonary arterial hypertension is a progressive and potentially fatal disease. Individuals living at higher altitude are exposed to lower barometric pressure and hypobaric hypoxemia. This may result in pulmonary vasoconstriction and contribute to disease progression. We sought to examine the relationship between living at moderately high altitude and pulmonary arterial hypertension characteristics.Methods Forty-two US centers participating in the Pulmonary Hypertension Association Registry enrolled patients who met the definition of WHO Group 1 pulmonary arterial hypertension. We utilized baseline data and patient questionnaire responses. Patients were divided into two groups: moderately high altitude residence (home ≥4000 ft) and low altitude residence (home <4000 ft) based on zip-code. Clinical characteristics, hemodynamic data, patient demographics, and patient reported quality of life metrics were compared.Results Controlling for potential confounders (age, sex at birth, body mass index, supplemental oxygen use, race, 100-day cigarette use, alcohol use, and pulmonary arterial hypertension medication use), subjects residing at moderately high altitude had a 6-min walk distance 32 m greater than those at low altitude, despite having a pulmonary vascular resistance that was 2.2 Wood units higher. Additionally, those residing at moderately high altitude had 3.7 times greater odds of using supplemental oxygen.Conclusion Patients with pulmonary arterial hypertension who live at moderately high altitude have a higher pulmonary vascular resistance and are more likely to need supplemental oxygen. Despite these findings, moderately high altitude Pulmonary Hypertension Association Registry patients have better functional tolerance as measured by 6-min walk distance. It is possible that a “high-altitude phenotype” of pulmonary arterial hypertension may exist. These findings warrant further study.

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Introduction:Elevated pulmonary artery wedge pressure (PAWP), a surrogate of left ventricular filling pressure, is associated with adverse outcomes in heart failure (HF). Few studies exist addressing the association of echocardiographic derived PAWP with exercise capacity, hospitalizations, and mortality.Hypothesis:We hypothesized that increasing PAWP derived non-invasively by echocardiography (echo) would be associated with reduced exercise capacity, increased hospitalization, and mortality among patients with chronic systolic HF.Methods:We analyzed the Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training (HF-ACTION) database with respect to baseline characteristics (age, gender, New York Heart Association [NYHA] class, and baseline exercise capacity (cardiopulmonary exercise test [CPET] exercise duration, CPET peak oxygen consumption [peak VO2], and 6-minute walk distance)), as well as clinical outcomes during 4 years of follow-up (all-cause mortality and the primary endpoint of survival free of death or hospitalization). PAWP was calculated using the Nagueh formula [PAWP = 1.24 * (E/e?) + 1.9] with e? = [(e?lateral+ e?septal) / 2]. Kaplan-Meier survival curves, multivariable Cox proportional hazards regression, and multivariable linear regression were used for analysis.Results:Among the 2019 patients in the dataset, 807 had complete variables for estimation of PAWP. The mean age was 58.6 ? 12.7 years, 28 % were female, and the mean PAWP was 15.8 ? 9.3 mmHg. After adjustment for age and gender, echo-derived PAWP was independently associated with both all-cause mortality (HR 1.02 per unit increase, 95% CI 1.002-1.032, P<0.0001) and the primary endpoint (HR 1.02 per 1 mm increase, 95% CI 1.009-1.027, P< 0.0001). PAWP also correlated with exercise parameters after covariate adjustment, including peak VO2 (adj. std. coef. = -0.25, P<0.0001) and 6-minute walk distance (adj. std. coef. = -0.12, P=0.0004).Conclusions:Echocardiographic derived PAWP is associated with higher all cause mortality, as well as reduced exercise capacity, increased hospitalization, and mortality in patients with chronic systolic HF.

Introduction:Sleep apnea is highly-prevalent in patients with atrial fibrillation (AF), and is considered an important risk factor for AF recurrence following cardioversion or catheter-based ablation. Obstructive sleep apnea (OSA) is the predominant sleep apnea type, and is most commonly linked to AF. However, recent cohort-based investigations have suggested a potential role for central sleep apnea (CSA) in incident AF.Hypothesis:We aimed to examine whether AF is predictive of CSA in patients undergoing polysomnography, and to quantify the burden of CSA events in this population.Methods:We retrospectively identified patients with and without a history of AF who underwent polysomnography at a single academic sleep center. OSA and CSA were defined as apnea hypopnea index (AHI) ?15 and central sleep apnea index (CSAI) ?5/hr, respectively. Mann-Whitney test was used to compare CSAI between patients with and without AF.Results:A total of 457 patients (male 56%, mean age 63 years, BMI 32.2, AF 229 patients) were included. Mean AHI was 25/hr, and mean CSAI was 1.6/hr. OSA and CSA were present in 54.5% and 8% of the cohort, respectively. While there was no difference in the prevalence of OSA between the AF and non-AF groups (57.2 vs. 51.8%, p=0.24), CSA was more common in the AF group (11.4% vs. 4.4%, p=0.006, Figure 1). In multivariable analysis, AF was predictive of CSA (OR 2.6 [1.1, 6.7], p=0.03), but not OSA. Male sex was predictive of both OSA (OR 1.8 [1.2, 2.7], p=0.002) and CSA (OR 2.5 [1.1, 5.9], p=0.03). No other factors, including HF, were predictive of CSA in this cohort.Conclusion:CSA prevalence and burden are low in patients with AF, but AF is independently associated with CSA. While causal association cannot be established, the findings suggest a role for CSA in the pathogenesis of AF.

Introduction:Advanced heart failure (AHF) is associated with poor contractile function, low pulse pressure, and central venous congestion.Hypothesis:Systemic pulse pressure (SPP) when indexed to central venous pressure (CVP) would be associated with adverse outcomes in AHF.Methods:We analyzed 165 patients with advanced decompensated heart failure from the ESCAPE trial database with complete hemodynamic data for calculation of SPP (systemic systolic pressure - diastolic pressure) / CVP. Cox proportional hazards regression was used to evaluate the association of SPP/CVP for the combined outcome of death, transplant, and left ventricular assist device implantation (DTxLVAD), as well as combined DTxLVAD and re-hospitalization (DTxLVADRH). We performed Cox proportional hazards regression to determine these associations and performed survival analysis using Kaplan-Meier analysis with the log-rank statistic.Results:Among 165 patients, the mean age was 56.7 years (SD +/- 13.6 years). The median SPP and SPP/CVP were 37.0 mm Hg (IQR 30-46) and 3.0 (IQR 1.8-5.2), respectively. Increasing SPP/CVP was associated with decreased risk of both DTxLVAD (HR 0.86, 95% CI 0.75-0.99, P=0.04) and DTxLVADRH (HR 0.93, 95% CI 0.88-0.98, P=0.005), although the effect on the hospitalization outcome was dominated by the SPP component of the ratio (P<0.0001). SPP/CVP below the median (<3.0) was associated with a nearly two-fold increased risk of DTxLVAD (HR 1.97, 95% CI 1.09-3.57, P=0.02) (Figure A). SPP below the median was also associated with a similarly increased risk for the DTxLVADRH outcome (HR 2.16, 95% CI 1.50-3.12, P<0.0001) (Figure B).Conclusions:Decreasing SPP/CVP, a marker of total vasculature pulsatility, is associated with worse outcomes in AHF patients. Further evaluation of SPP/CVP in guiding risk stratification in AHF is warranted.

Introduction:Patients with pulmonary hypertension (PH) have been shown to have a high prevalence of obstructive sleep apnea (OSA). However, prevalence of OSA is partly dependent on the threshold of apnea hypopnea index (AHI) used. In addition, it is uncertain whether traditional risk factors for OSA apply to patients with PH. We examined the prevalence of OSA and associated risk factors in patients with PH using two different AHI thresholds.Methods:We reviewed consecutive patients diagnosed with PH who underwent in-lab sleep study at a single academic medical center. Patients without hemodynamic data or sleep study with supplemental oxygen use or significant central sleep apnea were excluded. Patients were classified into pre- vs. post-capillary PH based on a pulmonary artery wedge pressure < or ? 15 mmHg, respectively. OSA was defined by AHI ? 15/hr (significant OSA [higher threshold]) or 5/hr (any OSA [lower threshold]). Traditional risk factors of OSA including age, sex and body mass index (BMI), as well as pre- vs. post-capillary PH group were entered into a logistic regression model. Hypertension and left ventricular systolic dysfunction (EF <40%) are also established risk factors for OSA and were tested separately using the same model.Results:A total of 86 patients (Age: 62? 16 years, Female 51%) including those with pre- (n=27) and post-capillary PH (n=59) were analyzed. Patients in the post-capillary PH group tended to be male (55 vs. 33%, P=0.05) and more obese (BMI [kg/m2]: 37 vs. 31, p=0.02) compared to the pre-capillary PH group. As a group, OSA was highly prevalent (significant OSA: 68%; any OSA: 89% with no significant difference in prevalence between the two PH groups). Age (per 10 years) (OR: 1.7 [1.2, 2.7], p=0.007), male sex (9.7 [2.8, 42.3, p=0.0008] and higher BMI (? 30 vs. <30) (10.0 [2.7-45], p=0.001), but not pre- vs. post, were associated with significant OSA. Results were similar for ?any OSA?. No associations were found between hypertension or left ventricular systolic dysfunction and OSA.Conclusions:OSA is highly prevalent regardless of using two different AHI thresholds and shares traditional risk factors for OSA in general population (but more exaggerated). A larger study is needed to better define risk factors of OSA based on PH subtypes.

Introduction:Sudden cardiac death (SCD) accounts for 40% of deaths overall in the end-stage renal disease (ESRD) population on hemodialysis (HD). Events are typically assumed to be fatal ventricular arrhythmias, but increasing evidence suggests bradyarrhythmias and asystole may be the major contributors to SCD in the HD population. Studies to date have excluded HD patients with cardiac implantable electronic devices (CIED), by which reliable rhythm analysis can be obtained with routine interrogation.Hypothesis:Determine the ventricular arrhythmia burden in hemodialysis patients with CIEDs versus controls with CIEDs.Methods:We identified 44 patients at a single tertiary care academic center with CIEDs either on HD (n= 22) or not on HD (n= 22). Device interrogations from 11/13/14 ? 3/15/19 were reviewed. For both groups, the dates, times, and duration of non-sustained ventricular tachycardia (NSVT), ventricular tachycardia (VT), and ventricular fibrillation (VF) episodes were recorded by reviewing the device interrogations available since implant.Results:HD patients experienced 204 ventricular arrhythmia events, while control patients experienced 164 episodes. The prevalence of primary prevention and secondary prevention ICDs was the same between groups (primary: 36.3%; secondary: 13.6%). In the HD group, 10/22 (45.4%) experienced any ventricular arrhythmia, compared to 14/22 (63.6%) patients in the control group (p = 0.226). There was no difference between HD patients and controls in the overall event rate (3.14 vs 3.31, p = 0.600), nor in the rates of ventricular arrhythmia subtypes (Table 1).Conclusions:There is no difference in ventricular arrhythmia burden between HD patients and controls monitored with CIEDs. Of HD patients experiencing ventricular arrhythmias, the vast majority are non-sustained events. These results support recent studies suggesting ventricular arrhythmias are unlikely to play a major role in SCD in ESRD patients on HD.

Background:P-wave indices (PWI) are electrocardiographic (ECG) markers of left atrial pathology. Recent community-based cohort studies have suggested that abnormal PWI are predictive of future ischemic strokes. However, it is unknown whether patients presenting with acute ischemic stroke in the clinical setting demonstrate abnormal PWI.Hypothesis:We hypothesized that PWI would be more abnormal in patients presenting with ischemic stroke than a comparable group without ischemic stroke.Methods:We retrospectively analyzed patients admitted with acute ischemic stroke (case) and patients followed in cardiology clinic (control) at a single tertiary care academic medical center. Patients with a history of prior stroke or atrial fibrillation were excluded. The first 12-lead ECG obtained on admission was used for cases and the most recent ECG available was used for controls. An ECG viewer program calculated the following PWI using lead V1: P-wave negative duration, P-wave negative amplitude (PNA), the product of the two (P terminal force, or PTF), and P-wave total duration. Logistic regression was performed to examine the association between continuous PWI and ischemic stroke.Results:A total of 288 patients (case n= 138, control n= 150) were included. The two groups were similar in baseline characteristics, though case patients were older (65.2 vs 61.1 years, p = 0.02) with a lower prevalence of obstructive sleep apnea (8.7% vs 28.7%, p = 0.001). In univariable analyses, only PNA was associated with ischemic stroke (OR for one-unit increase 1.01: [1.00, 1.02], p = 0.014). In multivariable analyses adjusting for age, sex, BMI, and hypertension, both PNA (OR 1.01: [1.00, 1.012, p = 0.009) and P-wave total duration (OR 1.01 [1.00, 1.02], p = 0.048) were associated with ischemic stroke. No associations were found with P-wave negative duration nor PTF.Conclusion:Patients who present with acute ischemic stroke have abnormalities in select PWI, namely PNA and P-wave total duration. These findings, derived from actual acute care presentations, support recent community-based cohort studies demonstrating an association between abnormal PWI and ischemic stroke. Larger clinical studies are necessary to evaluate the prognostic and predictive utility of PWI.

Introduction:We have recently shown that systemic arterial pulsatility index (SAPi = [systemic systolic pressure-systemic diastolic pressure]/pulmonary artery wedge pressure (PAWP) is associated with adverse outcomes in patients with systolic heart failure (HF)Hypothesis:SAPi, a metric of ventricular-arterial (VA) coupling would be associated with adverse outcomes in pulmonary arterial hypertension (PH)Methods:We evaluated SAPi in the National Institutes of Health PH registry for the association of 5-year probability of death using time to event analyses. We performed Cox proportional hazards regression and stratified Kaplan Meier analysis with evaluation of the log-rank statisticResults:Among 239 patients with complete data (mean age 36.1? 14.9 years, 62.2% female, mean pulmonary artery pressure was 61.1? 17.7 mmHg, the median SAPi was 5.7 (IQR 4.0-8.3). SAPi greater than median (5.7) was associated with better survival (HR 0.67, 95% CI 0.47-0.90, P=0.03) (Figure, top panel). SAPi as a continuous variable showed a trend for survival, P=0.06 (HR 0.96 per unit decrease in SAPi, 95% CI 0.933-1.002). SAPi was inversely correlated with RA pressure (r=-0.31, P<0.0001) and mean pulmonary arterial pressure (r=-0.14, P<0.0001). The association of SAPi with survival was dominated by the systemic pulse pressure (SPP) component, and SPP greater than median (45 mm Hg) was associated also with improved survival (HR 0.57, 95% CI 0.40-0.81, P=0.002) (Figure, lower panel)Conclusions:SAPi, a novel index of VA coupling, is associated with mortality in PH,but is mediated via a different mechanism to that previously reported in systolic HF. More studies are needed in the utility of SAPi as a prognostic tool in PH.

Introduction:Right ventricular (RV) failure is a determinant of mortality and symptom severity in pulmonary arterial hypertension (PAH). Pulmonary arterial elastance (PEa), calculated as pulmonary artery systolic pressure/stroke volume, is a marker of total RV afterload and reflects the resistive and pulsatile components of the arterial system. We have shown that higher PEa is associated with increased mortality but its impact on symptom severity is unknown.Hypothesis:We hypothesize that elevated PEa is associated with reduced exercise and functional capacity in patients with PAH.Methods:Using the National Institute of Health Primary PH (NIH-PPH) database, we evaluated the association of PEa with baseline functional status based on peak workload and NYHA classification. Multivariable linear regression and logistic regression models were used to determine these associations.Results:118 patients with complete variables were analyzed (median age 35 ? 16 years, 74.5% female, and 78.7% Caucasian). The median PEa was 1.76 mmHg/ml (IQR 1.42), median peak workload was 720 watts (IQR 469) and 52.5% had NYHA class 3 or 4 symptoms. In a multivariable linear regression model, one unit increase in PEa resulted in a 134.5 decrease in peak workload (95% CI 89.6, 179.0; p-value = .004). In a logistic regression model, increasing PEa, without adjustment, was associated with peak workload less than 720 (OR 3.10, 95% CI 1.8, 5.2; p-value < .0001) (Figure 1a). On multivariable adjustment, PEa remained an important predictor of peak workload < 720 (OR 3.56, 95% CI 1.15, 11.1; p-value = .01), with an AUC of .92 (Figure 1b). In a univariable logistic regression model, PEa predicted higher NYHA Class 3 or 4 symptoms, AUC of .69, p-value = .004, versus mean pulmonary artery pressure, AUC of .58, p-value = .43.Conclusions:PEa is independently associated with worsened functional and exercise capacity in PAH. Further studies are warranted to determine its utility in risk stratification in PAH.

Pulmonary arterial compliance (PAC), invasively assessed by the ratio of stroke volume to pulmonary arterial (PA) pulse pressure, is a sensitive marker of right ventricular (RV)-PA coupling that differs across the spectrum of pulmonary hypertension (PH) and is predictive of outcomes. We assessed whether the echocardiographically derived ratio of RV outflow tract velocity time integral to PA systolic pressure (RVOT-VTI/PASP) (a) correlates with invasive PAC, (b) discriminates heart failure with preserved ejection-associated PH (HFpEF-PH) from pulmonary arterial hypertension (PAH), and (c) is associated with functional capacity. We performed a retrospective cohort study of patients with PAH (n = 70) and HFpEF-PH (n = 86), which was further dichotomized by diastolic pressure gradient (DPG) into isolated post-capillary PH (DPG < 7 mmHg; Ipc-PH, n = 54), and combined post- and pre-capillary PH (DPG ≥ 7 mm Hg; Cpc-PH, n = 32). Of the 156 patients, 146 had measurable RVOT-VTI or PASP and were included in further analysis. RVOT-VTI/PASP correlated with invasive PAC overall (ρ = 0.61, P< 0.001) and for the PAH (ρ = 0.38, P= 0.002) and HFpEF-PH (ρ = 0.63, P< 0.001) groups individually. RVOT-VTI/PASP differed significantly across the PH spectrum (PAH: 0.13 [0.010–0.25] vs. Cpc-PH: 0.20 [0.12–0.25] vs. Ipc-PH: 0.35 [0.22–0.44]; P< 0.001), distinguished HFpEF-PH from PAH (AUC = 0.72, 95% CI = 0.63–0.81) and Cpc-PH from Ipc-PH (AUC = 0.78, 95% CI = 0.68–0.88), and remained independently predictive of 6-min walk distance after multivariate analysis (standardized β-coefficient = 27.7, 95% CI = 9.2–46.3; P= 0.004). Echocardiographic RVOT-VTI/PASP is a novel non-invasive metric of PAC that differs across the spectrum of PH. It distinguishes the degree of pre-capillary disease within HFpEF-PH and is predictive of functional capacity.

Upper airway obstruction is a potentially life-threatening emergency often encountered in the acute care, perioperative, and critical care settings. One important complication of acute obstruction is negative-pressure pulmonary edema (NPPE). We describe two cases of acute upper airway obstruction, both of which resulted in flash pulmonary edema complicated by acute hypoxic respiratory failure. Though NPPE was suspected, these patients were also found to have Takotsubo syndrome (TTS). Neither patient had prior cardiac disease, and both subsequently had a negative ischemic workup. Because TTS is a condition triggered by hyperadrenergic states, the acute airway obstruction alone or in combination with NPPE was the likely explanation for TTS in each case. These cases highlight the importance of also considering cardiogenic causes of pulmonary edema in the setting of upper airway obstruction, which we suspect generates a profound catecholamine surge and places patients at increased risk of TTS development.

Inferior vena cava (IVC) diameter and respirophasic variation are commonly used echocardiographic indices to estimate right atrial pressure. While dilatation of the IVC and reduced collapsibility have traditionally been associated with elevated right heart filling pressures, the significance of isolated IVC dilatation in the absence of raised filling pressures remains poorly understood. We present a case of an asymptomatic 28-year-old male incidentally found to have IVC dilatation, reduced inspiratory collapse, and normal right heart pressures.

IntroductionCongestive heart failure (CHF) is the most costly disease in the US. Readmission costs contribute significantly to this healthcare expenditure. While adherence to published guidelines has increased, readmission rates have not improved. There is an urgent need to identify clinical and process measures that improve care for CHF patients. Thirty day readmission rates have often been used by third party payers as a surrogate index for quality of care in the inpatients settings. This study looked at the relationship between preadmission patient characteristics and 30 day readmissions.