Impact of comorbid heart failure among hospitalized patients with sarcoidosis: A United States population-based cohort study.

Background: There is paucity of data regarding the impact of concomitant heart failure (HF) on the in-hospital outcomes among hospitalized sarcoidosis patients. We aim to investigate the factors associated with concomitant HF and its impact on in-hospital outcomes among hospitalized sarcoidosis patients. Methods: We utilized the 2018-2020 National Inpatient Sample (NIS) Database in conducting this study. Multivariable logistic and linear regression models were used to examine the factors associated with HF and hospital-associated outcomes among patients with sarcoidosis. Results: A total of 36,864 hospitalized patients with sarcoidosis were identified, of which 24.78 % (n = 9135/36,864) had concomitant HF. Factors associated with concomitant HF were age (aOR 1.03; 95 % CI: 1.02-1.03, p value ≤ 0.001), black race (aOR 1.74; 95 % CI: 1.47-2.05, p value ≤ 0.001), not being female (aOR 0.79; 95 % CI: 0.69-0.91, p value ≤ 0.001), and arrhythmias (aOR 2.50; 95 % CI: 2.10-2.98, p value ≤ 0.001) specifically atrial fibrillation and ventricular tachycardia. Comorbidities associated with concomitant HF in this population were hyperlipidemia, obesity, coronary artery disease, cardiac device implantation history, and chronic kidney disease stage 1-4. Concomitant HF was not an independent predictor of in-hospital mortality or length of stay (LOS). However, age (aOR 1.04; 95 % CI, 1.03-1.06; p ≤ 0.001) and arrhythmia burden (aOR 2.08; 95 % CI, 1.47-2.95; p ≤ 0.001), specifically ventricular tachycardia and fibrillation, were independently associated with in-hospital mortality among sarcoidosis patients. Conclusion: Traditional cardiovascular risk factors were associated with concomitant HF among hospitalized sarcoidosis patients. Moreover, concomitant HF among sarcoidosis patients was not significantly associated with in-hospital mortality or LOS.

Clinical characteristics and treatment of patients with central pulmonary embolism and right heart thrombus.

INTRODUCTION: Right heart thrombus (RHT), also known as clot in transit, is an uncommon finding in pulmonary embolism (PE) that is associated with increased inpatient mortality. To date, there is no consensus on the management of RHT. Therefore, we aim to describe the clinical features, treatments, and outcomes of patients with simultaneous RHT and PE. METHODS: This is a retrospective, cross-sectional, and single-center study of hospitalized patients with central PE who had RHT visualized on transthoracic echocardiography (TTE) from January 2012 to May 2022. We use descriptive statistics to describe their clinical features, treatments, and outcomes, including mechanical ventilation, major bleeding, inpatient mortality, length of hospital stay, and recurrent PE on follow-up. RESULTS: Of 433 patients with central PE who underwent TTE, nine patients (2%) had RHT. The median age was 63 years (range 29-87), most were African American (6/9), and females (5/9). All patients had evidence of RV dysfunction and received therapeutic anticoagulation. Eight patients received RHT-directed interventions, including systemic thrombolysis (2/9), catheter-directed suction embolectomy (4/9), and surgical embolectomy (2/9). Regarding outcomes, 4/9 patients were hemodynamically unstable, 8/9 were hypoxemic, and 2/9 were mechanically ventilated. The median length of hospital stay was six days (range 1-16). One patient died during hospital admission, and two patients had recurrent PE. CONCLUSION: We described the different therapeutic approaches and outcomes of patients with RHT treated in our institution. Our study adds valuable information to the literature, as there is no consensus on the treatment of RHT. HIGHLIGHTS: Right heart thrombus (RHT) was a rare finding in central pulmonary embolism. Most patients with RHT had evidence of RV dysfunction and pulmonary hypertension. Most patients received RHT-directed therapies in addition to therapeutic anticoagulation.

Cardiac Sarcoidosis With Elevated Cardiac Troponin Mimicking Acute Myocardial Ischemia: A Case Report.

Cardiac sarcoidosis (CS) is a disease entity with variable presentation causing significant morbidity and mortality. Concurrent signs of myocardial injury as evidenced by troponin elevation add to the complexity of an already challenging diagnosis. We present an unusual case of CS with elevated troponin I mimicking an acute ischemic cardiac event. A 48-year-old female presented with a two-month history of presyncope.  Electrocardiogram showed a bifascicular block with concomitant significant troponin I elevation. Two-dimensional echocardiography showed new-onset left ventricular systolic dysfunction with an ejection fraction of 40-45%. A heparin drip was initiated for possible non-ST-elevation myocardial infarction. Coronary angiography showed no evidence of epicardial coronary artery disease but did show an anomalous right coronary artery; however, CT angiography did not reveal any significant stenosis. Further, the telemetry monitor captured intermittent complete atrioventricular blocks. Due to concerns for an infiltrative cardiac disease, a cardiac magnetic resonance was done showing findings consistent with possible CS.  CT scan of the chest showed no radiographic evidence of pulmonary sarcoidosis. Fluorodeoxyglucose-positron emission tomography scan showed findings of active inflammation in the myocardium consistent with possible CS. The patient was treated for clinical CS with systemic corticosteroids and methotrexate. Follow-up six weeks later showed clinical improvement of symptoms. Our clinical case encompasses the unique variable presentation of CS including cardiac conduction abnormalities and left ventricular systolic dysfunction. Concomitant troponin I elevation can mimic myocardial ischemia, making the diagnosis more challenging. Treatment strategies aim to mitigate the long-term effects of CS on the heart; however, there is a paucity of data for appropriate pharmacological regimens.

Retrospective analyses of the outcomes among hospitalized liver cirrhosis patients with heart failure and COVID-19 infection: Insight from the National Inpatient Sample.

Background: There is paucity of data regarding the impact of Coronavirus Disease 2019 (COVID-19) infection on the outcomes of hospitalized liver cirrhosis (LC) patients with heart failure (HF). Methods: Utilizing the 2020 National Inpatient Sample (NIS) Database, we conducted a retrospective cohort study to investigate the outcomes of hospitalized LC patients with HF and COVID-19 infection, looking at its impact on in-hospital mortality, risk for acute kidney injury (AKI) and length of stay (LOS). Results: We identified a total of 10,810 hospitalized LC patients with HF, of which 1.39 % (n = 150/10,810) had COVID-19 infection. Using a stepwise survey multivariable logistic regression model that adjusted for patient and hospital level confounders, COVID-19 infection among hospitalized LC patients with HF was found to be an independent predictor of overall in-hospital mortality (aOR 3.73; 95 % CI, 1.58-8.79; p = 0.00) and risk for AKI (aOR 3.06; 95 % CI, 1.27-7.37; p = 0.01) compared to those without COVID-19 infection. However, there were comparable rates of LOS among LC patients with HF regardless of COVID-19 infection status. Moreover, AKI was found to be an independent predictor of longer LOS (coefficient 4.40, 95 % CI 3.26-5.38; p = 0.00). On subgroup analysis, diastolic HF was found to be associated with increased risk for in-hospital mortality (aOR 6.54; 95 % CI, 2.02-21.20; p = 0.00), development of AKI (aOR 3.33; 95 % CI, 1.12-9.91; p = 0.03) and longer LOS (coefficient 4.30, 95 % CI 0.79-9.45; p = 0.03). Conclusion: Concomitant COVID-19 infection among hospitalized LC patients with HF was associated with higher risk for in-hospital mortality and AKI but did not significantly affect hospital LOS.

Outcomes among ST-Elevation Myocardial Infarction (STEMI) patients with cardiogenic shock and COVID-19: A nationwide analysis.

Background: There is paucity of data regarding the characteristics and outcomes of patients admitted for ST Elevation Myocardial Infarction (STEMI) complicated by cardiogenic shock (CS) with concomitant Coronavirus Disease 2019 (COVID-19) infection. Methods: Using the National Inpatient Sample (NIS) Database for the year 2020, we conducted a retrospective cohort study to investigate the outcomes of patients who sustained STEMI-associated cardiogenic shock (STEMI-CS) with concomitant COVID-19 infection looking at its impact on in-hospital mortality and secondarily at the in-hospital procedure and intervention utilization rates as well as hospital length of stay. Results: We identified a total of 22,775 patients with STEMI-CS, of which 1.71 % (n = 390/22,775) had COVID-19 infection. Using a stepwise survey multivariable logistic regression model that adjusted for patient and hospital level confounders, concomitant COVID-19 infection among STEMI-CS patients was found to be an independent predictor of overall in-hospital mortality compared to those without COVID-19 (adjusted OR 2.10; 95 % confidence interval [CI], 1.30-3.40). STEMI-CS patients with concomitant COVID-19 infection had similar in-hospital utilization rates for percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG), extracorporeal membrane oxygenation (ECMO), percutaneous and durable left ventricular device, intra-arterial aortic balloon pump (IABP), renal replacement therapy (RRT), mechanical ventilation, as well as similar hospital lengths of stay. Conclusion: Concomitant COVID-19 infection was associated with higher in-hospital mortality rates among patients with cardiogenic shock related to STEMI but had similar in-hospital procedure and intervention utilization rates as well as hospital length of stay.

Primary Aldosteronism and Ischemic Heart Disease.

Cardiovascular disease, in particular ischemic heart disease is a major cause of morbidity and mortality worldwide. Primary aldosteronism is the leading cause of secondary hypertension, yet commonly under diagnosed, and represents a major preventable risk factor. In contrast to historical teaching, recent studies have shown that excess aldosterone production is associated with increased burden of ischemic heart disease disproportionate to the effects caused by hypertension alone. Aldosterone through its genomic and non-genomic actions exerts various detrimental cardiovascular changes contributing to this elevated risk. Recognition of primary hyperaldosteronism and understanding the distinctive pathophysiology of ischemic heart disease in primary aldosteronism is crucial to develop strategies to improve outcomes.

Use of direct oral anticoagulants in chronic thromboembolic pulmonary hypertension: a systematic review.

Direct oral anticoagulants (DOACs) are being increasingly used in patients with chronic thromboembolic hypertension (CTEPH), however, the data on their safety and efficacy are scarce and contradictory. We systematically searched MEDLINE and Google Scholar databases from January 2010 to January 2021 for studies of DOACs in CTEPH. Three observational studies, 2 abstracts and one case series met our inclusion criteria. While these studies reported similar or even less rates of major bleeding in patients receiving DOACs compared with vitamin K antagonists, there were concerns about the possibility of increased risk of venous thromboembolism recurrence with DOAC therapy. Further studies are warranted to better define the role of DOACs in CTEPH.

Prognostic Value of Left Ventricular Global Strain Analysis by Two-Dimensional Speckle-Tracking Echocardiography in Non-Hemodynamically Significant Intermediate Coronary Lesions.

Intermediate coronary lesions represent a major challenge for the invasive and noninvasive cardiologist. Left ventricular strain calculation by speckle tracking echocardiography has the capacity to analyze the motion of the cardiac tissue. This study aimed to evaluate its usefulness and prognostic significance in nonhemodynamically significant intermediate coronary lesions. We studied 247 patients who underwent a clinically indicated coronary angiogram. Each of the patients had a single nonrevascularized nonhemodynamically significant intermediate severity coronary lesion (ISCL) with a fractional flow reserve greater than 0.80. The left ventricular global longitudinal strain (GLS) was calculated using speckle-tracking echocardiography with TomTec 2D Cardiac Performance Analysis (Unterschleissheim, Germany). An abnormal GLS was defined as less than -20%. The primary endpoints were revascularization of the target lesion, admissions for major adverse cardiac events (MACE), and cardiac-related mortality, all within 2 years. On multivariate logistic regression data analysis, we found that patients with an ISCL and abnormal GLS had an increased risk for admissions due to MACE (odds ratio [OR] 1.06, P < 0.05, confidence interval [CI] 95%, 1.005-1.120], and an increased risk of cardiac-related death (OR 1.12, P < 0.05, CI 95% 1.012-1.275). There was no difference in the need for target lesion revascularization among individuals with normal and abnormal GLS (1.00, P 0.88, CI 95% .950-1.061). Left ventricular strain analysis by speckle-tracking echocardiography showed an independent prognostic value in patients with nonrevascularized nonhemodynamically significant coronary lesions.

The relationship between coronary artery disease and clinical outcomes in COVID-19: a single-center retrospective analysis.

INTRODUCTION: Recent studies have reported evidence that coronavirus disease 2019 (COVID-19) has disproportionately affected patients with underlying comorbidities. Our study aims to evaluate the impact of both cardiac and noncardiac comorbidities on a high-risk population with COVID-19 infection and coronary artery disease (CAD) compared to those without CAD. METHODS: This is a retrospective study of patients who tested COVID-19 positive via reverse transcriptase-PCR (RT-PCR) assay. We compared the characteristics and outcomes of patients with and without CAD. Population demographics, comorbidities and clinical outcomes were collected and analyzed. Multivariate logistic regression analysis was used to identify factors associated with inpatient mortality. RESULTS: A final sample population of 355 patients was identified, 77 of which had a known diagnosis of coronary artery disease. Our study population had a higher proportion of females, and those with CAD were significantly older. The rates of cardiovascular risk factors including hypertension, diabetes mellitus and chronic kidney disease, as well as heart failure and chronic obstructive pulmonary disease were significantly higher in the CAD population. Lactate dehydrogenase was the only inflammatory marker significantly lower in the CAD group, while troponin and brain natriuretic peptide were significantly higher in this population. Patients with CAD also had significantly higher inpatient mortality (31% vs 20%, P = 0.046) and need for renal replacement therapy (33% vs 11%, P < 0.0001) compared to the non-CAD group. However, only age [odds ratio 1.041 (1.017-1.066), P = 0.001] was significantly associated with mortality in the overall population after adjusting for demographics and comorbidities, while the presence of CAD was not independently associated with mortality. CONCLUSION: Patients with CAD and COVID-19 have higher rates of comorbidities, inpatient mortality and need for renal replacement therapy compared to their non-CAD counterparts. However, CAD in itself was not associated with mortality after adjusting for other covariates, suggesting that other factors may play a larger role in the increased mortality and poor outcomes in these patients.

Atrioventricular and Sinus Node Dysfunction in Stable COVID-19 Patients.

There are now well-documented cardiac complications of COVID-19 infection which include myocarditis, heart failure, and acute coronary syndrome resulting from coronary artery thrombosis or SARS-CoV-2-related plaque ruptures. There is growing evidence showing that arrhythmias are also one of the major complications. We report two patients with no known history of cardiac conduction disease who presented with COVID-19 symptoms, positive SARS-CoV-2 infection, and developed cardiac conduction abnormalities. Cardiac conduction system disease involving the sino-atrial (SA) node and atrioventricular (AV) node could be a manifestation of SARS-CoV-2 infection.

Polymorphic Ventricular Tachycardia with a Normal QTc Interval in a Patient with COVID-19 and Fever: Case Report.

Arrhythmias or conduction system disease are not the most common manifestation of COVID-19 infection in patients requiring hospital admission. Torsade de pointes typically occurs in bursts of self-limiting episodes with symptoms of dizziness and syncope. However, it may occasionally progress to ventricular fibrillation and sudden death. In this article, we report a case of COVID-19 patient who developed polymorphic ventricular tachycardia with torsade de pointes morphology with normal QTc interval in the setting of fever. An 81-year-old woman was admitted with symptoms of COVID-19. She was treated with hydroxychloroquine, azithromycin, and doxycycline at an outside facility and finished the treatment 5 days prior to admission to our facility. Her course was complicated by atrial fibrillation with rapid ventricular response requiring cardioversion. Later, she developed two episodes of polymorphic ventricular tachycardia with TdP morphology with normal QTc. There was a correlation with fever triggering the ventricular tachycardia. We advocated aggressive fever control given the QTc was normal and stable. Following fever control, the patient remained stable and had no abnormal rhythm. COVID-19 patients are prone to different arrhythmias including life-threatening ventricular arrhythmias with normal left ventricular systolic function and normal QTc, and they should be monitored for fever and electrolyte abnormality during their hospital stay.

Arrhythmia in COVID-19.

The current outbreak of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) also known as coronavirus disease 2019 (COVID-19) has quickly progressed to a global pandemic. There are well-documented cardiac complications of COVID-19 in patients with and without prior cardiovascular disease. The cardiac complications include myocarditis, heart failure, and acute coronary syndrome resulting from coronary artery thrombosis or SARS-CoV-2-related plaque ruptures. There is growing evidence showing that arrhythmias are also one of the major complications. Myocardial inflammation caused by viral infection leads to electrophysiological and structural remodeling as a possible mechanism for arrhythmia. This could also be the mechanism through which SARS-CoV-2 leads to different arrhythmias. In this review article, we discuss arrhythmia manifestations in COVID-19.

Association of frailty with all-cause mortality and bleeding among elderly patients with acute myocardial infarction: a systematic review and meta-analysis.

BACKGROUND: Frailty is a multidimensional syndrome that reflects the physiological reserve of elderly. It is related to unfavorable outcomes in various cardiovascular conditions. We conducted a systematic review and meta-analysis of the association of frailty with all-cause mortality and bleeding after acute myocardial infarction (AMI) in the elderly. METHODS: We comprehensively searched the databases of MEDLINE and EMBASE from inception to March 2019. The studies that reported mortality and bleeding in AMI patients who were evaluated and classified by frailty status were included. Data from each study were combined using the random-effects, generic inverse variance method of DerSimonian and Laird to calculate hazard ratio (HR), and 95% confidence interval (CI). RESULTS: Twenty-one studies from 2011 to 2019 were included in this meta-analysis involving 143,301 subjects (mean age 75.33-year-old, 60.0% male). Frailty status was evaluated using different methods such as Fried Frailty Index. Frailty was statistically associated with increased early mortality in nine studies (pooled HR = 2.07, 95% CI: 1.67-2.56, P < 0.001, I 2 = 41.2%) and late mortality in 11 studies (pooled HR = 2.30, 95% CI: 1.70-3.11, P < 0.001, I 2 = 65.8%). Moreover, frailty was also statistically associated with higher bleeding in 7 studies (pooled HR = 1.34, 95% CI: 1.12-1.59, P < 0.001, I 2 = 4.7%). CONCLUSION: Frailty is strongly and independently associated with bleeding, early and late mortality in elderly with AMI. Frailty assessment should be considered as an additional risk factor and used to guide toward personalized treatment strategies.

Myocardial injury and COVID-19: Possible mechanisms.

Coronavirus Disease 2019 (COVID-19) has quickly progressed to a global health emergency. Respiratory illness is the major cause of morbidity and mortality in these patients with the disease spectrum ranging from asymptomatic subclinical infection, to severe pneumonia progressing to acute respiratory distress syndrome. There is growing evidence describing pathophysiological resemblance of SARS-CoV-2 infection with other coronavirus infections such as Severe Acute Respiratory Syndrome coronavirus and Middle East Respiratory Syndrome coronavirus (MERS-CoV). Angiotensin Converting Enzyme-2 receptors play a pivotal role in the pathogenesis of the virus. Disruption of this receptor leads to cardiomyopathy, cardiac dysfunction, and heart failure. Patients with cardiovascular disease are more likely to be infected with SARS-CoV-2 and they are more likely to develop severe symptoms. Hypertension, arrhythmia, cardiomyopathy and coronary heart disease are amongst major cardiovascular disease comorbidities seen in severe cases of COVID-19. There is growing literature exploring cardiac involvement in SARS-CoV-2. Myocardial injury is one of the important pathogenic features of COVID-19. As a surrogate for myocardial injury, multiple studies have shown increased cardiac biomarkers mainly cardiac troponins I and T in the infected patients especially those with severe disease. Myocarditis is depicted as another cause of morbidity amongst COVID-19 patients. The exact mechanisms of how SARS-CoV-2 can cause myocardial injury are not clearly understood. The proposed mechanisms of myocardial injury are direct damage to the cardiomyocytes, systemic inflammation, myocardial interstitial fibrosis, interferon mediated immune response, exaggerated cytokine response by Type 1 and 2 helper T cells, in addition to coronary plaque destabilization, and hypoxia.

Wide unroofed coronary sinus and cryptogenic stroke: a case report.

BACKGROUND: Unroofed coronary sinus (UCS) is a rare congenital cardiac anomaly in which there is complete or partial absence of the roof of the coronary sinus (CS) resulting in a communication between the right and left atria. There are four types of UCS described in the literature. While usually asymptomatic and discovered incidentally on imaging, UCS can be the source of a brain abscess or paradoxical embolism. CASE SUMMARY: A 62-year-old gentleman presented to the emergency department with sudden onset of right-sided weakness and subsequent unresponsiveness. His brain computed tomography (CT) was consistent with left-sided stroke. Transthoracic echocardiography was remarkable for a dilated CS and an agitated saline study was suggestive of an UCS. A gated cardiac CT with coronary angiography confirmed a wide communication between the CS and left atrium. Right heart catheterization did not show evidence of left to right shunt. He had no abnormal rhythm on telemetry monitoring throughout his hospital stay. DISCUSSION: Unroofed coronary sinus is the least prevalent form of an atrial septal defect. Unroofed coronary sinus is usually asymptomatic and is diagnosed incidentally in imaging studies, however, it should be suspected in patients with cerebral emboli or evidence of left to right shunt with unexplained arterial desaturation. Transthoracic echocardiography is the most widely used imaging modality for the diagnosis of UCS but is limited in its ability to visualize the posterior cardiac structures such as the CS and pulmonary veins. Gated cardiac CT is a great diagnostic tool for UCS.

Transthyretin Cardiac Amyloidosis and Aortic Stenosis: Connection and Therapeutic Implications.

BACKGROUND: There is a growing interest in the observed significant incidence of transthyretin cardiac amyloidosis in elderly patients with aortic stenosis. Approximately, 16% of patients with severe aortic stenosis undergoing aortic valve replacement have transthyretin cardiac amyloidosis. Outcomes after aortic valve replacement appear to be worst in patients with concomitant transthyretin cardiac amyloidosis. METHODS: Publications in PubMed, Cochrane Library, and Embase databases were systematically searched from January 2012 to September 2018 using the keywords transthyretin, amyloidosis, and aortic stenosis. All studies published in English that reported the prevalence, association and outcomes of transthyretin cardiac amyloidosis in patients with aortic stenosis undergoing were included. RESULTS/CONCLUSION: The relationship between aortic stenosis and transthyretin cardiac amyloidosis is not well understood. A few studies have proven successful surgical management when both conditions coexist. This systematic review suggests that transthyretin cardiac amyloidosis is common in elderly patients with aortic stenosis and tend to have high mortality rates after AVR. The significant incidence of the two diseases occurring simultaneously warrants further investigation to improve management strategies in the future.

Trends and Outcomes of Atrial Fibrillation-Flutter Hospitalizations Among Heart Transplant Recipients (From the National Inpatient Sample).

Atrial fibrillation-flutter (AF) has been described in 10% to 24% of patients after heart transplant (HT). Data on AF hospitalizations after HT are limited to single-center experiences. To bridge this gap, we performed an analysis of admissions for AF in HT patients from the National Inpatient Sample (NIS) years 2000 to 2014. All hospitalizations with a primary diagnosis of 427.31 or 427.32 and V42.1 were used to identify hospitalizations with AF and previous HT respectively. Among a total of 211,961 HT related hospitalizations, 1,304 (0.62%) (955 males, 349 females, mean age 59 years, median CHA2DS2Vasc score 2 [Interquartile range 1 to 3]) were admitted with a primary diagnosis AF. Most hospitalizations were nonelective (80.17%). In-hospital mortality was 2.3% and the mean length of stay (LOS) was 3.7 days. Among those patients who were discharged from hospital, 85 % were discharged to home with self-care. Most commonly reported secondary diagnoses included hypertension (57.9%), diabetes (33%), renal failure (31.3%), and congestive heart failure (22%). The event rates for ischemic stroke and gastrointestinal bleeding in the same admission with the AF hospitalization were low (1.2% and 1.2% respectively). Cardioversion was performed in 37% and ablation in 11.2% of admissions. The adjusted median cost of hospitalization was $6478.7 (IQR $3561.8 to $12352.3) and did not change significantly during the study period. AF is a relatively infrequent cause of hospitalization among HT recipients. The number of hospitalizations, ablations, cardioversions, disposition, LOS, and cost of hospitalization for AF remained stable during the study period.

Renal implications of pulmonary arterial capacitance in acute heart failure with preserved ejection fraction.

Worsening renal function in patients with heart failure with preserved ejection fraction is associated with poor outcomes. Pulmonary arterial capacitance is a novel right heart catheterization derived hemodynamic metric representing pulmonary arterial tree distensibility and right ventricle afterload. Given the strong association between heart failure, pulmonary hypertension, and kidney function, the goal of this study is to investigate the correlation between Pulmonary arterial capacitance and long-term renal function in patients with heart failure with preserved ejection fraction. In this retrospective single center study, data from 951 patients with the diagnosis of heart failure, who underwent right heart catheterization were analyzed. Eight hundred and one patients with reduced ejection fraction, end-stage kidney disease on hemodialysis, acute myocardial infarction, and severe structural valvular disorders, were excluded. Pulmonary arterial capacitance was calculated as the stroke volume divided by pulmonary artery pulse pressure (mL/mmHg). Hemodynamic and clinical variables including baseline renal function were obtained at the time of the right heart catheterization, and renal function was also obtained at 3-5 years after right heart catheterization. The final cohort consisted of 150 subjects with a mean age 68 ( ± 14.2) years, 93 (62%) were female. The mean value for Pulmonary arterial capacitance was 2.82 ( ± 2.22) mL/mm Hg and the mean Glomerular Filtration Rate was 60.32 mL/min/l.73 m² ( ± 28.36). After multivariate linear regression analysis (including baseline Estimated Glomerular Filtration Rate as one of the variates), only age and Pulmonary arterial capacitance greater than 2.22 mL/mm Hg were predictors of long term Glomerular Filtration Rate. Pulmonary arterial capacitance as a novel right heart catheterization index could be a predictor of long-term renal function in patients with heart failure with preserved ejection fraction.

Trends, etiologies, and predictors of 90-day readmission after percutaneous ventricular assist device implantation: A national population-based cohort study.

Percutaneous ventricular assist devices (pVADs) are indicated to provide hemodynamic support in high-risk percutaneous interventions and cardiogenic shock. However, there is a paucity of published data regarding the etiologies and predictors of 90-day readmissions following pVAD use. We studied the data from the US Nationwide Readmissions Database (NRD) for the years 2013 and 2014. Patients with a primary discharge diagnosis of pVAD use were collected by searching the database for International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) procedural code 37.68 (Impella and TandemHeart devices). Amongst this group, we examined 90-day readmission rates. Comorbidities as identified by "CM_" variables provided by the NRD were also extracted. The Charlson Comorbidity Index was calculated using appropriate ICD-9-CM codes, as a secondary diagnosis. A 2-level hierarchical logistic regression model was then used to identify predictors of 90-day readmission following pVAD use. Records from 7074 patients requiring pVAD support during hospitalization showed that 1562 (22%) patients were readmitted within 90 days. Acute decompensated heart failure (22.6%) and acute coronary syndromes (11.2%) were the most common etiologies and heart failure (odds ratio [OR]: 1.39, 95% confidence interval [CI]: 1.17-1.67), chronic obstructive pulmonary disease (OR: 1.26, 95% CI: 1.07-1.49), peripheral vascular disease (OR: 1.305, 95% CI: 1.09-1.56), and discharge into short- or long-term facility (OR: 1.28, 95% CI: 1.08-1.51) were independently associated with an increased risk of 90-day readmission following pVAD use. This study identifies important etiologies and predictors of short-term readmission in this high-risk patient group that can be used for risk stratification, optimizing discharge, and healthcare transition decisions.

Transient Ischemic Dilation Ratio in Regadenoson, Single Isotope Gated Single-photon Emission Computed Tomography Myocardial Perfusion Imaging.

Single isotope 99mTc single-photon emission computed tomography-myocardial perfusion imaging (SPECT-MPI) is the most commonly used protocol for nuclear stress testing. Transient ischemic dilation of the left ventricle (TID) has been considered a specific marker of severe coronary artery disease (CAD). Recent publications have questioned the clinical utility of TID, specifically with regadenoson as a stressor and 4DM-SPECT software for TID analysis. These findings have not been demonstrated using other imaging packages. The goal of our study was to establish the TID threshold in the identification of Multi-vessel CAD using Quantitative Perfusion SPECT (QPS) software. Included in this study are 190 patients that had undergone regadenoson-stress, same day, single-isotope 99mTc MPI and had a coronary angiography within a designated 3-month period. QPS (Cedars-Sinai, LA, CA) automated image analysis software was used to calculate TID ratios which were compared across different CAD categories. Coronary angiograms were reviewed to identify both obstructive and nonobstructive CAD. The mean TID for patients with nonobstructive CAD (n = 91) was 1.02 ± 0.11, and the threshold for TID was 1.24. A receiver operating characteristic curve showed that TID had a poor discriminatory capacity to identify MVD (area under the curve 0.58) with a sensitivity of 3% and a specificity of 97%. In our study with regadenoson MPI in a predominantly African-American population, TID was found to be a poor predictor of MVD using QPS software. The reason is unclear but possibly related to the significant decline in the prevalence of severe CAD in the area where our study took place.