30-day readmission following urgent and elective transcatheter aortic valve replacement: A Nationwide Readmission Database analysis.

BACKGROUND: Transcatheter aortic valve replacement (TAVR) is being increasingly used for decompensated severe symptomatic aortic stenosis. Data on urgent and elective TAVR readmission is scarce in the literature. Here, we have performed a retrospective cohort study with the Nationwide Readmission Database of 2016 to identify the rate of 30-day all-cause readmission, common causes of readmission, and distribution of morbidity in index admission and readmission after urgent and elective TAVR. METHODS: We used International Classification of Diseases, Tenth Revision codes (02R.F38H, 02R.F38Z, 02R.F48Z) for identification of all TAVR procedures done in 2016 in patients >18 years old. We found 8379 patients who underwent urgent TAVR and 32,006 patients who underwent elective TAVR in 2016. RESULT: The mean age of patients undergoing urgent TAVR was 79 ± 9.97 years with 44.6% women. The mean age of patients undergoing elective TAVR was 80.7 ± 8.25 years with 46.2% women. We found the 30-day all-cause readmission rate of 15.5% and 9.5% in patients undergoing urgent and elective TAVR, respectively (p < 0.001). The cardiac cause was the predominant cause of readmission in both groups (43.77% vs. 42.11%, p = 0.57), followed by pulmonary cause, gastrointestinal (GI) cause, and renal cause. Among cardiac causes, congestive heart failure (CHF) was predominant cause of readmission and was similar in both groups (18.73 in urgent TAVR vs. 15.73 in elective TAVR, p = 0.12). CONCLUSION: We found that the all-cause 30-day readmission rate was higher in patients who had undergone urgent TAVR. Further studies are needed to better understand this difference.

Advances in the Pharmacogenomics of Antiplatelet Therapy.

BACKGROUND: Acute coronary syndrome (ACS) is a highly thrombotic state, and a sustained antiplatelet effect is vital to the prevention of thrombotic complications. Clopidogrel, the most widely used oral P2Y12 receptor antagonist in ACS, has attracted considerable attention because of significant variability in antiplatelet effect depending on the presence of CYP2C19 allele. Other P2Y12 receptor antagonists offer sustained and more predictable antiplatelet effects than clopidogrel albeit at an increased cost. Several studies have demonstrated the promising application of pharmacogenetics in choosing personalized antiplatelet therapy using the point-of-care genotype assays. AREAS OF UNCERTAINTY: Guidelines regarding the genotype-guided approach to the selection of antiplatelet therapy have been conflicting, and studies evaluating the effect of pharmacogenetic-guided selection of antiplatelet therapy on the outcomes have demonstrated mixed results. DATA SOURCES: A literature search was conducted using MEDLINE and EMBASE for studies reporting the association of pharmacogenetic-guided selection of antiplatelet therapy and the outcomes in patients with ACS until December 2018. RESULTS: Presence of specific CYP2C19 allele significantly influences clopidogrel metabolism and associated outcomes in patients with ACS. Thrombotic and bleeding complications are more common in patients with loss-of-function (LOF) and gain-of-function (GOF) alleles, respectively. Although the pharmacogenetic-guided approach to the selection of antiplatelet therapy appears promising in ACS, studies have shown conflicting results, and direct randomized evidence linking this approach with the better outcomes is lacking. CONCLUSIONS: Genotype-guided selection of antiplatelet therapy is expected to be useful in patients undergoing percutaneous coronary intervention (PCI) with a high risk of adverse outcomes. The patient-physician discussion should be an essential part of this decision-making process. Large-scale multicenter randomized controlled trials using the point-of-care genotype assay are needed to investigate this approach further before its use can be recommended in all comers.

Combined Neprilysin and RAS Inhibition in Cardiovascular Diseases: A Review of Clinical Studies.

The aim of this comprehensive review article is to emphasize on the possible exploration of a new therapeutic approach in the management of heart failure (HF) and other cardiovascular diseases: the renin-angiotensin-aldosterone system-neprilysin combination inhibitors, also called angiotensin receptor neprilysin inhibitor, valsartan/sacubitril (LCZ696). Sacubitril is an inhibitor of neutral endopeptidase (NEP) which degrades vasoactive peptides such as atrial natriuretic peptide and brain natriuretic peptide. Valsartan is an angiotensin receptor blocker which is usually used in hypertension. Although HF has been a global health burden, for decades there has been lack of novel therapeutic options as many trials failed due to potential side effects. With the published results of the landmark trial Prospective comparison of ARNI with ACEI to Determine the Impact on Global Mortality and morbidity in HF (PARADIGM-HF), a new direction in the treatment of HF is anticipated. This trial showed that LCZ696 was able to reduce the primary composite end point of cardiovascular death or HF hospitalization, and similar reduction was observed for cardiovascular death. This review article also highlights the results of 4 published trials of LCZ696 in both HTN and HF. After the results of PARADIGM-HF trial, the major challenge will be outcome in regular clinical practice, as subjects in the trial were mostly stable New York Heart Association class II patients with no comorbidities. In addition, many trials are simultaneously in progress regarding the use of LCZ696 in patients with diabetes, renal failure, and hepatic impairment. To conclude, sacubitril/valsartan significantly improved morbidity and mortality in patients with chronic HF, but it will need meticulous attention when used in real outpatient practice.

Relationship between chronic intermittent hypoxia and intraoperative mean arterial pressure in obstructive sleep apnea patients having laparoscopic bariatric surgery.

BACKGROUND: Recurrent nocturnal hypoxemia in obstructive sleep apnea enhances sympathetic function, decreases baroreceptor sensitivity, and weakens peripheral vascular responses to adrenergic signals. The authors hypothesized that the percentage of total sleep time spent at oxyhemoglobin saturation (SaO2) less than 90% and minimum nocturnal SaO2 on preoperative polysomnography are associated with decreased intraoperative mean arterial pressure. METHODS: The authors examined the records of all patients who had laparoscopic bariatric surgery at Cleveland Clinic between 2005 and 2009 and an available polysomnography study. The authors assessed the relationships between the percentage of total sleep time spent at SaO2 less than 90% and minimum nocturnal SaO2, and the time-weighted average of mean arterial pressure. The authors used multivariable regression models to adjust for prespecified clinical confounders. RESULTS: Two hundred eighty-one patients were included in the analysis. The average change in the time-weighted average of mean arterial pressure was -0.02 (97.5% CI, -0.08, 0.04) mmHg for each 1% absolute increase in the percentage of sleep time spent at SaO2 less than 90% (P = 0.50). The average change was -0.13 (97.5% CI, -0.27, 0.01) mmHg, for each 1% absolute decrease in the minimum SaO2 (P = 0.04 > significance criterion of 0.025, Bonferroni correction). An unplanned analysis estimated 1% absolute decrease in minimum SaO2 was associated with -0.22 (98.75% CI, -0.39, -0.04) mmHg, change in mean arterial pressure (P = 0.002) in the time period between endotracheal intubation and trocar insertion. CONCLUSION: Recurrent nocturnal hypoxemia in obstructive sleep apnea is not a risk marker for intraoperative hypotension.

The 2-year cost-effectiveness of 3 options to treat lumbar spinal stenosis patients.

Lumbar spinal stenosis (LSS) may result from degenerative changes of the spine, which lead to neural ischemia, neurogenic claudication, and a significant decrease in quality of life. Treatments for LSS range from conservative management including epidural steroid injections (ESI) to laminectomy surgery. Treatments vary greatly in cost and success. ESI is the least costly treatment may be successful for early stages of LSS but often must be repeated frequently. Laminectomy surgery is more costly and has higher complication rates. Minimally invasive lumbar decompression (mild(®) ) is an alternative. Using a decision-analytic model from the Medicare perspective, a cost-effectiveness analysis was performed comparing mild(®) to ESI or laminectomy surgery. The analysis population included patients with LSS who have moderate to severe symptoms and have failed conservative therapy. Costs included initial procedure, complications, and repeat/revision or alternate procedure after failure. Effects measured as change in quality-adjusted life years (QALY) from preprocedure to 2 years postprocedure. Incremental cost-effectiveness ratios were determined, and sensitivity analysis conducted. The mild(®) strategy appears to be the most cost-effective ($43,760/QALY), with ESI the next best alternative at an additional $37,758/QALY. Laminectomy surgery was the least cost-effective ($125,985/QALY).

Comparison of three techniques for ultrasound-guided femoral nerve catheter insertion: a randomized, blinded trial.

BACKGROUND: Ultrasound guidance for continuous femoral perineural catheters may be supplemented by electrical stimulation through a needle or through a stimulating catheter. The authors tested the primary hypothesis that ultrasound guidance alone is noninferior on both postoperative pain scores and opioid requirement and superior on at least one of the two. Second, the authors compared all interventions on insertion time and incremental cost. METHODS: Patients having knee arthroplasty with femoral nerve catheters were randomly assigned to catheter insertion guided by: (1) ultrasound alone (n = 147); (2) ultrasound and electrical stimulation through the needle (n = 152); or (3) ultrasound and electrical stimulation through both the needle and catheter (n = 138). Noninferiority between any two interventions was defined for pain as not more than 0.5 points worse on a 0 to 10 verbal response scale and for opioid consumption as not more than 25% greater than the mean. RESULTS: The stimulating needle group was significantly noninferior to the stimulating catheter group (difference [95% CI] in mean verbal response scale pain score [stimulating needle vs. stimulating catheter] of -0.16 [-0.61 to 0.29], P < 0.001; percentage difference in mean IV morphine equivalent dose of -5% [-25 to 21%], P = 0.002) and to ultrasound-only group (difference in mean verbal response scale pain score of -0.28 [-0.72 to 0.16], P < 0.001; percentage difference in mean IV morphine equivalent dose of -2% [-22 to 25%], P = 0.006). In addition, the use of ultrasound alone for femoral nerve catheter insertion was faster and cheaper than the other two methods. CONCLUSION: Ultrasound guidance alone without adding either stimulating needle or needle/catheter combination thus seems to be the best approach to femoral perineural catheters.

Unraveling the interaction between a glycolytic regulator protein EhPpdk and an anaphase promoting complex protein EhApc10: yeast two hybrid screening, in vitro binding assays and molecular simulation study.

The anaphase promoting complex (APC or cyclosome) is a major ubiquitin ligase that coordinates mitotic and G1 progression, acting as a major regulator of chromosome segregation. While the human APC contains fourteen subunits, it is yet to be explored in the pathogen Entamoeba histolytica. Our study reveals the existence of a single functional Apc10 homolog in E. histolytica, which acts as a processivity factor of ubiquitin ligase activity in human. A cDNA library generated from HM1:IMSS strain of E. histolytica was screened for interaction partners of EhApc10 in yeast two hybrid study. The novel interactor, a glycolytic enzyme, pyruvate phosphate dikinase (Ppdk) was found to interact with EhApc10 and further validated by in vitro assay. A comprehensive in silico study has emphasized the structural and functional aspects, encompassing physicochemical traits, predictive 3D structure modelling, validation of EhApc10-EhPpdk interaction through molecular docking and simulation. The interplay between a cell cycle protein and a glycolytic enzyme highlights the connection between cellular metabolism and the cell cycle regulatory mechanism. The study serves as the groundwork for future research on the non-mitotic role of APC beyond cell cycle.

EhSir2c, a Sir2 homolog from the human pathogen Entamoeba histolytica interacts with a DNA repair protein, EhRAD23: Protein-protein interaction, docking and functional study.

Chromosome segregation is a crucial phenomenon in the cell cycle and defects in genome segregation result in an abnormality in various cellular events. Unlike higher eukaryotes, chromosome segregation and a number of cell cycle events are unusual in the protozoan parasite Entamoeba histolytica (E. histolytica). Characterization of Sir2 proteins from E. histolytica may reveal its unique cellular events as they play role in diverse cellular processes including chromosome segregation. E. histolytica has four homologs of Sir2 proteins. EhSir2a and EhSir2b show sequence similarity towards eukaryotic Sir2 homologs, whereas EhSir2c and EhSir2d are more like prokaryotic sirtuins. Using both computational and experimental methods, EhSir2c has been characterized in this study. The three-dimensional structure of EhSir2c is predicted by homology modelling. The protein interactors of EhSir2c have been identified by yeast-two-hybrid screening against the cDNA library of E. histolytica. We have identified a novel interactor, EhRAD23 which is a homolog of UV excision repair protein RAD23. The interaction of EhSir2c and EhRAD23 was validated by pull-down assay. UV-C irradiation up-regulates the relative expression of EhSir2c, suggesting the necessity of EhSir2c in UV-induced stress in this parasite.Communicated by Ramaswamy H. Sarma.

The Emerging Role of FDG PET/CT in Diagnosing Endocarditis and Cardiac Device Infection.

Infective endocarditis and cardiac implantable electronic device infection (CIEDI) have witnessed an increasing incidence in clinical practice and associated with increasing health care expenditure. Expanding indications of CIED in various cardiovascular conditions have also contributed to the surge of these infections. Early diagnosis of these infections is associated with a favorable prognosis. Given the lack of a single definitive diagnostic method and the limitations of echocardiography, which is considered a central diagnostic imaging modality, additional imaging modalities are required. Recent studies have highlighted the diagnostic utility of FDG PET and CT. In this review article, we discuss the existing limitations of echocardiography, acquisition protocols of PET/CT, and indications of these advanced imaging modalities in infective endocarditis and CIEDI diagnosis.

In silico analysis of a Skp1 protein homolog from the human pathogen E. histolytica.

SCF complex consisting of Skp1, Cullins, F-box proteins, is the largest family of E3 ubiquitin ligases that promotes ubiquitination of many substrate proteins and controls numerous cellular processes. Skp1 is an adapter protein that binds directly to the F-box proteins. In this study, we have presented the first comprehensive analysis of the presence of peptides or proteins in the human pathogen Entamoeba histolytica having homology to Skp1protein. The occurrence of other protein components of the SCF complex has been identified from protein-protein interaction network of EhSkp1A. Studying the role of Skp1protein in this pathogen would help to understand its unique chromosome segregation and cell division which are different from higher eukaryotes. Further, owing to the development of resistance over several drugs that are currently available, there is a growing need for a novel drug against E. histolytica. Proteins from ubiquitin-proteasome pathway have received attention as potential drug targets in other parasites. We have identified four homologs of Skp1 protein in E. histolytica strain HM-1: IMSS. Molecular docking study between EhSkp1A and an F-box/WD domain-containing protein (EhFBXW) shows that the F-box domain in the N-terminal region of EhFBXW interacts with EhSkp1A. Therefore, the results of the present study shall provide a stable foundation for further research on the cell cycle regulation of E. histolytica and this will help researchers to develop new drugs against this parasite. Supplementary Information: The online version contains supplementary material available at 10.1007/s12639-022-01523-0.

Bempedoic acid and its role in contemporary management of hyperlipidemia in atherosclerosis.

Atherosclerotic heart disease is the leading cause of mortality and morbidity in the USA. Low density lipoprotein (LDL) has been the target for many hypolipidemic agents to modify atherosclerotic risk. Bempedoic acid is a novel hypolipidemic drug that inhibits the enzymatic activity of ATP citrate lyase in the cholesterol synthesis pathway. CLEAR Harmony, CLEAR Wisdom, CLEAR Tranquillity and CLEAR Serenity have shown safety and efficacy associated with long term administration of this drug. Studies have shown effectiveness in reducing LDL-C in both statin intolerant patients and in patients on maximally tolerated doses of statin. The fixed drug combination of bempedoic acid and ezetimibe in a recent phase III showed significant reduction in LDL compared with placebo, which might be a promising future for LDL reduction among statin intolerant patients. Bempedoic acid also reduced inflammatory markers like hs-CRP. Given these results, bempedoic acid alone and in combination with ezetimibe received the USA FDA approval for adults with heterozygous familial hypercholesterolaemia or established atherosclerotic cardiovascular disease. We present a comprehensive review exploring the underlying mechanism, pre-clinical studies, and clinical trials of bempedoic acid and discuss the potential future role of the drug in treating hyperlipidaemia.

A Brief Overview of Recurrent Pericarditis Management and the Potential of Rilonacept as a New Therapeutic Option.

Recurrent pericarditis affects 15-30% of patients after acute pericarditis. A large number of the patients with recurrent pericarditis can become corticosteroid dependent, leading to disease chronicity and drug dependence, with additional morbidity from long-term steroid use. Recent randomized trials indicate the efficacy of the interleukin-1 inhibitors anakinra and rilonacept in recurrent pericarditis, including colchicine-resistant and corticosteroid-dependent cases. In particular, rilonacept was assessed in the RHAPSODY clinical trial and found to be a potential treatment option that would decrease recurrent episodes, enabling patients to be weaned off steroids. Additionally, new data indicate that rilonacept should be considered as an option for patients with recurrent pericarditis, as add-on therapy to colchicine and nonsteroidal anti-inflammatory drugs, in place of steroids. We review the current management options for recurrent pericarditis as well as rilonacept as a prospective new addition to our armamentarium.

Eosinophilic Myocarditis: When Allergies Attack the Heart!

Eosinophilic myocarditis is a clinical condition whereby myocardial injury is mediated by eosinophilic infiltration. A number of underlying causes, including reactive, clonal, or idiopathic hypereosinophilic syndrome, may trigger eosinophilia. Disease presentation may vary from mild subclinical variants to fulminant myocarditis with thromboembolic complications, and in some cases, endomyocardial and valvular fibrosis may be seen. A detailed examination coupled with the use of multimodality imaging, and endomyocardial biopsy may help establish diagnosis. Treatment is aimed at symptomatic management and treating the underlying cause of eosinophilia, such as withdrawal of implicated drugs, antihelminthic therapy for infection, immunosuppression for autoimmune conditions, and targeted therapy with tyrosine kinase inhibitors in cases with clonal myeloid disorders.

In silico analysis and molecular identification of an anaphase-promoting complex homologue from human pathogen Entamoeba histolytica.

BACKGROUND: Amoebiasis, being endemic worldwide, is the second leading cause of parasite-associated morbidity and mortality after malaria. The human parasite Entamoeba histolytica is responsible for the disease. Metronidazole is considered as the gold standard for the treatment of amoebiasis, but this antibiotic is carcinogenic and the development of antibiotic resistance against E. histolytica is a major health concern. Chromosome segregation is irregular in this parasite due to the absence of a few cell cycle checkpoint proteins. Anaphase-promoting complex (APC/C or cyclosome) is an E3 ubiquitin ligase that synchronizes chromosome segregation and anaphase progression via the ubiquitin-proteasome system. Proteasome is considered to be an attractive drug target for protozoan parasites. For the present study, EhApc11 from E. histolytica, a homologue of Apc11 in humans, is selected for elucidating its structural and functional aspects by detailed in silico analysis and molecular methods. Its physicochemical characteristics, identification of probable interactors, 3D model and quality analysis are done using standard bioinformatics tools. cDNA sequence of EhAPC11 has been further cloned for molecular characterization. RESULT: Conserved domain analysis revealed that EhApc11 belongs to the RING (really interesting new gene) superfamily and has ligand binding capacity. Expression study in Escherichia coli BL21 (DE3) revealed that the molecular weight of glutathione S-transferase (GST)-tagged protein is ~ 36 kDa. CONCLUSION: EhApc11 is a hydrophilic, thermostable, extracellular protein with potent antigenicity. The study will serve as a groundwork for future in-depth analysis regarding the validation of protein-protein interaction of EhApc11 with its substrates identified by STRING analysis and the potential of EhApc11 to serve as an anti-amoebic drug target.

Transformation of CuS/ZnS nanomaterials to an efficient visible light photocatalyst by 'photosensitizer' graphene and the potential antimicrobial activities of the nanocomposites.

We report the growth of CuS/ZnS (CZS) nanoparticles (NPs) on the graphene sheet by a facile green synthesis process. The CuS/ZnS-graphene (CZSG) nanocomposites exhibit enhanced visible light photocatalytic activity towards organic dye (methylene blue) degradation than that of CZS nanoparticles. To find the reason for the enhanced photo-activity, we propose a new photocatalytic mechanism where graphene in the CZSG nanocomposites acts as a 'photosensitizer' for CZS nanoparticles. This distinctive photocatalytic mechanism is noticeably different from all other previous research works on semiconductor-graphene hybrid photocatalysts where graphene behaves as an electron reservoir to capture the electrons from photo-excited semiconductor. This novel idea of the photocatalytic mechanism in semiconductor-graphene photocatalysts could draw a new track in thinking for designing of graphene-based photocatalysts for solving environmental pollution problems and they also show remarkable antimicrobial activities.

The Role of Dapagliflozin in the Management of Heart Failure: An Update on the Emerging Evidence.

The burden and cost of heart failure management, primarily in the form of hospitalization in the setting of decompensated heart failure, continue to be some of the biggest clinical challenges in cardiovascular medicine. In recently published randomized controlled trials, including DAPA-HF, sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin was shown to reduce hospitalization from heart failure or mortality associated with cardiovascular causes, when added to existing guideline-directed medical therapy. The American College of Cardiology (ACC) released a Clinical Pathway guideline that recommends the use of dapagliflozin in clinical management of heart failure, with or without diabetes. Furthermore, the results of the DAPA-CKD trial broaden the utility of dapagliflozin as a therapeutic option in patients with advanced kidney disease. In this article, the authors explore the existing evidence on dapagliflozin in heart failure with reduced ejection fraction and highlight the need for further research on uses of dapagliflozin in the world of heart failure.

Contemporary narrative review on left atrial strain mechanics in echocardiography: cardiomyopathy, valvular heart disease and beyond.

Left atrial (LA) strain mechanics refer to the measurement of LA myocardial deformation expressed as a percentage, and have been gathering interest over the last decade with expanding research supporting their utility in multiple cardiovascular disorders. Measured through advanced dynamic imaging techniques which include tissue Doppler imaging (TDI) and two-dimensional (2D) speckle tracking echocardiography (STE), LA strain mechanics are affected by left ventricular diastolic dysfunction prior to the onset of functional and structural changes in the left ventricle (LV). There is a need for practising cardiologists to become more familiar with the clinical utility of LA strain mechanics. In this article, we begin by reviewing the physiologic function of the LA, using this as a basis for understanding LA strain mechanics. The focus of this review article is to provide a contemporary update on the utility of LA strain mechanics in a range of cardiovascular disorders, including atrial fibrillation (AF), hypertrophic cardiomyopathy (HCM), valvular pathologies, coronary artery disease (CAD) as well as systemic diseases, such as hypertension (HTN), obesity and diabetes mellitus (DM). This article also highlights the current limitations in more widespread clinical applications of LA strain mechanics, as well as outlining the future perspectives on the clinical applications of LA strain mechanics.

Serum Bilirubin and Coronary Artery Disease: Intricate Relationship, Pathophysiology, and Recent Evidence.

Coronary artery disease (CAD) is a major cause of morbidity, mortality, and healthcare expenditure. A number of environmental and genetic risk factors have been known to contribute to CAD. More recently, a number of studies have supported as well as opposed a possible protective benefit of bilirubin in CAD, since it has anti-inflammatory, antioxidant, and antiaggregatory properties that may reduce atherogenesis. It also shares associations with different forms of CAD, namely stable CAD, unstable angina pectoris, stable angina pectoris, and acute myocardial infarction. Lack of sufficient evidence, however, has failed to elucidate a causal relationship between serum bilirubin level and risk of CAD. Therefore, in this update, we attempted to simplify this intricate relationship between bilirubin and CAD, revisit the pathophysiology of disease, how bilirubin may be protective, and to summarize the findings of the current literature.

Does Insurance Effect the Outcome in Patients With Acute Coronary Syndrome?: An Insight from the Most Recent National Inpatient Sample.

Several studies have shown disparities in outcome in the patients with Acute coronary syndrome (ACS) based on several factors. Treatment might differ based on insurance type. Therefore, we retrospectively analyzed National Inpatient Sample (NIS 2016) data to identify the impact of different types of insurances on mortality outcome in patients admitted with ACS. ICD-CM-10 codes were used to identify hospital discharges with a principal diagnosis of ACS. Observations were stratified based on insurance (Medicare, Medicaid, Private, and No insurance). Primary and secondary outcomes were in-hospital mortality, length of stay and total cost. Any potential confounders were adjusted using multivariate logistic regression. STATA/IC 15.1 Stata Corp LLC was used for analysis. A total of 8,01,195 hospitalizations with the primary diagnosis of ACS were identified, of which 59.2% had Medicare, 9.72% had Medicaid, 26.8% had Private insurance, and 4.3% had no insurance. Higher odds of mortality were seen in the patients with Medicare, Medicaid, and Noninsured group. Adjusted Odds ratio for mortality in Medicare was 1.01 (confidence interval [CI]: 0.94-1.1; P = 0.65), in Medicaid was 1.16 (CI: 1.03-1.30; P = 0.01) and in uninsured group was 1.46 (CI: 1.26-1.69; P ≤ 0.01). However, the patients with private insurance adjusted odds ratio for mortality were 0.77 (CI: 0.70-0.84; P ≤ 0.01) compared to the patients with other insurance groups. Above results show that the disparity exists in the outcome of patients admitted with ACS based on their insurance types, particularly for Medicaid patients. We need further studies to understand the root cause of this disparity.

Anticoagulation in Pulmonary Arterial Hypertension: Do We Know the Answer?

The shear stress and hypoxia in the pulmonary artery in patients with pulmonary arterial hypertension(PAH) causes endothelial dysfunction, smooth muscle proliferation and activation of thrombotic pathways leading to in situ thrombosis. Targeting the thrombotic pathways is a proposed mechanism to slow disease progression and improve survival. Over the years, the survival in patients with PAH has improved due to multiple factors with the increased use of anticoagulation as one of them. Both European Respiratory Society/European Society of Cardiology and American College of Cardiology/American Heart Association guidelines make grade II recommendations for using anticoagulation in PAH. The guidelines are based on weak observational studies with high risk of bias which have only studied warfarin as the choice of anticoagulation. In this article, we review the pathophysiology, rationale and the current literature investigating the role of anticoagulation in PAH.