Strategy For Treatment Of Heart Failure Research Articles

Pharmacotherapeutic management of paediatric heart failure and ACE-I use patterns: a European survey

ObjectiveTo characterise heart failure (HF) maintenance pharmacotherapy for children across Europe and investigate how angiotensin-converting enzyme inhibitors (ACE-I) are used in this setting.MethodsA Europe-wide web-based survey was conducted between January...

Targeting Calpain for Heart Failure Therapy: Implications From Multiple Murine Models

Heart failure remains a major cause of morbidity and mortality in developed countries. There is still a strong need to devise new mechanism-based treatments for heart failure. Numerous studies have suggested the importance of the Ca2+-dependent protease calpain in cardiac physiology and pathology. However, no drugs are currently under development or testing in human patients to target calpain for heart failure treatment. Herein the data demonstrate that inhibition of calpain activity protects against deleterious ultrastructural remodeling and cardiac dysfunction in multiple rodent models of heart failure, providing compelling evidence that calpain inhibition is a promising therapeutic strategy for heart failure treatment.

MicroRNA-221/222 Family Counteracts Myocardial Fibrosis in Pressure Overload-Induced Heart Failure.

Pressure overload causes cardiac fibroblast activation and transdifferentiation, leading to increased interstitial fibrosis formation and subsequently myocardial stiffness, diastolic and systolic dysfunction, and eventually heart failure. A better understanding of the molecular mechanisms underlying pressure overload-induced cardiac remodeling and fibrosis will have implications for heart failure treatment strategies. The microRNA (miRNA)-221/222 family, consisting of miR-221-3p and miR-222-3p, is differentially regulated in mouse and human cardiac pathology and inversely associated with kidney and liver fibrosis. We investigated the role of this miRNA family during pressure overload-induced cardiac remodeling. In myocardial biopsies of patients with severe fibrosis and dilated cardiomyopathy or aortic stenosis, we found significantly lower miRNA-221/222 levels as compared to matched patients with nonsevere fibrosis. In addition, miRNA-221/222 levels in aortic stenosis patients correlated negatively with the extent of myocardial fibrosis and with left ventricular stiffness. Inhibition of both miRNAs during AngII (angiotensin II)-mediated pressure overload in mice led to increased fibrosis and aggravated left ventricular dilation and dysfunction. In rat cardiac fibroblasts, inhibition of miRNA-221/222 derepressed TGF-β (transforming growth factor-β)-mediated profibrotic SMAD2 (mothers against decapentaplegic homolog 2) signaling and downstream gene expression, whereas overexpression of both miRNAs blunted TGF-β-induced profibrotic signaling. We found that the miRNA-221/222 family may target several genes involved in TGF-β signaling, including JNK1 (c-Jun N-terminal kinase 1), TGF-β receptor 1 and TGF-β receptor 2, and ETS-1 (ETS proto-oncogene 1). Our findings show that heart failure-associated downregulation of the miRNA-221/222 family enables profibrotic signaling in the pressure-overloaded heart.

Shikonin ameliorates isoproterenol (ISO)-induced myocardial damage through suppressing fibrosis, inflammation, apoptosis and ER stress

Shikonin, isolated from the roots of herbal plant Lithospermum erythrorhizon, is a naphthoquinone. It has been reported to exert beneficial anti-inflammatory effects and anti-oxidant properties in various diseases. Isoproterenol (ISO) has been widely used to establish cardiac injury in vivo and in vitro. However, shikonin function in ISO-induced cardiac injury remains uncertain. In our study, we attempted to investigate the efficiency and possible molecular mechanism of shikonin in cardiac injury treatment induced by ISO. In vivo, C57BL6 mice were subcutaneously injected with 5mg/kg ISO to induce heart failure. And mice were given a gavage of shikonin (2 or 4mg/kg/d, for four weeks). Cardiac function, fibrosis indices, inflammation response, apoptosis and endoplasmic reticulum (ER) stress were calculated. Pathological alterations, fibrosis-, inflammation-, apoptosis- and ER stress-related molecules were examined. In ISO-induced cardiac injury, shikonin significantly ameliorated heart function, decreased myocardial fibrosis, suppressed inflammation, attenuated apoptosis and ER stress through impeding collagen accumulation, Toll like receptor 4/nuclear transcription factor κB (TLR4/NF-κB), Caspase-3 and glucose-regulated protein 78 (GRP78) signaling pathways activity, relieving heart failure in vivo. Also, in vitro, shikonin attenuated ISO-induced cardiac muscle cells by reducing fibrosis, inflammation, apoptosis and ER stress. Our findings indicated that shikonin treatment attenuated ISO-induced heart injury, providing an effective therapeutic strategy for heart failure treatment for future.

Fatigability, Exercise Intolerance, and Abnormal Skeletal Muscle Energetics in Heart Failure.

Among central and peripheral factors contributing to exercise intolerance (EI) in heart failure (HF), the extent to which skeletal muscle (SM) energy metabolic abnormalities occur and contribute to EI and increased fatigability in HF patients with reduced or preserved ejection fraction (HFrEF and HFpEF, respectively) are not known. An energetic plantar flexion exercise fatigability test and magnetic resonance spectroscopy were used to probe the mechanistic in vivo relationships among SM high-energy phosphate concentrations, mitochondrial function, and EI in HFrEF and HFpEF patients and in healthy controls. Resting SM high-energy phosphate concentrations and ATP flux rates were normal in HFrEF and HFpEF patients. Fatigue occurred at similar SM energetic levels in all subjects, consistent with a common SM energetic limit. Importantly, HFrEF New York Heart Association class II-III patients with EI and high fatigability exhibited significantly faster rates of exercise-induced high-energy phosphate decline than did HFrEF patients with low fatigability (New York Heart Association class I), despite similar left ventricular ejection fractions. HFpEF patients exhibited severe EI, the most rapid rates of high-energy phosphate depletion during exercise, and impaired maximal oxidative capacity. Symptomatic fatigue during plantar flexion exercise occurs at a common energetic limit in all subjects. HFrEF and HFpEF patients with EI and increased fatigability manifest early, rapid exercise-induced declines in SM high-energy phosphates and reduced oxidative capacity compared with healthy and low-fatigability HF patients, suggesting that SM metabolism is a potentially important target for future HF treatment strategies.

Current Treatment Strategies for Heart Failure: Role of Device Therapy and LV Reconstruction.

Medical care of heart failure (HF) begins with the determination of the cause of the heart failure and diagnosing potential reversible causes (i.e., coronary heart disease, hyperthyroidism, etc.). Medical therapy includes pharmacological and nonpharmacological strategies that limit and/or reverse the signs and symptoms of HF. Initial behavior modification includes dietary sodium and fluid restriction to avoid weight gain; and encouraging physical activity when appropriate. Optimization of medical therapy is the first line of treatment that includes the use of diuretics, vasodilators (i.e., ACE inhibitors or ARBs), beta blockers, and potentially inotropic agents and anticoagulation depending on the patient's severity of heart failure and LV dysfunction. As heart failure advances despite optimized medical management, cardiac resynchronization therapy (CRT), and implantable cardioverter defibrillators (ICDs) are appropriate device therapies. The development of progressive end-stage HF, despite maximal medical therapy, necessitates the consideration of mechanical circulatory devices such as ventricular assist devices (VADs) either as a bridge to heart transplantation or as destination therapy. Despite the advances in the treatment of heart failure, there is still a large morbidity and mortality associated with HF, thus the need to develop newer strategies for the treatment of HF.

Diagnostic, Prognostic, and Therapeutic Value of Circulating miRNAs in Heart Failure Patients Associated with Oxidative Stress.

Heart failure is a major public health problem especially in the aging population (≥65 years old), affecting nearly 5 million Americans and 15 million European people. Effective management of heart failure (HF) depends on a correct and rapid diagnosis. Presently, BNP (brain natriuretic peptide) or N-terminal pro-brain natriuretic peptide (NT-proBNP) assay is generally accepted by the international community for diagnostic evaluation and risk stratification of patients with HF. However, regardless of its widespread clinical use, BNP is still encumbered by reduced specificity. As a result, diagnosis of heart failure remains challenging. Although significant improvement happened in the clinical management of HF over the last 2 decades, traditional treatments are ultimately ineffective in many patients who progress to advanced HF. Therefore, a novel diagnostic, prognostic biomarker and new therapeutic approach are required for clinical management of HF patients. Circulating miRNAs seem to be the right choice for novel noninvasive biomarkers as well as new treatment strategies for HF. In this review, we briefly discuss the diagnostic, prognostic, and therapeutic role of circulating miRNAs in heart failure patients. We also mentioned our own technique of extraction of RNA and detection of circulating miRNAs from human plasma and oxidative stress associated miRNAs with HF.

From bedside to bench--meeting report of the 7th International Conference on cGMP "cGMP: generators, effectors and therapeutic implications" in Trier, Germany, from June 19th to 21st 2015.

During the past decade, our knowledge on the physiology, pathophysiology, basic pharmacology, and clinical pharmacology of the second messenger (cGMP) has increased tremendously. It is now well-established that cGMP, generated by soluble and particulate guanylate cyclases, is highly compartmentalized in cells and regulates numerous body functions. New cGMP-regulated physiological functions include meiosis and temperature perception. cGMP is involved in the genesis of numerous pathologies including cardiovascular, pulmonary, endocrine, metabolic, neuropsychiatric, eye, and tumor diseases. Several new clinical uses of stimulators and activators of soluble guanylate cyclase and of phosphodiesterase inhibitors such as heart failure, kidney failure, cognitive disorders, obesity bronchial asthma, and osteoporosis are emerging. The combination of neprilysin inhibitors-enhancing stimulation of the particulate guanylate cyclase pathway by preventing natriuretic peptide degradation-with angiotensin AT1 receptor antagonists constitutes a novel promising strategy for heart failure treatment. The role of oxidative stress in cGMP signaling, application of cGMP sensors, and gene therapy for degenerative eye diseases are emerging topics. It is anticipated that cGMP research will further prosper over the next years and reach out into more and more basic and clinical disciplines.

Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets.

The onset of heart failure is typically preceded by cardiac hypertrophy, a response of the heart to increased workload, a cardiac insult such as a heart attack or genetic mutation. Cardiac hypertrophy is usually characterized by an increase in cardiomyocyte size and thickening of ventricular walls. Initially, such growth is an adaptive response to maintain cardiac function; however, in settings of sustained stress and as time progresses, these changes become maladaptive and the heart ultimately fails. In this review, we discuss the key features of pathological cardiac hypertrophy and the numerous mediators that have been found to be involved in the pathogenesis of cardiac hypertrophy affecting gene transcription, calcium handling, protein synthesis, metabolism, autophagy, oxidative stress and inflammation. We also discuss new mediators including signaling proteins, microRNAs, long noncoding RNAs and new findings related to the role of calcineurin and calcium-/calmodulin-dependent protein kinases. We also highlight mediators and processes which contribute to the transition from adaptive cardiac remodeling to maladaptive remodeling and heart failure. Treatment strategies for heart failure commonly include diuretics, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers and β-blockers; however, mortality rates remain high. Here, we discuss new therapeutic approaches (e.g., RNA-based therapies, dietary supplementation, small molecules) either entering clinical trials or in preclinical development. Finally, we address the challenges that remain in translating these discoveries to new and approved therapies for heart failure.

Challenging aspects of treatment strategies in heart failure with preserved ejection fraction: "Why did recent clinical trials fail?".

Heart failure (HF) is the leading cause of hospitalization among older adults and the prevalence is growing with the aging populations in the Western countries. Epidemiologic reports suggest that approximately 50% of patients who have signs or symptoms of HF have preserved left ventricular ejection fraction. This HF type predominantly affects women and the elderly with other co-morbidities, such as diabetes, hypertension, and overt volume status. Most of the current treatment strategies are based on morbidity benefits such as quality of life and reduction of clinical HF symptoms. Treatment of patients with HF with preserved ejection fraction displayed disappointing results from several large randomized controlled trials. The heterogeneity of HF with preserved ejection fraction, understood as complex syndrome, seems to be one of the primary reasons. Here, we present an overview of the current management strategies with available evidence and new therapeutic approach from drugs currently in clinical trials, which target diastolic dysfunction, chronotropic incompetence, and risk factor management. We provide an outline and interpretation of recent clinical trials that failed to improve outcome and survival in patients with HF with preserved ejection fraction.

Treatment of Heart Failure with Reduced Ejection Fraction: Current Update

The prevalence of heart failure (HF) has been steadily increasing and it now creates an enormous social and economic burden. HF is a syndrome characterized by a high mortality rate, frequent hospitalization, a reduced quality of life, and a complex therapeutic regimen. In the last three decades, major progress in both the diagnosis and management of HF has taken place, and the pharmacologic and non-pharmacologic advances have led to a significant improvement in survival and symptoms in HF patients. After an accurate diagnosis, a proper HF management plan requires a multi-level team approach comprised of the correct combination of drug therapy, device therapy, and surgery, including heart transplantation. In this review, we focused on the pharmacologic and non-pharmacologic treatment strategies for HF with reduced ejection fraction. The goal was to develop treatment guidelines based on significant evidence derived from large clinical trials. (Korean J Med 2015;88:127-134)

Abstract 12651: Atrium Fibrosis and Inflammation: Impaired Atrial Natriuretic Peptide System in Experimental Heart Failure

Introduction: The cardiac atrium is an important endocrine organ which also releases natriuretic peptides (NPs). We reported that dysregulation of the proNP convertases, furin and corin, may disrupt NP progressing, causing atrial fibrosis in experimental heart failure (HF). Atrial fibrosis results in atrial arrhythmias and impairs the prognosis of human HF, therefore understanding mechanisms of atrial fibrosis may help in designing treatment strategies for HF. We sought to extend our studies into the entire NP system and global gene profiles including fibrotic and inflammatory pathways in experimental HF. Hypothesis: Components of the NP, pro-fibrotic and inflammatory system will be up-regulated in the atrium in HF. Methods: Experimental canine HF was induced by rapid right ventricular pacing at 240 bpm for 10 days. We examined hemodynamics, echo parameters, circulating neurohumoral factors, and global gene profiles using RT-PCR microarrays related to the NP system, fibrosis, growth factors, inflammation and cardiac hypertrophy in left atrium (LA) from normal and HF canines (n=4 of each). Results: Experimental HF was characterized by decreased % EF and LV radial strain, and increased circulating ANP, cGMP and aldosterone levels. HF LA weight significantly increased with fibrosis and interstitial edema compared to normals. Gene profile analyses showed increases in profibrotic cytokines and extracellular matrix related genes in LA. Increased ANP expression but also increased ANP degrading enzyme IDE and decreased proANP processing enzyme corin were also observed. Genes related to inflammatory cytokines such as TNF-alpha, members of the IL-6 family, MCP-1, and cell adhesion molecules were up-regulated in LA compared to normals. Conclusions: Experimental HF was characterized by on-going atrial fibrosis with increased circulating ANP levels. Although ANP gene expression increased in failing LA, impaired proANP processing and accelerated ANP degradation may impair any anti-fibrotic ANP effects. Further, atrium may be a source of inflammatory cytokines and pro-fibrotic growth factors which may advance organ damage in HF. Our studies suggest NP treatment, perhaps in a form less susceptible to IDE degradation, may be a novel therapeutic for HF.

Development and Use of a Human Induced Pluripotent Stem Cell Derived Cardiac Construct

Cell-based regenerative therapies hold promise in providing treatment strategies for heart failure. Previous work from our laboratory has shown that tissue engineered cardiac constructs enhance improvements in cardiac function by providing structural and nutrient support, potentially aiding in transplanted cell survival, integration and re-population of injured tissues. Our current studies focus on the development and testing of second-generation cardiac constructs utilizing high purity human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs).

Abstract 9: Development And Testing Of A Human Induced Pluripotetent Stem Cell Derived Cardiac Scaffold

Introduction: Cell-based regenerative therapies hold promise in providing treatment strategies for heart failure. Previous work from our laboratory has shown that tissue engineered cardiac constructs enhance improvements in cardiac function by providing structural and nutrient support, potentially aiding in transplanted cell survival, integration and re-population of injured tissues. Our current studies focus on the development and testing of second-generation cardiac constructs utilizing high purity human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs). Methods: High purity hiPSC-CMs were seeded and co-cultured onto a vicryl matrix embedded with biologically active human dermal fibroblasts. The hiPSC-CM constructs were maintained at 37°C and 5% CO2. Patches were constructed maintained as described for both in vitro and in vivo evaluation. Patches for in vivo evaluation were seeded, cultured and implanted onto the rat heart 3 weeks after left coronary artery ligation to assess improvements in LV function. Patches prepared for in vitro evaluation were seeded and cultured 1-10 days. Results: Patches constructed with hiPSC-CMs displayed synchronized and spontaneous contractions within 48hrs of culture which developed in robustness over time. At maximal robustness, contractions were visualized across the full thickness of the construct. Contractions were recorded at 36+5 beats BPM. In addition hiPSC-CM constructs respond to electrical stimulation with increased rate of contraction while maintaining their synchrony. Post pacing, the hiPSC-CM constructs return to their intrinsic rhythm. Conclusion: These findings show that high purity hiPSC-CMs can be seeded and co-cultured onto a vicryl and fibroblast construct in manner permitting adhesion and electromechanical coupling of the hiPSC-CMs to form a fully contractile construct. This is supported by the observation that the hiPSC-CMs contract spontaneously and in a synchronized manner in a directional fashion.

Outcomes after implantation of partial-support left ventricular assist devices in inotropic-dependent patients: Do we still need full-support assist devices?

Partial-support left ventricular assist devices (LVADs) represent a novel strategy for heart failure treatment. The Synergy Pocket Micro-pump (HeartWare Inc, Framingham, Mass), the smallest surgically implanted long-term LVAD, provides partial flow up to 4.25 L/min and was primarily designed for "less sick" patients with severe heart failure. This device is implanted minimally invasively without sternotomy or cardiopulmonary bypass. Early implantation in patients with Interagency Registry for Mechanically Assisted Circulatory Support class 4 and higher was shown to be feasible and associated with significantly improved hemodynamics and quality of life. The aim of this study was to present our experience with implementation of long-term partial circulatory support as a bridge to transplantation in patients with more advanced heart failure who were dependent preoperatively on inotropic support or intra-aortic balloon pump. In this observational study, only inotropic or intra-aortic balloon pump-dependent patients with end-stage heart failure were included (n = 12). These patients underwent Synergy device implantation between February 2012 and August 2013. The mean preoperative Interagency Registry for Mechanically Assisted Circulatory Support class was 2.17 ± 0.84 (class 1, 25%; class 2, 33%; class 3, 42%). The mean age was 46 ± 15 years, and 33% were female. Preoperatively, 4 patients (33%) had at least 1 previous sternotomy, 3 patients (25%) were supported with a balloon pump, 1 patient (8%) had a previous full-support LVAD, and 4 patients (33%) had cerebrovascular events in the past. After device implantation, there were no right ventricular failures, device-related infections, hemorrhagic strokes, arterial or venous thromboembolisms, or worsenings of aortic and mitral regurgitation observed over the follow-up. The mean follow up was 174 ± 171 days (range, 5-764 days; cumulative, 3199 days). One patient (8%) died, 3 patients (25%) successfully underwent transplantation, 1 device (8%) was explanted after myocardial recovery, and 5 patients (42%) are still on ongoing support. Two patients (17%) were upgraded to a full-support LVAD after 65 days of mean support. A total of 11 of 12 patients (92%) were discharged from the hospital and are presently alive. Left ventricular end-diastolic diameter was significantly reduced 3 months after device implantation. Partial LVAD support may be clinically efficacious in inotropic and intra-aortic balloon pump-dependent patients. On the basis of our experience and evidence of previous research, such patients may benefit from minimally invasive access, no need for sternotomy and cardiopulmonary bypass, a short implantation time, an easy exchange if necessary, and a lower risk of subsequent heart transplantation. Because the implantation is performed without sternotomy, device upgrade is feasible with a comparatively low operative risk and good clinical outcome. Our preliminary results show that partial-support devices may have the potential to replace full-support LVADs in the near future.

European Society of Cardiology (ESC) congress report from Barcelona 2014.

The Annual Congress of the European Society of Cardiology (ESC) was held in Barcelona from 30th August to 3rd September 2014. More than 30,300 attendees from around the world shared the latest original research, including 27 clinical Hot Line studies, 12 basic science Hot Lines, 15 clinical trial updates, 19 registry studies, and 4,597 abstracts. Many important issues were presented, including novel treatment strategies for heart failure, acute coronary syndrome, interventional treatment for structural heart disease, renal denervation, novel anticoagulant therapies, atrial fibrillation and so on. In addition, 5 new ESC clinical practice guidelines (ie, myocardial revascularization, non-cardiac surgery, acute pulmonary embolism, hypertrophic cardiomyopathy, and aortic disease) were launched. It should be noted that Japan has recently been ranked in the top position in terms of the number of abstract submissions. Based on these activities, the ESC Congress has been recognized as the dominant scientific and educational forum for healthcare professionals in cardiology. We report the highlights and several key presentations of the ESC Congress 2014. The scientific activities and growing contributions of Japanese cardiologists or cardiovascular surgeons enhance the favorable relationship between the ESC and the Japanese Circulation Society.

Noncardiovascular Death, Especially Infection, Is a Significant Cause of Death in Elderly Patients With Acutely Decompensated Heart Failure

BackgroundDespite marked improvements in treatment strategies for heart failure (HF), the mortality rate of elderly patients with HF is still high. Detailed causes of death have not been fully understood. Methods and ResultsWe studied 459 consecutive patients with acute decompensated HF (ADHF) emergently admitted to our hospital from 2007 to 2011. Patients were divided into 2 groups: <75 years old (younger group; n = 225) and ≥75 years old (elderly group; n = 234). All-cause death, cardiovascular death, and noncardiovascular death were assessed as adverse outcomes. Compared with the younger group, the elderly group was characterized by a higher proportion of women and hypertensive patients and higher left ventricular ejection fraction. During a mean follow-up of 20.7 months, a total of 174 patients (37.9%) died. All-cause death was significantly higher in the elderly group than in the younger group (46.6% vs 28.9%; P < .0001), and this difference was caused by an increase in noncardiovascular deaths (20.9% vs 9.3%; P < .001), especially deaths due to infection (10.7% vs 4.0%; P < .01). Cardiovascular deaths did not differ between the 2 groups. ConclusionsNoncardiovascular deaths, most of which were caused by infection, were frequent among elderly patients with ADHF.

The Challenge of Treating Heart Failure

Heart failure affects nearly 6 million people in the United States alone, 1 and the prevalence has reached alarming proportions. It is estimated that approximately 2% of Americans have heart failure, and 35% of cardiovascular deaths are directly related to heart failure. 1 The costs for treating patients with heart failure now approach $32 billion annually. 2 Successful and significant advances have been made in the treatment strategies for heart failure. Pharmacologic therapy includes agents such as β-blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers and aldosterone antagonists. Further advances in cardiac resynchronization therapy (CRT), cardiac transplantation, and mechanical circulatory support have provided additional options for patients with this debilitating and frequently fatal chronic illness. However, an important question is whether all patients are being afforded the same advantages of current treatment approaches. Are there groups of patients, as defined by sex, race, and ethnicity, being left behind?

Analysis of 10-year nationwide population-based data on sex differences in hospitalization for heart failure

Sex-related factors play an important role in the pathophysiology of heart failure (HF). However, trends in sex-related differences in hospital management for HF are not clear. We identified patients hospitalized for HF through a nationwide database (National Health Insurance in Taiwan), containing 722,272 subjects from 1999 to 2008. Higher incidences of diabetes mellitus (37 vs. 25%, p<0.001), thyroid dysfunction (2 vs. 0%, p<0.001), and transient cerebral ischemia (2 vs. 1%, p<0.05), as well as a lower incidence of chronic lung disease (14 vs. 22%, p<0.001) differentiated female HF patients from male HF patients. During this 10-year period, both percentage of HF hospitalization and age-adjusted HF rates significantly increased for total HF sample (1.92 vs. 2.49 ‰, p<0.05, and 20.44 vs. 27.38/100,000, p<0.05) and for female (1.76 vs. 2.86 ‰, p<0.05, and 20.94 vs. 32.12/100,000, p<0.05), but such changes did not occur among male patients (2.12 vs. 2.09 ‰, p>0.05, and 19.93 vs. 22.51/100,000, p>0.05). The age at the time of hospitalization and the length of the hospital stay increased significantly for all HF patients during the 10-year study period. However, the daily cost of hospitalization increased in males, but not in females. Compared to the survivors, patients who died were older and had a longer hospitalization and higher daily cost both in males and females. Through our analysis of the NHI database, we observed trends in factors related to hospitalization of HF patients in Taiwan that may be attributable to sex-related differences in the pathophysiology and treatment strategies for HF.

Using a high-fidelity patient simulator with first-year medical students to facilitate learning of cardiovascular function curves

Students are relying on technology for learning more than ever, and educators need to adapt to facilitate student learning. High-fidelity patient simulators (HFPS) are usually reserved for the clinical years of medical education and are geared to improve clinical decision skills, teamwork, and patient safety. Finding ways to incorporate HFPS into preclinical medical education represents more of a challenge, and there is limited literature regarding its implementation. The main objective of this study was to implement a HFPS activity into a problem-based curriculum to enhance the learning of basic sciences. More specifically, the focus was to aid in student learning of cardiovascular function curves and help students develop heart failure treatment strategies based on basic cardiovascular physiology concepts. Pretests and posttests, along with student surveys, were used to determine student knowledge and perception of learning in two first-year medical school classes. There was an increase of 21% and 22% in the percentage of students achieving correct answers on a posttest compared with their pretest score. The median number of correct questions increased from pretest scores of 2 and 2.5 to posttest scores of 4 and 5 of a possible total of 6 in each respective year. Student survey data showed agreement that the activity aided in learning. This study suggests that a HFPS activity can be implemented during the preclinical years of medical education to address basic science concepts. Additionally, it suggests that student learning of cardiovascular function curves and heart failure strategies are facilitated.