Ischemic Arrhythmias Research Articles

The Usefulness of Modified Mallampati Score and CT Upper Airway Volume Measurements in Diagnosing OSA among Patients with Breathing-Related Sleep Disorders

Background: Obstructive sleep apnea (OSA) is a condition causing restriction of the airflow through the upper airways during sleep, despite preserved inspiratory muscle activity. This may lead to the development of secondary hypertension, ischemic heart disease, myocardial infarction, and arrhythmia. Moreover, the prevalence of OSA is on the rise. Methods: Comparison of scores from the Berlin Questionnaire, modified Mallampati scores (MMP), pulse oximetry readings and Upper Airway Volume (UAV) data obtained from CBCT (Cone Beam Computed Tomography). The study group of 129 patients of both sexes reporting sleep-related breathing problems completed the Berlin Questionnaire, had their oxygen saturation (SpO2) measured with a PO40 pulse oximeter, and oropharyngeal tissues assessed according to MMP. CBCT scans were put into 3D Amira TM 3D computer analysisto obtain UAV values. Results: Snoring was associated with significantly higher BMI compared to non-snoring patients. Furthermore, snoring patients had higher heart rate, modified Mallampati score, and lower UAV than the non-snoring group. The multifactorial analysis showed MMP as a useful indicator of the risk of snoring (OR = 7.468 (3863–14, 507, p < 0.001)). Conclusions: The composition of MMP together with UAV and the Berlin questionnaire might be reliable indicators to assess the risk of snoring.

Dual-center experiences with interventional closure of patent foramen ovale: A medium-term follow-up study comparing two patient groups aged under and over 60 years.

BackgroundCurrent guidelines recommend interventional closure of patent foramen ovale (PFO) in patients with cryptogenic ischemic stroke who are under 60 years of age.HypothesisThe hypothesis of this study was to compare follow‐up results of PFO closure in patients over 60 years of age to those of patients under 60 years of age in order to determine whether the procedure is safe and effective for both age groups.MethodsWe included 293 patients who had a cryptogenic ischemic stroke and a PFO confirmed by transesophageal echocardiography (TEE) and who were scheduled for percutaneous closure of the PFO between 2014 and 2019. The device implantation was completed in all patients using an Amplatzer™, Occlutec™, or Cardia Ultrasept PFO occluder.ResultsFollow‐up TEE examinations were performed at intervals of 1, 3, and 6 months after implantation. Patients were followed for a median of 3.6 ± 1.2 years. Recurrent ischemic stroke or transient ischemic attack, cardiac death, arrhythmias, and residual shunt were reported equally in both groups.ConclusionsInterventional closure of PFO can be as safe and effective in patients over 60 years of age as it is in patients under 60 years of age regardless of the device used. In this older patient group, rigorous discussion and a case‐by‐case decision‐making process including cardiologists and neurologists is warranted to ensure optimal procedure selection.

Cardiac Myosin Activation with Omecamtiv Mecarbil in Systolic Heart Failure

BackgroundThe selective cardiac myosin activator omecamtiv mecarbil has been shown to improve cardiac function in patients with heart failure with a reduced ejection fraction. Its effect on cardiovascular outcomes is unknown.MethodsWe randomly assigned 8256 patients (inpatients and outpatients) with symptomatic chronic heart failure and an ejection fraction of 35% or less to receive omecamtiv mecarbil (using pharmacokinetic-guided doses of 25 mg, 37.5 mg, or 50 mg twice daily) or placebo, in addition to standard heart-failure therapy. The primary outcome was a composite of a first heart-failure event (hospitalization or urgent visit for heart failure) or death from cardiovascular causes.ResultsDuring a median of 21.8 months, a primary-outcome event occurred in 1523 of 4120 patients (37.0%) in the omecamtiv mecarbil group and in 1607 of 4112 patients (39.1%) in the placebo group (hazard ratio, 0.92; 95% confidence interval [CI], 0.86 to 0.99; P=0.03). A total of 808 patients (19.6%) and 798 patients (19.4%), respectively, died from cardiovascular causes (hazard ratio, 1.01; 95% CI, 0.92 to 1.11). There was no significant difference between groups in the change from baseline on the Kansas City Cardiomyopathy Questionnaire total symptom score. At week 24, the change from baseline for the median N-terminal pro–B-type natriuretic peptide level was 10% lower in the omecamtiv mecarbil group than in the placebo group; the median cardiac troponin I level was 4 ng per liter higher. The frequency of cardiac ischemic and ventricular arrhythmia events was similar in the two groups.ConclusionsAmong patients with heart failure and a reduced ejection, those who received omecamtiv mecarbil had a lower incidence of a composite of a heart-failure event or death from cardiovascular causes than those who received placebo. (Funded by Amgen and others; GALACTIC-HF ClinicalTrials.gov number, NCT02929329; EudraCT number, 2016-002299-28.)

Transcription Factor Meis1 Act As a New Regulator Of Ischemic Arrhythmias In Mice

Background: The principal voltage-gated Nam+ channel, NaV1.5 governs heart excitability and conduction. NaV1.5 dysregulation is responsible for ventricular arrhythmias and subsequent sudden cardiac death in post-infarct hearts. The transcription factor Meis1 plays an important role in determining differentiation fate and regenerative capability of cardiomyocytes. However, the functions of Meis1 in ischemic arrhythmias following myocardial infarction (MI) are still largely undefined. Here we set out to study whether Meis1 could act as a key regulator to mediate cardiac Na+ channels and arrhythmogenesis and its underlying mechanisms. Methods: Heart-specific Meis1 overexpression was established by AAV9 virus injection in C57BL/6 mice. The QTc interval, the incidence of ventricular arrhythmias and cardiac conduction velocity were evaluated by ECG, programmed electrical stimulation and optical mapping techniques respectively. The conventional patch clamp technique was used to study the I Na characteristics of isolated mouse ventricular myocytes. Findings: We found that forced expression of Meis1 rescued the prolongation of heart rate corrected QT (QTc) interval, produced anti-arrhythmic activity and improved epicardial conduction velocity in infarcted mouse hearts. Mechanistically, Meis1 may ameliorate cardiac electrophysiological remodeling as characterized by the decrease of INa current density and NaV1.5 expression in marginal zone of infarcted mouse hearts. Furthermore, in vitro studies showed that E3 ubiquitin ligase CDC20 led to the ubiquitination and degradation of Meis1, which blocked the transcriptional regulation of SCN5A. Interpretation: This study demonstrates that Meis1 overexpression can effectively inhibit the ventricular arrhythmia by regulating the transcription of SCN5A and cardiac electrical conductance in mouse ischemic heart, which provides new therapeutic strategies for malignant arrhythmias and sudden cardiac death following MI. Funding: This work was supported by the National Nature Science Foundation of China [Grant No. 81573425 and 81773733 to NW]. Declaration of Interest: None to declare. Ethical Approval: All animal experiments were performed along with the NIH guidelines (Guide for the care and use of laboratory animals, NIH Publication No. 85-23, revised 1996) and were conducted in accordance with the protocols approved by the Institutional Animal Care and Use Committee of Harbin Medical University.

Emerging Role of Mitophagy in the Heart: Therapeutic Potentials to Modulate Mitophagy in Cardiac Diseases.

The normal function of the mitochondria is crucial for most tissues especially for those that demand a high energy supply. Emerging evidence has pointed out that healthy mitochondrial function is closely associated with normal heart function. When these processes fail to repair the damaged mitochondria, cells initiate a removal process referred to as mitophagy to clear away defective mitochondria. In cardiomyocytes, mitophagy is closely associated with metabolic activity, cell differentiation, apoptosis, and other physiological processes involved in major phenotypic alterations. Mitophagy alterations may contribute to detrimental or beneficial effects in a multitude of cardiac diseases, indicating potential clinical insights after a close understanding of the mechanisms. Here, we discuss the current opinions of mitophagy in the progression of cardiac diseases, such as ischemic heart disease, diabetic cardiomyopathy, cardiac hypertrophy, heart failure, and arrhythmia, and focus on the key molecules and related pathways involved in the regulation of mitophagy. We also discuss recently reported approaches targeting mitophagy in the therapy of cardiac diseases.

Hyperleptinemia Results in Systemic Inflammation and the Exacerbation of Ischemia-Reperfusion Myocardial Injury: The Involvement of the JAK/STAT Pathway

Aim: Hyperleptinemia potentiates the effects of many atherogenic factors, such as inflammation, platelet aggregation, migration, hypertrophy, proliferation of vascular smooth muscle cells, and endothelial cell dysfunction. The present study analysed the effects of long-term hyperleptinemia in an in vivo myocardial ischemia-reperfusion model to demonstrate whether the in vivo deleterious effect also affects cardiac structure and function. Main methods: Rats by were subcutaneously administered leptin for 8 days to estimate the involvement of the JAK/STAT pathway. Data from 58 male Wistar rats were included in the final analysis. Myocardial infarction (MI) was modelled by the 30-minute ligation of the main left coronary artery followed by 120-minute reperfusion. Hemodynamic measurements, electrocardiography monitoring, echocardiography, myocardial infarct size and area at risk, blood biochemical parameters, leptin, IL-6, TNF-alpha, FGF-21, and cardiomyocyte morphology were measured. Statistical analyses were performed using IBM SPSS Statistics v.26. Key findings: Eight-day hyperleptinemia in rats led to increased an blood pressure and heart rate, myocardial hypertrophy, impaired LV function, an increased frequency of ischemic arrhythmias, dyslipidaemia, systemic inflammation, and an increased size of induced myocardial infarction. Significance: The blockade of the JAK/STAT signalling pathway effectively reversed the negative effects of leptin, including increased blood pressure and total cholesterol. Funding Information: The study has been supported by the grant from the Ministry of Science and Higher Education of the Russian Federation (agreement 075-15-2020-800). Declaration of Interests: None to declare. Ethics Approval Statement: This study was conducted in conformance with the policies and procedures detailed by the “Institutional Animal Care and Use Committee” (IACUC). All animal experimental protocols and procedures were reviewed and approved by the Committee for the Control of the Maintenance and Use of Laboratory Animals of the V. A. Almazov National Medical Research Center (date: 06-FEB-2020, application number: 20-01).

Comorbidity in patients with lymphoproliferative diseases

Purpose of the study. To make an informed assessment of comorbidity in patients with lymphoproliferative diseases. To evaluate the effectiveness of comorbidity scales CCI and CIRS-G in patients with lymphoproliferative diseases under treatment. To evaluate the effect of the conducted immunochemotherapy on the general comorbidity in this category of patients.Material and methods. Two scales were used for calculations: Charlson Comorbidity Index (CCI) and Cumulative Illness Rating Scale for Geriatrics (CIRS-G). 127 primary patients with lymphoproliferative diseases aged 19 to 95 years old (the average age was 51.4) were examined from January 2018 till October 2019. The distribution of patients was based on the types of diseases: non-Hodgkin’s lymphomas — 59 (46.46%), Hodgkin’s lymphoma — 35 (27.56%), multiple myeloma — 20 (15.77%), chronic lymphocytic leukemia — 7 (5.51%) people, Waldenstrom’s macroglobulinemia — 3 (2.36%); each of the following diseases: hairy cell leukemia, T-cell leukemia of large granular lymphocytes, T-cell prolymphocytic leukemia - 1, amounted to 0.78% each.Results. Comorbidity was detected in 46 patients who received immunotherapy, chemotherapy, combined chemoradiotherapy, which amounted to 36.22% of the total number of patients. Lesions of the peripheral and central nervous system — 20 (43.48%) patients, were diagnosed most frequently. Immunodefi ciency states — 19 (41.30%) people, came next, and diseases of the cardiovascular system — 12 (26.08%) patients, appeared to be least frequent.Conclusions. When recalculating comorbidity on the CCI and CIRS-G scales, a significant aggravation of comorbidity after treatment, an increase in moderate and severe comorbidity were noted. According to the effectiveness of the CCI and CIRS-G scales in the treated patients, comorbidity is evaluated only approximately, since the Charlson Comorbidity Index does not include polyneuropathy, immunodeficiency states, thrombosis, ischemic heart disease, cardiac arrhythmias, gastritis, and thromboembolic complications and immunodeficiency states are absent in the CIRS-G scale. It is advisable to develop scales for assessing comorbidity, free from disadvantages mentioned above.

The Contribution of Endothelial Dysfunction in Systemic Injury Subsequent to SARS-Cov-2 Infection.

SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) infection is associated, alongside with lung infection and respiratory disease, to cardiovascular dysfunction that occurs at any stage of the disease. This includes ischemic heart disease, arrhythmias, and cardiomyopathies. The common pathophysiological link between SARS-CoV-2 infection and the cardiovascular events is represented by coagulation abnormalities and disruption of factors released by endothelial cells, which contribute in maintaining the blood vessels into an anti-thrombotic state. Thus, early alteration of the functionality of endothelial cells, which may be found soon after SARS-CoV-2 infection, seems to represent the major target of a SARS CoV-2 disease state and accounts for the systemic vascular dysfunction that leads to a detrimental effect in terms of hospitalization and death accompanying the disease. In particular, the molecular interaction of SARS-CoV-2 with the ACE2 receptor located in the endothelial cell surface, either at the pulmonary and systemic level, leads to early impairment of endothelial function, which, in turn, is followed by vascular inflammation and thrombosis of peripheral blood vessels. This highlights systemic hypoxia and further aggravates the vicious circle that compromises the development of the disease, leading to irreversible tissue damage and death of people with SARS CoV-2 infection. The review aims to assess some recent advances to define the crucial role of endothelial dysfunction in the pathogenesis of vascular complications accompanying SARS-CoV-2 infection. In particular, the molecular mechanisms associated with the interaction of SARS CoV-2 with the ACE2 receptor located on the endothelial cells are highlighted to support its role in compromising endothelial cell functionality. Finally, the consequences of endothelial dysfunction in enhancing pro-inflammatory and pro-thrombotic effects of SARS-CoV-2 infection are assessed in order to identify early therapeutic interventions able to reduce the impact of the disease in high-risk patients.

Does night-time aircraft noise trigger mortality? A case-crossover study on 24886 cardiovascular deaths.

AimsIt is unclear whether night-time noise events, including from aeroplanes, could trigger a cardiovascular death. In this study, we investigate the potential acute effects of aircraft noise on mortality and the specific role of different night-time exposure windows by means of a case-crossover study design.Methods and resultsWe selected 24 886 cases of death from cardiovascular disease (CVD) from the Swiss National Cohort around Zürich Airport between 2000 and 2015. For night-time deaths, exposure levels 2 h preceding death were significantly associated with mortality for all causes of CVD [OR = 1.44 (1.03–2.04) for the highest exposure group (LAeq > 50 dB vs. <20 dB)]. Most consistent associations were observed for ischaemic heart diseases, myocardial infarction, heart failure, and arrhythmia. Association were more pronounced for females (P = 0.02) and for people living in areas with low road and railway background noise (P = 0.01) and in buildings constructed before 1970 (P = 0.36). We calculated a population attributable fraction of 3% in our study population.ConclusionOur findings suggest that night-time aircraft noise can trigger acute cardiovascular mortality. The association was similar to that previously observed for long-term aircraft noise exposure.

Fibronectin type III domain-containing 5 in cardiovascular and metabolic diseases: a promising biomarker and therapeutic target.

Cardiovascular and metabolic diseases are the leading causes of death and disability worldwide and impose a tremendous socioeconomic burden on individuals as well as the healthcare system. Fibronectin type III domain-containing 5 (FNDC5) is a widely distributed transmembrane glycoprotein that can be proteolytically cleaved and secreted as irisin to regulate glycolipid metabolism and cardiovascular homeostasis. In this review, we present the current knowledge on the predictive and therapeutic role of FNDC5 in a variety of cardiovascular and metabolic diseases, such as hypertension, atherosclerosis, ischemic heart disease, arrhythmia, metabolic cardiomyopathy, cardiac remodeling, heart failure, diabetes mellitus, and obesity.

The impact of proton therapy on cardiotoxicity following radiation treatment.

Cardiac disease following radiation therapy represents a major consideration in the treatment of a variety of malignancies. Damage to the heart can manifest in a variety of pathologies including ischemic cardiac disease, cardiomyopathy, valvular dysfunction, arrhythmias, and pericarditis. This damage has been shown to directly relate to cardiac radiation dose and to stem from a range of cellular pathways that are often related to fibrosis. The importance of minimizing radiation dose to the heart is especially critical in the pediatric population and when treating disease sites adjacent to the heart. Proton therapy represents a promising approach to minimize dose to normal tissues such as the heart. The cardiac dosimetry reductions due to proton therapy have been demonstrated in multiple cancers and further long-term follow-up will determine the clinical significance of these reductions to cardiac structures. Future approaches using advanced techniques such as FLASH therapy could provide even further benefit by reducing post-radiation fibrosis.

Obstructive Sleep Apnoea Syndrome: Continuous Positive Airway Pressure Therapy for Prevention of Cardiovascular Risk.

Obstructive sleep apnoea (OSA) syndrome is characterised by the presence of apnoea or obstructive hypopnoea during sleep, accompanied by hypoxia. It is estimated that the syndrome affects approximately 10% of men and 15% of women. Diagnosis and treatment rates have increased in recent years, but the condition remains undiagnosed in a high percentage of patients. Recent evidence suggests that OSA may increase the risk of cardiovascular disease. The relationship between OSA and cardiovascular disease can be explained, at least in part, by the coexistence of cardiovascular risk factors in the two pathologies, such as age, overweight, smoking and sedentary lifestyle. However, OSA has been independently associated with the risk of developing hypertension, cerebrovascular disease, ischaemic heart disease, heart failure and arrhythmias. Clinical trials that have evaluated the efficacy of continuous positive airway pressure (CPAP) treatment in primary and secondary cardiovascular prevention have not demonstrated a significant reduction in the incidence or recurrence of cardiovascular events. This article analyses the relationship between OSA and cardiovascular risk and discusses recent clinical trials on the efficacy of CPAP in primary and secondary cardiovascular prevention.

Telemedicine consultation for the clinical cardiologists in the era of COVID-19: present and future. Consensus document of the Spanish Society of Cardiology

The coronavirus disease 2019 (COVID-19) pandemic has changed how we view our consultations. To reduce the risk of spread in the most vulnerable patients (those with heart disease) and health personnel, most face-to-face consultations have been replaced by telemedicine consultations. Although this change has been rapidly introduced, it will most likely become a permanent feature of clinical practice. Nevertheless, there remain serious doubts about organizational and legal issues, as well as the possibilities for improvement etc. In this consensus document of the Spanish Society of Cardiology, we attempt to provide some keys to improve the quality of care in this new way of working, reviewing the most frequent heart diseases attended in the cardiology outpatient clinic and proposing some minimal conditions for this health care process. These heart diseases are ischemic heart disease, heart failure, and arrhythmias. In these 3 scenarios, we attempt to clarify the basic issues that must be checked during the telephone interview, describe the patients who should attend in person, and identify the criteria to refer patients for follow-up in primary care. This document also describes some improvements that can be introduced in telemedicine consultations to improve patient care.

A Soluble Epoxide Hydrolase Inhibitor Upregulated KCNJ12 and KCNIP2 by Downregulating MicroRNA-29 in a Mouse Model of Myocardial Infarction.

Soluble epoxide hydrolase inhibitors (sEHi) have anti-arrhythmic effects, and we previously found that the novel sEHi t-AUCB (trans-4[-4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid) significantly inhibited ventricular arrhythmias after myocardial infarction (MI). However, the mechanism is unknown. It's known that microRNA-29 (miR-29) participates in the occurrence of arrhythmias. In this study, we investigated whether sEHi t-AUCB was protective against ischemic arrhythmias by modulating miR-29 and its target genes KCNJ12 and KCNIP2. Male 8-week-old C57BL/6 mice were divided into five groups and fed distilled water only or distilled water with t-AUCB of different dosages for seven days. Then, the mice underwent MI or sham surgery. The ischemic region of the myocardium was obtained 24 hours after MI to detect miR-29, KCNJ12, and KCNIP2 mRNA expression levels via real-time PCR and KCNJ12 and KCNIP2 protein expression levels via western blotting. MiR-29 expression levels were significantly increased in the ischemic region of MI mouse hearts and the mRNA and protein expression levels of its target genes KCNJ12 and KCNIP2 were significantly decreased. T-AUCB prevented these changes dose-dependently. The sEHi t-AUCB regulates the expression levels of miR-29 and its target genes KCNJ12 and KCNIP2, suggesting a possible mechanism for its potential therapeutic application in ischemic arrhythmia.

Sex-dependent effect of perinatal hypoxia on cardiac tolerance to oxygen deprivation in adults.

Epidemiological studies have demonstrated a relationship between the adverse influence of perinatal development and increased risk of ischemic heart disease in adults. From negative factors to which the fetus is subjected, the most important is hypoxia. The fetus may experience hypoxic stress under different conditions, including pregnancy at high altitude, pregnancy with anemia, placental insufficiency, and heart, lung, and kidney disease. One of the most common insults during the early stages of postnatal development is hypoxemia due to congenital cyanotic heart defects. Experimental studies have demonstrated a link between early hypoxia and increased risk of ischemia/reperfusion injury (I/R) in adults. Furthermore, it has been observed that late myocardial effects of chronic hypoxia, experienced in early life, may be sex-dependent. Unlike in males, perinatal hypoxia significantly increased cardiac tolerance to acute I/R injury in adult females, expressed as decreased infarct size and lower incidence of ischemic arrhythmias. It was suggested that early hypoxia may result in sex-dependent programming of specific genes in the offspring with the consequence of increased cardiac susceptibility to I/R injury in adult males. These results would have important clinical implications, since cardiac sensitivity to oxygen deprivation in adult patients may be significantly influenced by perinatal hypoxia in a sex-dependent manner.

La consulta telemática para el cardiólogo clínico en tiempos de la COVID-19: presente y futuro. Documento de consenso de la Sociedad Española de Cardiología

The coronavirus disease 2019 (COVID-19) pandemic has changed how we view our consultations. To reduce the risk of spread in the most vulnerable patients (those with heart disease) and health personnel, most face-to-face consultations have been replaced by telemedicine consultations. Although this change has been rapidly introduced, it will most likely become a permanent feature of clinical practice. Nevertheless, there remain serious doubts about organizational and legal issues, as well as the possibilities for improvement etc. In this consensus document of the Spanish Society of Cardiology, we attempt to provide some keys to improve the quality of care in this new way of working, reviewing the most frequent heart diseases attended in the cardiology outpatient clinic and proposing some minimal conditions for this health care process. These heart diseases are ischemic heart disease, heart failure, and arrhythmias. In these 3 scenarios, we attempt to clarify the basic issues that must be checked during the telephone interview, describe the patients who should attend in person, and identify the criteria to refer patients for follow-up in primary care. This document also describes some improvements that can be introduced in telemedicine consultations to improve patient care.

Medical conditions in scuba diving fatality victims in Australia, 2001 to 2013.

This study identified pre-existing medical conditions among scuba diving fatalities in Australia from 2001 to 2013, inclusive, and assessed whether these conditions likely contributed to the deaths. The National Coronial Information System (NCIS) was searched for scuba diving-related cases during 2001-2013, inclusive. Coronial findings, witness and police reports, medical histories, and autopsy and toxicology reports were scrutinised for pre-existing medical conditions and autopsy findings. Predisposing factors, triggers, disabling agents, disabling injuries and causes of death were analysed using a validated template. There were 126 scuba diving-related fatalities identified during the study period. Forty-six (37%) divers were identified as having a significant medical condition which may have contributed to their incident. The most common condition was ischaemic heart disease (IHD) which had been diagnosed in 15 of the divers. Thirty-two (25%) deaths were attributed to cardiac disabling injuries (DI) such as ischaemic heart disease and arrhythmias, although a cardiac DI was thought likely in another six. Respiratory conditions were implicated in eight (6%) deaths, at least four associated with cerebral arterial gas embolism. At least 14 (11%) divers who had contributory pre-existing medical conditions had been cleared to dive by a medical practitioner within the year prior. Chronic health-related factors played a major role in almost half of these deaths; primarily cardiac conditions such as IHD and cardiac arrhythmias. Although fitness-to-dive (FTD) assessments have limitations, the high incidence of cardiac-related deaths indicates a need for 'older' divers to be medically assessed for FTD.

P1527SURVIVAL COMPARISON:HEMODIALYSIS VS PERITONEAL DIALYSIS: TEN YEARS OBSERVATIONAL STUDY

Abstract Background and Aims Survival comparison between peritoneal dialysis (PD) and hemodialysis (HD) is still controversial. While some retrospective studies have shown better survival in PD, particularly in the first year, others have not identified this difference. The only RCT published so far showed a 3-year mortality rate similar between two groups. However, the number of patients was too small to provide sufficient statistical power to identify any survival differences between the two dialysis techniques. Aim of this study was to compare HD and PD in term of survival rate and factors possibly involved in a ten-years observational study. Method We retrospectively evaluated all the incident patients that started a dialytic treatment, either HD or PD, due to uremia from 01-01-2008 to 31-12-2018 at the U.O. Nephrology ASST Spedali Civili of Brescia. Exclusion criteria were: duration of dialysis treatment less than 3 months, and previous dialytic treatment or kidney transplantation. For each patient anthropometric, clinical-anamnestic data and comorbidities at dialysis start were recorded. Results One thousand and six patients were identified. 130 patients were excluded due to dialysis treatment less than 3 months. A total 876 patients were analyzed. 77% of patients started dialysis on HD while 23% chose PD. Age was significantly higher in HD patients (69±15 vs 65±16 years; p&amp;lt;0.05). No differences were found in the incidence of: ischemic heart disease (HD 24%, PD 25%, p=0.90), diabetes (32% vs 32%, p=0.83), cancer (20% vs 17%, p=0.37), cardiac arrhythmia (20% vs 25%, p=0.08) and peripheral vascular disease (25% vs 25%, p=0.89). An increased incidence of COPD (HD 17% vs PD 8%, p&amp;lt;0.05) and hypertension (73% vs 87%, p&amp;lt;0.05) was present in PD patients. During follow-up, 17% of patients treated with PD shifted to HD due to catheter malfunction, recurrent infections, insufficient dialytic adequacy or ultrafiltration failure. Kidney transplants were performed more frequently in PD patients (HD 12%; PD 24%, p&amp;lt;0.05). At an intention to treat analysis of the data, univariate analysis showed better survival in PD patients (p&amp;lt;0.05, Figure 1). This difference was not confirmed at multivariate analysis (Figure 2), where age, cardiac arrhythmia, cirrhosis, diabetes and peripheral vascular disease were independently associated with an increased risk of mortality. No independent influence on mortality of the dialysis treatment modality was found. Conclusion This ten years observational study shows that HD and PD are similar in term of patient survival. Age and comorbidities seem to play the most important role in patient survival.

Abstract 318: Heart Failure and Osteoporosis- an Evidence Based Approach

Background: Heart disease occurs when there is reduced blood flow to the heart. It refers to a range of conditions that affect the heart. These conditions include ischemic heart disease (which can lead to acute myocardial infarction), angina, arrhythmia, atrial fibrillation, and heart failure, among others. Currently, there are 600,000 Canadians living with heart failure (HF) with 50,000 Canadians being diagnosed every year with HF. Community-based heart failure clinics have been proven to reduce hospitalizations, but Alberta has only one. The CHARM (Community Heart Failure Assessment, Rehabilitation and Management) clinic at Advanced Cardiology, Calgary, Alberta is a community based, charity funded clinic providing outpatient care, which is physician-directed but RN managed. We intended to investigate whether there was any relationship between patients with heart failure and their pre-disposition to osteoporosis and vice versa. Methods: We performed an observational case series with a retrospective chart review of 600 CHARM clinic patients who have been diagnosed with Heart Failure till June 2019. The primary endpoint was to look at CHARM clinic's prevalence of HF, patients who ever had Bone Mineral Density (BMD) done and if there was an intertwining relationship by comparing co-existence of heart failure with osteoporosis. Results: •Total # of pts above 65 years of age from a pool of 356 clinic pts = 169•Total # of pts above 65 years of age who had BMD done before June 2019 = 60•Total # of pts above 65 years of age who have Not had BMD done before June 2019 =108•Percentage of patients above 65 years of age who had BMD done before June 2019 = 35%•Percentage of patients above 65 years of age who have not had BMD done before June 2019 = 65%We also compared our finding with studies from Raymond b. Et al and Ezekowitz and it was found that out of 623 patients with Heart failure, 12% had moderate to severe vertebral compression fracture, 55% of those people have multiple fractures. It was seen that CHF patients with osteoporosis were the features that they were mostly female, Caucasian, smoker, obese, hypertensive, COPD, and patients with prevalence of diabetes. Conclusion: It was noticed from our clinic data that 65% of the patients with CHF did not have a BMD done (till June2019) and there by the presence of osteoporosis could have gone undiagnosed. What complicates CHF and osteoporosis is the age factor (mostly elderly), shared risk factors(factors include advanced age, hypovitaminosis D, renal disease and diabetes mellitus), medication use like (loop diuretics) and common pathogenic mechanisms(activation of the renin-angiotensin-aldosterone system) affect both HF and osteoporosis. It is to be noted that CHF is a major risk factor for mortality following fracture as the patient becomes immobile and it is important to carefully assess osteoporosis and take measures to reduce the risk of osteoporotic fractures.

Biological properties and clinical applications of berberine.

Berberine, an isoquinoline alkaloid isolated from the Chinese herb Coptis chinensis and other Berberis plants, has a wide range of pharmacological properties. Berberine can be used to treat many diseases, such as cancer and digestive, metabolic, cardiovascular, and neurological diseases. Berberine has protective capacities in digestive diseases. It can inhibit toxins and bacteria, including Helicobacter pylori, protect the intestinal epithelial barrier from injury, and ameliorate liver injury. Berberine also inhibits the proliferation of various types of cancer cells and impedes invasion and metastasis. Recent evidence has confirmed that berberine improves the efficacy and safety of chemoradiotherapies. In addition, berberine regulates glycometabolism and lipid metabolism, improves energy expenditure, reduces body weight, and alleviates nonalcoholic fatty liver disease. Berberine also improves cardiovascular hemodynamics, suppresses ischemic arrhythmias, attenuates the development of atherosclerosis, and reduces hypertension. Berberine shows potent neuroprotective effects, including antioxidative, antiapoptotic, and anti-ischemic. Furthermore, berberine exerts protective effects against other diseases. The mechanisms of its functions have been extensively explored, but much remains to be clarified. This article summarizes the main pharmacological actions of berberine and its mechanisms in cancer and digestive, metabolic, cardiovascular, and neurological diseases.