Abstract MP202: The Effects Of Maternal Hypothyroidism On Fetal And Adult Cardiac Function

Objectives: Maternal hypothyroidism (MH), a common clinical condition with a reported prevalence from 2.5% to 13%. MH could have an adverse effect on fetal cardiac development and adult heart function. However, there is a lack of systematic research for its effect on fetal and offspring’s development and cardiac function. This study aimed to determine the impact of MH on fetal and offspring’s organ structural and functional development at different gestation stages and during postnatal and puberty. Methods: MH model had been built through thyroidectomy (TX) with total thyroxine (TT4) under 1ng/dl after surgery. Pups from mice that underwent TX and Sham surgery were named THD (Deficient) and THN (Normal). Times of parturition and miscarriage from TX and Sham groups were recorded. Ultrasound was performed for fetuses and/or offspring to check the gestation, miscarriage, embryo arrest, development, malformation, and cardiac function. At different postnatal days, mice were euthanized for organ development evaluation. Result: TX mice had reduced parturition frequencies and smaller litter size but increased miscarriage frequency and malformed fetuses than the sham group. In addition, THD fetuses had smaller biparietal diameter (BPD) and abdominal circumference (AC) and significantly lower left ventricular ejection fraction (LVEF) on E14.5, but not at E18.5. Tei index, a parameter representing both systolic and diastolic cardiac function, was lower in THD fetuses than in THN fetuses at both E14.5 and E18.5. The cardiac systolic and diastolic function of female TX mice after a 9-month breeding period was also abnormal. The Postnatal T4 level was not significantly different between the two groups. On and after d21 after birth, THD mice had a higher heart weight/body weight ratio and lower LVEF still d21. Conclusion: MH impaired the development and cardiac function of the fetus and young adult. In addition, MH impaired the mother's fertility and depressed cardiac function.

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Abstract 14195: Impact of Leukocyte Filtration and Leukocyte Modulation on Recovery of Heart Function After Prolonged Cardiac Arrest Treated With ECPR in a Porcine Model

Circulation ◽

10.1161/circ.144.suppl_2.14195 ◽

2021 ◽

Vol 144 (Suppl_2) ◽

Author(s):

Jensyn VanZalen ◽

Takahiro Nakashima ◽

Annie Phillips ◽

Joseph Hill ◽

Alyssa Enciso ◽

...

Keyword(s):

Cardiac Arrest ◽

Cardiac Function ◽

Heart Function ◽

Randomized Study ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Control Group ◽

Swine Model ◽

Extracorporeal Cardiopulmonary Resuscitation ◽

Ventricular Ejection Fraction

Background: Extracorporeal cardiopulmonary resuscitation (ECPR) improves survival of patients with prolonged cardiac arrest (CA) that is refractory to standard CPR and ACLS. It has been proposed that ECPR accentuates inflammation after CA, potentially limiting its effectiveness. The benefits of leukocyte filters or leukocyte-modulating devices in conjunction with ECPR have not been studied. Hypothesis: When paired with ECPR, inflammation-modulating devices targeting leukocytes may improve recovery of cardiac function after prolonged cardiac arrest. Methods: In a randomized study, 24 swine (40±5kg) underwent 8min of untreated ventricular fibrillation CA followed by CPR with mechanical chest compressions and impedance threshold device for 30 min (total arrest time = 38min), immediately followed by 8h of ECPR with heparin anticoagulation and temperature maintained at 33°C. Group 1 (n=8) had standard ECPR system (control), Group 2 (n=8) had a leukocyte filter device (LF) added to the ECPR circuit, an and Group 3 (n=8) had a leukocyte modulation device (LMOD) added to the ECPR circuit. Recovery of cardiac function was measured using a cardiac resuscitablity score (CRS) and left ventricular ejection fraction (LVEF) via transthoracic echocardiography. Data was collected at baseline (prior CA) and after 8h of ECPR. Data analysis: single-factor ANOVA test (p<0.05 significance). Results: There were no statically significant differences between the groups in CRS (Control = 3.3 ± 2.4, LF = 4.0 ± 2.8, LMOD = 2.1 ± 2.6; p=0.37) or LVEF (Control = 59% ± 27%, LF = 49% ± 29% LMOD = 34% ± 38%: p=0.34) at 8 hours after ECPR initiation (Table 1). Discussion: In this swine model of prolonged cardiac arrest treated with ECPR, addition of a leukocyte filter or leukocyte modulation device to the ECPR circuit did not improve recovery of cardiac function during the first 8 hours after initiating ECPR.

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Abstract 314: Loss of Sarcospan has a Deleterious Effect on Cardiac Function in Aged Mice

Circulation Research ◽

10.1161/res.115.suppl_1.314 ◽

2014 ◽

Vol 115 (suppl_1) ◽

Author(s):

Michelle S Parvatiyar ◽

Jamie L Marshall ◽

Maria C Jordan ◽

Reginald T Nguyen ◽

Kenneth P Roos ◽

...

Keyword(s):

Cardiac Function ◽

Immune Cell ◽

Expression Profiles ◽

Weight Ratio ◽

Left Ventricular ◽

Calcium Handling ◽

Left Ventricular Ejection ◽

Adrenergic Stimulation ◽

Cardiac Sarcolemma ◽

Ventricular Ejection Fraction

Sarcospan (SSPN) has been shown to have an important role in stabilizing sarcolemmal dystrophin- and utrophin-glycoprotein adhesion complexes. Loss of sarcolemmal integrity leads to immune cell infiltration and inappropriate exchange of cellular contents with the extracellular milieu. Our laboratory has shown SSPN loss destabilizes skeletal muscle adhesion and reduces sarcolemmal dystrophin localization, whereas its complete loss due to mutation underlies development of Duchenne muscular dystrophy (DMD). Loss of dystrophin leads to cardiac dysfunction and early mortality in DMD patients. The role of SSPN in the heart is unknown. We present immunofluorescence data revealing reduction of dystrophin and the sarcoglycans with a coordinate increase of β1D integrin levels at the SSPN-null cardiac sarcolemma relative to WT. Also, SSPN loss decreases cardiac P-Akt levels, disrupting signaling promoting compensatory physiological hypertrophy. These studies suggest a fundamental role for SSPN in cardiac maintenance and function, since left ventricular mass increases with age and upon isoproterenol administration (0.8 mg/day for two wks). Aged SSPN-null mice developed hypertrophy, evidenced as increased heart/body weight ratio and left ventricular wall dimension. The SSPN-null mice lacked the characteristic initial rise in cardiac output, left ventricular ejection fraction (LvEF %), induced by chronic β-adrenergic stimulation. Functionally, aged SSPN-null hearts had an increased E/A ratio indicating restrictive ventricular filling and decreased fractional shortening F/S (%) upon isoproterenol administration. Aged untreated SSPN-null hearts had increased fibrosis compared to aged WT controls, however isoproterenol treated SSPN-null hearts displayed exacerbated fibrotic response compared to WT. To assess whether SSPN-null hearts have altered gene expression profiles during progression of pathogenesis, qRT-PCR will be utilized to measure differences in expression of fetal gene and calcium-handling proteins. In summary, we have found that SSPN has an important role in maintaining cardiac function, its loss exacerbates the hypertrophic response and localization of stabilizing adhesion complexes at the cardiac muscle sarcolemma.

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P3554CMR Fast-SENC intramyocardial LV & RV segmental strain helps manage cardioprotective therapy in patients exhibiting cardiotoxicity during cancer treatment

European Heart Journal ◽

10.1093/eurheartj/ehz745.0417 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

H Steen ◽

M Montenbruck ◽

P Wuelfing ◽

S Esch ◽

A K Schwarz ◽

...

Keyword(s):

Breast Cancer ◽

Heart Failure ◽

Cardiac Function ◽

Cancer Treatment ◽

Cancer Patients ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Ventricular Ejection Fraction ◽

The Impact

Abstract Background Cardiotoxicity during cancer treatment has become an acknowledged problem of chemotherapy medications and radiation therapy. Limitations of biomarkers and imaging tests such as echocardiography left ventricular ejection fraction (LVEF) hinder early detection of cardiotoxicity and proactive cardioprotective therapy. Once the heart is unable to compensate for subclinical dysfunction, systemic damage and remodeling occurs increasing the potential for heart failure. Fast-SENC segmental intramyocardial strain (fSENC) is a unique cardiac magnetic resonance imaging (CMR) test that regionally detects subclinical intramyocardial dysfunction in 1 heartbeat. This study evaluates the ability of fSENC to detect subclinical cardiotoxicity and manage cardioprotective therapy in cancer patients. Methods This single center, prospective Prefect Study was used to evaluate cardiotoxicity and the impact of cardioprotective therapy in Breast Cancer and Lymphoma patients (NCT03543228). fSENC was acquired with a 1.5T MRI and processed with the MyoStrain software to quantify intramyocardial strain. Segmental strain was measured in three short axis scans (basal, midventricular & apical) with 16LV/6RV longitudinal segments & three long axis scans (2-, 3-, 4-chamber) with 21LV/5RV circumferential segments. fSENC CMR was performed before chemotherapy, during and after anthracycline/taxan therapy, at 1 year follow-up, and as needed in between designated follow-up periods. Cardioprotective therapy was offered to patients meeting the definition of cardiotoxicity by the ESC Guidelines on Cardiotoxicity and/or ESMO Clinical Practice Guidelines or those observing a substantial decline in cardiac function. Comparisons were made with paired t-Test with a 95% confidence interval. Results Two hundred eight (208) CMRs were performed in fifty-two (52) patients (44 female). Patients had an average (± stdev) age of 53 (15) yrs, BMI of 26 (5) kg/m2; 77% had breast cancer, 23% had Lymphoma. fSENC CMRs required 11 (2) min total exam time. Figure 1 shows bar graphs of the % of normal LV myocardium (e.g. % LV MyoStrain Segments <−17%) at baseline and sequential follow-ups for patients without cardiotoxicity and with cardiotoxicity requiring cardioprotective therapy. Patients observing cardiotoxicity had a statistically significant decline in cardiac function measured by segmental fSENC (p=0.0002) which resolved after cardioprotective therapy. Figure 1 Conclusion Segmental fSENC intramyocardial strain detects subclinical cardiotoxicity during chemotherapy and impact of cardioprotective therapy. The ability to serve as a surrogate safety endpoint for chemotherapy or other pharmacological agents, and aid management of cardiotoxicity by serving as a surrogate efficacy endpoint for cardioprotection agents, dosage, and patient compliance may help physicians detect subclinical cardiac dysfunction, and proactively manage cancer patients to avoid early or late heart failure.

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P319Proliferative induced cardiomyocyte precursor cells obtained by direct reprogramming and transcriptional selection

European Heart Journal ◽

10.1093/eurheartj/ehz747.0154 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

D Bachamanda Somesh ◽

K Klose ◽

K Juerchott ◽

U Krueger ◽

D Kunkel ◽

...

Keyword(s):

Gene Expression ◽

Transcription Factors ◽

Cardiac Function ◽

Heart Function ◽

Cardiac Fibroblasts ◽

Gene Expression Pattern ◽

Left Ventricular ◽

Precursor Cells ◽

Left Ventricular Ejection ◽

Ventricular Ejection Fraction

Abstract Objective Enriched populations of proliferative induced cardiomyocyte precursors (iCMPs) generated from cardiac fibroblasts (CF) could represent a potential population for use in therapeutic application. We developed a protocol for generation of iCMPs from cardiac fibroblasts by genetic reprogramming followed by transcriptional selection and induced maturation. Methods Cardiac fibroblasts were reprogrammed into induced cardiomyocyte precursor cells (iCMPs) via transduction with cardiomyogenesis-related transcription factors Gata4, Mef2c, TBX5 and Myocd. Pure population of iCMPs were obtained by molecular beacons (MB) based selection of MYH6/7 expression. The transcriptome was profiled by RNA sequencing. For maturation iCMPs were treated with 5'-azacytidine and cultured in medium containing ascorbic acid and TGFβ1. The cells were monitored regularly for formation of sarcomere structures, cardiac marker expression and contractions. iCMPs were transplanted into MI mice and monitored for 6 weeks. At the end of 6 weeks, the mice were sacrificed and hearts were explanted and cryopreserved to examine the heart structure and scare size. Cardiac function was monitored by echocardiography. Results iCMPs expressed troponin T, α-actinin and myosin heavy chain (MHC) protein observed by immunocytology. These iCMPs could robustly proliferative and maintain a stable phenotype. Global transcriptome analysis revealed that the iCMP gene expression profile is unique from those of the parental CFs and adult CMs. With Gene Ontology (GO) analysis, we found that iCMPs show upregulation of genes associated with cardiac development, differentiation and morphogenesis while they showed downregulation of genes associated to cell-proliferation in comparison to their parental CFs. Evaluation of selected gene sets showed downregulation of non-myocyte genes, upregulation of transcription factors and upregulation of certain functional and structural genes like ion channel genes and contractile genes. Maturation studies showed that iCMPs gradually changed morphology after stimulation with 5-Aza, as seen in immunofluorescence staining. Cells expressing cTnT showed formation of sarcomeric striations. In vivo translational studies showed reduction of heart function in control groups treated with PBS or CF whereas the iCMPs group showed an improvement in function, reflected by left ventricular ejection fraction and fractional shortening as evaluated by echocardiography. Additionally we noticed an improvement in left ventricular wall thickness at diastole in mice transplanted with iCMPs. Conclusions Gene expression pattern suggests that these iCMPs represent an intermediate state of cardiogenic population that can be expanded to yield therapeutic cell doses. When transplanted to mouse hearts following myocardial infarction, they improved cardiac function.

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Heart failure in pregnancy: what is the long-term impact of pregnancy on cardiac function? A tertiary care centre experience and systematic review

Open Heart ◽

10.1136/openhrt-2021-001587 ◽

2021 ◽

Vol 8 (2) ◽

pp. e001587

Author(s):

Anudeep K Dodeja ◽

Francesca Siegel ◽

Katherine Dodd ◽

Marwan Ma'ayeh ◽

Laxmi S Mehta ◽

...

Keyword(s):

Heart Failure ◽

Left Ventricular Function ◽

Ventricular Function ◽

Heart Function ◽

Tertiary Care ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Major Adverse Cardiovascular Events ◽

Ventricular Ejection Fraction ◽

The Impact

BackgroundWomen with cardiomyopathy (CM) are often advised against pregnancy due to risk for major adverse cardiovascular events (MACE). However, the impact of CM subtype on maternal MACE is not understood, and so we sought to evaluate the influence of CM phenotype on maternal outcomes, as well as the effect on immediate and late left ventricular function.MethodsWe evaluated all pregnant women in our high-risk maternal cardiovascular programme (2009–2019). Composite maternal MACE included: death, inotrope use, left ventricular assist device, orthotopic heart transplant and/or escalation in transplant listing status, acute decompensated heart failure and sustained ventricular arrhythmia.ResultsAmong 875 women followed, 32 had CM (29±7 years old, left ventricular ejection fraction (LVEF) 41%±12%): 3 ischaemic CM (ICM), 10 peripartum CM (PPCM) and 19 non-ICM (NICM). MACE events occurred in 6 (18%) women (PPCM: 2 (33%), NICM: 4 (67%)). There was no difference in LVEF at baseline, however, women with MACE had significantly lower LVEF both early (LVEF: 27±5% vs . 41±2%, p<0.05) and late post partum (LVEF: 28±5% vs . 44±2%, p<0.01).ConclusionsIn this contemporary cohort of women with CM, maternal MACE rates were lower than previously reported, and were less common in PPCM as compared with ICM and NICM. Heart function in women with MACE was negatively impacted immediately after delivery and in late postpartum follow-up, suggesting that pregnancy itself likely has influence on future left ventricular function in women with underlying CM.

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The Cardio-Hepatic Relation in STEMI

Journal of Personalized Medicine ◽

10.3390/jpm11121241 ◽

2021 ◽

Vol 11 (12) ◽

pp. 1241

Author(s):

Lian Bannon ◽

Ilan Merdler ◽

Nir Bar ◽

Lior Lupu ◽

Shmuel Banai ◽

...

Keyword(s):

Myocardial Infarction ◽

Cardiac Function ◽

Cardiac Dysfunction ◽

Liver Enzymes ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Gamma Glutamyl Transferase ◽

Ventricular Ejection Fraction ◽

Glutamyl Transferase ◽

The Impact

Background: Hepatic injury secondary to congestive heart failure is well described, however, only limited data exist about the possible impact of acute cardiac dysfunction on the liver. We aimed to explore the possible cardio-hepatic interaction in patients with myocardial infarction. Material and methods: A single-center retrospective cohort study of 1339 ST elevation myocardial infarction (STEMI) patients who underwent primary coronary intervention between June 2012 to June 2019. Echocardiographic examinations were performed to assess left ventricular ejection fraction (LVEF) and central venous pressure (CVP). Patients were stratified into four groups by their LVEF and CVP levels: LVEF ≥ 45%, and CVP ≤ 10 mm/Hg (n = 853), LVEF < 45% with CVP ≤ 10 mm/Hg (n = 364), EF ≥ 45%, with CVP > 10 mm/Hg (n = 61), and LVEF < 45% with CVP > 10 mm/Hg (n = 61). Patients were evaluated for baseline and peak liver enzymes including alanine transaminase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), and bilirubin. Results: Greater severity of cardiac dysfunction was associated with worse elevation of liver enzymes. We found a graded increase in mean levels of maximal ALT, first and maximal ALP, and first and maximal GGT values. Using propensity score matching to estimate the impact of cardiac dysfunction on liver injury, we chose patients with the worst cardiac function parameters: (LVEF < 45% and CVP >10 mm/Hg; n = 61) and compared them to matched patients with better cardiac function (n = 45). We found a significantly higher level of maximal ALT, first and maximal ALP, and GGT values in the group with the worst cardiac function parameters (p < 0.05). Conclusions: Among patients with STEMI, the combination of decreased LVEF and venous congestion was associated with liver enzymes elevation suggesting a possible cardio-hepatic syndrome.

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Shenlijia Attenuates Doxorubicin-Induced Chronic Heart Failure by Inhibiting Cardiac Fibrosis

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2021/6659676 ◽

2021 ◽

Vol 2021 ◽

pp. 1-13

Author(s):

Xutao Sun ◽

Yunjia Song ◽

Ying Xie ◽

Jieru Han ◽

Fei Chen ◽

...

Keyword(s):

Heart Failure ◽

Chronic Heart Failure ◽

Cardiac Function ◽

Molecular Mechanisms ◽

Cardiac Fibrosis ◽

Heart Function ◽

Left Ventricular ◽

Protein Chip ◽

Left Ventricular Ejection ◽

Ventricular Ejection Fraction

Application of the anticancer drug doxorubicin (DOX) is restricted due to its adverse, cardiotoxic side effects, which ultimately result in heart failure. Moreover, there are a limited number of chemical agents for the clinical prevention of DOX-induced cardiotoxicity. Based on the theories of traditional Chinese medicine (TCM) on chronic heart failure (CHF), Shenlijia (SLJ), a new TCM compound, has been developed to fulfill multiple functions, including improving cardiac function and inhibiting cardiac fibrosis. In the present study, the protective effects and molecular mechanisms of SLJ on DOX-induced CHF rats were investigated. The CHF rat model was induced by intraperitoneal injection of DOX for six weeks with the cumulative dose of 15 mg/kg. All rats were then randomly divided into the control, CHF, CHF + SLJ (3.0 g/kg per day), and CHF + captopril (3.8 mg/kg per day) groups and treated for further four weeks. Echocardiography and the assessment of hemodynamic parameters were performed to evaluate heart function. A protein chip was applied to identify proteins with diagnostic values that were differentially expressed following SLJ treatment. The data from these investigations showed that SLJ treatment significantly improved cardiac function by increasing the left ventricular ejection fraction, improving the hemodynamic index, and inhibiting interstitial fibrosis. Protein chip analysis revealed that SLJ upregulated MCP-1, MDC, neuropilin-2, TGF-β3, thrombospondin, TIE-2, EG-VEGF/PK1, and TIMP-1/2/3 expressions and downregulated that of MMP-13. In addition, immunohistochemistry and western blot results further confirmed that SLJ promoted TIMP-1/2/3 and inhibited MMP-13 expression. The results of the present study suggest that SLJ was effective against DOX-induced CHF rats and is related to the improvement of heart function and ultrastructure and the inhibition of myocardial fibrosis.

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The enhanced effect and underlying mechanisms of mesenchymal stem cells with IL-33 overexpression on myocardial infarction

Stem Cell Research & Therapy ◽

10.1186/s13287-019-1392-9 ◽

2019 ◽

Vol 10 (1) ◽

Cited By ~ 3

Author(s):

Yueqiu Chen ◽

Jianfeng Zuo ◽

Weiqian Chen ◽

Ziying Yang ◽

Yanxia Zhang ◽

...

Keyword(s):

Myocardial Infarction ◽

Stem Cells ◽

T Cells ◽

Mesenchymal Stem Cells ◽

Cardiac Function ◽

Heart Function ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Therapeutic Effects ◽

Ventricular Ejection Fraction

Abstract Background Interleukin 33 is known to have an important influence in the process of myocardial infarction, and the immunoregulatory function of MSCs could be influenced by cell factors. In this study, we evaluated the therapeutic efficacy of IL-33-overexpressing bone marrow mesenchymal stem cells (IL33-MSCs) on myocardial infarction (MI) and detected the inflammatory level and cardiac function in rats. Methods and results First, we evaluated the proliferation of T cells and polarization of macrophages that had been co-cultured with Vector-MSCs or IL33-MSCs. Co-culture experiments indicated that IL33-MSCs reduced T cell proliferation and enhanced CD206+ macrophage polarization. Second, we determined the inflammation level and cardiac function of PBS-, Vector-MSC-, and IL33-MSC-injected rats. Echocardiography indicated that left ventricular ejection fraction (LVEF) was enhanced in IL33-MSC-injected rats compared with Vector-MSC-injected rats. Postmortem analysis of rat heart tissue showed reduced fibrosis and less inflammation in IL33-MSC-injected rats. Conclusion These studies indicated that the IL33-MSC injection improved heart function and reduces inflammation in rats with MI compared with PBS or Vector-MSC injections. Graphical Abstract IL-33 overexpression enhances the immunomodulatory function and therapeutic effects of MSCs on acute MI via enhancing the polarization of macrophages toward M2, enhancing the differentiation of CD4+ T cells toward CD4+IL4+Th2 cells, and finally, reducing heart inflammation and enhancing heart function.

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Biomarkers-based personalized follow-up in chronic heart failure improves patient’s outcomes and reduces care associate cost

Health and Quality of Life Outcomes ◽

10.1186/s12955-021-01779-9 ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Antonio Leon-Justel ◽

Jose I. Morgado Garcia-Polavieja ◽

Ana Isabel Alvarez-Rios ◽

Francisco Jose Caro Fernandez ◽

Pedro Agustin Pajaro Merino ◽

...

Keyword(s):

Heart Failure ◽

Hospital Admissions ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Secondary Outcome ◽

Ventricular Ejection Fraction ◽

Number Of Patients ◽

Ed Visits ◽

The Impact

Abstract Background Heart failure (HF) is a major and growing medical and economic problem, with high prevalence and incidence rates worldwide. Cardiac Biomarker is emerging as a novel tool for improving management of patients with HF with a reduced left ventricular ejection fraction (HFrEF). Methods This is a before and after interventional study, that assesses the impact of a personalized follow-up procedure for HF on patient’s outcomes and care associated cost, based on a clinical model of risk stratification and personalized management according to that risk. A total of 192 patients were enrolled and studied before the intervention and again after the intervention. The primary objective was the rate of readmissions, due to a HF. Secondary outcome compared the rate of ED visits and quality of life improvement assessed by the number of patients who had reduced NYHA score. A cost-analysis was also performed on these data. Results Admission rates significantly decreased by 19.8% after the intervention (from 30.2 to 10.4), the total hospital admissions were reduced by 32 (from 78 to 46) and the total length of stay was reduced by 7 days (from 15 to 9 days). The rate of ED visits was reduced by 44% (from 64 to 20). Thirty-one percent of patients had an improved functional class score after the intervention, whereas only 7.8% got worse. The overall cost saving associated with the intervention was € 72,769 per patient (from € 201,189 to € 128,420) and €139,717.65 for the whole group over 1 year. Conclusions A personalized follow-up of HF patients led to important outcome benefits and resulted in cost savings, mainly due to the reduction of patient hospitalization readmissions and a significant reduction of care-associated costs, suggesting that greater attention should be given to this high-risk cohort to minimize the risk of hospitalization readmissions.

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Review of Irish patients meeting ST elevation criteria during the COVID-19 pandemic

Open Heart ◽

10.1136/openhrt-2021-001716 ◽

2021 ◽

Vol 8 (2) ◽

pp. e001716

Author(s):

Luke Byrne ◽

Roisin Gardiner ◽

Patrick Devitt ◽

Caleb Powell ◽

Richard Armstrong ◽

...

Keyword(s):

Public Health ◽

Public Perception ◽

Coronary Intervention ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Control Group ◽

Ventricular Ejection Fraction ◽

St Elevation ◽

The Impact ◽

Transfer Times

IntroductionThe COVID-19 pandemic has seen the introduction of important public health measures to minimise the spread of the virus. We aim to identify the impact government restrictions and hospital-based infection control procedures on ST elevation myocardial infarction (STEMI) care during the COVID-19 pandemic.MethodsPatients meeting ST elevation criteria and undergoing primary percutaneous coronary intervention from 27 March 2020, the day initial national lockdown measures were announced in Ireland, were included in the study. Patients presenting after the lockdown period, from 18 May to 31 June 2020, were also examined. Time from symptom onset to first medical contact (FMC), transfer time and time of wire cross was noted. Additionally, patient characteristics, left ventricular ejection fraction, mortality and biochemical parameters were documented. Outcomes and characteristics were compared against a control group of patients meeting ST elevation criteria during the month of January.ResultsA total of 42 patients presented with STEMI during the lockdown period. A significant increase in total ischaemic time (TIT) was noted versus controls (8.81 hours (±16.4) vs 2.99 hours (±1.39), p=0.03), with increases driven largely by delays in seeking FMC (7.13 hours (±16.4) vs 1.98 hours (±1.46), p=0.049). TIT remained significantly elevated during the postlockdown period (6.1 hours (±5.3), p=0.05), however, an improvement in patient delays was seen versus the control group (3.99 hours (±4.5), p=0.06). There was no difference seen in transfer times and door to wire cross time during lockdown, however, a significant increase in transfer times was seen postlockdown versus controls (1.81 hours (±1.0) vs 1.1 hours (±0.87), p=0.004).ConclusionA significant increase in TIT was seen during the lockdown period driven mainly by patient factors highlighting the significance of public health messages on public perception. Additionally, a significant delay in transfer times to our centre was seen postlockdown.

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