Relative Risk Of Heart Failure Research Articles

Global, regional, and national burden of heart failure associated with atrial fibrillation

BackgroundHeart failure is a leading cause of mortality and morbidity worldwide, and Atrial fibrillation (AF) is among many modifiable risk factors for heart failure. No estimates are available on the magnitude of the burden of heart failure associated with AF, and this study estimated the global, regional, and national burdens associated with AF.MethodsWe used the comparative risk assessment method to estimate the disease burden in terms of prevalence and years lived with disability (YLD). The population-attributable fraction for heart failure and AF was calculated from prevalence estimates of AF and the recalculated relative risks of heart failure associated with AF from a systematic review summarising the longitudinal association between AF and outcomes. The burden of heart failure was retrieved from the Global Burden of Disease database.ResultsGlobally, 2.6% (95% uncertainty interval 1.3 to 4.7%) of the burden of heart failure is associated with AF. This was 1.5 (95% UI 0.6 to 3.2) million people in 2019, a 49.8% increase from 1990. The highest prevalence was from South-East Asia, East Asia and Oceania. The highest YLD was estimated for Central Europe, Eastern Europe and Central Asia. High-income countries showed a sharp decline in the age standardised prevalence and YLD rates from 1990 to 2019.ConclusionThe burden of heart failure associated with AF has increased substantially over the past two decades despite the advances in AF management. However, falling prevalence and YLD rates of heart failure associated with AF in high-income countries over time indicate that reducing this burden is possible.

Diabetes and heart failure associations in women and men: Results from the MORGAM consortium.

Diabetes and its cardiovascular complications are a growing concern worldwide. Recently, some studies have demonstrated that relative risk of heart failure (HF) is higher in women with type 1 diabetes (T1DM) than in men. This study aims to validate these findings in cohorts representing five countries across Europe. This study includes 88,559 (51.8% women) participants, 3,281 (46.3% women) of whom had diabetes at baseline. Survival analysis was performed with the outcomes of interest being death and HF with a follow-up time of 12 years. Sub-group analysis according to sex and type of diabetes was also performed for the HF outcome. 6,460 deaths were recorded, of which 567 were amongst those with diabetes. Additionally, HF was diagnosed in 2,772 individuals (446 with diabetes). A multivariable Cox proportional hazard analysis showed that there was an increased risk of death and HF (hazard ratio (HR) of 1.73 [1.58-1.89] and 2.12 [1.91-2.36], respectively) when comparing those with diabetes and those without. The HR for HF was 6.72 [2.75-16.41] for women with T1DM vs. 5.80 [2.72-12.37] for men with T1DM, but the interaction term for sex differences was insignificant (p for interaction 0.45). There was no significant difference in the relative risk of HF between men and women when both types of diabetes were combined (HR 2.22 [1.93-2.54] vs. 1.99 [1.67-2.38] respectively, p for interaction 0.80). Diabetes is associated with increased risks of death and heart failure, and there was no difference in relative risk according to sex.

Prevalence and characteristics of newly diagnosed heart failure in patients with shortness of breath after coronavirus infection

Aim. To determine the prevalence and show the features of the development of newly diagnosed heart failure (HF) in patients with dyspnea after a coronavirus disease 2019 (COVID-19).Material and methods. This clinical prospective observational study was conducted during 2020-2022. The study consecutively included 368 outpatients with shortness of breath, who applied to the clinic. Depending on the presence of prior COVID-19, the patients were divided into 2 groups: the first group consisted of 205 patients with shortness of breath after COVID-19, the second group — 163 patients without prior COVID-19. All patients underwent a clinical examination within 3 days after presentation with an assessment of outpatient records and other medical documents for the differential diagnosis of dyspnea. The severity of dyspnea was determined using the Modified Medical Research Council Dyspnoea Scale (mMRC). The diagnosis of HF was verified in accordance with the 2020 Russian Society of Cardiology guidelines and in some cases reclassified in accordance with the 2021European Society of Cardiology guidelines. For further analysis, 2 subgroups of patients with HF were identified depending on the presence and absence of prior COVID-19. The subgroup analysis excluded patients with acute heart failure, acute illness, and conditions requiring hospitalization and/or intensive care.Results. Among 368 patients who presented to the clinic with dyspnea during 2020-2022, 205 patients (55,7%) had COVID-19. The average period of treatment after COVID-19 was 3,5 [1,5; 22,4] months. Patients after COVID-19 applied earlier after the onset of dyspnea, which is associated with higher mMRC score. The prevalence of HF among patients with shortness of breath after COVID-19 was significantly higher than in patients without this pathology in history, and amounted to 19,0% vs 9,8% (p=0,021). Prior COVID-19 increased the relative risk (RR) of HF in patients with shortness of breath by 1,7 times. RR for HF in systolic blood pressure >140 mm Hg increased by 1,9 times, while in diastolic blood pressure >90 mm Hg — by 1,9 times, with the development of a hypertensive crisis — by 28%, with a heart rate >80 bpm at rest — by 1,4 times, with the development of type 2 diabetes — by 31%, in the presence of pulmonary fibrosis — by 2,3 times. Patients with shortness of breath after COVID-19 had more severe HF, both according to clinical tests and according to the blood concentration of N-terminal pro-brain natriuretic peptide (NT-proBNP), mainly with the preserved ejection fraction (EF) with a higher prevalence of left atrial (LA) enlargement in combination with a decrease in right ventricular (RV) systolic function and its dilatation. In patients after COVID-19 in the presence of chronic kidney disease, the RR for HF increased by 4,5 times; in the presence of C-reactive protein >4 mg/l — by 1,6 times.Conclusion. Every fifth patient with shortness of breath 3,5 months after COVID-19 had more severe HF, both according to clinical tests and according to blood NT- proBNP concentration, mainly with preserved EF with a higher prevalence of LA increase in combination with a decrease in RV systolic function and its dilatation. The risk of HF is interrelated with the female sex and multiple comorbidities.

Risk of heart failure in patients with type 2 diabetes receiving insulin therapy: a meta-analysis of observational studies

Aim. To compare the effect of insulin therapy and oral hypoglycemic agents (OHAs) on the risk of heart failure (HF) in patients with type 2 diabetes (T2D) using different databases.Material and methods. The systematic review and meta-analysis were carried out in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The analysis included studies that compared the risk of HF in T2D patients, depending on the OHA therapy in the presence of a group of patients receiving insulin therapy. The inclusion criteria were a duration of treatment of at least two years with at least 1000 included patients. The analysis did not include studies that compared the types and regimens of insulin therapy without a control group (antidiabetic drugs), which included patients with acute complications of type 2 diabetes and unstable conditions associated with comorbidities, in which no clinical outcomes were reported. Search was conducted in August 2022 using several databases (PubMed, Cochrane Central Register of Controlled Trials (CENTRAL) at the Cochrane Library, Elibrary) using the following keywords: heart failure development, 2 type diabetes mellitus, insulin.Results. Of the 1085 publications found in the search, 5 retrospective observational cohort clinical trials, including a total of 179777 patients with a mean duration of treatment of 67,2 months, met all criteria and were included in the analysis. Statistical analysis of the relative risk (RR) of HF in T2D patients receiving insulin therapy revealed a RR increase in all studies with a total RR using fixed effects model of 2,598 (95% confidence interval (CI), 2,346-2,878; p<0,001), while using the random effects model — 2,382 (95% CI, 1,565-3,626; p<0,001). When checking the statistical heterogeneity of the studies, a high heterogeneity was revealed (I2=93,8%).Conclusion. Meta-analysis of 5 retrospective observational studies including 179777 patients with T2D with a mean duration of treatment of 67,2 months showed that insulin therapy (without insulin glargine and degludec) in comparison with OHAs (without sodium-glucose cotransporter-2 inhibitors and glucagon-like peptide type 1 receptor agonists) significantly increased the RR for HF using a fixed effects model by 2,6 times, while using the random effects model — by 2,4 times (p<0,001 for both).

Clinical outcomes of myocarditis after SARS-CoV-2 mRNA vaccination in four Nordic countries: population based cohort study

ObjectiveTo investigate the clinical outcomes of myocarditis associated with mRNA vaccines against the SARS-CoV-2 virus compared with other types of myocarditis.DesignPopulation based cohort study.SettingNationwide register data from four Nordic countries...

Optimal cardiometabolic health and risk of heart failure in type 2 diabetes: an analysis from the Look AHEAD trial.

To evaluate the contribution of baseline and longitudinal changes in cardiometabolic health (CMH) towards heart failure (HF) risk among adults with type 2 diabetes (T2D). Participants of the Look AHEAD trial with T2D and without prevalent HF were included. Adjusted Cox models were used to create a CMH score incorporating target levels of parameters weighted based on relative risk for HF. The associations of baseline and changes in the CMH score with risk of overall HF, HF with preserved (HFpEF) and reduced ejection fraction (HFrEF) were assessed using Cox models. Among the 5080 participants, 257 incident HF events occurred over 12.4 years of follow-up. The CMH score included 2 points each for target levels of waist circumference, glomerular filtration rate, urine albumin-to-creatinine ratio, and 1 point each for blood pressure and glycated haemoglobin at target. High baseline CMH score (6-8) was significantly associated with lower overall HF risk (adjusted hazard ratio [HR], ref=low score (0-3): 0.31, 95% confidence interval [CI] 0.21-0.47) with similar associations observed for HFpEF and HFrEF. Improvement in CMH was significantly associated with lower risk of overall HF (adjusted HR per 1-unit increase in score at 4 years: 0.80, 95% CI 0.70-0.91). In the ACCORD validation cohort, the baseline CMH score performed well for predicting HF risk with adequate discrimination (C-index 0.70), calibration (chi-square 5.53, p=0.70), and risk stratification (adjusted HR [high (6-8) vs. low score (0-3)]: 0.35, 95% CI 0.26-0.46). In the Look AHEAD subgroup with available biomarker data, incorporating N-terminal pro-B-type natriuretic peptide to the baseline CMH score improved model discrimination (C-index 0.79) and risk stratification (adjusted HR [high (8-10) vs. low score (0-4)]: 0.18, 95% CI 0.09-0.35). Achieving target levels of more CMH parameters at baseline and sustained improvements were associated with lower HF risk in T2D.

Association of baseline and longitudinal changes in cardiometabolic health with risk of heart failure among adults with type 2 diabetes: an analysis from the Look AHEAD trial

Abstract Background Type 2 diabetes (T2D) is characterized by co-morbid cardiometabolic abnormalities and elevated heart failure (HF) risk. Purpose The purpose of this study was to evaluate the associations of baseline and longitudinal changes in cardiometabolic health with risk of HF among adults with T2D. Methods Adults with T2D enrolled in the Look AHEAD (Action for Health in Diabetes) trial without prevalent HF were included. Adjusted Cox models were used to create a cardiometabolic health score incorporating target levels of parameters weighted based on relative risk for HF. The associations of baseline, 1- and 4-year changes in the cardiometabolic health score with risk of overall HF, HF with preserved ejection fraction (HFpEF; EF≥50%), and HF with reduced EF (HFrEF; EF<50%) were assessed using adjusted Cox models. Results Of the 5,080 participants included, there were 257 incident HF events during 12.4-year follow-up. The cardiometabolic health score included 2-points each for target levels of waist circumference, glomerular filtration rate, urine albumin-to-creatinine ratio and 1-point each for blood pressure and hemoglobin A1c at target (Table 1). Higher baseline cardiometabolic health score was significantly associated with lower risk of overall HF (adjusted hazard ratio [aHR] per 1-unit higher score, 0.72 [95% CI, 0.66–0.79]) with similar associations observed for HFpEF and HFrEF (Table 2). Improvement in cardiometabolic health over 1- and 4-years was significantly associated with lower risk of overall HF (aHR per 1-unit increase in score at 1- and 4-years, 0.82 [95% CI, 0.73–0.92] and 0.80 [95% CI, 0.70–0.91], respectively). Conclusions Among adults with T2D, achieving target levels of more cardiometabolic health parameters at baseline and sustained improvements were associated with lower HF risk. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Institute of Diabetes and Digestive and Kidney Diseases

Effects of Gut Microbiota and Metabolites on Heart Failure and Its Risk Factors: A Two-Sample Mendelian Randomization Study.

IntroductionPrevious observational studies have indicated that gut microbiota and metabolites may contribute to heart failure and its risk factors. However, with the limitation of reverse causality and confounder in observational studies, such relationship remains unclear. This study aims to reveal the causal effect of gut microbiota and metabolites on heart failure and its risk factors.MethodsThis study collected summary statistics regarding gut microbiota and metabolites, heart failure, diabetes, hypertension, chronic kidney disease, myocardial infarction, atrial fibrillation, hypertrophic cardiomyopathy, dilated cardiomyopathy, coronary heart disease, valvular heart disease, and myocarditis. Two-sample Mendelian randomization analysis was performed using MR-Egger, inverse variance weighted (IVW), MR-PRESSO, maximum likelihood, and weighted median.ResultsResults from gene prediction showed that among all gut microbiota, candida, shigella, and campylobacter were not associated with higher incidence of heart failure. However, genetic prediction suggested that for every 1 unit increase in shigella concentration, the relative risk increased by 38.1% for myocarditis and 13.3% for hypertrophic cardiomyopathy. Besides, for every 1 unit increased in candida concentration, the relative risk of chronic kidney disease increased by 7.1%. As for intestinal metabolites, genetic prediction results suggested that for every 1 unit increase in betaine, the relative risk of heart failure and myocardial infarction increased by 1.4% and 1.7%, separately.ConclusionsThis study suggested new evidence of the relationship between gut microbiota and heart failure and its risk factors, which may shed light on designing microbiome- and microbiome-dependent metabolite interventions on heart failure and its risk factors in clinical trials in the future.

Contribution of inflammation to heart failure development in human immunodeficiency virus-infected patients

Aim. To determine the peculiarities of heart failure (HF) development in human immunodeficiency virus (HIV)-infected patients, depending on the blood concentration of C-reactive protein (CRP).Material and methods. This cross-sectional screening clinical trial included 100 patients hospitalized with HIV infection and a history of HF for 28 months. The patients were divided into 2 groups depending on blood CRP concentration. The cut-off point was CRP of 15 mg/l. The first group included 37 HIV-infected patients with HF and blood CRP <15 mg/l, while the second group — 63 HIV-infected patients with HF and CRP concentration ≥15 mg/l. The inclusion criteria were HIV infection and prior HF, stable medical state, taking into account the underlying disease that required hospitalization. The study did not include patients with acute cardiovascular diseases within prior 3 months, acute decompensated and acute heart failure, cancer, infectious diseases, conditions that required surgical intervention. N-terminal pro-brain natriuretic peptide (NT-proBNP) was determined in all patients.Results. Correlation analysis revealed a strong inverse relationship between the blood concentrations of NT-proBNP and CRP (r=-0,639; p<0,005). A ROC curve revealed the most optimal cut-off threshold of 9,8 mg/l (AUC=0,796, p<0,05), which ensures sensitivity of 92,9% (p<0,05) and specificity of 57,6% (p<0,05). The odds ratio (OR) of an increase in NT-proBNP >450 pg/ml, and hence the risk of acute decompensated HF in the presence of a CRP concentration of 1-9,8 mg/l in HIV-infected patients with HF was 44,73 (95% CI=8,62;311,10), while relative risk (RR) — 18,73 (95% CI=4,94;112,94). In the presence of in hospital inflammatory diseases and CRP ≥15 mg/l in HIV-infected patients and prior HF, the RR of acute decompensated HF is reduced by 88% (RR=0,12, 95% CI=0,03-0,33).Conclusion. CRP values from 1 to 9,8 mg/l in HIV-infected patients with HF are predictors of its severity, characterized by a higher incidence of HF with reduced ejection fraction, diastolic dysfunction and left ventricular hypertrophy without significant differences with patients who have CRP >9,8 mg/l. CRP concentration >9,8 mg/l in HIV-infected patients and prior HF indicates the development of an inflammatory process, and not a worsening of the HF course.

Risk of heart failure depending on the state of renal filtration function in patients with uncomplicated hypertension

Aim. To assess the risk of heart failure (HF) depending on the state of renal filtration function in patients with uncomplicated hypertension (HTN) without kidney dysfunction.Material and methods. This cross-sectional screening clinical trial consecutively included 176 outpatients with uncomplicated HTN and without chronic kidney disease (CKD). To assess the HF risk, the blood concentration of N-terminal pro-brain natriuretic peptide (NT-proBNP) was determined. To assess the renal filtration function, the blood serum concentration of creatinine and cystatin C was determined, followed by glomerular filtration rate (GFR) estimation using the CKDEPI equation with both parameters. Echocardiography was performed to assess the cardiac structural and functional state.Results. Correlation analysis revealed a moderate direct relationship between NT-proBNP and blood cystatin C concentration (r=0,370; p<0,005), as well as a moderate inverse relationship with GFR (CKD-EPIcre) and GFR (CKD-EPIcys) (r= -0,321; p<0,05 and r=-0,360; p<0,005, respectively). ROC curve for all available values of blood cystatin C revealed the most optimal cut-off threshold of 1016 ng/ml (AUC=0,726, p<0,001), which ensures the sensitivity of 72,2% (p<0,001) and specificity of 62,0% (p<0,001). ROC curve for all available GFR values (CKD-EPIcys) revealed a cut-off threshold of 74 ml/min/1,73 m2 (AUC=0,702, p=0,002) with a sensitivity and specificity of 55,6% and 74,7%, respectively (p=0,001 and p=0,001, respectively). Taking into account the cut-off points for cystatin C and GFRcys, the first group consisted of 73 (41,48%) patients with cystatin C ≥1016 ng/ml and GFR (CKD-EPIcys) ≤74 ml/min/1,73 m2, while the second one — 103 (58,52%) patients with cystatin C <1016 pg/ml and GFR (CKDEPIcys) >74 ml/min/1,73 m2. The presence of impaired glucose tolerance, left ventricular diastolic dysfunction (LV DD), LV hypertrophy and left atrial enlargement leads to an additional increase in HF risk in patients with uncomplicated HNT without CKD.Conclusion. The ROC analysis showed that cystatin C and cystatin C-based GFR (CKD-EPIcys) can be used as markers of HF risk in patients with uncomplicated HTN without CKD. With an increase in cystatin C ≥1016 ng/ml, the relative risk of HF is 2,99, while with a decrease in GFR (CKD-EPIcys) ≤74 ml/min/1,73 m2 — 1,26. The presence of impaired glucose tolerance, LV DD, LV hypertrophy and left atrial enlargement in patients with uncomplicated HTN without CKD with a cystatin C increase ≥1016 ng/ml and a decrease in GFR (CKD-EPIcys) ≤74 ml/min/1,73 m2 and below further increases the risk of developing CHF.

SGLT2 inhibitor dapagliflozin prevents atherosclerotic and cardiac complications in experimental type 1 diabetes.

IntroductionCardiovascular disease (CVD) is two to five times more prevalent in diabetic patients and is the leading cause of death. Therefore, identification of novel therapeutic strategies that reduce the risk of CVD is a research priority. Clinical trials showed that reduction in the relative risk of heart failure by sodium-glucose cotransporter 2 inhibitors (SGLT2i) are partly beyond their glucose lowering effects, however, the molecular mechanisms are still elusive. Here we investigated the role of SGLT2i dapagliflozin (DAPA) in the prevention of diabetes-induced cardiovascular complications.MethodsType 1 diabetes was induced with streptozotocin (65 mg/bwkg, ip.) in adult, male Wistar rats. Following the onset of diabetes rats were treated for six weeks with DAPA (1 mg/bwkg/day, po.).ResultsDAPA decreased blood glucose levels (D: 37±2.7 vs. D+DAPA: 18±5.6 mmol/L; p<0.05) and prevented metabolic decline. Aortic intima-media thickening was mitigated by DAPA. DAPA abolished cardiac hypertrophy, and myocardial damage. Cardiac inflammation and fibrosis were also moderated after DAPA treatment.ConclusionsThese data support the preventive and protective role of SGLT2i in diabetes-associated cardiovascular disease. SGLT2i may provide novel therapeutic strategy to hinder the development of cardiovascular diseases in type 1 diabetes, thereby improve the outcomes.

Abstract 11702: Sex Differences in Diabetic Cardiomyopathy: Greater Reduction in Myocardial Perfusion Reserve in Women Than Men Driven by Increased Resting Perfusion

Introduction: Type 2 diabetes (T2D) confers a higher relative risk of heart failure in women than men. Women also have a greater prevalence of heart failure with preserved ejection fraction (HFpEF), linked to microvascular dysfunction. We hypothesize that sex-specific differences are present in the pathophysiological alterations of myocardial structure, function, and perfusion associated with T2D. Methods: Cross-sectional case-control study. Participants underwent comprehensive cardiac phenotyping with echocardiography and cardiac magnetic resonance with adenosine stress/rest perfusion. Global myocardial perfusion was derived as a mean of three short axis slices. Image analysis was performed by two observers blinded to all participant information. Statistical analysis was performed with independent-sample T-tests or Mann-Whitney test. Results: Individuals with T2D (n=287, 41% female) were compared with age-matched controls (n=87, 41% female). Women with T2D were more obese than men (body mass index 35.7±7.2 vs 32.4±5.3 kg/m 2 , p&lt;0.05). Both women and men with T2D had increased left ventricular (LV) concentric remodelling (greater LV mass/volume ratio), impaired diastolic (higher E/e’) and systolic (lower global longitudinal strain) function compared to controls. LV mass index was significantly increased in women only. Comparing T2D and controls, stress perfusion was not significantly different in both sexes whereas resting perfusion was increased in women (1.4±0.6 vs 1.0±0.4 ml/min/g, p&lt;0.05) but not in men. Consequently, women with T2D have a lower myocardial perfusion reserve than men (2.6±0.9 vs 3.1±0.9, p&lt;0.001). Conclusions: In asymptomatic people with T2D, women have increased LV mass index and lower myocardial perfusion reserve than men, driven primarily by increased resting perfusion. These findings support the growing evidence that microvascular dysfunction partly explains the greater risk of HFpEF in women with T2D.

The risk of non-steroidal anti-inflammatory drug-induced heart failure in people with chronic kidney disease: a systematic review

AimTo examine the risk of non-steroidal anti-inflammatory drug-induced heart failure in patients with chronic kidney disease.MethodsEmbase, Medline, CENTRAL, Web of Science, and Google Scholar were searched for papers published in English between 1st January 1999 and 31st May 2020. Papers were included if some participants had chronic kidney disease, were exposed to non-steroidal anti-inflammatory drugs, and where heart failure was measured as an outcome. Papers were assessed for risk of bias using the Cochrane Risk of Bias 2 tool for randomised controlled trials, and ROBINS-I for observational studies.ResultsA total of 2480 independent papers were retrieved. Following abstract screening, 165 full texts were reviewed to identify seven eligible papers: two randomised controlled trials, four cohort studies, and one case-control study. For chronic kidney disease (stage 3–5), relative risk for heart failure ranged from 0.3 to 1.9 with 95% confidence interval 0.04 to 15.1. Results were not pooled due to study heterogeneity. We attributed bias to heterogenous populations studied, probable confounding due to partially adjusted risk estimates, and heterogenous measurement of the heart failure outcome.ConclusionOverall, there are only a few studies to refute or support an increased risk of heart failure associated with taking non-steroidal anti-inflammatory drugs in patients with chronic kidney disease, and therefore no robust evidence was available.

Women With Diabetes Are at Increased Relative Risk of Heart Failure Compared to Men: Insights From UK Biobank.

Aims: To investigate the effect of diabetes on mortality and incident heart failure (HF) according to sex, in the low risk population of UK Biobank. To evaluate potential contributing factors for any differences seen in HF end-point.Methods: The entire UK Biobank study population were included. Participants that withdrew consent or were diagnosed with diabetes after enrolment were excluded from the study. Univariate and multivariate cox regression models were used to assess endpoints of mortality and incident HF, with median follow-up periods of 9 years and 8 years respectively.Results: A total of 493,167 participants were included, hereof 22,685 with diabetes (4.6%). Two thousand four hundred fifty four died and 1,223 were diagnosed or admitted with HF during the follow up periods of 9 and 8 years respectively. Overall, the mortality and HF risk were almost doubled in those with diabetes compared to those without diabetes (hazard ratio (HR) of 1.9 for both mortality and heart failure) in the UK Biobank population. Women with diabetes (both types) experience a 22% increased risk of HF compared to men (HR of 2.2 (95% CI: 1.9–2.5) vs. 1.8 (1.7–2.0) respectively). Women with type 1 diabetes (T1DM) were associated with 88% increased risk of HF compared to men (HR 4.7 (3.6–6.2) vs. 2.5 (2.0–3.0) respectively), while the risk of HF for type 2 diabetes (T2DM) was 17% higher in women compared to men (2.0 (1.7–2.3) vs. 1.7 (1.6–1.9) respectively). The increased risk of HF in women was independent of confounding factors. The findings were similar in a model with all-cause mortality as a competing risk. This interaction between sex, diabetes and outcome of HF is much more prominent for T1DM (p = 0.0001) than T2DM (p = 0.1).Conclusion: Women with diabetes, particularly those with T1DM, experience a greater increase in risk of heart failure compared to men with diabetes, which cannot be explained by the increased prevalence of cardiac risk factors in this cohort.

Risk of heart failure depending on the structure and subclinical target organ damage in patients with hypertension

Aim. To determine the risk of heart failure (HF) in patients with hypertension (HTN) depending on the structure of subclinical target organ damage (TOD). Material and methods. The study included 234 patients with HTN without signs of HF. The mean age was 45,96±8,54 years. The patients underwent echocardiography with an assessment of myocardial mass index, ejection fraction, left ventricular diastolic function. Volumetric sphygmoplethysmography with determination of cardio-ankle vascular index (CAVI1) and carotid-femoral pulse wave velocity (PWVcf). Cystatin C blood concentration with the calculation of the glomerular filtration rate (GFR) was performed. NT-proBNP blood levels was also determined. Patients were divided into 4 groups depending on the presence and structure of subclinical TOD. The first group consisted of 74 (31,6%) patients without documented subclinical TOD; the second group — 99 (42,3%) patients with one subclinical TOD; the third group — 42 (18,0%) patients with two TOD; the fourth group -19 (8,1%) patients with three TOD. Results. Patients in the groups differed significantly in blood NT-proBNP concentration (p&lt;0,001). As the amount of TOD increased, NT-proBNP increased above the reference value 125 pg/ml (p=0,010). The odds ratio (OR) and relative risk (RR) of HF, determined by NT-proBNP concentration &gt;125 pg/ml, were significantly associated with the TOD structure compared to the group without confirmed TOD (p=0,035, p=0,21, p=0,044, respectively). Correlation analysis revealed direct relationships between the NT-proBNP level and TOD amount (r=0,56; p&lt;0,005), LVH (r=0,33; p&lt;0,005), cystatin C level (r=0,31; p&lt;0,005), CAVI1 and PWVcf (r=0,23; p&lt;0,005 and r=0,26; p&lt;0,005, respectively). Conclusion. The risk of HF in patients with hypertension depends on the presence and structure of subclinical TOD. With the involvement of one target organ, OR and RR for HF were 4,23 and 3,74, respectively (95% CI for OR, 1,09-19,19; for RR, 1,08-16,03); with the involvement of two target organs — 5,57 (95% CI, 1,2328,51) and 4,70 (95% CI, 1,21-21,84), respectively; with the multiple TOD — 6,31 (95% CI, 1,4-40,83) and 5,19 (95% CI, 1,04-27,95), respectively.

A population-based study of risk factors for heart failure in pediatric and adult-onset systemic lupus erythematosus

ObjectivesThe increased relative risk of heart failure (HF) from systemic lupus erythematosus (SLE) is greatest at younger ages, but the etiology remains unclear. We identified risk factors for HF in children and adults with SLE and evaluated associations between SLE manifestations and HF. MethodsIncident SLE cases without preceding HF were identified using Clinformatics DataMart® (OptumInsight, Eden Prairie, MN) US claims data (2000-2015), and categorized by age of SLE onset (children 5–17, young adults 18–24, adults 25–44 years old). The primary outcome was the first HF ICD-9-CM diagnosis code (428.x), categorized as early-onset (< 6 months) or delayed-onset. Multivariable logistic regression was used to identify factors associated with early or delayed-onset HF. Cox proportional hazards regression was used to identify time-dependent associations between the onset of SLE manifestations and incident HF. ResultsThere were 523 (2.3%) HF cases among 1,466 children, 2,163 young adults and 19,349 adults age 25–44 with SLE. HF in children and young adults was early-onset in 50% and 60% of cases, respectively, compared to 35% of cases in adults 25–44 years old. There was a temporal association between incident myopericarditis and valvular disease diagnoses and early-onset HF, whereas nephritis and hypertension were more strongly associated with delayed-onset HF. Black race remained independently associated with a 1.5-fold increased HF risk at any time. ConclusionHypertension remains an important traditional CV risk factor across all ages and should be managed aggressively even in younger patients with SLE. Cardiac dysfunction due to acute cardiac manifestations of SLE may contribute to the very high relative incidence of early HF diagnoses among younger SLE patients. Therefore, future prospective studies will need to address heterogeneity in the types and severity of heart failure in order to determine etiology and which patients should be monitored.

Ivabradine Improves Cardiac Function and Increases Exercise Capacity in Patients with Chronic Heart Failure.

To systematically review and conduct a meta-analysis of the ivabradine-induced improvement in cardiopulmonary function, exercise capacity, and primary composite endpoints in patients with chronic heart failure (CHF).This study was a systematic review and meta-analysis.Databases, including PubMed, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), and Clinical Trials and European Union Clinical Trials, were searched for randomized placebo-controlled trials. The efficacy and safety of ivabradine treatment in patients with CHF were assessed and compared to those of the standard anti-heart failure treatment. Review Manager 5.3 software was used to analyze the relative risk (RR) for dichotomous data and the mean difference (MD) for continuous data.In total, 22 studies with 24,562 patients were included. Cardiopulmonary function analysis showed that treatment with added ivabradine reduced the heart rate (MD = -17.30, 95% confidence interval (CI): 19.52--15.08, P < 0.00001), significantly increased the left ventricular ejection fraction (LVEF) (MD = 3.90, 95% CI: 0.40-7.40, P < 0.0001), and led to a better New York Heart Association (NYHA) classification. Ivabradine significantly reduced the minute ventilation/carbon dioxide production (VE/VCO2) (MD = -2.68, 95% CI: -4.81--0.55, P = 0.01) and improved the peak VO2 (MD = 2.80, 95% CI: 1.05-4.55, P = 0.002) and the exercise capacity, including the exercise duration with a submaximal load (MD = 7.82, 95% CI: -2.57--18.21, P < 0.00001) and the 6-minute walk distance. The RR of cardiovascular death or worsening heart failure was significantly decreased (RR = 0.93, 95% CI: 0.87--0.98, P = 0.01) in the patients treated with ivabradine. Additionally, the RRs of heart failure and hospitalization also decreased (RR = 0.91, 95% CI: 0.85--0.97, P = 0.006; RR = 0.86, 95% CI: 0.79--0.93, P = 0.0002). Safety analysis showed no significant difference in the RR of severe adverse events between the ivabradine group and the standard anti-heart failure treatment group (P = 0.40). However, ivabradine significantly increased the RR of visual symptoms in CHF patients (RR = 3.82, 95% CI: 1.80--8.13, P = 0.0005).Existing evidence showed that adding ivabradine treatment significantly improved the cardiopulmonary function and increased the exercise capacity of patients with CHF. Adding ivabradine to the standard anti-heart failure treatment reduced the mortality and hospitalization risk and improved the quality of life. Finally, ivabradine significantly increased the RR of visual symptoms in CHF patients.This is the first systematic review and meta-analysis to focus on the efficacy of ivabradine, which improved the cardiac function and increased the exercise capacity in patients with chronic heart failure (CHF). Therefore, this study will help evaluate the quality of life after adding ivabradine to the treatment of patients with CHF, even though there are differences in the standard for resting heart rate, left ventricular ejection fraction (LVEF), and New York Heart Association (NYHA) class in the included studies. This hybrid effect might be smaller when analyzed separately but might have a higher heterogeneity when analyzed in multiple studies.

1269-P: Assessing the Performance of the UKPDS 82 Risk Equations to Predict Cardiovascular Events in the DECLARE-TIMI 58 Trial Population

Risk equations (RE) from the UK Prospective Diabetes Study (UKPDS) remain the most commonly used within economic models of type 2 diabetes mellitus (T2DM). However, clinical practice has evolved since UKPDS reported and the applicability of these RE to contemporary T2DM patients is uncertain. The Dapagliflozin Effect on Cardiovascular Events (DECLARE)-TIMI 58 trial assessed cardiovascular (CV) outcomes in a broad T2DM population treated with dapagliflozin (DAPA) versus placebo (PLA). This study aimed to assess the performance of the UKPDS 82 RE in the DECLARE-TIMI 58 population. RE for myocardial infarction (MI), heart failure (HF) and stroke were applied to baseline characteristics and 12-month effects of DAPA versus PLA on HbA1c, weight and blood pressure from DECLARE-TIMI 58. Predicted annual probabilities were converted to event rates per 1,000-person years and associated relative risks (RR) for DAPA versus PLA derived for comparison to trial outcomes. Due to misalignment of the UKPDS and DECLARE-TIMI 58 endpoints, predictions of congestive heart failure were compared to observed incidence of hospitalization for HF and stroke to ischemic stroke, respectively. Predicted (study reported) rates per 1,000 person years for MI, HF and stroke were 8.15 (11.7), 2.47 (6.20) and 3.28 (6.90) for DAPA, and 8.53 (13.2), 2.59 (8.50) and 3.46 (6.80) for PLA. Predicted RR of MI, HF and stroke for DAPA versus PLA were 0.96, 0.95, 0.95, respectively, compared to reported hazard ratios of 0.89 (95% CI: 0.77, 1.01), 0.73 (0.61, 0.88) and 1.01 (0.84, 1.21) in DECLARE-TIMI 58. UKPDS 82 RE did not predict the reduction in CV events demonstrated for DAPA versus PLA based on risk factor improvements observed in DECLARE-TIMI 58. These findings add to a growing body of evidence that suggests the CV effects of sodium-glucose co-transporter inhibitors such as DAPA cannot be fully described via treatment-induced changes in conventional prognostic factors. Disclosure P. McEwan: Consultant; Self; AstraZeneca. Employee; Self; Health Economics and Outcomes Research Ltd. V. Foos: Employee; Self; Health Economics and Outcomes Research Ltd., IQVIA. H. Bennett: Consultant; Self; AstraZeneca. Employee; Self; Health Economics and Outcomes Research Ltd. B. Kartman: Employee; Self; AstraZeneca. Stock/Shareholder; Self; AstraZeneca. C. Edmonds: Employee; Self; AstraZeneca. I.A. Gause-Nilsson: Employee; Self; AstraZeneca. Funding AstraZeneca

ABO blood type and risk of porcine bioprosthetic aortic valve degeneration: SWEDEHEART observational cohort study

ObjectiveBlood type A antigen on porcine aortic bioprostheses might initiate an immune reaction leading to an increased frequency of structural valve deterioration in patients with blood type B or O....

Association Between Cardiorespiratory Fitness and Risk of Heart Failure: A Meta-Analysis

Evidence emerges that cardiorespiratory fitness (CRF) might be implicated in the development of heart failure (HF). This meta-analysis aimed to quantify the association between CRF exposed at baseline and HF risk with dose-response analysis and to assess whether CRF changes over time are correlated with alterations in HF risk. Cohort studies that assessed the association between CRF and risk of HF in subjects without baseline HF were included. Study-specific multivariate-adjusted relative risks (RRs) with 95% confidence intervals (CIs) were pooled using a random-effects model. Ten studies from 8 articles were included, enrolling 8987 incident HF cases from 154,598 participants. The RR of HF per 1-metabolic equivalent (MET) higher CRF at baseline was 0.82 (95% CI 0.80-0.84) in the overall population. The RRs were similar in men (0.82, 95% CI 0.80-0.85) and women (0.81, 95% CI 0.78-0.84), and remained minorly changed in patients with existing diabetes, hypertension, or cardiovascular disease at entry. No evidence of a nonlinear relationship between CRF at baseline and risk of HF was observed (Pnonlinearity = .18). The RR of HF per 1-MET increase in CRF over time was 0.79 (95% CI 0.67-0.93), and the measurement of CRF provided incremental value to the prediction of HF beyond conventional models. High or increased CRF resulted in reduced risk of HF in a dose-dependent manner, supporting the necessity to increase CRF to prevent HF in clinical practice.