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Post‐traumatic stress disorder (PTSD) is an independent risk factor for incident heart failure, but the underlying cardiac mechanisms remained elusive. Impedance cardiography (ICG), especially when measured during stress, can help understand the underlying psychophysiological pathways linking PTSD with heart failure. We investigated the association between PTSD and ICG‐based contractility metrics (pre‐ejection period (PEP) and Heather index (HI)) using a controlled twin study design with a laboratory‐based traumatic reminder stressor. PTSD status was assessed using structured clinical interviews. We acquired synchronized electrocardiograms and ICG data while playing personalized‐trauma scripts. Using linear mixed‐effects models, we examined twins as individuals and within PTSD‐discordant pairs. We studied 137 male veterans (48 pairs, 41 unpaired singles) from Vietnam War Era with a mean (standard deviation) age of 68.5(2.5) years. HI during trauma stress was lower in the PTSD vs. non‐PTSD individuals (7.2 vs. 9.3 [ohm/s2], p =.003). PEP reactivity (trauma minus neutral) was also more negative in PTSD vs. non‐PTSD individuals (−7.4 vs. −2.0 [ms], p =.009). The HI and PEP associations with PTSD persisted for adjusted models during trauma and reactivity, respectively. For within‐pair analysis of eight PTSD‐discordant twin pairs (out of 48 pairs), PTSD was associated with lower HI in neutral, trauma, and reactivity, whereas no association was found between PTSD and PEP. PTSD was associated with reduced HI and PEP, especially with trauma recall stress. This combination of increased sympathetic activation and decreased cardiac contractility combined may be concerning for increased heart failure risk after recurrent trauma re‐experiencing in PTSD. Our study employed an innovative technique involving replaying scripts from previous traumas in veterans with and without post‐traumatic stress disorder (PTSD) to study the potential relationship of trauma‐induced stress and cardiac pathophysiology. This is the first investigation to examine the association of PTSD and impedance cardiogram‐based contractility metrics during a trauma recall. We found robust relationships between PTSD and worsened cardiac contractility, as well as increased sympathetic activation, particularly during trauma reminders. [ABSTRACT FROM AUTHOR]

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

Abstract Aims Heart failure (HF) is associated with several metabolic changes, but it is unknown whether distinct components of the circulating metabolome may be related to cardiac structure and function, and with incident HF in the community. Methods and results We assayed 217 circulating metabolites in 2336 Framingham Study participants (mean age 55 ± 10 years, 53% women) without HF at baseline. We used linear and Cox regression to relate concentrations of metabolites to left ventricular (LV) diastolic dimension, LV wall thickness, LV ejection fraction, left atrial dimension, LV ventricular mass, and aortic root size cross‐sectionally and to incident HF prospectively. Bonferroni‐adjusted P‐values

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; p74 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.

Aims: Congestion is a cardinal feature of untreated heart failure (HF) and might be detected by ultrasound (US) before overt clinical signs appear. Methods and results: We investigated the prevalence and clinical associations of subclinical congestion in 238 patients with at least one clinical risk factor for HF (diabetes, ischaemic heart disease, or hypertension) using three US variables: (i) inferior vena cava (IVC) diameter; (ii) jugular vein distensibility (JVD) ratio (the ratio of the jugular vein diameter during the Valsalva manoeuvre to that at rest); (iii) the number of B‐lines from a 28‐point lung US. US congestion was defined as IVC diameter > 2.0 cm, JVD ratio < 4.0 or B‐lines count > 14. The prevalence of subclinical congestion (defined as at least one positive US marker of congestion) was 30% (13% by IVC diameter, 9% by JVD ratio and 13% by B‐line quantification). Compared to patients with no congestion on US, those with at least one marker had larger left atria and higher plasma concentrations of natriuretic peptides. Patients with raised plasma N‐terminal pro‐B‐type natriuretic peptide/B‐type natriuretic peptide had a lower JVD ratio (7.69 vs. 8.80; P = 0.05) and more often had at least one lung B‐line (74% vs. 63%; P = 0.05). However, plasma natriuretic peptide concentrations were more closely related to left atrial volume than other US measures of congestion. Conclusions: Subclinical evidence of congestion by US is common in patients with clinical risk factors for HF. Whether these measurements provide additional value for predicting the development of HF and its prevention deserves consideration. [ABSTRACT FROM AUTHOR]

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 (p125 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

Aims: Heart failure (HF) is associated with several metabolic changes, but it is unknown whether distinct components of the circulating metabolome may be related to cardiac structure and function, and with incident HF in the community. Methods and results: We assayed 217 circulating metabolites in 2336 Framingham Study participants (mean age 55 ± 10 years, 53% women) without HF at baseline. We used linear and Cox regression to relate concentrations of metabolites to left ventricular (LV) diastolic dimension, LV wall thickness, LV ejection fraction, left atrial dimension, LV ventricular mass, and aortic root size cross‐sectionally and to incident HF prospectively. Bonferroni‐adjusted P‐values <0.05 denoted statistical significance. Circulating concentrations of kynurenine [β = −0.12 cm per standard deviation (SD) increment in normalized residual of metabolite, P = 7.3 × 10−8] and aminoadipate (−0.11 cm per SD increment, P = 2.61 × 10−5) were associated with left ventricular diastolic dimension, phosphatidylcholine (carbon:double bound = 38:6) with left atrial dimension (0.10 cm per SD increment, P = 9.7 × 10−6), and cholesterol ester (carbon:double bound = 20:5) with left atrial dimension (0.10 cm per SD increment, P = 1.4 × 10−5) in multivariable‐adjusted models. During an average follow‐up of 15.8 (range 0.02–23.2) years, 113 participants (5%) were diagnosed with HF with reduced ejection fraction and 106 individuals (5%) with HF with preserved ejection fraction. In multivariable analyses, concentrations of phosphatidylcholine (hazard ratio 0.63, P = 1.3 × 10−5) and ornithine (hazard ratio 1.44, P = 0.00014) were associated with HF with reduced ejection fraction. Conclusions: Several metabolites, including the vasoactive metabolite kynurenine, were related to cardiac structure and function in our sample. Additional research is warranted to confirm our observations and investigate if these metabolites can risk stratify ambulatory individuals. [ABSTRACT FROM AUTHOR]

Aim: To evaluate use of CIED-generated Heart Failure Risk Score (HFRS) alerts in an integrated, multi-disciplinary approach to HF management. Methods: We undertook a prospective, single centre outcome study of patients implanted with an HFRS-enabled Medtronic CIED, generating a “high risk” alert between November 2018 and November 2020. All patients generating a “high risk” HFRS alert were managed within an integrated HF pathway. Alerts were shared with local HF teams, prompting patient contact and appropriate intervention. Outcome data on health care utilisation (HCU) and mortality were collected. A validated questionnaire was completed by the HF teams to obtain feedback. Results: 367 “High risk” alerts were noted in 188 patients. The mean patient age was 70 and 49% had a Charlson Comorbidity Score of >6. Mean number of alerts per patients was 1.95 and 44 (23%) of patients had >3 “high risk” alerts in the follow up period. Overall, 75 (39%) patients were hospitalised in the 4–6-week period of the alert; 53 (28%) were unplanned of which 24 (13%) were for decompensated HF. A total of 33 (18%) patients died in the study period. Having three or more alerts significantly increased the risk of hospitalisation for heart failure (HR 2.5, CI 1.1–5.6 p = 0.03). The feedback on the pathway was positive. Conclusions: Patients with “high risk” alerts are co-morbid and have significant HCU. An integrated approach can facilitate timely risk stratification and intervention. Intervention in these patients is not limited to HF alone and provides the opportunity for holistic management of this complex cohort.

Background: Patients with type 2 diabetes mellitus (T2DM) are at high risk of heart failure. A summary of the effects of blood glucose-lowering drugs other than glitazones on the risk of heart failure in routine clinical practice is lacking. The objective of this study was to conduct a systematic review and meta-analysis of observational studies on the risk of heart failure when using blood glucose-lowering drugs. Methods: We systematically identified and reviewed cohort and case–control studies in which the main exposure of interest was noninsulin blood glucose-lowering medications in patients with T2DM. We searched Medline, Embase, and the Cochrane Library to identify publications meeting prespecified eligibility criteria. The quality of included studies was assessed with the Newcastle-Ottawa Scale and the RTI item bank. Results were combined using fixed and random-effects models when at least 3 independent data points were available for a drug-drug comparison. Results: The summary relative risk of heart failure in rosiglitazone users versus pioglitazone users (95% CI) was 1.16 (1.05-1.28) (5 cohort studies). Heterogeneity was present (I2 = 66%). For new users (n = 4) the summary relative risk was 1.21 (1.14-1.30) and the heterogeneity was reduced (I2 = 31%);. The summary relative risk for rosiglitazone versus metformin was 1.36 (95% CI, 1.17-1.59) (n=3). The summary relative risk (95% CI) of heart failure in sulfonylureas users versus metformin users was 1.17 (95% CI, 1.06-1.29) (5 cohort studies; I2 = 24%) and 1.22 (1.02-1.46) when restricted to new users (2 studies). Information on other comparisons was very scarce. Information on dose and duration of treatment effects was lacking for most comparisons. Few studies accounted for disease severity; therefore, confounding by indication might be present in the majority of the within-study comparisons of this meta-analysis. Conclusions: Use of glitazones and sulfonylureas was associated with an increased risk of heart failure compared with metformin use. However, indication bias cannot be ruled out. Ongoing large multidatabase studies will help to evaluate the risk of heart failure in treated patients with diabetes, including those using newer blood glucose-lowering therapies. [ABSTRACT FROM AUTHOR]

Aim: To evaluate use of CIED-generated Heart Failure Risk Score (HFRS) alerts in an integrated, multi-disciplinary approach to HF management. Methods: We undertook a prospective, single centre outcome study of patients implanted with an HFRS-enabled Medtronic CIED, generating a "high risk" alert between November 2018 and November 2020. All patients generating a "high risk" HFRS alert were managed within an integrated HF pathway. Alerts were shared with local HF teams, prompting patient contact and appropriate intervention. Outcome data on health care utilisation (HCU) and mortality were collected. A validated questionnaire was completed by the HF teams to obtain feedback. Results: 367 "High risk" alerts were noted in 188 patients. The mean patient age was 70 and 49% had a Charlson Comorbidity Score of >6. Mean number of alerts per patients was 1.95 and 44 (23%) of patients had >3 "high risk" alerts in the follow up period. Overall, 75 (39%) patients were hospitalised in the 4–6-week period of the alert; 53 (28%) were unplanned of which 24 (13%) were for decompensated HF. A total of 33 (18%) patients died in the study period. Having three or more alerts significantly increased the risk of hospitalisation for heart failure (HR 2.5, CI 1.1–5.6 p = 0.03). The feedback on the pathway was positive. Conclusions: Patients with "high risk" alerts are co-morbid and have significant HCU. An integrated approach can facilitate timely risk stratification and intervention. Intervention in these patients is not limited to HF alone and provides the opportunity for holistic management of this complex cohort. [ABSTRACT FROM AUTHOR]

Although dipeptidyl peptidase (DPP)-4 inhibitors have been reported to have a neutral effect on thromboembolic vaso-occlusive events in large-scale trials, they act to potentiate several endogenous peptides that can exert deleterious cardiovascular effects. Experimentally, DPP-4 inhibitors may augment the ability of glucagon-like peptide-1 to stimulate cyclic adenosine monophosphate in cardiomyocytes, and potentiation of the effects of stromal cell-derived factor-1 by DPP-4 inhibitors may aggravate cardiac fibrosis. These potentially deleterious actions of DPP-4 inhibitors might not become clinically apparent if these drugs were to promote sodium excretion. However, the natriuretic effect of DPP-4 inhibitors is modest, because they act on the distal (rather than proximal) renal tubules. Accordingly, both clinical trials and observational studies have reported an increase in the risk of heart failure in patients with type 2 diabetes who were receiving DPP-4 inhibitors. This risk may be muted in trials with a high prevalence of metformin use or with low and declining background use of insulin and thiazolidinediones. Still, the most vulnerable patients (i.e., those with established heart failure) were not well represented in these studies. The only trial that specifically evaluated patients with pre-existing left ventricular dysfunction observed important drug-related adverse structural and clinical effects. In conclusion, an increased risk of worsening heart failure appears to be a class effect of DPP-4 inhibitors, even in patients without a history of heart failure. Additional clinical trials are urgently needed to elucidate the benefits and risks of DPP-4 inhibitors in patients with established left ventricular dysfunction., (Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)