Evidence Of Structural Heart Disease Research Articles

Association between heart failure and cerebral collateral flow in large vessel occlusive ischemic stroke

BackgroundCerebral collateral circulation plays a crucial role in determining the extent of brain ischemia in large vessel occlusive (LVO) stroke. Heart failure (HF) is known to cause cerebral hypoperfusion, yet the relationship between HF and robustness of collateral flow has not been well described. MethodsConsecutive patients with middle cerebral and/or internal carotid LVO who underwent endovascular thrombectomy (EVT) between 2012 and 2020 were included. Single-phase head CTA prior to EVT was used to assess collateral status (poor <50 % filling; good ≥50 %). Classification of HF by left ventricular ejection fraction (LVEF) on echocardiogram was used where HF with reduced ejection fraction (HFrEF) had LVEF ≤40 %, HF with preserved EF (HFpEF) had LVEF ≥50 % with evidence of structural heart disease, and no HF had LVEF≥50 % without structural heart disease. Multivariable logistic regression analyses were performed to evaluate the association between HF and poor collaterals. ResultsWe identified 235 patients, mean age was 69 ± 15 years; initial NIHSS was 18 ± 7. Of these, 107 (45.5 %) had HF and 105 (44.7 %) had poor collaterals. Those with HF were likely to have poor collaterals compared to those without HF (56.1 % vs 35.2 %, P = 0.001). There was a dose-dependent relationship between EF and poor collaterals: adjusted odds of poor collaterals were 1.63 and 2.45 in HFpEF and HFrEF, compared to those without HF (trend P = .018). ConclusionPatients with HFrEF are more likely to have poor cerebral collaterals. Further study is needed to explore the pathomechanisms. Optimization of HF may improve cerebral collaterals and enhance EVT outcomes.

Finerenone in patients with heart failure with mildly reduced or preserved ejection fraction: Rationale and design of the FINEARTS-HF trial.

Steroidal mineralocorticoid receptor antagonists (MRAs), spironolactone and eplerenone, are strongly recommended in the treatment of patients with chronic heart failure (HF) with reduced left ventricular ejection fraction (LVEF), but the balance of efficacy and safety in those with higher LVEF has not been well established. Broad use of steroidal MRAs has further been limited in part due to safety concerns around risks of hyperkalaemia, gynecomastia, and kidney dysfunction. These risks may be mitigated by the unique pharmacological properties of the non-steroidal MRA finerenone. The FINEARTS-HF trial is designed to evaluate the long-term efficacy and safety of the selective non-steroidal MRA finerenone among patients with HF with mildly reduced or preserved ejection fraction. FINEARTS-HF is a global, multicentre, event-driven randomized trial evaluating oral finerenone versus matching placebo in symptomatic patients with HF with LVEF ≥40%. Adults (≥40 years) with HF with New York Heart Association class II-IV symptoms, LVEF ≥40%, evidence of structural heart disease, and diuretic use for at least the previous 30 days were eligible. All patients required elevated natriuretic peptide levels: for patients in sinus rhythm, N-terminal pro-B-type natriuretic peptide (NT-proBNP) ≥300 pg/ml (or B-type natriuretic peptide [BNP] ≥100 pg/ml) were required, measured within 30 days (in those without a recent worsening HF event) or within 90 days (in those with a recent worsening HF event). Qualifying levels of NT-proBNP or BNP were tripled if a patient was in atrial fibrillation at screening. Estimated glomerular filtration rate <25 ml/min/1.73 m2 or serum potassium >5.0 mmol/L were key exclusion criteria. Patients were enrolled irrespective of clinical care setting (whether hospitalized, recently hospitalized, or ambulatory). The primary endpoint is the composite of cardiovascular death and total (first and recurrent) HF events. The trial started on 14 September 2020 and has validly randomized 6001 participants across 37 countries. Approximately 2375 total primary composite events are targeted. The FINEARTS-HF trial will determine the efficacy and safety of the non-steroidal MRA finerenone in a broad population of hospitalized and ambulatory patients with HF with mildly reduced or preserved ejection fraction. ClinicalTrials.gov NCT04435626 and EudraCT 2020-000306-29.

Baseline characteristics of patients with heart failure with mildly reduced or preserved ejection fraction: The FINEARTS-HF trial.

To describe the baseline characteristics of participants in the FINEARTS-HF trial, contextualized with prior trials including patients with heart failure (HF) with mildly reduced and preserved ejection fraction (HFmrEF/HFpEF). The FINEARTS-HF trial is comparing the effects of the non-steroidal mineralocorticoid receptor antagonist finerenone with placebo in reducing cardiovascular death and total worsening HF events in patients with HFmrEF/HFpEF. Patients with symptomatic HF, left ventricular ejection fraction (LVEF) ≥40%, estimated glomerular filtration rate ≥ 25 ml/min/1.73 m2, elevated natriuretic peptide levels and evidence of structural heart disease were enrolled and randomized to finerenone titrated to a maximum of 40 mg once daily or matching placebo. We validly randomized 6001 patients to finerenone or placebo (mean age 72 ± 10 years, 46% women). The majority were New York Heart Association functional class II (69%). The baseline mean LVEF was 53 ± 8% (range 34-84%); 36% of participants had a LVEF <50% and 64% had a LVEF ≥50%. The median N-terminal pro-B-type natriuretic peptide (NT-proBNP) was 1041 (interquartile range 449-1946) pg/ml. A total of 1219 (20%) patients were enrolled during or within 7 days of a worsening HF event, and 3247 (54%) patients were enrolled within 3 months of a worsening HF event. Compared with prior large-scale HFmrEF/HFpEF trials, FINEARTS-HF participants were more likely to have recent (within 6 months) HF hospitalization and greater symptoms and functional limitations. Further, concomitant medications included a larger percentage of sodium-glucose cotransporter 2 inhibitors and angiotensin receptor-neprilysin inhibitors than previous trials. FINEARTS-HF has enrolled a broad range of high-risk patients with HFmrEF and HFpEF. The trial will determine the safety and efficacy of finerenone in this population.

Ventricular tachycardia-without structural heart disease: History

This article focuses on ventricular arrythmias without evidence for structural heart disease. There are many different reasons for this type of arrythmia and there is still agap of knowledge. Starting with the first description of this disease, we present the diagnosis and management with medication, and finally catheter ablation procedures from the beginning to how it is currently treated and how it possibly will be treated in the near future.

Effects of dapagliflozin in heart failure with preserved ejection fraction and chronic obstructive pulmonary disease: an analysis of the DELIVER trial

Abstract Introduction Chronic obstructive pulmonary disease (COPD) is a common comorbidity in heart failure (HF) with preserved ejection fraction (HFpEF) and associated with worse outcomes. Purpose We investigated the relationship between COPD status and outcomes, and the efficacy of dapagliflozin, compared with placebo, according to COPD status in patients with heart failure (HF) with preserved ejection fraction (HFpEF) randomized in DELIVER. Methods A total of 6,263 patients with HF with New York Heart Association functional class II-IV, left ventricular ejection fraction &amp;gt;40%, evidence of structural heart disease, and elevated N-terminal pro–B-type natriuretic peptide levels were randomized to dapagliflozin or placebo. Clinical outcomes and the effect of dapagliflozin, according to COPD status at baseline, were examined. The primary outcome was a composite of cardiovascular death or worsening HF. Results Of the 6,261 patients with data on baseline COPD, 692 (11.1%) had a history of COPD. Compared with patients without COPD, those with COPD were older, more often men and current smokers, and they had a higher BMI, but lower systolic blood pressure. Patients with COPD also had a longer duration of HF, a higher rate of prior HF hospitalization, higher NT-proBNP, and worse NYHA functional class and KCCQ-TSS. The risk of the primary endpoint was higher in patients with COPD compared with those without COPD (adjusted HR: 1.29 (95% CI: 1.09-1.52). The benefit of dapagliflozin on the primary outcome was consistent irrespective of COPD status: no COPD, HR: 0.82 (95% CI: 0.72-0.93); COPD, HR: 0.84 (95% CI: 0.63-1.12) (Pinteraction = 0.92). Consistent effects were observed for HF hospitalization, cardiovascular death, and all-cause mortality (Table). Dapagliflozin, as compared with placebo, increased (improved) the KCCQ-TSS from baseline to 8 months to a similar extent in patients with and without COPD (Pinteraction = 0.75) (Table). Adverse events and treatment discontinuation were not more frequent with dapagliflozin than with placebo irrespective of COPD status. Conclusions COPD is common in patients with HFpEF and associated with worse outcomes. Dapagliflozin reduced the risk of worsening HF or cardiovascular death, and improved symptoms, similarly in patients with and without COPD. In addition, dapagliflozin was safe and well-tolerated, irrespective of COPD status.

A rapid wide complex tachycardia

A rapid wide complex tachycardia

Abstract WMP65: Association Between Heart Failure And Collateral Flow In Large Vessel Occlusive Ischemic Stroke

Introduction: Collateral circulation plays a crucial role in determining the extent of brain tissue ischemia and functional outcome in large vessel occlusive (LVO) stroke. Heart failure (HF) is known to cause cerebral hypoperfusion, yet the relationship between HF and robustness of collateral flow has not been well described. Here we hypothesized that HF is associated with poor collateral flow and functional outcome in patients presenting with LVO treated with mechanical thrombectomy (MT). Methods: A single center retrospective study of patients presenting with LVO ischemic stroke who underwent MT between 2012-2020 was done. Single-phase CTA of head prior to MT was used to assess collateral status with poor status defined as ≤ 50% filling and good status as &gt;50% filling. Classification of HF by left ventricular ejection fraction (LVEF) on echocardiogram was used where HF with reduced ejection fraction (HFrEF) had LVEF ≤40%, HF with preserved EF (HFpEF) had LVEF ≥50% with evidence of structural heart disease, and no HF was LVEF≥50% without structural heart disease. Functional outcome was modified Rankin scale (mRS) at 90 days with scores of 0-2 representing good outcome and 3-6 representing poor outcome. Multivariable logistic regression analyses were performed to evaluate the association between HF and poor collaterals after adjusting for vascular risk factors. Results: We identified 235 patients, mean age was 69 ±15 years, median NIHSS was 18, and 45.5% had HF (HFrEF 12.8%, HFmrEF 4.7%, HFpEF 28.1%) while 54.5% had no HF. Poor collaterals were seen in 47.7%, and those with HF were likely to have poor collaterals compared to those without HF (56.1% vs 35.1%, P=.001). There was a dose-dependent relationship between severity of HF and poor collaterals: adjusted odds of poor collaterals were 1.63 and 2.45 in HFpEF and HFrEF, compared to those without HF (trend p=.018). Patients with poor collaterals were likely to have poor outcome at 3 months compared to those with good collaterals (75.0% vs 57.8%; p=.015). Conclusion: Patients with HFrEF were twice as likely to have poor collaterals. This study demonstrated a likely mechanism for poor outcomes seen in ischemic stroke with HF, future studies may explore whether optimization of HF may augment collaterals to improve outcomes.

Efficacy and safety of dapagliflozin in patients with heart failure with mildly reduced or preserved ejection fraction by baseline glycaemic status (DELIVER): a subgroup analysis from an international, multicentre, double-blind, randomised, placebo-controlled trial

Type 2 diabetes and prediabetes are risk factors for heart failure and adverse heart failure outcomes. The Dapagliflozin Evaluation to Improve the Lives of Patients with Preserved Ejection Fraction Heart Failure (DELIVER) trial showed that dapagliflozin was associated with a reduction in the primary outcome of worsening heart failure or cardiovascular mortality in patients with heart failure with mildly reduced or preserved ejection fraction. We aimed to assess the efficacy and safety of oral dapagliflozin in these patients by their baseline glycaemia categories. DELIVER was an international, multicentre, double-blind, randomised, placebo-controlled trial done in 350 health-care centres and hospitals across 20 countries. Patients aged 40 years or older with New York Heart Association class II-IV, left ventricular ejection fraction of more than 40%, elevated natriuretic peptides (N-terminal pro B-type natriuretic peptide ≥300 pg/mL or ≥600 pg/mL for patients in atrial fibrillation or flutter), and evidence of structural heart disease were randomly assigned (1:1) to 10 mg dapagliflozin or placebo, administered orally, and followed up for a median of 2·3 years (IQR 1·7-2·8). The primary outcome, a composite of time from randomisation to first worsening heart failure events (defined as an unplanned hospitalisation or urgent heart failure visit requiring intravenous therapy) or cardiovascular death, in participants with type 2 diabetes (history of or identified by HbA1c ≥6·5% [48 mmol/mol] at baseline) or prediabetes (HbA1c 5·7 to <6·5% [39 mmol/mol to <48 mmol/mol] at baseline) was compared with those with normoglycaemia (HbA1c <5·7% [39 mmol/mol]). Efficacy of dapagliflozin versus placebo was assessed according to glycaemic status and based on HbA1c as a continuous measure. The full-analysis set comprised all patients who were randomly assigned to study treatment, with patients analysed according to their randomised treatment assignment, irrespective of the treatment received (ie, intention to treat). The safety analysis set comprised patients who were randomly assigned to study treatment and who took at least one dose of investigational product, with patients analysed according to the treatment actually received. This trial is registered with ClinicalTrials.gov, NCT03619213. Between Sept 1, 2018, and Jan 18, 2021, 6263 patients were randomly assigned to oral dapagliflozin (n=3131) or placebo (n=3132). Of these patients, 1175 had normoglycaemia, 1934 had prediabetes, and 3150 had type 2 diabetes and were included in the glycaemia subgroup analysis (3515 [56·2%] of 6263 patients were men and 4435 [70·9%] were White). The incidence rate of the primary outcome was 6·9 per 100 patient-years in the normoglycaemia subgroup (reference), increasing to 7·6 per 100 patient-years in the prediabetes subgroup (hazard ratio 1·09 [95% CI 0·90-1·31]) and 10·1 per 100 patient-years in the type 2 diabetes subgroup (1·46 [1·24-1·73]; p<0·0001 for trend). Dapagliflozin reduced the risk of the primary outcome versus placebo in each subgroup (hazard ratio 0·77 [95% CI 0·57-1·04], log-rank p=0·088, for patients with normoglycaemia, 0·87 [0·69-1·08], log-rank p=0·21, for patients with prediabetes, and 0·81 [0·69-0·95], log-rank p=0·0077, for patients with type 2 diabetes; pinteraction=0·82) and across the continuous HbA1c range (pinteraction=0·85). Volume-related or renal serious adverse events or adverse events leading to discontinuation of the study drug, hypoglycaemia, and amputations were not differentially affected by treatment in any of the glycaemia categories. In patients with heart failure with mildly reduced or preserved ejection fraction, oral dapagliflozin improved heart failure outcomes to a similar extent in three glycaemia subgroups: normoglycaemia, prediabetes, and type 2 diabetes. Moreover, the heart failure benefits of dapagliflozin seem to be consistent across a continuous glycaemic range. AstraZeneca.

Point-of-care NT-proBNP for the screening of PREGnancy-related Heart Failure – the PREG-HF study

Abstract Introduction Cardiovascular disease is an important cause of maternal mortality worldwide. However, diagnosing heart failure (HF) during pregnancy remains challenging. Patients with HF present with symptoms that are often attributed to the physiological changes of pregnancy. Although the measurement of natriuretic peptides (such as NT-proBNP) has been recommended as a cost-effective screening test for HF, its value in predicting underlying structural heart disease on echocardiography during pregnancy is unclear. Purpose To evaluate the accuracy of point-of-care (POC) NT-proBNP to predict echocardiographic evidence of structural heart disease in pregnant women. Methods All consecutive consenting pregnant women with symptoms of HF (New York Heart Association functional class [NYHA FC] II–IV), who underwent echocardiography at Groote Schuur Hospital (a tertiary hospital in South Africa) between 1 March 2021 and 15 March 2022 were recruited and compared with asymptomatic pregnant women (NYHA FC I). Demographic and obstetric data were collected, as well as clinical and echocardiographic parameters. POC NT-proBNP was measured; a receiver operating characteristic (ROC) curve was used to determine the level of NT-proBNP that would have the best predictive value for detecting structural heart disease on echocardiography. Results We included 121 women with a median age of 31.3 years (IQR 24.9–36.4) and a median gravidity of 3 (2–4), mostly in their third trimester of pregnancy (75.2%). Symptomatic women (66.1%) presented mainly with dyspnoea (92.5%) and fatigue (73.8%). Most common signs of HF were peripheral oedema (46.8%), jugular venous distension (17.7%) and pulmonary crackles (17.7%). Overall, the median POC NT-proBNP was 98pg/ml (60–506) but was not statistically different between symptomatic and asymptomatic participants. However, NT-proBNP levels were significantly elevated in those with left ventricular (LV) dilatation (376 [86–744] vs 65 [60–191], p=0.001), left atrial enlargement (395 [65–744] vs 60 [59–108], p&amp;lt;0.001), LV systolic dysfunction (510 [113–1668] vs 65 [60–210], p&amp;lt;0.001), diastolic dysfunction (300 [77–1450] vs 78 [60–257], p=0.031), mitral regurgitation (167 [60–672] vs 78 [60–243], p=0.038) and pericardial effusion (440 [81–1031] vs 71 [60–243], p=0.011) (Figure 1). An NT-proBNP of &amp;lt;200pg/ml had the highest negative predictive value (83%) to rule out structural heart disease (AUC 0.68 [0.59–0.77]). Patients with NT-proBNP of ≥200pg/ml were at increased risk of having echocardiographic evidence of structural heart disease (diagnostic odds ratio 4.9 [95% confidence interval 2.0–11.7]). Conclusion In this cohort of pregnant women with symptoms suggestive of HF, POC NT-proBNP identified those with structural heart disease with acceptable discrimination. POC NT-proBNP testing might be particularly useful as a screening test in settings where pregnant women do not readily have access to echocardiography. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): World Heart Federation Salim Yusuf Emerging Leaders Programme

Atrial Fibrillation and Dapagliflozin Efficacy in Patients With Preserved or Mildly Reduced Ejection Fraction

BackgroundAtrial fibrillation (AF) is common in heart failure (HF), is associated with worse outcomes compared with sinus rhythm, and may modify the effects of therapy. ObjectivesThis study examined the effects of dapagliflozin according to the presence or not of AF in the DELIVER (Dapagliflozin Evaluation to Improve the LIVEs of Patients With PReserved Ejection Fraction Heart Failure) trial. MethodsA total of 6,263 patients with HF with New York Heart Association functional class II-IV, left ventricular ejection fraction >40%, evidence of structural heart disease, and elevated N-terminal pro–B-type natriuretic peptide levels were randomized to dapagliflozin or placebo. Clinical outcomes and the effect of dapagliflozin, according to AF status, were examined. The primary outcome was a composite of cardiovascular death or worsening HF. ResultsOf the 6,261 patients with data on baseline AF, 43.3% had no AF, 18.0% had paroxysmal AF, and 38.7% had persistent/permanent AF. The risk of the primary endpoint was higher in patients with AF, especially paroxysmal AF, driven by a higher rate of HF hospitalization: no AF, HF hospitalization rate per 100 person-years (4.5 [95% CI: 4.0-5.1]), paroxysmal AF (7.5 [95% CI: 6.4-8.7]), and persistent/permanent AF (6.4 [95% CI: 5.7-7.1]) (P < 0.001). The benefit of dapagliflozin on the primary outcome was consistent across AF types: no AF, HR: 0.89 (95% CI: 0.74-1.08); paroxysmal AF, HR: 0.75 (95% CI: 0.58-0.97); persistent/permanent AF, HR: 0.79 (95% CI: 0.66-0.95) (Pinteraction = 0.49). Consistent effects were observed for HF hospitalization, cardiovascular death, all-cause mortality, and improvement in the KCCQ-TSS. ConclusionsIn DELIVER, the beneficial effects of dapagliflozin compared with placebo on clinical events and symptoms were consistent, irrespective of type of AF at baseline. (Dapagliflozin Evaluation to Improve the LIVEs of Patients With PReserved Ejection Fraction Heart Failure. [DELIVER]; NCT03619213)

Psychological Aspects of Syncopes and Possible Association with Recurrency-The Role of Implantable Loop Recorders.

Syncopes are a very common phenomenon and have a high recurrence rate. The differentiation between the psychogenic and physical, especially of arrhythmic origin, remains difficult. In many cases, an implantable loop recorder is used for the detection of possible arrhythmias, leading to syncopes. Yet, the existing literature suggests that psychological factors may play a significant role in recurrent syncopes. We aimed at analyzing the potential role of several psychological factors on the recurrence of arrhythmic or non-arrhythmic syncopes. Methods and results: A total of 119 patients, who had received an implantable loop recorder for recurrent syncopes at our center between 01/2018 and 12/2021, participated in this retrospective cohort study. Anxiety, depression and quality of life were assessed using extensively validated questionnaires (GAD-7, PHQ-9 and SF-12). The mean follow-up after loop recorder implantation was 710 ± 430 days and 50% of patients were female. The mean patient age was 54.8 ± 18.6 years. Most patients had no evidence of structural heart disease (84%), and normal LV function (92%). A statistical analysis revealed that the presence of structural heart disease was the strongest predictor for arrhythmic syncope during follow-up. In patients with non-arrhythmic syncopes, we found significantly higher levels of anxiety (GAD-7 score: 2.5 ± 2.6 vs. 4.8 ± 4.3) and depression (PHQ-9 score: 3.9 ± 3.6 vs. 6.8 ± 5.1), and a lower quality of life (SF-12 score: 33.7 ± 6.4 vs. 29.6 ± 7.8). Discussion: We identified factors as contributors to a better identification of patients at risk for arrhythmic as well as non-arrhythmic syncopes. Especially anxious or depressive symptoms may hinted at non-arrhythmic causes of syncope. However, the study was limited by its retrospective design and low patient number. Further trials should likewise combine the diagnostic yield of loop recorders with psychometric evaluations before implantation and combine it with additional diagnostic measures, such as video monitoring, to further examine the role of psychological factors in the pathomechanism and treatment of syncope.

New Variant in Placophilin-2 Gene Causing Arrhythmogenic Myocardiopathy.

Introduction: Arrhythmogenic cardiomyopathy (ACM) is an inherited disease characterized by progressive fibroadipose replacement of cardiomyocytes. Its diagnosis is based on imaging, electrocardiographic, histological and genetic/familial criteria. The development of the disease is based mainly on desmosomal genes. Knowledge of the phenotypic expression of each of these genes will help in both diagnosis and prognosis. The objective of this study is to describe the genotype–phenotype association of an unknown PKP2 gene variant in a family diagnosed with ACM. Methods: Clinical and genetic study of a big family carrying the p.Tyr168* variant in the PKP2 gene, in order to demonstrate pathogenicity of this variant, causing ACM. Results: Twenty-two patients (proband and relatives) were evaluated. This variant presented with high arrhythmic load at an early age, but without evidence of structural heart disease after 20 years of follow-up, with low risk in predictive scores. We demonstrate evidence of its pathogenicity. Conclusions: The p.Tyr168* variant in the PKP2 gene causes ACM with a high arrhythmic load and with an absence of structural heart disease. This fact emphasizes the value of knowing the phenotypic expression of each variant.

Dronedarone for the treatment of atrial fibrillation with concomitant heart failure with preserved and mildly reduced ejection fraction: a post-hoc analysis of the ATHENA trial.

AimsLimited therapeutic options are available for the management of atrial fibrillation/flutter (AF/AFL) with concomitant heart failure (HF) with preserved (HFpEF) and mildly reduced ejection fraction (HFmrEF). Dronedarone reduces the risk of cardiovascular events in patients with AF, but sparse data are available examining its role in patients with AF complicated by HFpEF and HFmrEF.Methods and resultsATHENA was an international, multicentre trial that randomized 4628 patients with paroxysmal or persistent AF/AFL and cardiovascular risk factors to dronedarone 400 mg twice daily versus placebo. We evaluated patients with (i) symptomatic HFpEF and HFmrEF (defined as left ventricular ejection fraction [LVEF] >40%, evidence of structural heart disease, and New York Heart Association class II/III or diuretic use), (ii) HF with reduced ejection fraction (HFrEF) or left ventricular dysfunction (LVEF ≤40%), and (iii) those without HF. We assessed effects of dronedarone versus placebo on death or cardiovascular hospitalization (primary endpoint), other key efficacy endpoints, and safety. Overall, 534 (12%) had HFpEF or HFmrEF, 422 (9%) had HFrEF or left ventricular dysfunction, and 3672 (79%) did not have HF. Patients with HFpEF and HFmrEF had a mean age of 73 ± 9 years, 37% were women, and had a mean LVEF of 57 ± 9%. Over a mean follow‐up of 21 ± 5 months, dronedarone consistently reduced risk of death or cardiovascular hospitalization (hazard ratio 0.76; 95% confidence interval 0.69–0.84) without heterogeneity based on HF status (p interaction >0.10). This risk reduction in the primary endpoint was consistent across the range of LVEF (as a continuous function) in HF without heterogeneity (p interaction = 0.71). Rates of death, cardiovascular hospitalization, and HF hospitalization each directionally favoured dronedarone versus placebo in HFpEF and HFmrEF, but these treatment effects were not statistically significant in this subgroup.ConclusionsDronedarone is associated with reduced cardiovascular events in patients with paroxysmal or persistent AF/AFL and HF across the spectrum of LVEF, including among those with HFpEF and HFmrEF. These data support a rationale for a future dedicated and powered clinical trial to affirm the net clinical benefit of dronedarone in this population.

Baseline Characteristics of Patients With HF With Mildly Reduced and Preserved Ejection Fraction: DELIVER Trial

ObjectivesThis report describes the baseline clinical profiles and management of DELIVER (Dapagliflozin Evaluation to Improve the Lives of Patients With Preserved Ejection Fraction Heart Failure) trial participants and how these compare with those in other contemporary heart failure with preserved ejection fraction trials. BackgroundThe DELIVER trial was designed to evaluate the effects of the sodium-glucose cotransporter–2 inhibitor dapagliflozin on cardiovascular death, heart failure (HF) hospitalization, or urgent HF visits in patients with HF with mildly reduced and preserved left ventricular ejection fraction (LVEF). MethodsAdults with symptomatic HF and LVEF >40%, with or without type 2 diabetes mellitus, elevated N-terminal pro–B-type natriuretic peptide (NT-proBNP) levels, and evidence of structural heart disease were randomized to dapagliflozin 10 mg once daily or matching placebo. ResultsA total of 6,263 patients were randomized (mean age: 72 ± 10 years; 44% women; 45% type 2 diabetes mellitus; 45% with body mass index ≥30 kg/m2; and 57% with history of atrial fibrillation or flutter). Most participants had New York Heart Association functional class II symptoms (75%). Baseline mean LVEF was 54.2 ± 8.8% and median NT-proBNP of 1,399 pg/mL (IQR: 962 to 2,210 pg/mL) for patients in atrial fibrillation/flutter compared with 716 pg/mL (IQR: 469 to 1,281 pg/mL) in those who were not. Patients in both hospitalized and ambulatory settings were enrolled, including 10% enrolled in-hospital or within 30 days of a hospitalization for HF. Eighteen percent of participants had HF with improved LVEF. ConclusionsDELIVER is the largest and broadest clinical trial of this population to date and enrolled high-risk, well-treated patients with HF with mildly reduced and preserved LVEF. (Dapagliflozin Evaluation to Improve the Lives of Patients With Preserved Ejection Fraction Heart Failure [NCT03619213])

Abstract 11661: Associations of Macronutrient and Sodium Intake With Cardiac Structure and Function in the Hispanic Community Health Study/Study of Latinos

Introduction: Dietary macronutrient balance and reduced sodium intake are key modifiable risk factors for prevention of cardiovascular disease. Pre-heart failure (HF) (evidence of structural heart disease or abnormal cardiac function) is an independent risk factor for incident clinical HF development. We assessed associations of macronutrient and sodium intake with cardiac structure and function from the Echocardiographic Study of Latinos (Echo-SOL), an ancillary study of the Hispanic Community Health Study/Study of Latinos (HCHS/SOL). Hypothesis: We hypothesized that higher intake of protein and lower intake of fat, carbohydrate and sodium would be associated with healthier cardiac structure and function. Methods: Cross-sectional data from HCHS/SOL interviews were analyzed among 1818 adults (57% female, mean age 56 ± 0.17) with complete echo assessments. Intake of carbohydrates, proteins, fats, and sodium in relation to total caloric intake was derived from two 24-hour recalls. Associations between nutrients and pre-HF outcomes were estimated via simple linear regression as well as ANOVA across quintiles of each nutrient. All analyses were weighted and account for complex survey design. Results: Mean ± SE macronutrient intake for the overall target population was 52.3 ± 0.1% carbohydrates, 17.1 ± 0.05% protein, and 29.7 ± 0.1% fat. Mean dietary sodium intake was 3,107.2 ± 47.7mg. Higher percent of total daily calories from carbohydrates was associated with lower LV mass (-13.7g per 5%, p&lt;0.01) and lower e’ velocity (-0.37cm/s per 5%, p&lt;0.01). Higher fat consumption was associated with higher LV mass (11.23g per 5%, p&lt;0.01). No significant associations were seen with protein intake. Higher sodium intake was associated with higher LV mass (1.35g per 100mg, p&lt;0.01) and lower ejection fraction (-0.091% per 100mg, p&lt;0.01). Quintile analysis confirmed the presence and monotonicity of the observed associations. Conclusions: Our results suggest that a macronutrient balance favoring higher carbohydrate and lower fat consumption along with reduced sodium intake is associated with better cardiac structure and function. These findings have important implications for HF prevention. Future studies should explore the role of specific nutrient types.

Antidromic His capture during ventricular entrainment of an orthodromic AV re-entrant tachycardia. What is the mechanism?

A 32-year-old lady was evaluated for recurrent episodes of palpitation. During one of the palpitation episodes a regular narrow QRS tachycardia was documented, and it got terminated with the administration of IV adenosine. The baseline 12 lead electrocardiogram (ECG) did not show any manifest preexcitation. There was no evidence of structural heart disease by echocardiogram. Patient underwent an electrophysiology [EP] study after informed consent. Quadripolar catheters were placed at the His region and right ventricular (RV) apex. A decapolar catheter was placed in the coronary sinus (CS) with CS 9,10 dipoles at CS OS region and CS 1,2 dipoles at CS distal region (at 3 O clock of mitral anulus). A mapping & ablation catheter was positioned at right atrial (RA) appendage. Baseline atrial and ventricular pacing protocols could not be performed as both atrial and ventricular pacing were easily inducing a regular narrow QRS tachycardia. Ventricular pacing manoeuvres including delivery of His refractory premature ventricular extra (PVE) stimulus [Figure 1] & ventricular overdrive pacing (VOD) [Figure 2 & 3] were performed during the tachycardia from the right ventricular (RV) apex. Antidromic His capture during VOD of orthodromic AV re-entry had occurred, which was unusual and might be expected to terminate AV re-entrant tachycardia rather than entrain it. Why did this not happen? This article is protected by copyright. All rights reserved.

Presence of dysfunction and myocardial remodeling in patients with premature ventricular complex-induced cardiomyopathy - a cardiovascular MR study

Abstract Funding Acknowledgements Type of funding sources: None. Background Premature ventricular complexes (PVCs) in the absence of underlying structural heart disease are considered to be benign. However, cardiac dysfunction has been observed in patients with a high PVC burden. The characterization of a PVC-induced cardiomyopathy with structural remodeling including myocardial fibrosis and the determination of a specific PVC burden leading to subclinical cardiac dysfunction remains to be determined. Objectives We aimed to evaluate cardiac function, remodeling and myocardial fibrosis patterns in patients with PVCs using cardiac magnetic resonance imaging (CMR). Additionally, we aimed to determine a PVC cut-off value leading to subclinical cardiac dysfunction. Methods Patients who underwent CMR and 24-hour, 12-lead ECG monitoring (Holter ECG) within six months were retrospectively studied. Patients with evidence of structural heart disease were excluded. The cohort was subdivided based on the number of PVCs in Holter ECG; Group-1 = 0-100, Group-2 = 100-5000 and Group-3 &amp;gt; 5000 PVCs. CMR parameters were extracted from our local databank. Myocardial strain was measured using feature tracking. For quantification of myocardial fibrosis, T1 mapping and late gadolinium enhancement (LGE) were investigated. Z-scores were calculated in order to combine T1 values from a 1.5 and 3Tesla CMR vendor. Results 443 patients (52 ± 20 years, 45% females) were included in the study. Compared to Group-1, Group-3 revealed a significantly reduced LV-EF, an increased indexed LV-EDV and increased indexed LV-ESV, indicating cardiac dysfunction and LV enlargement. PVCs frequency was inversely correlated with LV-EF (r=-0.23, p &amp;lt; 0.001) and positively correlated with indexed LV-EDV (r = 0.13; p &amp;lt; 0.01). Feature tracking showed significantly higher global circumferential strain (GCS) indicating subclinical dysfunction. Global T1 times were significantly prolonged in Group-3. Elevated global T1 Z-scores were found in Group-2 and Group-3 compared to Group-1. Significantly more intramural LGE was present in Group-2. The PVC cut-off value characterized by reduced GCS was defined by 216 PVCs (AUC = 0.61, p = 0.02). Conclusion CMR revealed cardiac dysfunction, left ventricular enlargement and diffuse myocardial fibrosis in patients with PVC in the absence of structural heart disease. These changes indicate the development of a PVC-induced cardiomyopathy depending on the PVC burden. Interestingly, subclinical myocardial dysfunction was determined at already low PVC frequencies. Further investigations are necessary in order to examine the influence of different origins of PVCs and the development of structural remodeling.

Native T1 mapping for differential diagnosis of left ventricular hypertrophy

Abstract Funding Acknowledgements Type of funding sources: None. Purpose The aim of this study was to investigate native T1 mapping cardiac magnetic resonance (CMR) tomography for the differential diagnosis of left ventricular (LV) hypertrophy. Background Mapping techniques are useful to characterize myocardial tissue abnormalities, particularly cardiac amyloidosis. However, specific cut-off values to differentiate LV hypertrophic phenotypes on 3.0 tesla CMR scanners have not been established, yet. Methods We retrospectively identified patients in the CMR database of Leipzig university hospital with increased LV wall thickness (≥12mm diameter at end-diastole) who were referred for the evaluation of LV hypertrophy or ischemia between 2017 and 2020 on a 3T scanner (Philips Achieva). Patients with suspected or confirmed myocarditis were excluded. Diagnosis of cardiac amyloidosis was made by either biopsy or non-invasively by bone scintigraphy and screening for monoclonal gammopathy. T1 mapping was measured as global mean value from 3 short axis slices of the LV. Results 128 consecutive patients were included in the study. 31 subjects without evidence of structural heart disease served as healthy control. The final diagnosis was cardiac amyloidosis in 24 patients (5 patients with light-chain, 18 with transthyretin amyloidosis, 1 undetermined), hypertrophic cardiomyopathy in 24, and hypertensive heart disease in 80 patients. Mean age of patients was 65 ± 13years, 84% were male. LV mass was increased in patients with LV hypertrophy compared to healthy control (p &amp;lt; 0.001). Native T1 values of the LV myocardium were higher in patients with cardiac amyloidosis (1409 ± 59ms, p &amp;lt; 0.0001 vs. all other groups) compared to healthy control (1225 ± 21ms), patients with hypertrophic cardiomyopathy (HCM; 1263 ± 43ms) and hypertensive heart disease (HHD; 1257 ± 41ms) (Figure). Patients with hypertrophic cardiomyopathy and hypertensive heart disease did not differ in their native T1 values, but both groups were increased compared to healthy control (p &amp;lt; 0.01). Receiver operating characteristic analysis of native T1 values demonstrated an area under the curve for the detection of cardiac amyloidosis of 0.9954 (p &amp;lt; 0.0001) vs. hypertrophic cardiomyopathy, hypertensive heart disease and healthy control. The optimal cut-off value was 1341ms, with a sensitivity of 100% and a specificity of 97%. Conclusion Native T1 mapping has high diagnostic accuracy for the diagnosis of cardiac amyloidosis among patients with LV hypertrophy. These data need confirmation in a prospective clinical trial. Study ID DRKS00022048

Universal Definition and Classification of Heart Failure: A Report of the Heart Failure Society of America, Heart Failure Association of the European Society of Cardiology, Japanese Heart Failure Society and Writing Committee of the Universal Definition of Heart Failure

In this document, we propose a universal definition of heart failure (HF) as the following: HF is a clinical syndrome with symptoms and or signs caused by a structural and/or functional cardiac abnormality and corroborated by elevated natriuretic peptide levels and or objective evidence of pulmonary or systemic congestion. We propose revised stages of HF as: At-risk for HF (Stage A) , for patients at risk for HF but without current or prior symptoms or signs of HF and without structural or biomarkers evidence of heart disease. Pre-heart failure (Stage B) for patients without current or prior symptoms or signs of HF but evidence of structural heart disease or abnormal cardiac function, or elevated natriuretic peptide levels. HF (Stage C) for patients with current or prior symptoms and/or signs of HF caused by a structural and/or functional cardiac abnormality. Advanced HF (Stage D) for patients with severe symptoms and/ or signs of HF at rest, recurrent hospitalizations despite guideline-directed management and therapy (GDMT) , refractory or intolerant to GDMT, requiring advanced therapies such as consideration for transplant, mechanical circulatory support, or palliative care. Finally, we propose a new and revised classification of HF according to left ventricular ejection fraction (LVEF) . The classification includes HF with reduced EF (HFrEF) : HF with LVEF ≤ 40%; HF with mid-range EF (HFmrEF) : HF with LVEF 41-49%; HF with preserved EF (HFpEF) : HF with LVEF ≥ 50%; and HF with improved EF (HFimpEF) : HF with a baseline LVEF ≤ 40%, a ≥ 10 point increase from baseline LVEF, and a second measurement of LVEF > 40.

Contact-force monitoring increases accuracy of right ventricular voltage mapping avoiding “false scar” detection in patients with no evidence of structural heart disease

PurposeElectroanatomical mapping (EAM) could increase cardiac magnetic resonance imaging (CMR) sensitivity in detecting ventricular scar. Possible bias may be scar over-estimation due to inadequate tissue contact. Aim of the study is to evaluate contact-force monitoring influence during EAM, in patients with idiopathic right ventricular arrhythmias. Methods20 pts (13 M; 43 ± 12 y) with idiopathic right ventricular outflow tract (RVOT) arrhythmias and no structural abnormalities were submitted to Smarttouch catheter Carto3 EAM. Native maps included points collected without considering contact-force. EAM scar was defined as area ≥1 cm2 including at least 3 adjacent points with signal amplitude (bipolar <0.5 mV, unipolar 3,5 mV), surrounded by low-voltage border zone. EAM were re-evaluated offline, removing points collected with contact force <5 g. Finally, contact force-corrected maps were compared to the native ones. ResultsAn EAM was created for each patient (345 ± 85 points). After removing poor contact points, a mean of 149 ± 60 points was collected. The percentage of false scar, collected during contact force blinded mapping compared to total volume, was 6.0 ± 5.2% for bipolar scar and 7.1 ± 5.9% for unipolar scar, respectively. No EAM scar was present after poor contact points removal. Right ventricular areas analysis revealed a greater number of points with contact force < 5 g acquired in free wall, where reduced mean bipolar and unipolar voltage were recorded. ConclusionsTo date this is the first work conducted on structurally normal hearts in which contact-force significantly increases EAM accuracy, avoiding “false scar” related to non-adequate contact between catheter and tissue.