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Abstract Hydralazine and nitrate combination was the first treatment that showed improved survival of patients with heart failure with reduced left ventricular ejection fraction (HFREF) in the Vasodilator Heart Failure Trial (V-HeFT trial) in 1986. This showed a 34% reduction of mortality at 2 years of follow-up in patients with advanced heart failure (New York Heart Association Class IV). The angiotensin-converting enzyme inhibitor (ACEi), beta-blockers, mineralocorticoid receptor antagonists, and most recently sacubitril–valsartan have superseded the combination of hydralazine and nitrates. However, the latter combination does have a place bridging the survival gap of Black patients with HFREF when added to their standard therapy. This was demonstrated in the African-American Heart Failure Trial (A-HeFT trial) in 2004 when the risk reduction in the Black patients was 43% compared with that in the placebo. This combination may have a potential use in patients with contraindications to the use of ACEi, angiotensin receptor blockers, and sacubitril–valsartan. This is suggested by both the European Society of Cardiology (ESC) Guidelines and the guidelines of the National Institute for Health and Care Excellence (NICE). In this perspective, the role of the combination of hydralazine and nitrates in the treatment of HFREF is reviewed through a synopsis of the evidence base consisting of three randomized controlled studies, several further analyses of subgroups within those trials, a systemic review, and two large observational studies of registry cohorts. The place of the combination in the treatment cascades proposed by heart failure guidelines of the ESC and NICE is explored. This perspective is to remind us of their appropriate roles, particularly given the findings of underuse of this combination in people of African ancestry in Europe.

Aims The clinical reliability of echocardiographic surrogate markers of left ventricular filling pressures (LVFPs) across different cardiovascular pathologies remains unanswered. The main objective was to evaluate the evidence of how effectively different echocardiographic indices estimate true LVFP. Methods and results Design: this is a systematic review and meta‐analysis. Data source: Scopus, PubMed and Embase. Eligibility criteria for selecting studies were those that used echocardiography to predict or estimate pulmonary capillary wedge pressure or left ventricular end‐diastolic pressures. Twenty‐seven studies met criteria. Only eight studies (30%) reported both correlation coefficient and bias between non‐invasive and invasively measured LVFPs. The majority of studies (74%) recorded invasive pulmonary capillary wedge pressure as a surrogate for left ventricular end‐diastolic pressures. The pooled correlation coefficient overall was r = 0.69 [95% confidence interval (CI) 0.63–0.75, P < 0.01]. Evaluation by cohort demonstrated varying association: heart failure with preserved ejection fraction (11 studies, n = 575, r = 0.59, 95% CI 0.53–0.64) and heart failure with reduced ejection fraction (8 studies, n = 381, r = 0.67, 95% CI 0.61–0.72). Conclusions Echocardiographic indices show moderate pooled association to invasively measured LVFP; however, this varies widely with disease state. In heart failure with preserved ejection fraction, no single echocardiography‐based metric offers a reliable estimate. In heart failure with reduced ejection fraction, mitral inflow‐derived indices (E/e′, E/A, E/Vp, and EDcT) have reasonable clinical applicability. While an integrated approach of several echocardiographic metrics provides the most promise for estimating LVFP reliably, such strategies need further validation in larger, patient‐specific studies.

Objective The 2020/2021 National Heart Failure Audit found prescribing rates of beta‐blockers, angiotensin‐converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARBs) and mineralocorticoid receptor antagonists (MRAs) were below target levels in individuals with heart failure with reduced ejection fraction (HFrEF). In Sheffield Teaching Hospitals (STH), prescribing rates of this triple therapy (TT) were below the national average. The aim of this study was to evaluate the impact of patients’ frailty and comorbidities on TT prescribing rates. Methods We analysed the clinical details of individuals with a diagnosis of moderate or severe HFrEF admitted to STH between May 2021 and December 2021. Patients’ electronic notes, investigations and heart failure specialist nurses’ assessments were reviewed. Results Electronic records of 310 patients were reviewed. About 45.5% were discharged on appropriate TT, compared to 52% nationally. Prescribing rates were 84.2% for beta‐blockers and 61.3% for ACE‐i/ARB/ARNIs, compared to national levels of 91% and 84%, respectively. The prescribing rate for MRA was 63.4%, which is higher than the national average (61%). About 92.6% of those not on TT had a documented clinical reason, with the commonest being ‘poor renal function’ (45.6%) and ‘low systolic blood pressure’ (25.5%). Those not on TT had a greater mean clinical frailty score (4.4 vs. 3.0, p < 0.001), were older (78.4 vs. 67.1, p < 0.001) and had worse 12‐month readmission (p < 0.001) and mortality rates (p < 0.001). Conclusions Patients’ frailty and comorbidities play a significant role in HFrEF‐prescribing patterns. Identifying and addressing the barriers to optimal HFrEF treatment may improve prescribing rates and patient outcomes.

Cardiac magnetic resonance (CMR) is emerging as an important tool in the assessment of heart failure with preserved ejection fraction (HFpEF). This study sought to investigate the prognostic value of multiparametric CMR, including left and right heart volumetric assessment, native T1-mapping and LGE in HFpEF. In this retrospective study, we identified patients with HFpEF who have undergone CMR. CMR protocol included: cines, native T1-mapping and late gadolinium enhancement (LGE). The mean follow-up period was 3.2 ± 2.4 years. We identified 86 patients with HFpEF who had CMR. Of the 86 patients (85% hypertensive; 61% males; 14% cardiac amyloidosis), 27 (31%) patients died during the follow up period. From all the CMR metrics, LV mass (area under curve [AUC] 0.66, SE 0.07, 95% CI 0.54–0.76, p = 0.02), LGE fibrosis (AUC 0.59, SE 0.15, 95% CI 0.41–0.75, p = 0.03) and native T1-values (AUC 0.76, SE 0.09, 95% CI 0.58–0.88, p < 0.01) were the strongest predictors of all-cause mortality. The optimum thresholds for these were: LV mass > 133.24 g (hazard ratio [HR] 1.58, 95% CI 1.1–2.2, p < 0.01); LGE-fibrosis > 34.86% (HR 1.77, 95% CI 1.1–2.8, p = 0.01) and native T1 > 1056.42 ms (HR 2.36, 95% CI 0.9–6.4, p = 0.07). In multivariate cox regression, CMR score model comprising these three variables independently predicted mortality in HFpEF when compared to NTproBNP (HR 4 vs HR 1.65). In non-amyloid HFpEF cases, only native T1 > 1056.42 ms demonstrated higher mortality (AUC 0.833, p < 0.01). In patients with HFpEF, multiparametric CMR aids prognostication. Our results show that left ventricular fibrosis and hypertrophy quantified by CMR are associated with all-cause mortality in patients with HFpEF.

Aims Clinical outcomes for patients suspected of having heart failure (HF) who do not meet the diagnostic criteria of any type of HF by echocardiography remain unknown. The aim of this study was to investigate the clinical predictors of all‐cause mortality in patients with suspected HF, a raised N‐terminal pro‐b‐type natriuretic peptide (NTproBNP) and who do not meet the diagnostic criteria of any type of HF by echocardiography. Methods and results Relevant data were taken from the Sheffield HEArt Failure (SHEAF) registry (222349P4). The inclusion criteria were presence of symptoms raising suspicion of HF, NTproBNP > 400 pg/mL, and preserved left ventricular function. Exclusion criteria were any type of HF by echocardiography. The outcome was defined as all‐cause mortality. Cox proportional‐hazards regression model was used to investigate the association between the survival time of patients and clinical variables; 1031 patients were identified with NTproBNP > 400 pg/mL but who did not have echocardiographic evidence of HF. All‐cause mortality was 21.5% (222 deaths) over the mean follow‐up (FU) period of 6 ± 2 years. NTproBNP was similar in patients who were alive or dead (P = 0.96). However, age (HR 1, P < 0.01), chronic kidney disease (CKD, HR 1.2, P < 0.01), chronic pulmonary obstructive disease (COPD, HR 1.6, P < 0.01), dementia (HR 5.9, P < 0.01), male gender (HR 1.4, P < 0.01), first‐degree atrioventricular block (HR 2.1, P < 0.01), left axis deviation (HR 1.6, P = 0.04), and diabetes (HR 1.4, P = 0.03) were associated with all‐cause mortality. In multivariate regression, age, gender, CKD stage, COPD, and dementia were independently associated with mortality. In patients with NTproBNP > 627 pg/mL, NYHA class predicted death (II, 19.6%; III, 27.4%; IV, 66.7%; P < 0.01). Conclusions Patients with no HF on echocardiography but raised NTproBNP suffer excess mortality particularly in the presence of certain clinical variables. Age, male gender, worsening CKD stage, presence of COPD, and dementia are independently associated with all‐cause mortality in these patients. An NTproBNP > 627 pg/mL coupled with NYHA class could identify patients at greatest risk of death.

BackgroundIn health, women have a lower haemoglobin than men and their prevalence of both anaemia and iron deficiency may be higher, especially if they have heart failure. The erythropoietic response to iron might also differ between the sexes. We used data from a randomised trial (IRONMAN) of intravenous (IV) ferric derisomaltose (FDI) to investigate these issues.MethodsPatients with a diagnosis of heart failure, a left ventricular ejection fraction ≤45%, and either a TSAT <20% or serum ferritin <100 µg/L were included. Haemoglobin for women had to be in the range of 9-13 g/dL and for men 9-14g/dL. Patients were randomised to receive IV ferric derisomaltose (FDI) or not. Neither the patient nor investigator was blinded. The main endpoints of interest were changes in haemoglobin at 4 months and 12 months and the primary endpoint of the trial (the rate of the composite outcome of heart failure hospitalisations or cardiovascular death expressed as events per 100 patient-years). Analyses were conducted by intention to treat, stratified by sex. A further analysis was conducted for patients with a TSAT <20%.ResultsOf 1,137 patients randomised, 300 were women. Women and men were of similar age (73 vs 74 years), predominantly in NYHA class II, with similar values for NT-proBNP, LVEF, eGFR, ferritin and TSAT. However, haemoglobin was lower in women (11.8 [11.0 to 12.4] g/dL] compared to men (12.3 [11.3 to 13.0] g/dL).The increases in haemoglobin with FDI compared to control was similar for women at 4 months (+0.8 [+0.5 to +1.2] g/dL) and 12 months (+0.8 [+0.4 to +1.3] g/dL) compared to men ((+0.5 [+0.3 to +0.7] g/dL) and (+0.5 [+0.3 to +0.8] g/dL) respectively.The hazard ratio for the primary endpoint for men was 0.81 (0.63 to 1.03) and for women 0.77 (0.42 to 1.42), the wider confidence intervals reflecting the smaller population and fewer events. The results were similar when restricted to patients with a TSAT <20%.ConclusionsThe increase in haemoglobin with IV FDI and its effect on the primary endpoint rate are similar for men and women.Abstract 144 Table 1Prevalence of iron deficiency and response to IV iron according to sex in a randomised trial of intravenous iron (IRONMAN)malefemale Baseline N= 837300 Age74 (67,80)72 (65,78) NYHA II (%)479 (57)169 (56) CAD NT-proBNP1785(936,3788)N=4231414(780,2659)N=142 BNP414 (212,715)N=152285 (188,598)N=45 TSAT 16 (11,20)15 (10,19) Ferritin52 (31,87)42 (27,79) LVEF33 (25, 37)35 (27,39) eGFR51 (38,69)51 (39,68) Haemoglobin Baseline12.3(11.3,13.0)11.8(11.0,12.4) Follow-up UCFDIDiff/RRUCFDIDiff/RR Haemoglobin month 412.4(1.5)12.9(1.4)0.5(0.3,0.7)11.7(1.1)12.6(1.3)0.9(0.6,1.2) Haemoglobin month 1212.6 (1.7)13.1 (1.4)0.6 (0.3,0.8)11.7(1.1)12.4 (1.4)0.7(0.3,1.1) Delta haemoglobin month 40.2 (1.3)0.8(1.3)0.5(0.3,0.7)0.1(1.0)0.9(1.5)0.8(0.5,1.2) Delta haemoglobin month 120.3 (1.6)0.9 (1.4)0.5 (0.3,0.8)-0.0 (1.2)0.8 (1.5)0.8 (0.4,1.3) Primary Endpoint recurrent events, rate (per 100 patient years) and rate ratio. All314 (29.8)257 (23.5)0.81 (0.63,1.03)148 (21.3)129 (17.4)0.77 (0.42,1.42) TSAT <20% TSAT <20% onlymalefemale Baseline N= 629238Age74 (67,79)73 (65,78)NYHA II (%)336 (53)129 (54)CADNT-proBNP1986(1001,4241)N=2941492(802,2954)N=107BNP440 (220,726)N=121302(194,608) n-36TSAT 13(9,17)13(9,16)Ferritin51 (29,104)39 (24,81)LVEF31 (25,36)35(27,39)eGFR51(37,68)51(39,68)Haemoglobin Baseline12.1(11.1,12.9)11.7(10.8,12.3) Follow-up UCFDIDiff/RRUCFDIDiff/RRHaemoglobin month 412.3(1.5)12.9(1.5)0.6 (0.3,0.9)11.7(1.1)12.7(1.4)0.9(0.6,1.3)Haemoglobin month 1212.6 (1.8)13.1(1.4)0.6(0.2,0.9)11.7(1.2)12.4(1.5)0.7(0.3,1.2)Delta haemoglobin month 40.3(1.3)1.0(1.4)0.7(0.4,0.9)0.2(1.0)1.2(1.6)1.0(0.6,1.4)Delta haemoglobin month 120.5(1.8)1.1(1.4)0.6(0.2,0.9)0.1(1.2)1.0(1.6)1.0(0.5,1.5)Primary Endpoint recurrent events, rate (per 100 patient years) and rate ratio.240(32.6)191(24.1)0.75(0.57,1.00)84(23.1)63(22.5)0.94(0.55,1.63)Conflict of InterestNone

Abstract Background Myeloid sarcoma, also known as chloroma, is a pathologic diagnosis for an extramedullary proliferation of blasts of one or more of the myeloid lineages. It is an uncommon manifestation of acute myeloid leukaemia (AML), although the diagnosis may occur prior to or after diagnosis of AML. Cardiac infiltration by myeloid sarcoma is extremely rare, and of the few published cases, a diagnosis of leukaemia was almost always already present. Case summary This is a 52-year-old patient admitted to the hospital with acute shortness of breath, with a large amorphous mass found on computed tomography scan invading the myocardium and causing heart failure. Echocardiography demonstrated multiple cardiac masses. A bone marrow biopsy was non-diagnostic. An endomyocardial biopsy confirmed a cardiac primary myeloid sarcoma. The patient was successfully treated with chemotherapy with complete resolution of the cardiac infiltration and of the heart failure. Discussion We present this rare case of primary cardiac myeloid sarcoma and discuss current literature relevant to this effectively unique presentation. We discuss the use of endomyocardial biopsy in the diagnosis of cardiac malignancy and the advantages of early diagnosis and management of this unusual cause of heart failure.

Two-dimensional (2D) methods of assessing mitral inflow velocities are pre-load dependent, limiting their reliability for evaluating diastolic function. Left ventricular (LV) blood flow kinetic energy (KE) derived from four-dimensional flow cardiovascular magnetic resonance imaging (4D flow CMR) may offer improvements. It remains unclear whether 4D LV blood flow KE parameters are associated with physiological factors, such as age when compared to 2D mitral inflow velocities. Fifty-three healthy volunteers underwent standard CMR, plus 4D flow acquisition. LV blood flow KE parameters demonstrated good reproducibility with mean coefficient of variation of 6 ± 2% and an accuracy of 99% with a precision of 97%. The LV blood flow KEi EDV E/A ratio demonstrated good association to the 2D mitral inflow E/A ratio (r = 0.77, P < 0.01), with both decreasing progressively with advancing age (P < 0.01). Furthermore, peak E-wave KEi EDV and A-wave KEi EDV displayed a stronger association to age than the corresponding 2D metrics, peak E-wave and A-wave velocity (r = −0.51 vs −0.17 and r = 0.65 vs 0.46). Peak E-wave KEi EDV decreases whilst peak A-wave KEi EDV increases with advancing age. This study presents values for various LV blood flow KE parameters in health, as well as demonstrating that they show stronger and independent correlations to age than standard diastolic metrics.

Background Myocardial infarction (MI) leads to complex changes in left ventricular (LV) haemodynamics that are linked to clinical outcomes. We hypothesize that LV blood flow kinetic energy (KE) is altered in MI and is associated with LV function and infarct characteristics. This study aimed to investigate the intra-cavity LV blood flow KE in controls and MI patients, using cardiovascular magnetic resonance (CMR) four-dimensional (4D) flow assessment. Methods Forty-eight patients with MI (acute-22; chronic-26) and 20 age/gender-matched healthy controls underwent CMR which included cines and whole-heart 4D flow. Patients also received late gadolinium enhancement imaging for infarct assessment. LV blood flow KE parameters were indexed to LV end-diastolic volume and include: averaged LV, minimal, systolic, diastolic, peak E-wave and peak A-wave KEi EDV . In addition, we investigated the in-plane proportion of LV KE (%) and the time difference (TD) to peak E-wave KE propagation from base to mid-ventricle was computed. Association of LV blood flow KE parameters to LV function and infarct size were investigated in all groups. Results LV KEi EDV was higher in controls than in MI patients (8.5 ± 3 μJ/ml versus 6.5 ± 3 μJ/ml, P  = 0.02). Additionally, systolic, minimal and diastolic peak E-wave KEi EDV were lower in MI ( P  < 0.05). In logistic-regression analysis, systolic KEi EDV (Beta = − 0.24, P  < 0.01) demonstrated the strongest association with the presence of MI. In multiple-regression analysis, infarct size was most strongly associated with in-plane KE ( r  = 0.5, Beta = 1.1, P  < 0.01). In patients with preserved LV ejection fraction (EF), minimal and in-plane KEi EDV were reduced ( P  < 0.05) and time difference to peak E-wave KE propagation during diastole increased ( P  < 0.05) when compared to controls with normal EF. Conclusions Reduction in LV systolic function results in reduction in systolic flow KEi EDV . Infarct size is independently associated with the proportion of in-plane LV KE. Degree of LV impairment is associated with TD of peak E-wave KE. In patient with preserved EF post MI, LV blood flow KE mapping demonstrated significant changes in the in-plane KE, the minimal KEi EDV and the TD. These three blood flow KE parameters may offer novel methods to identify and describe this patient population.

Background Hyponatraemia is a common problem in patients with heart failure. It can be difficult to treat, especially in the presence of the patient’s needs for diuresis and manipulation of the renin–angiotensin–aldosterone system (RAAS). Case summary This concerns a 74-year-old woman with follicular lymphoma and severe global left ventricular systolic dysfunction secondary to treatment with R-CHOP chemotherapy. She presented a difficult challenge in the management of her decompensated heart failure alongside hyponatraemia as low as 113 mmol/L. This was resistant to standard treatment. The resistance to usual measures necessitated treatment with Tolvaptan, a selective arginine vasopressin V2 inhibitor used to treat hyponatraemia in syndrome of inappropriate anti-diuretic hormone. This, along with a strict fluid restriction of 500 mL/day, resolved the patient’s hyponatraemia and enabled her discharge home on tolerated heart failure treatment. She has now remained stable for almost 12 months. Discussion The potential causes of hyponatraemia are discussed along with the role of Tolvaptan in its management.