1,721,174 research outputs found
Reduced occurrence of appropriate therapy for ventricular arrhythmias after beta-blocker uptitration following implant of a primary prevention CRT-defibrillator
No full textBackground: Absence of beta-blocker use independently predicts appropriate therapy. Following cardiac resynchronisation therapy (CRT) implant, reverse remodelling and protection against bradycardia allows for beta-blocker dose uptitration. The differential dosing effects on the occurrence of a first episode of appropriate therapy in primary prevention CRT-defibrillator (CRT-D) patients remains unstudied. Methods and Results: Changes in beta-blocker dose following CRT-D in consecutive primary prevention patients implanted between 2008 and 2015 were retrospectively studied. Beta-blocker dose was expressed as percent of target dose. Uptitration of beta-blocker dose following implant was calculated as the change in percent of target dose between implant and 6-months follow-up. Results from a prospectively maintained database of all device analysis were used to determine the occurrence of appropriate therapy. A total of 162 patients (68 +/- 8 years) were studied. One hundred and ten (68%) patients underwent uptitration (mean 47 +/- 19% in target dose) and 52 (32%) remained on a stable beta-blocker dose. During 37 +/- 22 months follow-up, the cumulative percent of appropriate therapy was 31% in patient receiving no-uptitration versus 10% in the uptitrated patients (p < 0.001). After correction for known predictors of appropriate therapy, uptitration was independently associated with an OR = 0.263 (CI = 0.103-0.675; p = 0.001) for the occurrence of appropriate therapy. Every 1%-increase in target dose for beta-blocker associated with a significant lower risk for appropriate therapy, OR = 0.982 (CI = 0.965-0.999; p = 0.042). Conclusion: Following implantation of a primary prevention CRT-D, uptitration of beta-blockers associated with a reduced occurrence of a first episode of appropriate therapy for ventricular arrhythmias. An inverse dose-response effect was seen between beta-blocker dose and appropriate therapy.Martens, P (reprint author), Ziekenhuis Oost Limburg, Dept Cardiol, Schiepse Bos 6, B-3600 Genk, Belgium.
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Contemporary choice of glucose lowering agents in heart failure patients with type 2 diabetes
No full textBackground: The choice of glucose lowering agent in heart failure (HF)-patients can have a strong effect on HF-related adverse events, with some classes increasing and other classes reducing the risk. Little data is available about the choice of glucose lowering agents in HF-patients with type-2-diabetes. Methods: We performed a cross-sectional single centre point analysis of all patients with both a diagnoses of HF and type-2-diabetes followed in a tertiary HF-clinic. Medical records were used to determine the choice of current glucose lowering agent. Data at the time of cross-sectional analysis was used to determine potential eligibility to a sodium-glucose-linked-transporter-2-inhibitor (SGLT2-inhibitor) based on the enrolment criteria of the EMPAREG-OUTCOME-trial. Results: A total of 571 HF-patients with diabetes were assessed on June the first 2017. The majority of patients were either managed with one or two glucose lowering agents (43% respectively 34%), with metformin (N = 391;61%), Insulin (N = 278;49%) and sulfonylurea (N = 259;45%) being the most frequently employed treatments. SGLT2-inhibitor use was low (N = 7;1%). According to trial criteria 184 patients (32%) qualified for an SGLT2-inhibitor. With main reasons for ineligibility being a HbA1C = 2 glucose lowering agents from a class other than SGLT-2-inhibiton. Conclusion: Despite potential eligibility, SGLT2-inhibition remains an underused glucose lowering agent in this contemporary HF-population. Additional research is necessary on optimising its implementation in clinical practice, which might include switching glucose lowering therapies in patients at HbA1C-target.Pieter Martens is supported by a doctoral fellowship by the Research Foundation – Flanders (FWO, grant-number: 1127917N). Pieter Martens, and Wilfried Mullens are researchers for the Limburg Clinical Research Program (LCRP) UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk (LSM), Hasselt University, Ziekenhuis Oost-Limburg and Jessa Hospital.Martens, P (corresponding author), Ziekenhuis Oost Limburg, Dept Cardiol, Schiepse Bos 6, B-3600 Genk, Belgium.
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Mode of Death in Octogenarians Treated With Cardiac Resynchronization Therapy
No full textBackground: Cardiac resynchronization therapy (CRT) improves morbidity and mortality in heart failure with reduced ejection fraction (HFrEF) and electrical dyssynchrony. CRT patients in clinical practice are older compared with clinical trials. Objective: To investigate clinical response, reverse remodeling, outcome, and mode of death in octogenarians receiving CRT. Methods: Baseline characteristics, change in New York Heart Association (NYHA) functional class, reverse ventricular remodeling, heart failure readmissions, all-cause mortality, and mode of death were evaluated in CRT patients with comparison between octogenarians and nonoctogenarians. In addition, annual mortality rates of octogenarians undergoing CRT were compared with age-matched control subjects from the general population with the use of national actuarial tables. Results: A total of 686 patients, including 178 octogenarians (26%), were followed for 38 +/- 22 months. Octogenarians exhibited a similar change in NYHA functional class (P = .640), left ventricular ejection fraction increase (P = .796), and decrease in end-diastolic (P = .441) and end-systolic (P = .312) diameter compared with their younger counterparts undergoing CRT. Octogenarians had a higher all-cause mortality risk (P < .001), but heart failure readmission risk did not differ (hazard ratio 0.916, 95% confidence interval 0.638-1.313; P = .632). A higher proportion of noncardiac deaths was observed in octogenarians (74%) versus younger patients (50%; P = .022), with worsening heart failure rather than malignant tachyarrhythmia being the main cardiac cause of death. Compared with an age-matched sample from the general population, octogenarians receiving CRT had an equivalent annual mortality rate (log-rank test: P = .444). Conclusions: Octogenarians retain the ability to mount a significant symptomatic and ventricular remodeling response after CRT, resulting in survival similar to the general age-matched population.Pieter Martens, Petra Nijst, and Wilfried Mullens are researchers for the Limburg Clinical Research Program UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk, Hasselt University, Ziekenhuis Oost-Limburg, and Jessa Hospital
The importance of dose optimisation in the treatment of iron deficiency in heart failure
No full textBackground: Treatment with ferric carboxymaltose (FCM) is limited to 1 g during one administration, which is insufficient in patients with a higher body weight or low haemoglobin (Hb). As a consequence, under-dosing might be common in clinical practice, yet the consequences remain unstudied.Methods: We retrospectively assessed all HFrEF-patients with iron-deficiency (ferritin <100 µg/l or between 100 and 300 µg/l if TSAT < 20%) receiving treatment with FCM between 2015 and 2017. This time-frame was chosen as during this we used a 1-g FCM-regimen for all patients (unless Hb = 14-15 mg/dl, than 500 mg). We compared the actual given dose versus the calculated target dose (according to the SmPC, with the difference between both being the dose deficit). We assessed the impact of dose deficits on clinical and biochemical status after 12 weeks.Results: A total of 211 HFrEF patients were analysed. The actual given dose FCM was 918 ± 188 mg, while the calculated target dose was 1308 ± 470 mg. In 121(61%) patients, a standard dose of 1-g FCM resulted in a dose deficit, of whom 93 had a dose deficit of 500 mg and 35 had a dose deficit of 1000 mg. Follow-up was available in 81% of patients (median = 12 weeks). A dose deficit of 500 mg was associated with a 4.93 higher odds, while a dose deficit of 1000 mg was associated with a 7.78 higher odds of residual iron deficiency. After adjusting for baseline NYHA-class, a dose deficit was associated with less symptomatic improvement. During 442 ± 292 days of follow-up, 68 patients were readmitted with heart failure and 15 patients died. In an univariate model (but not in a multivariate model), a dose deficit was associated with adverse clinical outcome.Conclusion: A majority of HFrEF patients with iron deficiency require doses exceeding 1 g of FCM, and thus require follow-up appointments to correct a residual dose deficit. A residual dose deficit is associated with less functional and biochemical improvement.status: Publishe
Prevalence of underlying gastrointestinal malignancies in iron-deficient heart failure
No full textAIMS: Anaemia and iron deficiency (ferritin level < 100 or 100-300 μg/L with transferrin saturation < 20%) are prevalent in heart failure. Mechanistically, iron deficiency is linked to poor intestinal uptake, increased intestinal loss, and chronic inflammation. However, the prevalence of underlying gastrointestinal malignancies is not established in iron-deficient heart failure with or without anaemia. METHODS AND RESULTS: Patients followed up in a single-centre, heart failure database with baseline registration of haemoglobin and iron status were retrospectively evaluated. The proportion of patients undergoing upper and lower gastrointestinal endoscopy between inclusion and censoring was determined. Afterwards, the prevalence of biopsy that confirmed intestinal malignancies in relation to baseline iron and haemoglobin status was determined. Anaemia was defined as a haemoglobin level <12 g/dL, and iron deficiency according to the aforementioned criteria. Of the 1197 patients in the database, 699 (59%) patients underwent full endoscopic workup over a mean follow-up of 50 ± 27 months. A total of 50 intestinal malignancies were identified (n = 42, 84%, in iron-deficient vs. n = 8, 16%, non-iron-deficient patients; P < 0.001). The prevalence of intestinal malignancies was non-statistically different in iron-deficient patients with anaemia (n = 12/129, 9.3%) or without anaemia (n = 30/287, 10.5%; P = 0.551). The prevalence was much lower in patients without iron deficiency with anaemia (n = 5/83, 6%) or without anaemia (n = 3/200, 1.5%). In patients with iron deficiency but without anaemia (a group in which the role of endoscopic workup is less established), ferritin levels carried an inverse diagnostic capacity in detecting patients with an underlying malignancy (area under the curve = 0.741, P < 0.001). A ferritin level < 56 μg/L had the best acuity, detecting malignancies with a sensitivity of 80% and a specificity of 71%. CONCLUSIONS: Endoscopic evaluation is warranted in heart failure patients with iron-deficient anaemia given the high prevalence of underlying intestinal malignancies, as advised by gastroenterology guidelines. However, additional research is needed assessing the best approach to patients with iron deficiency without anaemia, given the high occurrence of intestinal malignancies in these patients. A lower ferritin level could potentially help stratify the need for an endoscopic workup in these patients.sponsorship: P.M. is supported by a doctoral fellowship by the Research Foundation - Flanders (FWO, grant-number: 1127917N). P.M. and W.M. are researchers for the Limburg Clinical Research Program (LCRP) UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk (LSM), Hasselt University, Ziekenhuis Oost-Limburg and Jessa Hospital. (Research Foundation - Flanders (FWO)|1127917N, foundation Limburg Sterk Merk (LSM), Hasselt University, Ziekenhuis Oost-Limburg, Jessa Hospital)status: Publishe
Impact of Systemic Venous Congestion in Heart Failure
No full textSystemic venous congestion is one of the hallmarks of the syndrome of heart failure that results from activation of different deleterious neurohormonal pathways. Apart from contributing to patients’ symptoms and hospital admissions, growing evidence suggests that congestion itself drives further heart failure progression. In addition, systemic venous congestion exerts detrimental effects on other organs (such as kidneys and liver) due to ineffective organ perfusion. Endothelial cell activation, altered ventricular geometry, and functional mitral insufficiency are among the proposed mechanisms. Diuretics and vasodilators remain the mainstay of treatment options, mostly because of poor understanding of the underlying cardiorenal mechanisms involved. Recently, ultrafiltration has emerged as an invasive treatment option in the setting of diuretic resistance. Congestion ideally should be prevented, often initially through water and salt restriction. Early detection, possibly with the help of novel implantable sensor technology, may allow for early detection and intervention long before overt congestion is established
Cardiovascular Volume Reserve in Patients with Heart Failure and Reduced Ejection Fraction
No full textThis study aimed to investigate the relationship between intravascular volume and intracardiac filling pressures in stable HF patients with reduced ejection fraction (HFrEF). A total of 40 HFrEF patients (LVEF 36 +/- 10%) (10 subjects with a pulmonary artery catheter) underwent intravascular volume expansion with 1 L hydroxyl-ethyl-starch over 3 h with coinciding intravascular volume measurements (technetium (99 tc)-labeled red blood cell technique). Intravascular blood volume increased from 5.0 +/- 1.0 L to 5.7 +/- 1.0 L (p < 0.0001). No change in clinical status, echocardiographic indices, or cardiac filling pressures was noticed. Invasively measured right atrial pressure and pulmonary arterial wedge pressure increased significantly immediately after start of infusion (4 +/- 2 mmHg to 8 +/- 4 mmHg; p = 0.01 and 10 +/- 3 mmHg to 15 +/- 6 mmHg; p = 0.01, respectively), decreased afterwards, and remained stable for 3 h (6 +/- 2 mmHg and 14 +/- 4 mmHg, respectively). The accuracy of cardiac filling pressure estimates to predict intravascular volume expansion was low (all AUC < 0.65).P.N is supported by The Frans Van de Werf Fund for Clinical Cardiovascular Research. P.N., P.M., and W.M. are researchers for the Limburg Clinical Research Program (LCRP) UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk (LSM), Hasselt University, Ziekenhuis Oost-Limburg, and Jessa Hospital. P.N. and M.D. are supported by a research grant provided by Vision4Life-Sciences.Nijst, P (reprint author), Ziekenhuis Oost Limburg, Dept Cardiol, Schiepse Bos 6, B-3600 Genk, Belgium, Hasselt Univ, Doctoral Sch Med & Life Sci, Diepenbeek, Belgium.
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The importance of developing hyperkalaemia in heart failure during long-term follow-up
No full textBackground:Hyperkalaemia is a potentially life-threatening condition. Furthermore, it is one of the main reasons for discontinuation and dose reduction of renin-angiotensin-aldosterone system inhibitors (RAASi) in clinical practice. However, exact data on the prevalence and consequences of occurrence of hyperkalaemia when taking RAASi in a dedicated heart failure care setting are scarce. Methods:Consecutive patients diagnosed with heart failure from a single tertiary hospital between August 2000 and May 2017 were retrospectively evaluated. Primary endpoint was the development of hyperkalaemia (>= 5.5 mmol/L) at any moment during follow-up. Results:About 396 patients were included in the current analysis (mean follow-up 6.9 years). 26% (n = 104) and 12% (n = 46) of patients developed hyperkalaemia (>= 5.5 mmol/L and >= 6.0 mmol/L, respectively). Diabetes mellitus (OR = 1.80, 95% CI = 1.03-3.19) and baseline creatinine (mg/dL) (OR = 2.37, 95% CI = 2.37-3.85) were independent risk factors for hyperkalaemia. Development of hyperkalaemia was associated with 6.5 higher odds for recurrence. Only 10% developed hyperkalaemia during up-titration of RAASi, while 90% developed during later follow-up on stable doses of RAASi. hyperkalaemia was not associated with worse outcome after multivariate adjustment for baseline co-morbidities. However, hyperkalaemia was associated with discontinuation and lower doses of MRAs during follow-up (p = 0.007). Discontinuation of MRA due to hyperkalaemia was associated with an increase in all-cause mortality in HFrEF patients (HR = 1.77, 95% CI = 1.05-2.99). Conclusions:Approximately, one-fourth of patients developed hyperkalaemia during follow-up which was associated with a lower MRA dose during follow-up. Discontinuation of MRA, but not hyperkalaemia itself, was associated with an increased risk of all-cause mortality and heart failure admission in HFrEF patients.Pieter Martens is supported by a doctoral fellowship by the Research Foundation - Flanders (FWO, grant-number: 1127917N). Pieter Martens, Petra Nijst, and Wilfried Mullens are researchers for the Limburg Clinical Research Program (LCRP) UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk (LSM), Hasselt University, Ziekenhuis Oost-Limburg and Jessa Hospital. Pieter Martens has received consultancy fees from and an unrestricted research grant from Vifor Pharma.Martens, P (corresponding author), Ziekenhuis Oost Limburg, Dept Cardiol, Schiepse Bos 6, B-3600 Genk, Belgium.
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Insights into implementation of sacubitril/valsartan into clinical practice
No full textBackgroundSacubitril/valsartan significantly reduced heart failure hospitalization and mortality in PARADIGM-HF (Prospective Comparison of Angiotensin Receptor-Neprilysin Inhibitor With an Angiotensin-Converting Enzyme Inhibitor to Determine Impact on Global Mortality and Morbidity in Heart Failure). However, real-world data from its use are lacking. Methods and resultsWe retrospectively assessed all baseline and follow-up data of consecutive heart failure patients with reduced ejection fraction receiving therapy with sacubitril/valsartan for Class I recommendation between December 2016 and July 2017. Baseline characteristics and dose titration of sacubitril/valsartan were compared between patients in clinical practice and in PARADIGM-HF. A total of 120 patients (81% male) were switched from angiotensin-converting enzyme inhibitor or angiotensin receptor blocker to sacubitril/valsartan. A total of 20.1% of patients received dose uptitration. Patients were treated with an equipotential dose of renin-angiotensin system blockers before and after uptitration of sacubitril/valsartan (5729% vs. 53 +/- 29% of target dose indicated by European Society of Cardiology guidelines; P=0.286). However, they received a lower dose of sacubitril/valsartan in comparison with those in the PARADIGM-HF (219 +/- 12 vs. 375 +/- 75mg; P<0.001). In comparison with the patients receiving sacubitril/valsartan in PARADIGM-HF, patients in clinical practice were older and had a higher serum creatinine, higher New York Heart Association functional classification, and lower left ventricular ejection fraction (all P-value <0.05). Even in comparison with patients who experienced dropout during the run-in phase of PARADIGM-HF, real-world patients exhibited baseline characteristics indicative of more disease severity. Patients were at high absolute baseline risk for adverse outcome as illustrated by the EMPHASIS-HF (Eplerenone in Mild Patients Hospitalization and Survival Study in Heart Failure) risk score of 6 (inter-quartile range 3), in comparison with 5 (inter-quartile range 4) in PARADIGM-HF. After initiation of sacubitril/valsartan, New York Heart Association class significantly improved (P<0.001), but systolic blood pressure dropped more than was reported in PARADIGM-HF (7.1 +/- 8.0 vs. 3.2 +/- 0.4mmHg; P<0.001). ConclusionsPatients in clinical practice exhibit baseline characteristics associated with more severe disease, which might lead to prescription of lower doses. Nevertheless, patients in clinical practice are at high risk of adverse outcome as illustrated by the EMPHASIS-HF risk score, underscoring the large potential for sacubitril/valsartan therapy to reduce the risk of heart failure hospitalization and all-cause mortality.Research Foundation - Flanders (FWO) [1127917N]; foundation Limburg Sterk Merk (LSM); Hasselt University; Ziekenhuis Oost-Limburg; Jessa Hospita
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