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4,008 results for “Heart failure”
Early left atrial dysfunction in idiopathic pulmonary fibrosis patients without chronic right heart failure
<p>Raw data related to the article.</p> <p>Abstract</p> <p>No data are actually available regarding the left atrial (LA) functional assessment by two-dimensional speckle tracking<br> echocardiography (2D-STE) in early-stage idiopathic pulmonary fibrosis (IPF). The primary end-point of our study was to<br> assess whether global LA peak strain (GLAPS), measured by 2D-STE analysis, may detect early alterations in LA function<br> in IPF patients without right heart failure (RHF). Between September 2017 and January 2019, 50 consecutive IPF patients<br> (73.8 ± 6.8 years, 36 males) without chronic RHF and 30 controls matched by age, sex and cardiovascular risk factors, were<br> enrolled in an observational retrospective case–control study. All patients underwent a complete echocardiographic study<br> implemented with 2D-STE analysis. GLAPS, left ventricular (LV) global longitudinal strain (GLS), right atrial (RA) reservoir<br> strain (GSA+) and right ventricular (RV)-GLS were obtained in each patient. LVFP were significantly increased in<br> IPF patients in comparison to controls (average E/e′ ratio 14.4 ± 3.0 vs 9.6 ± 1.5, p < 0.0001), while LV-GLS was slightly<br> reduced in IPF patients compared to controls (19.4 ± 3.6% vs 21.0 ± 2.2%, p = 0.03).Moreover, GLAPS was significantly<br> impaired in IPF patients in comparison to controls (18.4 ± 3.7% vs 28.4 ± 5.6%, p < 0.0001).Finally, the two groups of<br> patients did not show any statistically significant difference in both RA-GSA + (23.9 ± 3.7% vs 24.5 ± 4.0%, p = 0.49)<br> and RV-GLS (− 22.6 ± 3.3% vs − 23.5 ± 3.0%, p = 0.22). Notably, LV-GLS was strongly inversely correlated both with<br> RV/LV basal diameter ratio and TRV in IPF patients (r = − 0.87 and − 0.82, respectively) but not in controls (r = − 0.29<br> and − 0.27, respectively). This finding highlights a likely process of ventricular interdependence in non-advanced IPF, with<br> consequent LV diastolic dysfunction and secondary impairment in LV-GLS and GLAPS. Early LA reservoir dysfunction in<br> IPF patients may be secondary to LV diastolic dysfunction induced by ventricular interdependence and may develop before<br> RV diastolic and systolic dysfunction.</p>
Do the remodeling effects of sacubitril/valsartan treatment depend upon heart failure duration?
<p>Aims The angiotensin receptor and neprilysin inhibitor (ARNI) sacubitril/valsartan (LCZ696) is recommended for the treatment of patients with heart failure in New York Heart Association (NYHA) class II–III and left ventricular ejection fraction (LVEF) 35% or less. We examined the effects of sacubitril/valsartan on cardiac remodeling and their correlation with heart failure duration in patients enrolled in our heart failure clinic from March 2017 to December 2019. <br> Methods Echocardiographic and clinical/laboratory data were collected at baseline and at 6-month and 12-month follow-up visits in 69 patients (age 67+/-12 years, disease duration 8.4W5.8 years, 93% men).<br> Results At both time points, mean NYHA class, NT-proBNP level, LVEF, LV end-systolic volume, and estimated systolic pulmonary pressure significantly (P<0.05) improved versus baseline, as did the proportion of patients with diastolic dysfunction grade 3 or functional mitral regurgitation grade 3–4. In the subgroup with mean disease duration less than 8.5 years (n = 40), there was a significant improvement in all variables at both time points; in this group, a recovery of right ventricular function was also seen at the 12-month follow-up. On the contrary, patients with heart failure duration of at least 8.5 years (n=29) showed only a slight improvement in LVEF and mitral regurgitation at 12 months. There were no significant changes in renal function and/or potassium levels in all patients. <br> Conclusion In patients with a relatively short disease duration, sacubitril/valsartan was associated with a strong favorable remodeling of the left ventricle and improvement in pulmonary circulation.</p>
Raw data of "Old and new equations for maximal heart rate prediction in patients with heart failure and reduced ejection fraction on beta-blockers treatment: results from the MECKI score data set"
<p>AIMS: Predicting maximal heart rate (MHR) in heart failure with reduced ejection fraction (HFrEF) still remains a major concern. In such a context, the Keteyian equation is the only one derived in a HFrEF cohort on optimized beta-blockers treatment. Therefore, using the Metabolic Exercise combined with Cardiac and Kidney Indexes (MECKI) data set, we looked for a possible MHR equation, for an external validation of Keteyien formula and, contextually, for accuracy of the historical MHR formulas and their relationship with the HR measured at the anaerobic threshold (AT). METHODS AND RESULTS: Data from 3487 HFrEF outpatients on optimized beta-blockers treatment from the MECKI data set were analyzed. Besides excluding all possible confounders, the new equation was derived by using HR data coming from maximal cardiopulmonary exercise test. The simplified derived equation was [109-(0.5*age) + (0.5*HR rest) + (0.2*LVEF)-(5 if haemoglobin &lt;11 g/dL)]. The R2 and the standard error of the estimate were 0.24 and 17.5 beats min-1 with a mean absolute percentage error (MAPE) = 11.9%. The Keteyian equation had a slightly higher MAPE = 12.3%. Conversely, the Fox and Tanaka equations showed extremely higher MAPE values. The range 75-80% of MHR according to the new and the Keteyian equations was the most accurate in identifying the HR at the AT (MAPEs = 11.3-11.6%). CONCLUSION: The derived equation to estimate the MHR in HFrEF patients, by accounting also for the systolic dysfunction degree and anaemia, improved slightly the Keteyian formula. Both formulas might be helpful in identifying the true maximal effort during an exercise test and the intensity domain during a rehabilitation programme.</p>
Respiratory patterns and baroreflex function in heart failure
<p>Dataset to reproduce tables 1, 2 and 3 of the paper "Respiratory patterns and baroreflex function in heart failure" published on Scientific Reports</p>
NCOA4-mediated ferritinophagy exacerbates heart failure by releasing free iron to promote GPX4-mediated ferroptosis
<p>Heart failure (HF) is typically characterized by high mortality and disability rates. The pathogenesis of HF is complex and multifactorial,the exact pathophysiology of HF remains to be fully elucidated. In our research group, we have discovered that autophagy is a crucial mechanism underlying the development of heart failure, and abnormal iron metabolism (such as ferroptosis) is closely associated with the occurrence and progression of cardiovascular diseases.Thus, through the construction of a rat model of heart failure following myocardial infarction and an H/R H9C2 cell model, we have conducted studies and found that NCOA4, through the classical autophagy pathway mediated by ATG5/ATG7 and in association with LC3B, plays a role in mediating ferritinophagy, controlling the degradation of ferritin. This modulation regulates the concentrations of cellular free iron and labile iron pool, suppresses GPX4 expression, promotes lipid peroxidation and oxidative stress, induces ferroptosis, and exacerbates the severity of heart failure. Our proposed hypothesis elucidates the mechanisms by which autophagy, NCOA4-mediated ferritinophagy, and GPX4-mediated ferroptosis contribute to the development of heart failure under conditions of myocardial ischemia and hypoxia. It helps reconcile many previously contradictory viewpoints and provides a viable pathway for the treatment of post-myocardial infarction heart failure.</p>
Variability in pulmonary diffusing capacity in heart failure
<p>Raw datA of the paper Variability in pulmonary diffusing capacity in heart failure</p>
The right side of the circulation in not secondary heart failure with preserved ejection fraction: an elephant in the room?
<p>raw data </p>
Current Limitations of Invasive Exercise Hemodynamics for the Diagnosis of Heart Failure With Preserved Ejection Fraction
<p>raw data ex-hemo protocol</p>
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