scholarly journals Long-Term Administration of Neuropeptide Y in the Subcutaneous Infusion Results in Cardiac Dysfunction and Hypertrophy in Rats

2015 ◽  
Vol 37 (1) ◽  
pp. 94-104 ◽  
Author(s):  
Rong Zhang ◽  
Huifang Niu ◽  
Xiaohui Kang ◽  
Tao Ban ◽  
Hong Hong ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Cardiac Remodeling ◽  
Cardiac Dysfunction ◽  
Diastolic Pressure ◽  
Heart Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Mitogen Activated Protein Kinase ◽  
Elevated Plasma

Background/Aims: The purpose of the present study was to clarify whether chronically elevated plasma neuropeptide Y (NPY) might affect heart function and cardiac remodeling in rats. Methods: Male Wistar rats were administered NPY (85 μg for 30 days) by mini-osmotic pump subcutaneously implanted between the scapulae. Associated indices for heart function, cardiac remodeling and hypertrophy were evaluated. Results: Compared to the sham group, the baseline systolic blood pressure (SBP) in rats administered NPY was significantly increased; cardiac function was significantly decreased, as indicated by reduced ejection fraction (EF), left ventricular end-systolic pressure (LVESP), maximum change velocity of left ventricular pressure in the isovolumic contraction or relaxation period (±dp/dtmax) and increased left ventricular end-diastolic pressure (LVEDP); hematoxylin-eosin (H&E) staining detection displayed enlarged cell areas and a consistent increase in heart-to-body weight ratios (HW/BW) was observed; quantitative real time PCR (qRT-PCR) and Western blot analysis showed markedly increased expressions of β-myosin heavy chain (β-MHC), calcineurin (CaN) and phosphorylated p38 proteins, while no changes were found in the expressions of p38 total protein and the phosphorylations of JNK and ERK. Conclusion: This study reported for the first time that long-term elevated plasma concentration of NPY could induce cardiac dysfunction and cardiac hypertrophy and this phenomenon could, in part, be mediated by the Ca2+/CaM-dependent CaN pathway and p38 mitogen-activated protein kinase (MAPK) signal pathway in rats.

scholarly journals Involvement of Sirtuins and Klotho in Cardioprotective Effects of Exercise Training Against Waterpipe Tobacco Smoking-Induced Heart Dysfunction

2021 ◽  
Vol 12 ◽  
Author(s):  
Samaneh Sadat Alavi ◽  
Siyavash Joukar ◽  
Farzaneh Rostamzadeh ◽  
Hamid Najafipour ◽  
Fatemeh Darvishzadeh-mahani ◽  
...  
Keyword(s):  
Exercise Training ◽  
Tobacco Smoking ◽  
Diastolic Pressure ◽  
Heart Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Smoke Inhalation ◽  
Control Group ◽  
Heart Dysfunction ◽  
Waterpipe Tobacco Smoking

Despite its negative effect on the cardiovascular system, waterpipe smoking (WPS) is currently popular worldwide, especially among youth. This study investigated the effects of moderate endurance exercise on heart function of rats exposed to WPS and its possible mechanism. The animals were randomly divided into four groups: control group (CTL), the exercise group (Ex) which trained for 8 weeks, the waterpipe tobacco smoking group (S) exposed to smoke inhalation (30 min per day, 5 days each week, for 8 weeks), and the group that did exercise training and received waterpipe tobacco smoke inhalation together (Ex + S). One day after the last session of Ex and WPS, cardiac pressures and functional indices were recorded and calculated. The levels of SIRT1, SIRT3, Klotho, Bax, and Bcl-2 in the serum and heart, the expression of phosphorylated GSK3β of heart tissue, and cardiac histopathological changes were assessed. WPS reduced systolic pressure, +dP/dt max, -dP/dt max, and heart contractility indices (P < 0.001 vs. CTL) and increased cardiac tissue lesions (P < 0.05 vs. CTL) and end diastolic pressure and Tau index (P < 0.001 vs. CTL) of the left ventricle. Exercise training normalized the left ventricular end diastolic pressure, +dP/dt max, and contractility index. Also, exercise improved the levels of SIRT1, SIRT3, Klotho, and Bcl-2 and reduced Bax level in the heart. The findings showed that WPS causes left ventricular dysfunction. Moderate exercise prevented WPS-induced heart dysfunction partly through its anti-apoptotic features and activation of the sirtuins and Klotho pathways.

Absence of meal-induced insulin sensitization (AMIS) in aging rats is associated with cardiac dysfunction that is protected by antioxidants

2011 ◽  
Vol 111 (3) ◽  
pp. 704-714 ◽  
Author(s):  
Zhi Ming ◽  
Dallas J. Legare ◽  
W. Wayne Lautt
Keyword(s):  
Cardiac Dysfunction ◽  
Insulin Action ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Sprague Dawley ◽  
Antioxidant Treatment ◽  
Aging Rats ◽  
Progressive Development

We have previously demonstrated that progressive development of absence of meal-induced insulin sensitization (AMIS) leads to postprandial hyperglycemia, compensatory hyperinsulinemia, resultant hyperlipidemia, increased oxidative stress, and obesity, progressing to syndrome X in aging rats. The present study tested the hypothesis that progressive development of AMIS in aging rats further resulted in deterioration in cardiac performance. Anesthetized male Sprague-Dawley rats were tested at 9, 26, and 52 wk to determine their dynamic response to insulin and cardiac function. Dynamic insulin sensitivity was determined before and after atropine to quantitate hepatic insulin sensitizing substance (HISS)-dependent and -independent insulin action. Cardiac performance was evaluated using a Millar pressure-volume conductance catheter system. AMIS developed with age, as demonstrated by significant decrease in HISS-dependent insulin action, and this syndrome was increased by sucrose supplementation and inhibited by the antioxidant treatment. Associated with progressive development of AMIS, aging rats showed impaired cardiac performance, including the reduction in cardiac index, heart rate, dP/d tmax, dP/d tmin, ejection fraction and decreased slope of left ventricular end-systolic pressure-volume relationship, and increased relaxation time constant of left ventricular pressure as well as increased left ventricular end-diastolic pressure. Total peripheral vascular resistance also increased with age. Sucrose supplementation and antioxidant treatment, respectively, potentiated and attenuated cardiac dysfunction associated with age. In addition, poor cardiac performance correlated closely with the development of AMIS. These results indicate that AMIS is the first metabolic defect that leads to homeostatic disturbances and dysfunctions, including cardiovascular diseases.

scholarly journals Longitudinal Reinforcement of Acute Myocardial Infarcts Improves Function by Transmurally Redistributing Stretch and Stress

2019 ◽  
Vol 142 (2) ◽  
Author(s):  
Ana Cristina Estrada ◽  
Kyoko Yoshida ◽  
Samantha A. Clarke ◽  
Jeffrey W. Holmes
Keyword(s):  
Diastolic Pressure ◽  
Heart Function ◽  
Systolic Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Published Data ◽  
Longitudinal Reinforcement ◽  
Wide Range ◽  
Volume Relationship ◽  
Pressure Volume Relationship

Abstract A wide range of emerging therapies, from surgical restraint to biomaterial injection to tissue engineering, aim to improve heart function and limit adverse remodeling following myocardial infarction (MI). We previously showed that longitudinal surgical reinforcement of large anterior infarcts in dogs could significantly enhance systolic function without restricting diastolic function, but the underlying mechanisms for this improvement are poorly understood. The goal of this study was to construct a finite element model that could match our previously published data on changes in regional strains and left ventricular function following longitudinal surgical reinforcement, then use the model to explore potential mechanisms for the improvement in systolic function we observed. The model presented here, implemented in febio, matches all the key features of our experiments, including diastolic remodeling strains in the ischemic region, small shifts in the end-diastolic pressure–volume relationship (EDPVR), and large changes in the end-systolic pressure–volume relationship (ESPVR) in response to ischemia and to patch application. Detailed examination of model strains and stresses suggests that longitudinal reinforcement reduces peak diastolic fiber stretch and systolic fiber stress in the remote myocardium and shifts those peaks away from the endocardial surface by reshaping the left ventricle (LV). These findings could help to guide the development of novel therapies to improve post-MI function by providing specific design objectives.

Involvement of cardiomyocyte apoptosis in myocardial injury of hereditary epileptic rats

2013 ◽  
Vol 91 (10) ◽  
pp. 804-811 ◽  
Author(s):  
Fan Chen ◽  
Yong-gang Cao ◽  
Han-ping Qi ◽  
Lei Li ◽  
Wei Huang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Myocardial Injury ◽  
Caspase 3 ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Cardiomyocyte Apoptosis ◽  
Mitogen Activated Protein Kinase ◽  
Catecholamine Level

Many clinical cases have been reported where epilepsy profoundly influenced the pathophysiological function of the heart; however, the underlying mechanisms were not elucidated. We use the tremor (TRM) rat as an animal model of epilepsy to investigate the potential mechanisms of myocardial injury. Cardiac functions were assessed by arrhythmia score, heart rate, heart:body mass ratio, and hemodynamic parameters including left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), and maximum rate of left ventricular pressure rise and fall (+dp/dtmax and –dp/dtmax). Catecholamine level was detected by HPLC. Apoptotic index was estimated by TUNEL assay. The expressions of Bcl-2, Bax, caspase-3, extracellular signal-regulated protein kinase (ERK), c-Jun NH2-terminal protein kinases (JNK), and p38 were evaluated by Western blot. The results indicated that there existed cardiac dysfunction and cardiomyocyte apoptosis, accompanied by increasing catecholamine levels in TRM rats. Further investigation revealed that apoptosis was mediated by reducing Bcl-2, upregulating Bax, and activating caspase-3. Additional experiments demonstrated that P-ERK1/2 was decreased, whereas P-JNK and P-p38 were up-regulated. Our results suggest that the sympathetic nervous system activation and cardiomyocyte apoptosis are involved in the myocardial injury of TRM rats. The mechanisms of apoptosis might be associated with the activation of the mitochondria-initiated and the mitogen-activated protein kinase pathways.

scholarly journals Initial Effects of the Left Ventricular Repair by Plication May Not Last Long in a Rat Ischemic Cardiomyopathy Model

Circulation ◽  
2001 ◽  
Vol 104 (suppl_1) ◽  
Author(s):  
Takeshi Nishina ◽  
Kazunobu Nishimura ◽  
Sadatoshi Yuasa ◽  
Senri Miwa ◽  
Takuya Nomoto ◽  
...  
Keyword(s):  
Ischemic Cardiomyopathy ◽  
Sham Group ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Long Term Results ◽  
Lv Function ◽  
Long Term Effects ◽  
Second Surgery

Background Long term effects of left ventricle (LV) repair surgery (LVR) for ischemic cardiomyopathy are not well understood. Methods and Results Sixty-nine rats developed ischemic cardiomyopathy with large akinetic LV area 4 weeks after the left anterior descending artery was ligated. In a second surgery 4 weeks later, 33 rats underwent LVR by plication of the akinetic LV area (LVR group), and 36 underwent rethoracotomy alone (sham group). No medication was used in either group. All rats survived the second surgery. LV end-diastolic dimension as measured by echocardiography, LV fractional shortening, and the maximal end-systolic pressure-volume relationship (E max ) as calculated from the data by catheter-tipped manometer and echocardiography improved in the LVR group after the second surgery, but LV end-diastolic dimension and E max gradually deteriorated as time passed. LV end-diastolic pressure improved 1 week after LVR but rose significantly 4 weeks after LVR. Brain natriuretic peptide mRNA was lower in the LVR group than in the sham group 1 week after LVR but not 4 weeks postoperatively. Conclusions Initial improvement in LV function and neurohormonal status after LVR did not last for 4 weeks in this rat model when untreated medically. The mechanism of deterioration should be elucidated to improve long-term results of LVR.

Effects of free fatty acids and dichloroacetate on isolated working diabetic rat heart

1991 ◽  
Vol 261 (4) ◽  
pp. H1053-H1059 ◽  
Author(s):  
T. A. Nicholl ◽  
G. D. Lopaschuk ◽  
J. H. McNeill
Keyword(s):  
Fatty Acids ◽  
Heart Rate ◽  
Cardiac Function ◽  
Free Fatty Acids ◽  
Cardiac Dysfunction ◽  
Glucose Oxidation ◽  
Heart Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Diabetic Heart

It is well established that cardiac dysfunction independent of atherosclerosis develops in both humans and animals with diabetes mellitus. The etiology is complex, involving many different processes, one of which may be increased fatty acid utilization and/or a concomitant decrease in glucose utilization by the diabetic heart. We compared control and 6-wk streptozotocin (STZ)-induced diabetic isolated working rat hearts and were able to demonstrate cardiac dysfunction in the diabetic as assessed by depressed heart rate (HR), heart rate peak systolic pressure product (HR.PSP), left ventricular developed pressure (LVDP), and rate of pressure rise (+dP/dt). Paralleling depressed cardiac function in the diabetic were hyperglycemia, hyperlipidemia, and decreased body weight gain compared with age-matched controls. The addition of free fatty acids, in the form of 1.2 mM palmitate, to the isolated working heart perfusate had no effect on either control or diabetic heart function, with the exception of a depressive effect on +dP/dt of diabetic hearts. But diabetic hearts perfused with palmitate-containing perfusate plus the glucose oxidation stimulator dichloroacetate (DCA) showed a marked improvement in function. HR and HR.PSP in spontaneously beating hearts, as well as LVDP and +dP/dt in paced hearts were all restored to control heart values in diabetic hearts perfused in the presence of DCA. Creatine phosphate and ATP levels were similar under all perfusion conditions, thus eliminating energy stores as the limiting factor in heart function. Results indicate that DCA will acutely reverse diabetic cardiac function depression. Therefore glucose oxidation depression in the diabetic heart may be a significant factor contributing to cardiac dysfunction.

Abstract 64: Conditional Knockout of Activin Like Kinase-1 (ALK-1) Leads to Heart Failure Without Maladaptive Remodeling

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Kevin Morine ◽  
Vikram Paruchuri ◽  
Xiaoying Qiao ◽  
Emily Mackey ◽  
Jonathan Levine ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Remodeling ◽  
Cardiac Fibrosis ◽  
Type I Collagen ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Conditional Knockout ◽  
Type I ◽  
Total Body Mass

Activin like kinase 1 (ALK1) mediates signaling via the TGFb family of ligands. ALK1 activity promotes endothelial proliferation and migration. Reduced ALK1 activity is associated with arteriovenous malformations. No studies have examined the effect of global ALK1 deletion on indices of cardiac remodeling. We hypothesized that reduced levels of ALK1 promote maladaptive cardiac remodeling. Methods: We employed an ALK1 conditional knockout mice (cKO) harboring the ROSA26-CreER knock-in allele whereby a single dose of intraperitoneal tamoxifen triggered ubiquitous Cre recombinase mediated excision of floxed ALK1 alleles. Tamoxifen treated wild-type (WT-Tam; n=5) and vehicle treated ALK1-cKO mice (cKO-Veh; n=5) served as controls for tamoxifen treated ALK1-cKO mice (cKO-Tam; n=15). Results: ALK1 cKO-Tam mice demonstrated reduced 14-day survival compared to cKO-Veh controls (33% vs 100%, respectively, p<0.01). Seven days after treatment, ALK1 cKO mice began to exhibit reduced left ventricular (LV) fractional shortening, progressive LV dilation, and gastrointestinal bleeding. After 14 days total body mass was reduced, but LV and lung mass increased in cKO-Tam not cKO-Veh mice. Peak LV systolic pressure, contractility, and arterial elastance were reduced, but LV end-diastolic pressure and stroke volume increased in cKO-Tam, not cKO-Veh mice. LV ALK1 mRNA and protein levels were reduced in cKO-Tam, not cKO-Veh mice. LV levels of other TGFb-family ligands and receptors (ALK5, TBRII, BMPRII, Endoglin, BMP7, BMP9, and TGFB1) were unchanged between groups. Cardiomyocyte area and LV levels of BNP were increased in cKO-Tam mice, but LV levels of b-MHC, SerCA, and calcineurin were unchanged. No increase in cardiac fibrosis Type I collagen, CTGF, or PAI-1 levels were observed between groups. No differences were observed for any variable studied between cKO-Veh and WT-Tam mice. Conclusion: Global deletion of ALK1 is associated with the development of high output heart failure without maladaptive remodeling. Future studies exploring the functional role of ALK1 in cardiac remodeling are required.

scholarly journals Clinical value and role of microRNA-29c-3p in sepsis-induced inflammation and cardiac dysfunction

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Bingyu Zhang ◽  
Lin Yu ◽  
Ying Sheng
Keyword(s):  
Inflammatory Response ◽  
Roc Curve ◽  
Cardiac Dysfunction ◽  
Troponin I ◽  
Diastolic Pressure ◽  
Cecal Ligation ◽  
Systolic Pressure ◽  
Diagnostic Value ◽  
Left Ventricular ◽  
Tnf Α

Abstract Background The goal of this study was to investigate the diagnostic value of miR-29c-3p in sepsis and its role in sepsis-induced inflammatory response and cardiac dysfunction. Methods Serum level of miR-29c-3p was detected by qRT-PCR. The ROC curve was used to evaluate the diagnostic value of miR-29c-3p for Sepsis. The cecal ligation and puncture method (CLP) was used to establish a rat sepsis model. To assess cardiac function, left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP) and maximum rate of rise/fall of left ventricle pressure (± dp/dtmax) in different experimental groups were detected, and the serum cardiac troponin I (cTnI), creative kinase isoenzyme MB (CK-MB) were measured by ELISA. Meanwhile, TNF-α, IL-1β, and IL-6 were detected by ELISA to assess the level of inflammatory response in animals. Results miR-29c-3p level was upregulated in sepsis patients. ROC curve revealed that miR-29c-3p had the ability to distinguish sepsis patients from healthy controls. Cardiac dysfunction and inflammation were observed in sepsis rat, which were characterized by the decrease of LVSP and + dp/dtmax, the increase of LVEDP, − dp/dtmax, cTnI, CK-MB, TNF-α, IL-1β, IL-6. All effects were reversed by the injection of miR-29c-3p antagomir. Logistics regression analysis manifested miR-29c-3p is an independent factor in the occurrence of cardiac dysfunction in sepsis patients. Conclusions miR-29c-3p has potential as a biomarker for the diagnosis of sepsis, and inhibition of miR-29c-3p expression in animal models reduced sepsis-induced cardiac dysfunction and inflammatory response.

scholarly journals d-Propranolol protects against oxidative stress and progressive cardiac dysfunction in iron overloaded rats

2012 ◽  
Vol 90 (9) ◽  
pp. 1257-1268 ◽  
Author(s):  
Jay H. Kramer ◽  
Christopher F. Spurney ◽  
Micaela Iantorno ◽  
Constantine Tziros ◽  
Joanna J. Chmielinska ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Mass ◽  
Cardiac Dysfunction ◽  
Diastolic Pressure ◽  
Heart Function ◽  
Treated Group ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Cardiac Inflammation

d-Propranolol (d-Pro: 2–8 mg·(kg body mass)–1·day–1) protected against cardiac dysfunction and oxidative stress during 3–5 weeks of iron overload (2 mg Fe–dextran·(g body mass)–1·week–1) in Sprague–Dawley rats. At 3 weeks, hearts were perfused in working mode to obtain baseline function; red blood cell glutathione, plasma 8-isoprostane, neutrophil basal superoxide production, lysosomal-derived plasma N-acetyl-β-galactosaminidase (NAGA) activity, ventricular iron content, and cardiac iron deposition were assessed. Hearts from the Fe-treated group of rats exhibited lower cardiac work (26%) and output (CO, 24%); end-diastolic pressure rose 1.8-fold. Further, glutathione levels increased 2-fold, isoprostane levels increased 2.5-fold, neutrophil superoxide increased 3-fold, NAGA increased 4-fold, ventricular Fe increased 4.9-fold; and substantial atrial and ventricular Fe-deposition occurred. d-Pro (8 mg) restored heart function to the control levels, protected against oxidative stress, and decreased cardiac Fe levels. After 5 weeks of Fe treatment, echocardiography revealed that the following were depressed: percent fractional shortening (%FS, 31% lower); left ventricular (LV) ejection fraction (LVEF, 17%), CO (25%); and aortic pressure maximum (Pmax, 24%). Mitral valve E/A declined by 18%, indicating diastolic dysfunction. Cardiac CD11b+ infiltrates were elevated. Low d-Pro (2 mg) provided modest protection, whereas 4–8 mg greatly improved LVEF (54%–75%), %FS (51%–81%), CO (43%–78%), Pmax (56%–100%), and E/A >100%; 8 mg decreased cardiac inflammation. Since d-Pro is an antioxidant and reduces cardiac Fe uptake as well as inflammation, these properties may preserve cardiac function during Fe overload.

scholarly journals Prediction of long-term survival in haemoglobinopathies: insights from cardiac imaging and ferritin

2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
V Kamperidis ◽  
M Vlachou ◽  
Z Pappa ◽  
D Pantelidou ◽  
T Karamitsos ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Term Survival ◽  
Long Term Survival ◽  
Ventricular Systolic Pressure ◽  
Survival Status ◽  
Funding Sources

Abstract Funding Acknowledgements Type of funding sources: None. Aims.The data on echocardiography, cardiac magnetic resonance (CMR) and ferritin predicting long-term survival in haemoglobinopathies are scarce. The current study evaluated the association of these parameters with the 10-years survival in haemoglobinopathies. Methods.This prospective study included stable consecutive haemoglobinopathy patients .Demographics, ferritin, echocardiography and CMR parameters were prospectively collected. Results. In total, 83 patients (mean age 38.4 ± 12.0 years, 46% male) with haemoglobinopathies were included and dichotomized based on their survival status after a follow-up of 9.8 ± 1.4 years. Patients who died were older (45.3 ± 11.6 vs 37.1 ± 11.7 years, p = 0.025), had higher ferritin levels (2498 vs 754 ng/ml, p = 0.001), higher right ventricular systolic pressure (RVSP) (41 ± 10 vs 31 ± 11mmHg, p = 0.001), more frequently elevated left ventricular (LV) end-diastolic pressure (70 vs 35%, p = 0.039) and lower CMR T2* values (23 ± 12 vs 35 ± 12ms, p = 0.007). Older age (HR: 1.053, p = 0.018), ferritin &gt;2000ng/ml (HR: 3.517, p = 0.03), and &gt;950ng/ml (HR: 11,135, p = 0.02), elevated LV end-diastolic pressure (HR: 3.977, p = 0.046), RVSP &gt;34mmHg(HR: 10,134, p = 0.003), CMR T2* &lt;20msec (HR: 4.900, p = 0.018) and &lt;36msec (HR: 9.376, p = 0.035) were associated with increased all-cause mortality. A baseline model including age was created andit became more predictive of worse survival by adding RVSP &gt;34mmHg than elevated LV end-diastolic pressure (C index 0.777 vs. 0.757 respectively) or ferritin &gt;950ng/ml than &gt;2000ng/ml (C index 0.805 vs. 0.770 respectively) or CMR T2*&lt;36msec than &lt;20msec (C index 0.825 vs. 0.810 respectively). Conclusions. In haemoglobinopathy patients, RVSP &gt;34mmHg, ferritin &gt;2000ng/ml and CMR T2* &lt;20ms were associated with worse long term survival.In the current era of advanced chelation therapy, aiming for ferritin &lt;950ng/ml and CMR T2* &gt;36ms appears to improve their prognosis. Abstract Figure.

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