Exjade® Reduces Cardiac Iron Burden in Chronically Transfused β-Thalassemia Patients: An MRI T2* Study.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2781-2781 ◽  
Author(s):  
J. Wood ◽  
A.A. Thompson ◽  
C. Paley ◽  
B. Kang ◽  
P. Giardina ◽  
...  

Abstract Introduction: Despite the routine use of iron chelation therapy, cardiac iron overload results in cardiomyopathy, congestive heart failure and death in approximately 71% of pts with β-thalassemia. Recent MRI studies suggest that the kinetics of cardiac iron uptake and elimination differ from that of liver. Furthermore, different chelators appear to exhibit unique profiles of relative heart and liver iron removal. Deferasirox (DFX; Exjade®) is a once-daily oral iron chelator with demonstrated efficacy in reducing liver iron. In addition, preclinical and single-institution clinical studies have demonstrated cardiac iron removal. This study is a prospective, single-arm multi-institutional trial designed to evaluate the effect of DFX on cardiac iron in pts with β-thalassemia major. Here, we report preliminary results from the first 15 pts who completed 6 months of treatment. Methods: This ongoing study will enroll 30 pts at 4 US centers. DFX is administered at 30–40 mg/kg/day for 18 months. Entry criteria include MRI evidence of cardiac iron (T2* <20 ms) and normal left ventricular ejection fraction (LVEF ≥56%). Serum ferritin is assessed monthly and MRI assessments for liver iron concentration (LIC), cardiac T2* and LVEF are assessed every 6 months. Labile plasma iron (LPI), serum creatinine, biochemical and hematological status are being monitored. Results: At the time of this analysis, 15 of 17 pts had 6 months of evaluation; all were dosed at 30 mg/kg/day. One of the excluded pts was found ineligible (LVEF <56% at baseline) and the other developed cardiac failure prior to 6 months and was switched to continuous DFO (deferoxamine). This pt had markedly elevated cardiac iron (T2*=1.8 ms) at enrollment. All results are reported as mean±SEM (range) unless otherwise stated. Baseline: All 15 evaluable pts (3 male, 12 female; aged 10–43 years) received ≥150 lifetime transfusions. Ferritin was 4927±987 ng/mL (395–10751; n=12). Cardiac T2* was 9.8±1.13 ms (5.0–16.1), LIC was 16.6±4.27 mg/g dw (3.6–62.3) and ejection fraction was 61.2±1.83%. LPI was 0.72±0.28 μmol/L (n=11) and 33% of pts started with abnormal LPI (≥0.5 μmol/L). 6 Month results: At 6 months, the mean decrease in ferritin was 516 ng/mL; 14 of 15 (93%) pts had decreases in hepatic and cardiac iron. The mean reductions in cardiac and hepatic iron were 17.8% (P=0.0136) and 27.0% (P=0.0027), respectively (Figure). There was no change in LVEF by MRI. All patients had normal LPI at 6 months; for pts with abnormal LPI at baseline, the mean LPI dropped from 1.6±0.3 to 0.26±0.1 μmol/L (P=0.003). No pts developed creatinine >upper limit of normal. Four pts had abnormal transaminases on ≥2 occasions but all 4 were abnormal at baseline. Conclusions: The 30 mg/kg/day dose was well tolerated and led to negative cardiac and liver iron balance in 93% of pts. These results are encouraging given this heavily iron-overloaded and heavily transfused population of β-thalassemia pts. Ongoing assessments over 12 and 18 months will elucidate if DFX continues to improve cardiac iron burden and maintain/improve cardiac function in severely iron-overloaded pts. Figure Figure

Blood ◽  
2010 ◽  
Vol 116 (4) ◽  
pp. 537-543 ◽  
Author(s):  
John C. Wood ◽  
Barinder P. Kang ◽  
Alexis Thompson ◽  
Patricia Giardina ◽  
Paul Harmatz ◽  
...  

AbstractWe present results from a prospective, multicenter, open-label, single-arm study evaluating response of cardiac and liver iron to deferasirox therapy for 18 months. Twenty-eight patients with abnormal T2* and normal left ventricular ejection fraction were enrolled from 4 US centers. All patients initially received deferasirox doses of 30 to 40 mg/kg per day. Patients were severely iron overloaded: mean liver iron concentration (LIC) 20.3 mg Fe/g dry weight, serum ferritin 4417 ng/mL, and cardiac T2* 8.6 ms. In the intent-to-treat population, 48% reached the primary endpoint (cardiac T2* improvement at 18 months, P = not significant). There were 2 deaths: 1 from congestive heart failure and 1 from sepsis. In the 22 patients completing the trial, LIC and cardiac T2* improvements were 16% (P = .06) and 14% (P = .07), respectively. Cardiac T2* improvement (13 patients) was predicted by initial LIC, final LIC, and percentage LIC change, but not initial cardiac T2*. Cardiac iron improved 24% in patients having LIC in the lower 2 quartiles and worsened 8.7% in patients having LIC in the upper 2 quartiles. Left ventricular ejection fraction was unchanged at all time points. Monotherapy with deferasirox was effective in patients with mild to moderate iron stores but failed to remove cardiac iron in patients with severe hepatic iron burdens. This study was registered at www.clinicaltrials.gov as #NCT00447694.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3873-3873 ◽  
Author(s):  
Dudley Pennell ◽  
John B Porter ◽  
Maria Domenica Cappellini ◽  
Chi-Kong Li ◽  
Yesim Aydinok ◽  
...  

Abstract Background: Heart failure secondary to myocardial siderosis remains the main cause of death in regularly transfused patients (pts) with β-thalassemia, hence the importance of using a chelator that can reduce cardiac iron. Deferasirox (Exjade®), a once-daily, oral iron chelator, has demonstrated removal of cardiac iron in preclinical and small clinical studies. The EPIC trial is a 1-yr, multicenter prospective longitudinal study, and is the largest of its kind for any chelation therapy. Here we report the EPIC cardiac sub-study, which evaluates the cardiac efficacy of deferasirox in β-thalassemia pts with myocardial siderosis. Methods: The sub-study of EPIC included pts with β-thalassemia aged ≥10 yrs who were eligible for enrollment in the core trial and who had magnetic resonance (MR) myocardial T2* >5–<20 ms (indicating cardiac siderosis), left ventricular ejection fraction (LVEF) ≥56%, serum ferritin (SF) >2500 ng/mL, MR (R2) liver iron concentration (LIC) >10 mg Fe/g dw, and a lifetime minimum of 50 transfused blood units. Deferasirox was initiated at 30 mg/kg/d and subsequent dose adjustments of 5–10 mg/kg/d were based on changes in SF, month-6 cardiac T2* and safety parameters. The primary endpoint was the change in myocardial T2* from baseline to 1 yr. Secondary endpoints included change in LVEF, SF and LIC at 1 yr. Results: Enrolled into this sub-study were 114 pts (54 M, 60 F; mean 20.9±7.3 yrs), of whom the baseline myocardial T2* was <10 ms in 47 (41%), and 10–20 ms in 67 (59%). Mean baseline LIC was 28.2±10.0 mg Fe/g dw, median SF 5235 ng/mL, and the mean amount of transfused blood in the previous yr 185 mL/kg. 68% of pts had received prior deferoxamine (DFO) and 32% DFO/deferiprone combination therapy. Mean actual deferasirox dose over 1 yr was 32.6 mg/kg/d. At 1 yr, the myocardial T2* improved significantly from a (geometric mean ± coefficient of variation) baseline of 11.2 ms ±40.5% to 12.9 ms ±49.5% (P<0.0001), representing an increase by a factor of 1.16 from baseline. Significant increases from 7.4 ms ±19.4% to 8.2 ms ±25.6% (P=0.0002) and from 14.6 ms ±20.9% to 17.4 ms ±31.2% (P<0.0001) were also noted in pts with baseline T2* <10 and 10–20 ms, respectively. Improvement in T2* (>4% increase) was seen in 69.5%; no change in 14.3%; and worsening (>4% decrease) in 16.2%. LVEF remained stable throughout the study: 67.4±5.7% to 67.1±6.0% (P=ns). Overall both mean LIC and median SF were reduced significantly from baseline by −6.6±9.9 mg Fe/g dw and −1257 ng/mL (P<0.0001 for both). Treatment was completed in 105 pts (92.1%) with 4 discontinuations due to AEs (3.5%) and 5 for other reasons (4.4%). No pts died during the study. Most investigator-assessed drug-related AEs (78.6%) were mild-to-moderate in severity; rash was the most common (n=15; 13.2%). Two drug-related serious AEs (one nephritis leading to acute renal failure and one renal tubular disorder) were reported which eventually resolved following drug discontinuation. In total, 5 pts (4.4%) had an increase in serum creatinine >33% above baseline and the upper limit of normal (ULN) on two consecutive visits; there were no progressive increases. Two (1.8%) pts had an increase in alanine aminotransferase >10×ULN on two consecutive visits; levels were already elevated in these pts. Conclusions: In β-thalassemia pts with myocardial siderosis, deferasirox at a mean dose of 32.6 mg/kg/d over 1 yr removes iron from the heart. The statistically significant improvement in myocardial T2* was associated with maintained ejection fraction. Concomitantly, a significant decrease in hepatic and total body iron burden was also seen. Deferasirox treatment was generally well tolerated. Ongoing one-yr extension of this sub-study will elucidate further the cardiac efficacy of deferasirox.


Blood ◽  
2010 ◽  
Vol 115 (12) ◽  
pp. 2364-2371 ◽  
Author(s):  
Dudley J. Pennell ◽  
John B. Porter ◽  
Maria Domenica Cappellini ◽  
Amal El-Beshlawy ◽  
Lee Lee Chan ◽  
...  

Cardiac iron overload causes most deaths in β-thalassemia major. The efficacy of deferasirox in reducing or preventing cardiac iron overload was assessed in 192 patients with β-thalassemia in a 1-year prospective, multicenter study. The cardiac iron reduction arm (n = 114) included patients with magnetic resonance myocardial T2* from 5 to 20 ms (indicating cardiac siderosis), left ventricular ejection fraction (LVEF) of 56% or more, serum ferritin more than 2500 ng/mL, liver iron concentration more than 10 mg Fe/g dry weight, and more than 50 transfused blood units. The prevention arm (n = 78) included otherwise eligible patients whose myocardial T2* was 20 ms or more. The primary end point was the change in myocardial T2* at 1 year. In the cardiac iron reduction arm, the mean deferasirox dose was 32.6 mg/kg per day. Myocardial T2* (geometric mean ± coefficient of variation) improved from a baseline of 11.2 ms (± 40.5%) to 12.9 ms (± 49.5%) (+16%; P < .001). LVEF (mean ± SD) was unchanged: 67.4 (± 5.7%) to 67.0 (± 6.0%) (−0.3%; P = .53). In the prevention arm, baseline myocardial T2* was unchanged from baseline of 32.0 ms (± 25.6%) to 32.5 ms (± 25.1%) (+2%; P = .57) and LVEF increased from baseline 67.7 (± 4.7%) to 69.6 (± 4.5%) (+1.8%; P < .001). This prospective study shows that deferasirox is effective in removing and preventing myocardial iron accumulation. This study is registered at http://clinicaltrials.gov as NCT00171821.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3882-3882 ◽  
Author(s):  
John C Wood ◽  
Alexis A. Thompson ◽  
Carole Paley ◽  
Barinder Kang ◽  
Patricia Giardina ◽  
...  

Abstract Introduction: Despite the availability of iron chelation therapy, accumulation of excess iron in the heart results in cardiomyopathy, congestive heart failure (CHF) and death in approximately 71% of transfused patients with β-thalassemia (β-thal) major. In preclinical and single-institution clinical studies, Exjade®(deferasirox, DFX) has demonstrated efficacy in decreasing cardiac iron. This ongoing study evaluates the effects of DFX on cardiac iron and left ventricular ejection fraction (LVEF) in patients (pts) with β-thal major in a prospective, single-arm, multi-center trial using cardiac MRI T2*. Here, we report preliminary results from patients who have completed 12 or 18 months of treatment. Methods: Twenty-eight pts were enrolled at four US centers. DFX was administered at 30–40 mg/kg/day for 18 months. Entry criteria included MRI evidence of cardiac iron (T2* <20 ms) and normal LVEF (≥56%). Serum ferritin (SF) was assessed monthly and MRI assessments for liver iron concentration (LIC), cardiac T2* and LVEF were done every 6 months. Serum creatinine (SCr), biochemical and hematological status were also monitored. All results are reported as mean±SE (range) unless otherwise stated. Results: At the time of analysis, 18 pts had 12-month evaluations and 12 pts had 18-month evaluations. Five pts discontinued (one non-compliance, two patient decisions, and two deaths). Both deaths were considered unrelated to DFX treatment; the first patient enrolled with markedly elevated baseline cardiac iron (T2*=1.8 ms) and died secondary to CHF. The second patient death was due to sepsis and multi-organ failure. Baseline: All 18 evaluable pts (three male, 15 female; aged 10–44 years) received ≥150 lifetime transfusions. SF was 4324±912 ng/mL (395–16,249). Cardiac T2* was 9.6±0.97 ms (4.6–16.1), LIC was 18.7±3.8 mg Fe/g dry weight (dw; 3.6–62.3) and LVEF was 61.7±1.0%. 12-Month results: At 12 months, 7/18 pts were on 40 mg/kg/day. 12/18 pts (67%) had an increase in cardiac T2* with a mean difference of 2.2 ms (18%; P=0.025). 13/18 pts (72%) had a decrease in LIC with a mean difference of 2.4 mg Fe/g dw (25%; P=0.032). LVEF remained stable. SF fell by 583 ng/mL (n=18; 22%; P=0.147). 18-Month results: At 18 months, 3/12 pts were on 40 mg/kg/day. 10/12 pts (83%) had an increase in cardiac T2* with a mean difference of 4.1 ms (35%; P=0.001). 11/12 pts (92%) had a decrease in LIC with a mean reduction of 4.7 mg Fe/g dw (50%; P=0.003). Mean LVEF trended upward from 61.5 to 63.3% (n=13; P=0.2). SF fell by 1373 ng/mL (n=11; 46%, P=0.006). Safety data from pts (n=25) treated with 30–40 mg DFX were in line with previous studies. The most common drug-related adverse events (AEs; eight pts; 32%) were gastrointestinal in nature. 1/25 patients experienced a suspected SAE (hospitalization due to abdominal pain and vomiting) but completed the study. One patient developed SCr >upper limit of normal (ULN). Two pts (8%) had abnormal transaminases (≥5×ULN) on ≥2 occasions but both had abnormal values at baseline. Conclusions: DFX monotherapy significantly improved cardiac and liver iron after 12 and 18 months. Overall, doses from 30–40 mg/kg/day were well tolerated. Cardiac T2* improvement rates were 1.5–1.9% per month, which is comparable to other monotherapy trials. A trend towards improved LVEF was seen in patients completing 18 months of therapy; however, a larger, long-term study will be required to confirm whether DFX can significantly improve cardiac function in this population. Figure Figure


2021 ◽  
Vol 10 (9) ◽  
pp. 1829
Author(s):  
Marcin Wełnicki ◽  
Iwona Gorczyca ◽  
Wiktor Wójcik ◽  
Olga Jelonek ◽  
Małgorzata Maciorowska ◽  
...  

Background: Hyperuricemia is an established risk factor for cardiovascular disease, including atrial fibrillation (AF). The prevalence of hyperuricemia and its clinical significance in patients with already diagnosed AF remain unexplored. Methods: The Polish Atrial Fibrillation (POL-AF) registry includes consecutive patients with AF hospitalized in 10 Polish cardiology centers from January to December 2019. This analysis included patients in whom serum uric acid (SUA) was measured. Results: From 3999 POL-AF patients, 1613 were included in the analysis. The mean age of the subjects was 72 ± 11.6 years, and the mean SUA was 6.88 ± 1.93 mg/dL. Hyperuricemia was found in 43% of respondents. Eighty-four percent of the respondents were assigned to the high cardiovascular risk group, and 45% of these had SUA >7 mg/dL. Comparison of the extreme SUA groups (<5 mg/dL vs. >7 mg/dL) showed significant differences in renal parameters, total cholesterol concentration, and left ventricular ejection fraction (EF). Multivariate regression analysis showed that SUA >7 mg/dL (OR 1.74, 95% CI 1.32–2.30) and GFR <60 mL/min/1.73 m2 (OR 1.94, 95% CI 1.46–2.48) are significant markers of EF <40% in the study population. Female sex was a protective factor (OR 0.74, 95% CI 0.56–0.97). The cut-off point for SUA with 60% sensitivity and specificity indicative of an EF <40% was 6.9 mg/dL. Conclusions: Although rarely assessed, hyperuricemia appears to be common in patients with AF. High SUA levels may be a significant biomarker of reduced left ventricular EF in AF patients.


EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
M Ben Kilani ◽  
P Jacon ◽  
A Carabelli ◽  
S Venier ◽  
P Defaye

Abstract Funding Acknowledgements Type of funding sources: Private company. Main funding source(s): P. JACON consultant: Boston Scientific France Introduction The implantable cardioverter defibrillator (ICD) is the most effective therapy for prevention of sudden cardiac death in high-risk patients with heart failure and reduced ejection fraction (HFrEF). The subcutaneous implantable cardioverter defibrillator (S-ICD) has been considered as a comparable and relatively safer alternative to transvenous ICD in patients (pts) without pacing indication. Purpose Our aim was to assess the clinical "real-life" outcomes of S-ICD in patients with HFrEF and primary or secondary prevention, over a long-term follow-up (FU) period after S-ICD implantation. Methods All pts with HFrEF (left ventricular ejection fraction ≤35%) implanted with a S-ICD and a FU above 6 months were included in a cross-sectional monocentric study. Pts were followed by remote monitoring. Results 88 pts were included (52 ± 12.8 years old, male 87.5%). Indications were: primary 92% and secondary 8% prevention  (ischemic cardiopathy 46%; dilated 46%; hypertrophic 5%; congenital 2%; valvular 1%). The mean left ventricular ejection fraction was 27%. 9 pts had a previous transvenous ICD implanted, but required revision because of infection or lead defects. The mean FU period was 33 ± 18 months with a mortality rate of 10% (S-ICD-related death secondary to inappropriate (inap) shocks for one patient). 5 pts underwent S-ICD system extraction after a mean FU period of 30 ± 21 months. Reasons were infectious complication (1 pt), pacing indication (2 pts) and S-ICD lead dysfunction (2 pts). Extraction after heart transplant was performed in 4 pts. During FU, 18 pts (20.5%) experienced at least one therapy: 8 pts (9%) with appropriate (ap) (3.3% per year) and 11 pts (12%) with inap shocks (4.36% per year). A total number of 24 ap shocks have been observed (3 ± 4 ap shocks per patient, several shocks for 3 pts), the first shock occurred after a mean FU period of 24 ± 14 months. 2 pts were referred to VT ablation and no recurrence of events was observed after medical therapy modification for the other pts. For the 11 pts with inap shocks, time to the first event was 19 ± 20 months. Reasons were: supraventricular arrhythmias (18%), T wave (36%) and noise (54%) oversensing. There was 1.8 ± 1.6 shock per patient with several shocks for 4 pts. Among pts with inap shocks, 2 pts required S-ICD system extraction, 1 pt died, while reprogramming and medical therapy options were efficient in other pts. Conclusion In pts with HFrEF at high risk of sudden cardiac death, S-ICD has proven to be effective in treating ventricular arrhythmias. However, more investigations must be conducted to explain the real-life high rate of inappropriate therapies. Abstract Figure. Survival-free from therapies curve


Author(s):  
Parisa Gholami ◽  
Shoutzu Lin ◽  
Paul Heidenreich

Background: BNP testing is now common though it is not clear if the test results are used to improve patient care. A high BNP may be an indicator that the left ventricular ejection fraction (LVEF) is low (<40%) such that the patient will benefit from life-prolonging therapy. Objective: To determine how often clinicians obtained a measure of LVEF (echocardiography, nuclear) following a high BNP value when the left ventricular ejection fraction (LVEF) was not known to be low (<40%). Methods and Results: We reviewed the medical records of 296 consecutive patients (inpatient or outpatient) with a BNP values of at least 200 pg/ml at a single medical center (tertiary hospital with 8 community clinics). A prior diagnosis of heart failure was made in 65%, while 42% had diabetes, 79% had hypertension, 59% had ischemic heart disease and 31% had chronic lung disease. The mean age was 73 ± 12 years, 75% were white, 10% black, 15% other and the mean BNP was 810 ± 814 pg/ml. The LVEF was known to be < 40% in 84 patients (28%, mean BNP value of 1094 ± 969 pg/ml). Of the remaining 212 patients without a known low LVEF, 161 (76%) had a prior LVEF >=40% ( mean BNP value of 673 ± 635 pg/ml), and 51 (24%) had no prior LVEF documented (mean BNP 775 ± 926 pg/ml). Following the high BNP, a measure of LVEF was obtained (including outside studies documented by the primary care provider) within 6 months in only 53% (113 of 212) of those with an LVEF not known to be low. Of those with a follow-up echocardiogram, the LVEF was <40% in 18/113 (16%) and >=40% in 95/113 (84%). There was no significant difference in mean initial BNP values between those with a follow-up LVEF <40% (872 ± 940pg/ml), >=40% (704 ± 737 pg/ml), or not done (661 ± 649 pg/ml, p=0.5). Conclusions: Follow-up measures of LVEF did not occur in almost 50% of patients with a high BNP where the information may have led to institution of life-prolonging therapy. Of those that did have a follow-up study a new diagnosis of depressesd LVEF was noted in 16%. Screening of existing BNP and LVEF data and may be an efficient strategy to identify patients that may benefit from life-prolonging therapy for heart failure.


Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 5110-5110
Author(s):  
Amal M. El-Beshlawy ◽  
Mona Mohamed Hamdy ◽  
Mona Elgamrawy ◽  
Khaled Abdel Azim ◽  
Doria Salem ◽  
...  

Abstract Abstract 5110 Introduction Myocardial siderosis in thalassemia major remains the leading cause of death in developing countries. Once heart failure develops, the outlook is usually poor with precipitous deterioration and death. Cardiovascular magnetic resonance (CMR) technology can measure cardiac iron deposition directly using the magnetic relaxation time T2*. This allows earlier diagnosis and treatment and help to reduce mortality from this cardiac affection. Patients and Methods 89 β thalassemia patients (10 to 43 years, mean age of 20.78±6.36) were recruited in this study. All patients were receiving chelation therapy of subcutaneous desferroxamine. Evaluation of hemosiderosis was based on CMR, liver magnetic resonance R2 and serum ferritin. Results T2* values ranged between 4.3 to 53.8 ms with a mean of 28.50±11.74 ms among our study group. The left ventricular ejection fraction (LVEF) as measured by CMR ranged between 55 and 78%; mean=67.66±4.69%.and liver iron concentration (LIC) ranged between 1.5 to 56 mg/g dry weight with a mean of 26.13±13.37 mg/g. Serum ferritin varied among our study group from 533 to 22363ng/ml; mean=4514.27±2847.58ng/ml with 83.15% above 2500ng/ml. The prevalence of myocardial siderosis (T2*<20ms) among our patients was 22/89 patients (24.7%) aged 20.86±7.54 years with a mean T2* value of 12.718±4.36ms and LVEF of 68.59 ±5.84%. LIC and serum ferritin results were 30.85±13.48 mg/g and 6122.86±4185.67ng/ml respectively. There was no correlation between T2* results and the age, LVEF, LIC and serum ferritin of this group (P=0.651, P=0.085, P=0.999 and P=0.627 respectively). Those patients with severe cardiac siderosis (T2*<10ms) constituted 7/89 (7.9%) with a mean age of 18.43±4.35 years. Although these patients had a mean T2* of 7.8±1.73 ms, the LVEF value was 65.14±6.20 % and only one patient had clinical cardiac disease (T2*=4.3 ms and LVEF =55%). LIC and serum ferritin results were 29.84±16.99mg/g and 7202.14±6953.79ng/ml respectively. In this group of severe cardiac siderosis, T2* was not correlated to age (P=0.5), LVEF (P=0.144), LIC (P=0.969) and serum ferritin (P=0.818). Conclusion Low prevalence of myocardial siderosis in the Egyptian thalassemic patients in spite of the very high serum ferritin. In severely iron overloaded patients the cardiac function was not affected. T2* is the best test that can identify at risk patients who can be treated with optimization of their chelation protocols. The possibility of a genetic component for the susceptibility of cardiac iron loading in our population should be considered. Disclosures No relevant conflicts of interest to declare.


1988 ◽  
Vol 29 (2) ◽  
pp. 175-178 ◽  
Author(s):  
H. Kelbæk ◽  
J. H. Svendsen ◽  
J. Aldershvile ◽  
K. Folke ◽  
S. L. Nielsen

The stroke volume (SV) was determined by first passage radionuclide cardiography and the left ventricular ejection fraction (LVEF) by multigated radionuclide cardiography in 20 patients with ischemic heart disease. The results were evaluated against those obtained by the invasive dye dilution or thermodilution and left ventricular cardioangiographic techniques. In a paired comparison the mean difference between the invasive and radionuclide SV was −1 ml (SED 3.1) with a correlation coefficient of 0.83 (p<0.01). Radionuclide LVEF values also correlated well with cardioangiographic measurements, r=0.93 (p<0.001). LVEF determined by multigated radionuclide cardiography was, however, significantly lower than when measured by cardioangiography, the mean difference being 6 per cent (p<0.001). These findings suggest that radionuclide determinations of SV and LVEF are reliable. The discrepancy between the non-invasive and invasive LVEF values raises the question, whether LVEF is overestimated by cardioangiography or underestimated by radionuclide cardiography.


Sign in / Sign up

Export Citation Format

Share Document