scholarly journals Reduced in vivo high-energy phosphates precede Adriamycin-induced cardiac dysfunction

2010 ◽  
Vol 299 (2) ◽  
pp. H332-H337 ◽  
Author(s):  
M. Y. Maslov ◽  
V. P. Chacko ◽  
G. A. Hirsch ◽  
A. Akki ◽  
M. K. Leppo ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Ejection Fraction ◽  
High Energy ◽  
Left Ventricular ◽  
Peak Filling Rate ◽  
High Energy Phosphates ◽  
Cardiac Energetics ◽  
Filling Rate ◽  
Lv Dysfunction

Adriamycin (ADR) is an established, life-saving antineoplastic agent, the use of which is often limited by cardiotoxicity. ADR-induced cardiomyopathy is often accompanied by depressed myocardial high-energy phosphate (HEP) metabolism. Impaired HEP metabolism has been suggested as a potential mechanism of ADR cardiomyopathy, in which case the bioenergetic decline should precede left ventricular (LV) dysfunction. We tested the hypothesis that murine cardiac energetics decrease before LV dysfunction following ADR (5 mg/kg ip, weekly, 5 injections) in the mouse. As a result, the mean myocardial phosphocreatine-to-ATP ratio (PCr/ATP) by spatially localized 31P magnetic resonance spectroscopy decreased at 6 wk after first ADR injection (1.79 ± 0.18 vs. 1.39 ± 0.30, means ± SD, control vs. ADR, respectively, P < 0.05) when indices of systolic and diastolic function by magnetic resonance imaging were unchanged from control values. At 8 wk, lower PCr/ATP was accompanied by a reduction in ejection fraction (67.3 ± 3.9 vs. 55.9 ± 4.2%, control vs. ADR, respectively, P < 0.002) and peak filling rate (0.56 ± 0.12 vs. 0.30 ± 0.13 μl/ms, control vs. ADR, respectively, P < 0.01). PCr/ATP correlated with peak filling rate and ejection fraction, suggesting a relationship between cardiac energetics and both LV systolic and diastolic dysfunction. In conclusion, myocardial in vivo HEP metabolism is impaired following ADR administration, occurring before systolic or diastolic abnormalities and in proportion to the extent of eventual contractile abnormalities. These observations are consistent with the hypothesis that impaired HEP metabolism contributes to ADR-induced myocardial dysfunction.

scholarly journals Left Ventricular Magnetic Resonance Imaging Strain Predicts the Onset of Duchenne Muscular Dystrophy–Associated Cardiomyopathy

2020 ◽  
Vol 13 (11) ◽  
Author(s):  
Saira Siddiqui ◽  
Tarek Alsaied ◽  
Sarah E. Henson ◽  
Janvi Gandhi ◽  
Priyal Patel ◽  
...  
Keyword(s):  
Cardiac Magnetic Resonance ◽  
Duchenne Muscular Dystrophy ◽  
Magnetic Resonance ◽  
Muscular Dystrophy ◽  
Ejection Fraction ◽  
Radial Strain ◽  
Left Ventricular ◽  
3 Dimensional ◽  
Lv Dysfunction ◽  
Lv Ejection Fraction

Background: Early detection of left ventricular (LV) dysfunction before the onset of overt Duchenne muscular dystrophy–associated cardiomyopathy (DMDAC) may direct clinical management to slow onset of dysfunction. We aimed to assess whether LV strain will predict those who develop DMDAC. Methods: We performed a single center retrospective case control study of patients with Duchenne muscular dystrophy who underwent serial cardiac magnetic resonance between 2006 and 2019. Patients with Duchenne muscular dystrophy with an LV ejection fraction ≥55% on ≥1 cardiac magnetic resonance were identified and grouped into age-matched +DMDAC and –DMDAC. Within 3 years, +DMDAC had a subsequent cardiac magnetic resonance with a decline in LV ejection fraction ≥10% and absolute LV ejection fraction ≤50%. −DMDAC maintained an LV ejection fraction ≥55% on serial cardiac magnetic resonances. Two-dimensional and 3-dimensional global radial strain, global circumferential strain (GCS), and global longitudinal strain were measured using tissue tracking software and their ability to predict DMDAC onset was assessed. Multivariable analysis adjusted for late gadolinium enhancement. Results: Thirty +DMDAC and 30 age-matched −DMDAC patients were included with a total of 164 studies analyzed. Before DMDAC onset, 2-dimensional global radial strain and GCS were significantly worse in +DMDAC compared with −DMDAC (25.1±6.0 versus 29.0±6.3, P =0.011; −15.4%±2.4 versus −17.3%±2.6, P =0.003). Three-dimensional GCS and global radial strain had similar findings. Among strain measures, 3-dimensional GCS had the highest area under the curve to predict DMDAC in our cohort. These findings persisted after adjusting for the presence of late gadolinium enhancement. Conclusions: Reduced global radial strain and GCS may predict those at risk for developing DMDAC before onset of LV dysfunction and its clinical utility warrants further exploration.

A non-Invasive Technique for Continuous Monitoring of Left Ventricular Function Using a New Solid State Mercuric Iodide Radiation Detector

1984 ◽  
Vol 66 (5) ◽  
pp. 551-556 ◽  
Author(s):  
A. Lahiri ◽  
J. C. W. Crawley ◽  
R. I. Jones ◽  
M. J. Bowles ◽  
E. B. Raftery
Keyword(s):  
Solid State ◽  
Ejection Fraction ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Left Ventricular ◽  
Peak Filling Rate ◽  
Left Ventricular Ejection ◽  
Mercuric Iodide ◽  
Filling Rate ◽  
Non Invasive

1. A miniature solid-state mercuric iodide (HgI2) nuclear probe detector has been developed in conjunction with a computerized nuclear probe (Nuclear Stethoscope) to enable continuous noninvasive monitoring of left ventricular function using 99Tc-labelled equilibrium blood pool techniques. 2. Left ventricular ejection fraction was measured in 54 patients undergoing radionuclide angiography with a gamma-camera and with the Nuclear Stethoscope and a good correlation was obtained between both techniques (r = 0.94, n = 54, P < 0.001). 3. The prototype mercuric iodide detector was compared with the sodium iodide detector of the Nuclear Stethoscope and a study in 41 consecutive patients demonstrated a good correlation for the measurement of ejection fraction, ejection rate, peak filling rate and time to peak filling rate (r = 0.94, 0.89, 0.90 and 0.78 respectively). 4. It may be possible to adapt the mercuric iodide detector for continuous non-invasive monitoring of left ventricular performance in critically ill patients and during physiological or pharmacological interventions.

scholarly journals Effect of Myocardial Fibrosis on Left Ventricular Function in Rheumatic Mitral Stenosis: A Preliminary Study with Cardiac Magnetic Resonance

2018 ◽  
Vol 38 (4) ◽  
pp. 202-206
Author(s):  
Elen Elen ◽  
Celly A. Atmadikoesoemah ◽  
Manoefris Kasim
Keyword(s):  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Ejection Fraction ◽  
Myocardial Fibrosis ◽  
Mitral Stenosis ◽  
Left Ventricular ◽  
Lv Function ◽  
Fibrotic Tissue ◽  
Rheumatic Mitral Stenosis ◽  
Lv Dysfunction

Background: Left ventricular (LV) dysfunction was frequently found in rheumatic mitral stenosis. Myocardial fibrosis had been revealed in rheumatic heart disease and could be associated with LV dysfunction. We evaluate myocardial fibrosis profile related to LV function in rheumatic mitral stenosis with cardiac magnetic resonance (CMR). Methods: Eighteen patients with severe rheumatic mitral stenosis without history of coronary artery disease or its risk factors underwent 1.5T CMR examination. LV ejection fraction (LVEF), right ventricular ejection fraction (RVEF), myocardial fibrotic tissue were evaluated with CMR. Other hemodynamic data was derived from echocar­diography results. Results: These patients (40.4±10.5 years old, 72.2% female, 66.7% atrial fibrillation) had LVEF of 50.9±15.9% and RVEF of 37.7±13.9%. Volume of fibrotic tissue in these patients were 16.6 (5.5-55.8)%. In multivariate analysis, volume of fibrotic tissue was a significant predictor of LVEF that myocardial fibrotic tissue of 1% was associated with LVEF reduction of 0.87% (95% CI 0.51%-1.24%). Conclusion: LV function was determined by the extent of myocardial fibrosis in rheu­matic mitral stenosis.   Abstrak Latar Belakang: Disfungsi ventrikel kiri (LV) sering ditemukan pada mitral stenosis rematik. Fibrosis miokardium ditemukan pada penyakit jantung rematik. Fibrosis miokardium pada penyakit jantung rematik juga dihubungkan dengan disfungsi LV. Kami mengevaluasi profil fibrosis miokardium yang berhubungan dengan fungsi LV pada mitral stenosis rematik dengan cardiac magnetic resonance (CMR). Metode: Dilakukan pemeriksaan 1.5T CMR pada delapanbelas pasien dengan mitral stenosis rematik berat tanpa riwayat penyakit jantung koroner atau faktor resikonya. Fraksi ejeksi LV (LVEF), fraksi ejeksi RV (RVEF), dan jaringan fibrotik miokardium dievaluasi menggunakan CMR. Data hemodinamik lainnya didapatkan dari pemeriksaan ekokardiografi. Hasil: Pasien tersebut (40.4±10.5 tahun, 72.2% perempuan, 66.7% fibrilasi atrium) memiliki LVEF 50.9±15.9% dan RVEF 37.7±13.9%. Vol­ume jaringan fibrotic pada pasien tersebut adalah 16.6 (5.5-55.8)%. Dalam analisis multivariat, volume jaringan fibrotic adalah prediktor LVEF yang signifikan yaitu 1% jaringan fibrotic miokardium dihubungkan dengan menurunan LVEF sebesar 0.87% (95% CI 0.51%-1.24%). Kesimpulan: Fungsi LV dipengaruhi seberapa besar fibrosis miokardium pada mitral stenosis rematik

scholarly journals The von Hippel-Lindau Chuvash mutation in mice alters cardiac substrate and high-energy phosphate metabolism

2016 ◽  
Vol 311 (3) ◽  
pp. H759-H767 ◽  
Author(s):  
Mary Slingo ◽  
Mark Cole ◽  
Carolyn Carr ◽  
Mary K. Curtis ◽  
Michael Dodd ◽  
...  
Keyword(s):  
Gene Expression ◽  
Magnetic Resonance ◽  
Genetic Disorder ◽  
High Energy ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Resonance Spectroscopy ◽  
Ventricular Ejection Fraction ◽  
Hif Pathway

Hypoxia-inducible factor (HIF) appears to function as a global master regulator of cellular and systemic responses to hypoxia. HIF pathway manipulation is of therapeutic interest; however, global systemic upregulation of HIF may have as yet unknown effects on multiple processes. We used a mouse model of Chuvash polycythemia (CP), a rare genetic disorder that modestly increases expression of HIF target genes in normoxia, to understand what these effects might be within the heart. An integrated in and ex vivo approach was employed. Compared with wild-type controls, CP mice had evidence (using in vivo magnetic resonance imaging) of pulmonary hypertension, right ventricular hypertrophy, and increased left ventricular ejection fraction. Glycolytic flux (measured using [3H]glucose) in the isolated contracting perfused CP heart was 1.8-fold higher. Net lactate efflux was 1.5-fold higher. Furthermore, in vivo 13C-magnetic resonance spectroscopy (MRS) of hyperpolarized [13C1]pyruvate revealed a twofold increase in real-time flux through lactate dehydrogenase in the CP hearts and a 1.6-fold increase through pyruvate dehydrogenase. 31P-MRS of perfused CP hearts under increased workload (isoproterenol infusion) demonstrated increased depletion of phosphocreatine relative to ATP. Intriguingly, no changes in cardiac gene expression were detected. In summary, a modest systemic dysregulation of the HIF pathway resulted in clear alterations in cardiac metabolism and energetics. However, in contrast to studies generating high HIF levels within the heart, the CP mice showed neither the predicted changes in gene expression nor any degree of LV impairment. We conclude that the effects of manipulating HIF on the heart are dose dependent.

scholarly journals Abnormal energetics and ATP depletion in pressure-overload mouse hearts: in vivo high-energy phosphate concentration measures by noninvasive magnetic resonance

2009 ◽  
Vol 297 (1) ◽  
pp. H59-H64 ◽  
Author(s):  
Ashish Gupta ◽  
V. P. Chacko ◽  
Robert G. Weiss
Keyword(s):  
Magnetic Resonance ◽  
Pressure Overload ◽  
High Energy ◽  
Atp Depletion ◽  
New Method ◽  
Resonance Spectroscopy ◽  
Mouse Heart ◽  
High Energy Phosphates ◽  
External Reference

31P magnetic resonance spectroscopy (MRS) offers a unique means to noninvasively quantify the major cardiac high-energy phosphates, creatine phosphate (PCr) and adenosine 5′-triphosphate (ATP), that are critical for normal myocardial contractile function and viability. Spatially localized 31P MRS has been used to quantify the in vivo PCr-to-ATP ratio (PCr/ATP) of murine hearts, including those with pressure-overload hypertrophy induced by thoracic aortic constriction (TAC). To date, there has been no approach for measuring the absolute tissue concentrations of PCr and ATP in the in vivo mouse heart that promise a better understanding of high-energy metabolism. A method to quantify in vivo murine myocardial concentrations of PCr and ATP using an external reference is described, validated, and applied to normal and TAC hearts. This new method does not prolong the scan times in mice beyond those previously required to measure PCr/ATP. The new method renders an [ATP] of 5.0 ± 0.9 (mean ± SD) and [PCr] of 10.4 ± 1.4 μmol/g wet wt in normal mouse hearts ( n = 7) and significantly lower values in TAC hearts ( n = 10) of 4.0 ± 0.8 and 6.7 ± 2.0 μmol/g wet wt for [ATP] ( P < 0.04) and [PCr] ( P < 0.001), respectively. The in vivo magnetic resonance [ATP] results are in good agreement with those obtained using an in vitro enzyme luminescent assay of perchloric acid extracts of the same hearts. In conclusion, a validated 31P MRS method for quantifying [ATP] and [PCr] in the in vivo mouse heart using spatial localization and an external reference is described and used to demonstrate significant reductions in not only PCr/ATP but [ATP] in hypertrophied TAC hearts.

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