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Introduction The phosphocreatine-to-adenosine triphosphate ratio (PCr/ATP) is a sensitive marker of the energetic state of the heart and can be reliably measured non-invasively using 31Phosphorus magnetic resonance spectroscopy (31P-MRS). Derangements in cardiac energetics are a distinctive feature in the pathophysiology of several cardiac diseases, and thus potential therapeutic targets. Purpose We sought to compare cardiac PCr/ATP across a range of cardiac pathologies. Methods Using a 3D chemical shift 31P spectral acquisition we recorded PCr/ATP in 515 participants: athletes (n=17), healthy controls with normal weight (n=148), overweight (n=67) and with obesity (n=73), diabetes (n=23), heart failure with preserved ejection fraction (HFpEF) (n=33), heart failure with reduced ejection fraction (HFrEF) (n=63), amyloid (n=9), severe aortic stenosis (AS) (n=29), severe mitral regurgitation (MR) (n=18), and hypertrophic cardiomyopathy (HCM) (n=35). Results A spectrum of myocardial PCr/ATP exists ranging from normal in athletes (2.23±0.28) and those with normal weight (2.05±0.38) to severely impaired in severe MR (1.56±0.32) and cardiac amyloid (1.34±0.19, Figure 1). Despite normal systolic function (all LVEF >57%) those living with obesity and diabetes have lower PCr/ATP than normal (all p Conclusions We demonstrate a spectrum of energetic deficit in cardiac disease and this is affected by not only myocardial pathology but also by obesity and age. Derangements in myocardial energetics are present in myocardial pathologies independent of underlying aetiology. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): We acknowledge support from the British Heart Foundation Oxford Center of Research Excellence.

Supplemental Digital Content is available in the text., Background: Why some but not all patients with severe aortic stenosis (SevAS) develop otherwise unexplained reduced systolic function is unclear. We investigate the hypothesis that reduced creatine kinase (CK) capacity and flux is associated with this transition. Methods: We recruited 102 participants to 5 groups: moderate aortic stenosis (ModAS) (n=13), SevAS, left ventricular (LV) ejection fraction ≥55% (SevAS-preserved ejection fraction, n=37), SevAS, LV ejection fraction 0.99). Accompanying the fall in CK flux, total CK and citrate synthase activities and the absolute activities of mitochondrial-type CK and CK-MM isoforms were also lower (P

Aims We sought to determine if myocardial energetics could distinguish obesity cardiomyopathy as a distinct entity from dilated cardiomyopathy. Methods and results Sixteen normal weight participants with dilated cardiomyopathy (DCMNW), and 27 with DCM and obesity (DCMOB), were compared to 26 normal weight controls (CTLNW). All underwent cardiac magnetic resonance imaging and 31P spectroscopy to assess function and energetics. Nineteen DCMOB underwent repeat assessment after a dietary weight loss intervention. Adenosine triphosphate (ATP) delivery through creatine kinase (CK flux) was 55% lower in DCMNW than in CTLNW (P = 0.004), correlating with left ventricular ejection fraction (LVEF, r = 0.4, P = 0.015). In contrast, despite similar LVEF (DCMOB 41 ± 7%, DCMNW 38 ± 6%, P = 0.14), CK flux was two-fold higher in DCMOB (P < 0.001), due to higher rate through CK [median kf 0.21 (0.14) vs. 0.11 (0.12) s−1, P = 0.002]. During increased workload, the CTLNW heart increased CK flux by 97% (P < 0.001). In contrast, CK flux was unchanged in DCMNW and fell in DCMOB (by >50%, P < 0.001). Intentional weight loss was associated with positive left ventricular remodelling, with reduced left ventricular end-diastolic volume (by 8%, P < 0.001) and a change in LVEF (40 ± 9% vs. 45 ± 10%, P = 0.002). This occurred alongside a fall in ATP delivery rate with weight loss (by 7%, P = 0.049). Conclusions In normal weight, DCM is associated with reduced resting ATP delivery. In obese DCM, ATP demand through CK is greater, suggesting reduced efficiency of energy utilization. Dietary weight loss is associated with significant improvement in myocardial contractility, and a fall in ATP delivery, suggesting improved metabolic efficiency. This highlights distinct energetic pathways in obesity cardiomyopathy, which are both different from dilated cardiomyopathy, and may be reversible with weight loss.

Cardiac proton spectroscopy (1H‐MRS) is widely used to quantify lipids. Other metabolites (e.g. creatine and choline) are clinically relevant but more challenging to quantify because of their low concentrations (approximately 10 mmol/L) and because of cardiac motion. To quantify cardiac creatine and choline, we added water‐suppression cycling (WSC) to two single‐voxel spectroscopy sequences (STEAM and PRESS). WSC introduces controlled residual water signals that alternate between positive and negative phases from transient to transient, enabling robust phase and frequency correction. Moreover, a particular weighted sum of transients eliminates residual water signals without baseline distortion. We compared WSC and the vendor's standard ‘WET’ water suppression in phantoms. Next, we tested repeatability in 10 volunteers (seven males, three females; age 29.3 ± 4.0 years; body mass index [BMI] 23.7 ± 4.1 kg/m2). Fat fraction, creatine concentration and choline concentration when quantified by STEAM‐WET were 0.30% ± 0.11%, 29.6 ± 7.0 μmol/g and 7.9 ± 6.7 μmol/g, respectively; and when quantified by PRESS‐WSC they were 0.30% ± 0.15%, 31.5 ± 3.1 μmol/g and 8.3 ± 4.4 μmol/g, respectively. Compared with STEAM‐WET, PRESS‐WSC gave spectra whose fitting quality expressed by Cramér‐Rao lower bounds improved by 26% for creatine and 32% for choline. Repeatability of metabolite concentration measurements improved by 72% for creatine and 40% for choline. We also compared STEAM‐WET and PRESS‐WSC in 13 patients with severe symptomatic aortic or mitral stenosis indicated for valve replacement surgery (10 males, three females; age 75.9 ± 6.3 years; BMI 27.4 ± 4.3 kg/m2). Spectra were of analysable quality in eight patients for STEAM‐WET, and in nine for PRESS‐WSC. We observed comparable lipid concentrations with those in healthy volunteers, significantly reduced creatine concentrations, and a trend towards decreased choline concentrations. We conclude that PRESS‐WSC offers improved performance and reproducibility for the quantification of cardiac lipids, creatine and choline concentrations in healthy volunteers at 3 T. It also offers improved performance compared with STEAM‐WET for detecting altered creatine and choline concentrations in patients with valve disease., A water‐suppression cycling (WSC) module was added to STEAM and PRESS single‐voxel spectroscopy pulse sequences. We report an improvement in the accuracy and repeatability in the quantification of low concentration metabolites like creatine and choline in the myocardium using WSC compared with the vendor's standard WET water suppression. This allowed us to detect a significant decrease in creatine levels in patients with symptomatic aortic stenosis in less than half the scan time compared with the vendor's standard WET water suppression.

Cardiac metabolism and function are intrinsically linked. High-energy phosphates occupy a central and obligate position in cardiac metabolism, coupling oxygen and substrate fuel delivery to the myocardium with external work. This insight underlies the widespread clinical use of ischaemia testing. However, other deficits in high-energy phosphate metabolism (not secondary to supply-demand mismatch of oxygen and substrate fuels) may also be documented, and are of particular interest when found in the context of structural heart disease. This review introduces the scope of deficits in high-energy phosphate metabolism that may be observed in the myocardium, how to assess for them, and how they might be interpreted.

We appreciate the interest and comments by Mahmood in regards to our recent article (1). In this study we have shown not only that cardiac energetics are impaired early in the aortic stenosis (AS) disease process, being present in a group of patients with moderate aortic stenosis, but also that transition to systolic failure in severe AS is not dependent on further energetic decline. Whilst Mahmood points out correctly that energetic impairment was not a “necessary correlate of systolic failure as assessed by LV ejection fraction (LVEF)” this does not imply that it is unrelated. We would like to clarify that as ATP demands increase with AS severity, a reduction in the capacity to deliver ATP to the myocardium, as established early in the process of AS, could increase susceptibility to systolic failure when the increasing ATP demand exceeds supply.

Purpose Phosphorus spectroscopy (31P-MRS) is a proven method to probe cardiac energetics. Studies typically report the phosphocreatine (PCr) to adenosine triphosphate (ATP) ratio. We focus on another 31P signal: inorganic phosphate (Pi), whose chemical shift allows computation of myocardial pH, with Pi/PCr providing additional insight into cardiac energetics. Pi is often obscured by signals from blood 2,3-diphosphoglycerate (2,3-DPG). We introduce a method to quantify Pi in 14 min without hindrance from 2,3-DPG. Methods Using a 31P stimulated echo acquisition mode (STEAM) sequence at 7 Tesla that inherently suppresses signal from 2,3-DPG, the Pi peak was cleanly resolved. Resting state UTE-chemical shift imaging (PCr/ATP) and STEAM 31P-MRS (Pi/PCr, pH) were undertaken in 23 healthy controls; pH and Pi/PCr were subsequently recorded during dobutamine infusion. Results We achieved a clean Pi signal both at rest and stress with good 2,3-DPG suppression. Repeatability coefficient (8 subjects) for Pi/PCr was 0.036 and 0.12 for pH. We report myocardial Pi/PCr and pH at rest and during catecholamine stress in healthy controls. Pi/PCr was maintained during stress (0.098 ± 0.031 [rest] vs. 0.098 ± 0.031 [stress] P = .95); similarly, pH did not change (7.09 ± 0.07 [rest] vs. 7.08 ± 0.11 [stress] P = .81). Feasibility for patient studies was subsequently successfully demonstrated in a patient with cardiomyopathy. Conclusion We introduced a method that can resolve Pi using 7 Tesla STEAM 31P-MRS. We demonstrate the stability of Pi/PCr and myocardial pH in volunteers at rest and during catecholamine stress. This protocol is feasible in patients and potentially of use for studying pathological myocardial energetics.

Rationale: The recent development of hyperpolarized 13 C magnetic resonance spectroscopy has made it possible to measure cellular metabolism in vivo, in real time. Objective: By comparing participants with and without type 2 diabetes mellitus (T2DM), we report the first case-control study to use this technique to record changes in cardiac metabolism in the healthy and diseased human heart. Methods and Results: Thirteen people with T2DM (glycated hemoglobin, 6.9±1.0%) and 12 age-matched healthy controls underwent assessment of cardiac systolic and diastolic function, myocardial energetics ( 31 P-magnetic resonance spectroscopy), and lipid content ( 1 H-magnetic resonance spectroscopy) in the fasted state. In a subset (5 T2DM, 5 control), hyperpolarized [1- 13 C]pyruvate magnetic resonance spectra were also acquired and in 5 of these participants (3 T2DM, 2 controls), this was successfully repeated 45 minutes after a 75 g oral glucose challenge. Downstream metabolism of [1- 13 C]pyruvate via PDH (pyruvate dehydrogenase, [ 13 C]bicarbonate), lactate dehydrogenase ([1- 13 C]lactate), and alanine transaminase ([1- 13 C]alanine) was assessed. Metabolic flux through cardiac PDH was significantly reduced in the people with T2DM (Fasted: 0.0084±0.0067 [Control] versus 0.0016±0.0014 [T2DM], Fed: 0.0184±0.0109 versus 0.0053±0.0041; P =0.013). In addition, a significant increase in metabolic flux through PDH was observed after the oral glucose challenge ( P Conclusions: This work represents the first demonstration of the ability of hyperpolarized 13 C magnetic resonance spectroscopy to noninvasively assess physiological and pathological changes in cardiac metabolism in the human heart. In doing so, we highlight the potential of the technique to detect and quantify metabolic alterations in the setting of cardiovascular disease.

Background: Obesity is strongly associated with exercise intolerance and the development of heart failure. Whereas myocardial energetics and diastolic function are impaired in obesity, systolic function is usually preserved. This suggests that the rate of ATP delivery is maintained, but this has never been explored in human obesity. We hypothesized that ATP transfer rate through creatine kinase (CK) ( k f CKrest ) would be increased, compensating for depleted energy stores (phosphocreatine/ATP), but potentially limiting greater ATP delivery during increased workload. We hypothesized that these changes would normalize with weight loss. Methods: We recruited 80 volunteers (35 controls [body mass index 24±3 kg/m 2 ], 45 obese [body mass index 35±5 kg/m 2 ]) without coexisting cardiovascular disease. Participants underwent body composition analysis, magnetic resonance imaging of abdominal, liver, and myocardial fat content, left ventricular function, and 31 P magnetic resonance spectroscopy to assess phosphocreatine/ATP and CK kinetics, at rest and during dobutamine stress. Obese volunteers were assigned to a dietary weight loss intervention, before reexamination. Results: At rest, although myocardial phosphocreatine/ATP was 14% lower in obesity (1.9±0.3 versus 2.2±0.2, P k f Ckrest was 33% higher (0.23±0.07 s –1 versus 0.16±0.08 s –1 , P =0.002), yielding no difference in overall resting ATP delivery (obese 2.5±0.9 µmol·g –1 ·s –1 versus control 2.2±1.1 µmol·g –1 ·s –1 , P =0.232). In controls, increasing cardiac workload led to an increase in both k f CK (+86%, P P k f CK ( P =0.117) or ATP delivery ( P =0.608). This was accompanied by reduced systolic augmentation (absolute increase in left ventricular ejection fraction, obese +16±7% versus control +21±4%, P =0.031). Successful weight loss (–11±5% body weight) was associated with improvement of these energetic changes such that there was no significant difference in comparison with controls. Conclusions: In the obese resting heart, the myocardial CK reaction rate is increased, maintaining ATP delivery despite reduced phosphocreatine/ATP. During increased workload, although the nonobese heart increases ATP delivery through CK, the obese heart does not; this is associated with reduced systolic augmentation and exercise tolerance. Weight loss reverses these energetic changes. This highlights myocardial energy delivery through CK as a potential therapeutic target to improve symptoms in obesity-related heart disease, and a fascinating modifiable pathway involved in the progression to heart failure, as well.

The energy starvation hypothesis proposes that maladaptive metabolic remodeling antedates, initiates, and maintains adverse contractile dysfunction in heart failure (HF). Better understanding of the cardiac metabolic phenotype and metabolic signaling could help identify the role metabolic remodeling plays within HF and the conditions known to transition toward HF, including “pathological” hypertrophy. In this review, we discuss metabolic phenotype and metabolic signaling in the contexts of pathological hypertrophy and HF. We discuss the significance of alterations in energy supply (substrate utilization, oxidative capacity, and phosphotransfer) and energy sensing using observations from human and animal disease models and models of manipulated energy supply/sensing. We aim to provide ways of thinking about metabolic remodeling that center around metabolic flexibility, capacity (reserve), and efficiency rather than around particular substrate preferences or transcriptomic profiles. We show that maladaptive metabolic remodeling takes multiple forms across multiple energy-handling domains. We suggest that lack of metabolic flexibility and reserve (substrate, oxidative, and phosphotransfer) represents a final common denominator ultimately compromising efficiency and contractile reserve in stressful contexts.

Introduction Myocardial creatine kinase (CK) activity represents an important metabolic reserve: it correlates closely with contractile reserve and post-ischaemic function, keeps cytosolic [ADP] low, and optimises the free energy for ATP hydrolysis. It may also contribute to the transition to failure in the heart hypertrophied by chronic haemodynamic overload; modest up-regulation has been shown to be cardio-protective. Total CK activity measurement requires chemical freeze-and-extract methods, which destroy tissue, precluding repeated measures. To date, non-invasive assessments of human myocardial CK flux (calculated as kf × [PCr], where kf is the pseudo-first-order forward rate constant measured by 31P-magnetic resonance spectroscopy (MRS) have not assessed creatine content or total CK activity. Thus we aimed to validate kf measurement against total CK activity and investigate predictors of CK activity. Methods 39 subjects (median age 71, range 43–84) undergoing clinically indicated cardiac surgery had CK total activity measured from LV biopsy. 31 had severe AS (10 with impaired LVEF); 2 had severe primary MR; 5 had severe mitral stenosis (2 with impaired LVEF) and 1 had an LA mass. 35 of 39 contributed triplicate datasets: CK total activity, kf (31P-MRS TRiST sequence at 3T) and LV volumes (cine-MRI, 3T Siemens). 27 had severe AS (8 with impaired LVEF); other groups were the same. Exclusion criteria were prior myocardial infarction and flow-limiting coronary disease. Flash-frozen LV biopsies obtained within 15 min of cardiopulmonary bypass were analysed for CK total activity, total creatine, and citrate synthase (CS) activity (a marker of oxidative phosphorylation capacity). Results Multiple, novel correlations were observed between CK total activity (IU/mg protein) and CS activity (r=0.87, p=9e-13), total creatine (r=0.59, p=8e-5), kf (r=0.42, p=0.013), total creatine × kf (r=0.64, p=4e-5), LVESVi (r=−0.52, p=8e-4), LVEF (r=0.48, p=0.002) and LVMi (r=−0.42, p=0.009) (Panels A-E) (LVEDVi and non-indexed counterparts were also significant correlates.) The most predictive linear regression model incorporating elements of the CK rate equation included total creatine (nmol/mg protein), kf (/s), and kf × LVESVi (ml/m2) (adjusted R2=0.56, beta=0.426, 0.618, −1.968 and p=0.001, 5e-5, 0.003 respectively, Panel F). Figure 1 Conclusions These results are the first evidence of agreement between non-invasive estimates of human cardiac CK activity (kf) and freeze-extracted chemical methods. The key original finding is that it is feasible to attempt to predict CK capacity in vivo by using a combination of techniques (creatine by 1H MRS, CK kf by 31P-MRS and LVESVi by cine imaging). The key insight is that CK capacity is best estimated not simply from what the rate equation would predict (creatine and kf), but that other factors relating to failing contractility reduce CK activity independently from creatine content and enzyme kf. Acknowledgement/Funding British Heart Foundation Clinical Research Training Fellowship (FS/15/80/31803) and Programme Grant (RG/18/12/34040).

Introduction The transition to systolic failure in severe aortic stenosis (AS) increases mortality. There are currently no reliable markers of transition, and the guideline LVEF Methods 19 patients with severe AS, LVEF ≥55% (AS-pEF, mean±SD LVEF 63±5%, mean gradient 48±14 mmHg) and 10 with severe AS, LVEF Results When compared to controls, both CK total activity and CS activity were lower in AS-pEF (by 27% and 23% respectively, both p AS-rEF was associated with further reduction in both CK and CS activities (by 32% and 22% respectively, both p When median mitochondria-sarcomere ATP diffusion distances were plotted against CK total activity a strong positive correlation was observed (r=0.86, p=0.003, Panel F). This suggests a compensatory reduction in diffusion distance develops when CK activity falls. Conclusions Transition to failure in severe AS is associated with lower oxidative capacity and maximal ATP delivery capacity through CK. Despite compensatory falls in ATP diffusion distance and altered CK isozyme expression, these changes may underlie susceptibility to EF decline in AS. Acknowledgement/Funding British Heart Foundation Clinical Research Training Fellowship (FS/15/80/31803) and Programme Grant (RG/18/12/34040).

Introduction Obesity is associated with diminished myocardial energetic stores, as determined by PCr/ATP, and this is restored with weight loss. We have previously demonstrated that the creatine kinase rate constant (kfCK) is elevated in obesity, which may represent a compensatory mechanism preserving ATP delivery. We hypothesised that intentional weight loss would reduce the requirement for increased enzyme activity, and hence kfCK would fall. Methods 31 obese individuals (53±13 years, 11 male, BMI 37±5 kg/m-2) underwent comprehensive metabolic phenotyping including MR (3 T, Siemens) for abdominal, hepatic and myocardial fat, and cardiac MR for structure and function. Triple Repetition time Saturation Transfer (TRiST) 31P magnetic resonance spectroscopy was used to measure kfCK. Participants then underwent repeat testing following a dietary weight loss intervention. Results Mean BMI in the cohort fell from 37±5 kg/m-2 to 33±6 kg/m-2 (p Conclusion We demonstrate that dietary weight loss in an obese population is associated with a fall in kfCK. It has previously been shown that weight loss in this population is associated with an increase in the PCr/ATP ratio. Our findings may reflect a recalibration of the required kfCK in the context of replenished substrate pool (i.e. higher PCr levels). The impact of weight loss in diseases with more profound myocardial energetic deficit must be investigated to establish its safety.

Introduction Obesity is associated with improved prognosis in heart failure, despite diminished myocardial energetic stores. It has been shown that reduced ATP transfer from the mitochondrion to the myofibril via creatine kinase is related to increased mortality. Given that the creatine kinase rate constant (kfCK) is elevated in obesity in the absence of cardiovascular disease, we hypothesised that the rate of ATP transfer would also be raised in obese heart failure. Methods 43 individuals (14 normal weight (BMI 30 kg/m2)) with DCM (EF 25%–45%) underwent MR imaging (3 T Siemens) of visceral, hepatic and myocardial lipid, and cardiac structure and function. They also underwent Triple Repetition time Saturation Transfer (TRiST) 31P magnetic resonance spectroscopy, to calculate apical myocardial kfCK. Results Obese DCM participants had greater BMI (37±5 kg/m2 compared to 23±3 kg/m2, p However, kfCK was significantly higher in the obese group compared to normal weight (0.17±0.08s-1 compared to 0.08±0.07s-1, p=0.002). kfCK was significantly correlated with visceral fat volume (r=0.473, p=0.008). Conclusion Here we demonstrate that myocardial kfCK is higher in obese DCM, despite identical cardiac parameters to the control group. It has previously been shown that low kfCK is associated with heart failure events and mortality. Utilising multinuclear MRS to demonstrate the reverse in obesity, we propose this as a novel energetic basis underlying the obesity paradox.

Background Very Low Calorie Diets (VLCD) in obesity are an effective weight loss intervention that rapidly reduce liver fat and improve peripheral insulin resistance. We hypothesised that improved peripheral glycaemic control would be accompanied by initial impairment of cardiac function as hepatic fat stores are mobilised and taken up by the myocardium. Methods 14 obese volunteers (4 male, 49±15 years, BMI 36.2±5.9 kg m-2) underwent body composition analysis and MR scanning for abdominal visceral and liver fat, LV structure and function, 1H-MRS to measure myocardial triglyceride content (MTGC), and echocardiography for diastolic function (E/E’), before and one week into a VLCD (800 kcal/day). Results 7 days of VLCD led to significant reductions in total body fat, visceral and hepatic fat, and insulin resistance. However, MTGC rose from 1.74±0.99% to 3.02±1.70% (p=0.030), and there was a reduction in both systolic function (LVEF 67±3% to 62±5%, p=0.014; peak radial strain 51±8% to 42±9%, p=0.005) and diastolic function (e/e’ 8.5±1.6 to 10.3±3.5, p=0.034). The change in MTGC at one week correlated with change in diastolic function (r=0.729, p=0.017). However at 8 weeks (n=6), changes in MGTC as well as cardiac function had returned to normal. Conclusions We demonstrate for the first time in healthy obese individuals that a 7 day period of severe caloric restriction results in accumulation of myocardial fat which is associated with impairment of both systolic and diastolic LV function at this timepoint, despite a significant improvement in hepatic fat and whole body insulin sensitivity.

Background Obesity is associated with impaired myocardial energetics (reduced phosphocreatine to adenosine triphosphate ratio (PCr/ATP)). However, LV systolic function is usually preserved, suggesting that the rate of ATP delivery to the contractile apparatus may be maintained. We hypothesised that the forward rate constant of the creatine kinase (CK) reaction would increase to compensate for the reduced substrate pool. Methods 145 participants across a range of BMIs were recruited. All underwent CMR at 3T to determine LV geometry and function. Group A (75 individuals) underwent 31 P-MRS to assess PCr/ATP. The remaining 70 (group B) – 51 obese (BMI 36.1±5.3), and 19 normal weight (BMI 23.9±3.9) – underwent Triple Repetition time Saturation Transfer 31P-MRS to determine CK kf. Results Body fat mass and PCr/ATP were negatively correlated in group A (r=−0.457, p Conclusions We studied the effect of obesity on CK kinetics in the human heart, and have demonstrated that, despite a fall in PCr/ATP with increasing body fat, the CK reaction rate is higher in obesity than in normal weight. This may reflect a compensatory increase in CK activity to maintain ATP delivery rates and attempt to preserve cardiac function despite a diminished substrate pool.

Cardiovascular imaging is key for the assessment of patients with heart failure. Today, cardiovascular magnetic resonance imaging plays an established role in the assessment of patients with suspected and confirmed heart failure syndromes, in particular identifying aetiology. Its role in informing prognosis and guiding decisions around therapy are evolving. Key strengths include its accuracy; reproducibility; unrestricted field of view; lack of radiation; multiple abilities to characterise myocardial tissue, thrombus and scar; as well as unparalleled assessment of left and right ventricular volumes. T2* has an established role in the assessment and follow-up of iron overload cardiomyopathy and a role for T1 in specific therapies for cardiac amyloid and Anderson–Fabry disease is emerging.

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