Benjamin Hewins

The relationship between interstitial fibrosis and contractile function in HCM: a combined T1-mapping and CSPAMM tagging study

Background Interstitial fibrosis is a pathological hallmark of hypertrophic cardiomyopathy (HCM) and is thought to contribute to the abnormal myocardial mechanics seen in this patient group. T1-mapping now allows interstitial fibrosis to be detected non-invasively. Replacement fibrosis as identified by late gadolinium enhancement imaging has been associated with abnormal cardiac mechanics in HCM. However, the relationship between interstitial fibrosis and contractile function in HCM has not been previously explored. We assessed the association between interstitial fibrosis as assessed by T1-mapping and contractile function as determined by continuous spatial modulation of magnetisation (CSPAMM) tagging, hypothesising that increased fibrosis would correlate with abnormal myocardial strain. Methods Twelve HCM patients free of significant comorbidity and 16 controls were studied. CMR was undertaken on a 1.5T Siemens Avanto (Siemens, Erlangen, Germany). Tagged images were acquired at the mid-ventricle using aC SPAMM sequence (Field of View: 300mm, slice thickness 6mm, tag separation 7mm, typical TR/TE 30/ 1.26ms, Flip Angle 20°, 20 phases). Peak circumferential (Ecc) and radial (Err) strains were determined using inTag (Creatis, Lyon, France). Mid-ventricular short-axis T1 maps were acquired using the Modified Look-Locker Inversion Recovery sequence pre-gadolinium bolus and then at 5, 7, 9, 11, 15, 20 and 25 minutes. Signal intensity-time curves for myocardial and blood pool regions of interest were used to determine T1 relaxation times through a non-linear curve-fit (CMR42, Circle Cardiovascular Imaging, Calgary, Canada). The partition coefficient at equilibrium, an index of fibrosis, was determined by plotting the reciprocal of myocardial T1 times at equilibrium against those for the blood pool and calculating the slope of the resultant linear regression line. Results HCM patients were older than the controls and there was a preponderance of men. In keeping with their diagnosis, HCM patients had significantly higher indexed LV mass and wall thickness than controls (Table 1). The partition coefficient was significantly higher in HCM patients than controls (mean ±SD: 0.439 ±0.230 for HCM vs 0.281 ±0.071 for controls, P=0.02). Whilst peak global Ecc was significantly lower in the HCM group relative to the controls (0.173 ±0.041 vs 0.226 ±0.025, P<0.001), there was no significant difference with respect to peak global Err (0.154 ±0.06 vs 0.134 ±0.051, P=0.25). No significant association was found between the partition coefficient and either circumferential or radial strain. Conclusions The partition coefficient for gadolinium was significantly raised in patients with HCM relative to controls, however, no association was found between this and local contractile function. This implies that interstitial fibrosis alone may not account for the perturbations in myocardial mechanics seen in patients with HCM and that alternative mechanisms should be explored.

Cardiac effects of anabolic steroid use amongst recreational body builders - a CMR study

Background Abuse of anabolic steroids to induce skeletal muscle hypertrophy is widespread amongst recreational bodybuilders, however, the cardiac effects of such drugs have not been systematically documented. The ability of cardiovascular magnetic resonance (CMR) to image the myocardium in any plane and achieve full myocardial coverage renders it the gold standard for assessing LV volumes and mass.We sought to investigate the cardiac effects of anabolic steroid use with CMR hypothesising that significant hypertrophy and distinct LV remodelling would be seen in steroid users relative to non-users. Methods

Effects of anabolic steroid use on myocardial perfusion in body-builders: a quantitative cardiovascular magnetic resonance Study

Methods Twenty one body-builders were studied 14 anabolic steroid users and 7 controls matched for age and training history. First pass CMR perfusion imaging was performed on a 1.5T Avanto (Siemens, Erlangen, Germany) after adenosine-induced hyperemia (140 mcg/kg/min) and at rest using a hybrid echo-planar imaging sequence. Images of the base, mid-ventricle and apex were acquired and the myocardium was divided into 16 segments as well as endocardial and epicardial layers. After image registration, a modified Fermi-constrained deconvolution algorithm was applied pixel-wise to quantify absolute MBF. Late gadolinium enhancement (LGE) imaging was performed as well as standard assessment of ventricular volumes, function and LV mass. Data were analysed using a linear mixed effects model.

Role of T1 and T2-mapping in assessing the myocardial interstitium in hypertrophic cardiomyopathy: a cardiovascular magnetic resonance study

Background Fibrosis is thought to play an important role in the pathogenesis of the adverse sequelae of hypertrophic cardiomyopathy (HCM). Late gadolinium enhancement (LGE) cardiovascular magnetic resonance detects replacement fibrosis but cannot presently detect interstitial fibrosis. The latter is thought to be a very early feature of HCM and can be triggered by inflammation, which can also expand the size of the myocardial interstitium. We sought to determine whether extracellular volume (ECV) mapping by T1-relaxometry in concert with T2mapping can identify interstitial changes in HCM and whether these were related to myocardial edema.

PREVALENCE AND SIGNIFICANCE OF CORONARY MICROVASCULAR DYSFUNCTION IN HYPERTROPHIC CARDIOMYOPATHY: A CARDIOVASCULAR MAGNETIC RESONANCE STUDY

Abnormalities of the coronary microvasculature are thought to be a histological hallmark of hypertrophic cardiomyopathy (HCM). We sought to determine the prevalence of microvascular ischemia in HCM using stress perfusion cardiovascular magnetic resonance (CMR) and to assess its relationship to

Potential of pre-contrast T1 mapping as a marker of interstitial fibrosis in severe aortic stenosis

circumferential max strain (r=0.43, p=0.03), angle δ strain (r=0.78, p=0.001), and motion magnitude peak strain (r=0.87, p<0.001); and with increased septal wall thickness (r=-0.61, p<0.001) and left atrial dilatation (r=0.55, p=0.001). Conclusions

Multimodality assessment of aortic stenosis severity in Transcatheter Aortic Valve Implantation (TAVI): comparison between cardiovascular magnetic resonance, transesophageal and transthoracic echocardiography

Multimodality assessment of aortic stenosis severity in Transcatheter Aortic Valve Implantation (TAVI): comparison between cardiovascular magnetic resonance, transesophageal and transthoracic echocardiography Andrew Jabbour, Tevfik F Ismail, Ali Vazir, Isabelle Roussin, Ankur Gulati, Francisco Alpendurada, Sameer Zaman, Oluwatosin Sotubo, Saman S Zaman, Benjamin Hewins, Simon Davies, Sanjay K Prasad, Susanna Price, Michael B Rubens, Neil Moat, Raad H Mohiaddin

Role of inflammation in the pathogenesis of hypertrophic cardiomyopathy: a T2-mapping CMR study

Background Hypertrophic cardiomyopathy (HCM) is associated with increased myocardial fibrosis and collagen deposition. Collagen reduces cardiovascular magnetic resonance (CMR) derived T2 times, however, the inflammatory milieu required for its deposition is often associated with localised oedema. Focal areas of high T2 signal intensity have been reported in association with areas of late gadolinium enhancement (LGE) in patients with HCM. However, this previous work has relied upon the subjective visual assessment of local changes in signal intensity. We hypothesised that quantitative CMR T2mapping would reveal marked differences in myocardial T2 characteristics in patients with HCM relative to controls. Methods Twenty-two consecutive patients with HCM (15 male, age 55.8±8.7 years) but no co-morbidity and 22 healthy controls (9 male, age 49.3±13.1 years) were studied. For each subject, a short axis mid-ventricular slice was acquired using a 1.5T Avanto (Siemens Healthcare, Erlangen, Germany). A breath-hold T2-prepared singleshot steady-state free precession (SSFP) sequence was used to produce three T2-weighted images with different T2 preparation times (0 ms, 24 ms, 55 ms). Parallel imaging was used to reduce the imaging time and motioncorrection was applied to improve the accuracy of T2 measurement. T2 maps were produced by fitting the signal intensity-time exponential decay curve using a linear 2-parameter model after logarithmic transformation (CMRtools, Cardiovascular Imaging Solutions, London, UK). An inversion recovery prepared gradient echo sequence with the inversion time optimised to null normal myocardium was used 10 minutes after intravenous gadolinium contrast (Gadovist, Bayer-Schering, Berlin, Germany, 0.1 mmol/kg) to detect late enhancement. Imaging was repeated in an orthogonal phase encoding direction to exclude artifact. Results There were no significant differences in baseline demographic characteristics between HCM and control patients. LV-wall thickness, indexed LV mass and ejection fraction were significantly higher in HCM patients (Table 1). In keeping with LV hypertrophy, the LV volumes were significantly smaller. None of the healthy controls exhibited any late enhancement whereas 18 (82%) HCM patients had areas of mid-wall enhancement, predominantly in the areas of hypertrophy. T2 times in patients with HCM were similar to controls with no evidence of any significant differences (HCM 54.1±2.5ms versus Controls 54.1±1.6ms, P=0.97). Conclusions