Evaluation of Brugada syndrome by cardiac magnetic resonance.

Brugada syndrome (BrS) has been originally considered to occur in structural normal hearts. However recent pathological and imaging data suggest that structural and functional changes may be present in this syndrome. This study was designed to elucidate whether any macroscopic heart abnormality is detectable in patients with BrS. For this purpose we used cardiac magnetic resonance (CMR). Twenty-nine patients displaying the BrS type-1 ECG pattern and 29 healthy controls underwent CMR (1.5 Tesla). Left (LV) and right ventricular (RV) dimensions, function and regional contractility were evaluated. Late-gadolinium-enhancement (LGE) imaging was obtained in 24 patients. We found no difference between BrS patients and controls regarding LV and RV dimensions and ejection fraction. RV wall motion abnormalities (WMA) were detected in 19 patients (65.5%) and in 22 control subjects (75.9%). The majority of these WMA were attributable to areas of hypokinesia and found in the RV inferior wall. None of the patients showed LGE. No differences were detected between controls and the different subgroups of BrS patients according to symptoms, family history and spontaneous type-1 ECG pattern. BrS patients do not differ from normal subjects with regard to dimensions and global function of both LV and RV. BrS patients may show RV-WMA, however similar changes are also present in healthy subjects and may therefore represent a physiological behaviour of RV. The lack of LGE further confirms the absence of myocardial structural damage. Our results indicate that BrS seems to occur in individuals with structurally and functionally normal heart.

Three-dimensional simultaneous strain-volume analysis describes left ventricular remodelling and its progression: a pilot study.

AIMS: Three-dimensional (3D)-echocardiography speckle imaging allows the evaluation of frame-by-frame strain and volume changes simultaneously. The aim of the present investigation was to describe the strain-volume combined assessment in different patterns of cardiac remodelling. METHODS AND RESULTS: Fifty patients received a 3D acquisition. Patients were classified as follows: healthy subjects (CNT), previous AMI, and normal ejection fraction (EF; group A); ischaemic cardiomyopathy with reduced EF (group B); hypertrophic/infiltrative cardiomyopathy (group C). Values of 3D strain were plotted vs. volume for each frame to build a strain-volume curve for each case. Peak of radial, longitudinal, and circumferential systolic strain (Rεp, Lεp, and Cεp, respectively), slopes of the curves (RεSl, LεSl, CεSl), and strain to end-diastolic volume (EDV) ratio (Rε/V, Lε/V, Cε/V) were computed for the analysis. Strain-volume curves of the CNT group were steep and clustered, whereas, due to progressive dilatation and reduction of strains, progressive flattening could be demonstrated in groups A and B. Quantitative data supported visual assessment with progressive lower slopes (P< 0.05 for RεSl, CεSl, P= 0.06 for LεSl) and significantly lower ratios (P< 0.01 for Rε/V, Lε/V, and Cε/V). Group C showed an opposite behaviour with slopes and ratios close to those of normal subjects. Correlation coefficients between EDV and slopes of the curves were significant for all the directions of strain (CεSl: r = 0.891; RєSl: r = 0.704; LєSl: r = 0.833; P< 0.0001 for all). CONCLUSION: We measured left ventricular volumes and strain by 3D-echo and obtained strain-volume curve to evaluate their behaviour in remodelling. A distinctive and progressive pattern consistent with pathophysiology was observed. The analysis here shown could represent a new non-invasive method to assess myocardial mechanics and its relationship with volumes.