Relationship between echocardiographic and functional parameters in patients with heart failure undergoing cardiopulmonary exercise test.

BACKGROUND: HF patients typically show effort intolerance due to a reduction in peak exercise oxygen (peak VO2) consumption, which is related to inability to adapt systolic function to increased demand. Left ventricular ejection fraction (EF) is a surrogate marker of cardiac contractility and a powerful predictor of adverse prognosis in chronic heart failure (HF). The aim of the study was to explore the relationship between EF and other echocardiographic findings with peak VO2 in a population of HF individuals undergoing cardiopulmonary exercise testing (CPX). METHODS: We evaluated 101 patients (61% hypertensives, 74% with documented coronary artery disease) undergoing both resting echocardiography and symptom-limited CPX. RESULTS: Mean age was 58±13 years, 83% were males. Mean EF was 55±12%; 20% of the patients showed EF<40%. Mean test duration was 9.4±2.2 min. Average peak VO2 was 21±6 mL/kg/min. Peak VO2 showed a robust positive correlation with EF (R=0.42, P<0.001). Other independent predictors of peak VO2 were age, male sex, height and tricuspidal anular plane systolic excursion (TAPSE), this latter reflecting right ventricular dysfunction. When subjects were dichotomized according to predicted peak VO2values, those with higher-than-predicted peak VO2 showed significantly lower VE/VCO2 slope, and higher values of both oxygen pulse and VO2/WR slope. CONCLUSIONS: EF and TAPSE are associated with peak VO2 in HF patients independently from age, sex and height. The evaluation of potentially relevant mechanisms affecting exercise capacity in HF patients requires further investigation.

Cortical lesion load associates with progression of disability in multiple sclerosis.

Cortical inflammatory lesions have been correlated with disability and cortical atrophy in multiple sclerosis. The extent to which cortical lesion load is associated with longer-term physical and cognitive disability in different multiple sclerosis phenotypes has not yet been investigated. Thus, a 5-year prospective longitudinal study was carried on in a large group of patients with multiple sclerosis. Three hundred and twelve consecutive patients suffering from multiple sclerosis (157 relapsing remitting, 35 paediatric, 45 benign, 44 primary progressive and 31 secondary progressive) were enrolled in a 5-year prospective clinical and neuroimaging study. Several magnetic resonance parameters (including cortical lesion number and volume, contrast-enhancing cortical lesions and grey matter atrophy) were analysed to find associations with clinical and cognitive outcomes. Patients with high cortical lesion load had higher Expanded Disability Status Scale increase (median = 1.5; range = 0-3) during the study than both patients with low cortical lesion load (median = 1.0; range = 1-3, P < 0.001) and without cortical lesions (median = 0.5; range = -1 to 2, P < 0.001). Compared with clinically stable patients, 101 (32.4%) patients showing clinical progression at 5 years had the highest rate of cortical lesion accumulation (P < 0.001). Stepwise regression analysis revealed significant and independent contributions from age (ß = 0.55), cortical lesion volume (ß = 0.58), T(2) white matter lesion volume (ß = 0.34) and grey matter fraction (ß = 0.42) as predictors (final model with r(2 )= 0.657, P < 0.001) of Expanded Disability Status Scale change. Disease duration (ß = 0.52, P < 0.001), cortical lesion volume (ß = 0.67, P < 0.001), grey matter fraction (ß = 0.56, P < 0.001) and T(2) white matter lesion volume (ß = 0.31, P = 0.040) at baseline were found to be independent predictors of cognitive status at the end of the study. While confirming the relevance of cortical pathology in all multiple sclerosis phenotypes, but benign, our study suggests that grey matter and white matter changes in multiple sclerosis occur, at least, partly independently, and that grey matter, more than white matter, damage is associated with physical and cognitive disability progression. Thus, the combination of grey and white matter parameters gives a more comprehensive view of multiple sclerosis pathology and allows a better understanding of the progressive phase of the disease, which, however, seems more related to cortical damage than to subcortical white matter changes.

No MRI evidence of cortical lesions in neuromyelitis optica.

BACKGROUND: Neuromyelitis optica (NMO) is a severe inflammatory demyelinating disease of the CNS in which a pathogenic role of anti-aquaporin-4 (AQP4) antibodies has been suggested. Although AQP4 is expressed in human cortex, recent histologic studies have failed to find any evidence of cortical demyelination in NMO. OBJECTIVE: To evaluate, in vivo, the occurrence of focal and diffuse cortical pathology in NMO. METHODS: We studied 30 patients with NMO, 30 patients with relapsing-remitting multiple sclerosis (RRMS), and 30 normal controls (NC). RRMS and NC were age- and gender-matched to NMO. The presence of cortical lesions (CLs) was evaluated on double inversion recovery sequence and cortical thickness (CTh) by the application of Freesurfer on 3 volumetric fast field echo T1-weighted images. RESULTS: No CL was observed in NC or in NMO, while 83 CLs were identified in 20/30 (66.7%) patients with RRMS. Although NMO did not differ from NC in the global CTh, a mild thinning was observed in some cortical areas (postcentral [p = 0.018], precentral [p = 0.009], and calcarine [p = 0.015] gyri) and in the thalamus (p = 0.036). Global and regional cortical thickness was significantly decreased in RRMS compared to both NMO and NC. DISCUSSION: Our in vivo data further suggest that the immune-mediated pathologic process occurring in NMO spares most of the cortex. NMO differs from multiple sclerosis, where CLs and atrophy are frequently found, even in early disease phases. Thus, MRI analysis of the cortex may be a potential diagnostic tool, especially in ambiguous cases.