Atrial reservoir function by strain rate imaging in asymptomatic mitral stenosis: prognostic value at 3 year follow-up.

AIMS: Assessment of left and right systolic atrial reservoir function in asymptomatic mitral stenosis (MS) by strain and strain rate imaging (SRI) and their prognostic power at 3 year follow-up was the purpose of this study. There is clear indication to treat (by surgery or percutaneous valvotomy) symptomatic patients with MS, whereas for the asymptomatic ones, the question is much debated. So, we need new echocardiographic parameters helpful for the management of asymtomatic patients. Atrial reservoir function by SRI could help in evaluation of these patients. METHODS AND RESULTS: Fifty-three asymptomatic patients with MS and 53 healthy controls were evaluated by the standard echo-Doppler study [mitral valve (MV) area, mean gradient, systolic pulmonary pressure, left atrial (LA) width, LA volumes, LA compliance index] and by Doppler myocardial imaging (velocity, strain, and SR of both atria). The endpoint at 3 year follow-up was symptoms, hospitalization for cardiac cause, atrial fibrillation, thrombo-embolic events, valvular surgery, or percutaneous commissurotomy. LA width, volumes, and systolic pulmonary pressure were significantly increased in MS patients (P < 0.001). Atrial myocardial velocities and deformation indices were significantly compromised in MS patients (P < 0.0001). Significant correlation was found between atrial myocardial velocity and MV area (by pressure half-time method: P = 0.019, R = 0.41; by planimetric method: P = 0.016, R = 0.43). Peak systolic LA myocardial strain and SR were significantly correlated with atrial volumes (strain: P = 0.03, R = -0.28; SR: P = 0.0008, R = -0.42), with atrial compliance index (strain: P = 0.04, R = 0.26; SR: P = 0.04, R = 0.16), with atrial ejection fraction (strain: P < 0.0001, R = 0.56; SR: P = 0.03, R = 0.43). At 3 year follow-up, 22 (41%) patients had events. Comparing the MS patients who had events during the 3 year follow-up with those who did not, the former had bigger LA volumes, although these parameters did not reached a significant value, whereas atrial myocardial systolic SR was significantly impaired in patients with events. In multivariate analysis, the best predictor of adverse events was LA peak systolic SR average (P = 0.04; coefficient: 0.113; SE: 0.055; cut-off value of 1.69 s(-1) for LA peak systolic SR average) with a sensitivity of 88%, specificity of 80.6%, area under the receiver operating characteristic curve of 0.852 (SE: 0.048; 95% CI: 0.74-0.93, P = 0.0001). CONCLUSION: Atrial myocardial deformation properties, assessed by SRI, are abnormal in asymptomatic patients with rheumatic MS. The degree of this impairment is predictor of events in a 3 year follow-up. SRI could be helpful in decision-making of asymtomatic patients with MS.

Noninvasive evaluation of arterial abnormalities in young patients with neurofibromatosis type 1.

Neurofibromatosis regroups at least two different autosomal dominant genetic disorders: neurofibromatosis type 1 (NF1) and neurofibromatosis type 2 (NF2). Vascular disease is an underestimated complication of NF1. Few studies are available on this, all based on case reports. Neurofibromin, NF1 protein product, has also been detected in aortic smooth muscle. The purpose of this study was to evaluate the physical properties of the vessels, by measuring the carotid-femoral pulse wave velocity (PWV). This parameter was assessed by the Complior, a new noninvasive, validated device, used to screen a large population. The authors studied 64 neurofibromatosis patients (34 boys and 30 girls) with a mean age of 12 years (range 5-25 years). To investigate the presence of vascular lesions, aortic stiffness was evaluated by carotid-femoral PWV by using an automatic processor (Complior). They compared data from the PWV with a control group (30 healthy children, 17 boys and 13 girls, mean age 11 years, range 5-23 years). The calculated mean PWV in the control group was 6.5 +/- 1.15 m/s. The mean PWV of the 64 young patients with NF1 was 6.3 +/- 1.02 m/s. There was no difference between the two groups (p=0.39). Nevertheless, analysis of the linear regression has shown a linear relationship between systolic blood pressure (SBP) and PWV in the control group, while in NF1 patients this relationship is not present. The authors suggest that the coexistence of different factors, such as intimal proliferation, thinning media, fragmentation of the elastic tissue, irregularity, stenosis and tortuosity of the vessels, dysplasia of the small vessels, that counterbalance PWV, normalize the mean value. They emphasize the importance of a careful vascular evaluation, using noninvasive method, such as Complior. This device is well accepted by NF1 patients.

[TNF alpha and heart failure]. / TNF alpha e scompenso cardiaco.

Tumor necrosis factor alpha (TNF alpha) is a cytokine with proinflammatory properties which produces negative inotropic effects on the heart. It is produced in a variety of conditions such as septic shock, acute myocarditis, reperfusion injury, and congestive hear failure (CHF). This production is probably due to activation of immune elements localized in the heart or periphery, or both. TNF alpha acts by binding to two specific receptors: TNF-R1 and TNF-R2. These two proteins have different effects. TNF-R1 has cytotoxic and antiviral activity, induces fibroblast proliferation, and mediates apoptosis. TNF-R2 is involved in septic shock and in lymphocyte proliferation. They both have negative inotropic effect on the heart. It has been showed that these receptors are down-regulated in congestive heart failure, while their soluble forms (sTNF-R1 and sTNF-R2) increase with the severity of symptoms. However the significance of this increase is still unclear. The role of Fas, a receptor protein that induces apoptosis, is also examined. Fas and its ligand have homologies respectively with TNF alpha and TNF-R. Also the soluble form of Fas (sFas) increases in relation to heart failure and is related to soluble forms of the similar receptor family, therefore it is possible that the same stimuli lead the three receptors to act together. SFas, as well as sTNF receptors, may play an important role in CHF.