Indexed left atrial volume is a more sensitive indicator of filling pressures and left heart function than is anteroposterior left atrial diameter.

INTRODUCTION: Left atrial (LA) size is an indicator of the pressure to which it is chronically subjected. Although guidelines recommend measuring it using volume indexed to body surface, the anteroposterior diameter is still normally used. AIM: To evaluate which of these measurements correlates better with atrial pressure-related echocardiographic parameters. METHODS: Atrial diameter and volume, together with parameters of systolic function, diastolic function, pressure, and degree of mitral regurgitation, were measured in 121 consecutive outpatients. RESULTS: Atrial diameter correlated with its indexed volume (r: 0.69) with a low degree of agreement for detecting dilation (Kappa: 0.51). Atrial diameter was related to the parameters associated with atrial pressure: E/E' (r: 0.44), pulmonary vein systolic/diastolic rates quotient (r: 0.25) and degree of mitral regurgitation (r: 0.19). The correlations improved when volume indexed to body surface was measured (r: 0.52; 0.38 and 0.44, respectively). In a multiple regression analysis that included E/E', pulmonary vein flow and degree of mitral regurgitation, LA diameter depended entirely on E/E' (r: 0.44; B: 0.04; P: 0.000). The relationship improved when the diameter was corrected for body surface or the volume was measured (r: 0.54 and 0.54, respectively), and in particular when volume indexed to body surface was measured (r: 0.66). In this case, pulmonary vein flow (B: 6.8; P: 0.03), degree of mitral regurgitation (B: 5.2; P: 0.000) and E/E' ratio (B: 0.8; P : 0.000) were included in the equation. CONCLUSIONS: Indexed atrial volume correlates better with LA pressure surrogates than the anteroposterior diameter, even when this is corrected for body surface.

Atorvastatin modifies the protein profile of circulating human monocytes after an acute coronary syndrome.

Aggressive treatment with high-dose atorvastatin reduces more effectively the incidence of cardiovascular events than moderate statin therapy. The mechanism of this benefit has not been fully elucidated. In order to know the potential effects of statin treatment on the protein expression of circulating monocytes in acute coronary syndrome (ACS) patients, a proteomic analysis of these cells was carried out by 2-DE and MS. Twenty-five patients with non-ST-elevation acute coronary syndrome (NSTEACS) were randomized, the fourth day after admission, to receive ATV 80 mg/dL (n = 14) or conventional treatment (CT) (n = 11), for two months. Blood was withdrawn at the end of the treatment, and monocytes were extracted for proteomic analysis and their protein expression patterns determined. Age, sex, total cholesterol, LDL, HDL, triglycerides, body mass index, presence of hypertension, diabetes, and smoking status were not significantly different between the two groups of patients. The expression of 20 proteins was modified by intensive ATV. Among the most relevant results stand out the normalization by intensive ATV treatment of the expression of proteins that modulate inflammation and thrombosis such as protein disulfide isomerase ER60 (PDI), Annexin I, and prohibitin, or that have other protective effects as HSP-70. Thus, this approach shed light at the molecular level of the beneficial mechanisms of anti-atherothrombotic drugs.

Circulating human monocytes in the acute coronary syndrome express a characteristic proteomic profile.

We examined the proteome of circulating monocytes of patients with acute coronary syndrome at different times in comparison to that of patients with stable coronary artery disease. On admission, the expression of 18 spot proteins was altered, 10 of which were totally absent. This pattern changed progressively, and at 6 months, there were no differences with the monocyte proteome of stable patients.