ABSTRACT
Background: It has been proved that there is an inspiratory muscle dysfunction in mitral stenosis; Although its causes still remain unknown. Aim: to evaluate the effect of percutaneous balloon mitral valvuloplasty (PMV) on inspiratory muscle performance (IMP) in patients with mitral stenosis (mitral area < 1.5 cm2). Patients and methods: We studied IMP in 8 patients (35 ñ 10 years) before and 3 months after successful PMV. Inspiratory muscle strength was studied by measuring maximal statistical inspiratory mouth pressure (MIP). Endurance was evaluated using a two minute incremental threshold loading test in order to obtain the maximal sustainable inspiratory pressure (SIP), with the maximal sustainable load (MSL) the patients could sustain for 2 minutes. Results: Mitral valvuloplasty increased mean cardiac index from 3.1 ñ 0.3 to 4.15 ñ 0.3 l/min/m2 (p<0.01), and significantly decreased mean pulmonary and capillary pressures. The MIP value(118 ñ 6 cmH2O), similar to that of normal group, increased to 137 ñ 7 cmH2O (p<0.01). SIP and maximal sustainable load were 52 ñ 3 cmH2O and 294 ñ 29 g respectively, lower than normal subjects (p<0.05) They increased after PMV to 80 ñ 3 cmH2O and 463 ñ 26 g respectively (p<0.001). Conclusions: PMV improved inspiratory muscle function in patients with severe mitral stenosis, probably secondary to a decrease work of breath and improvement of ventricular function
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Catheterization/statistics & numerical data , Mitral Valve Stenosis/surgery , Respiratory Physiological Phenomena , Vital Capacity/physiology , Anthropometry , Inspiratory Capacity/physiology , Muscle Weakness/physiopathology , Hemodynamics/physiology , Respiratory Muscles/physiopathology , Airway Resistance/physiologyABSTRACT
Background: High density lipoproteins are an heterogeneous population of particles. Two main subpopulations have been identified, one contains Apo A-I and Apo A-II and is denominated LpA-I:A-II and another one contains only Apo A-I and is denominated LpA-I. Aim: To measure the concentrations of these particles in patients with stable coronary artery disease. Patients and Methods: Serum lipids, A-I and B apolipoproteins, LpA-I, LpA-I:A-II and LpB particles were measured in 73 men aged 33 to 82 years with angiographically documented coronary artery disease (CAD) and 33 control subjects aged 39 to 76 years. LpA-I, LpA-I:A-II and LpB were measured by a noncompetitive enzyme linked immunoassay using previously characterized monoclonal antibodies against ApoA-I, ApoA-II and apoB. Results: Patients with CAD had significantly higher mean levels of LDL cholesterol than the control group (p= 0.038). The mean concentration of LpA-I particles in patients with CAD was significantly lower (p= 0.031) than in control subjects, while the concentration of LpA-I:A-II particles was significantly higher (p=0.016). The percentage of coronary stenosis correlated negatively with LpA-I and positively with LpA-I:A-II. The best relative risk (RR) indicator in these patients was LDL-cholesterol. The relative risk increases 2.5 fold when LpA-I falls below the cut-off level. Likewise, the relative risk increases 3-fold when LpA-I:A-II raises over the cut-off level. Conclusions: Our findings indicate that the quantification of LpA-I and LpA-I:A-II particles might allow a more accurate evaluation of the CAD risk than HDL cholesterol. LpA-I might represent the antiatherogenic fraction of HDL