Valve prosthesis-patient mismatch: hemodynamic, echocardiographic and clinical consequences.

OBJECTIVES: The purpose is to evaluate in vivo at rest and under stress conditions hemodynamic performance of the small size St. Jude Medical Regent (SJMR) prosthetic valve in patients with a body surface area (BSA) of 1.8 ± 0.11 m(2) and to define the role of valve prosthesis- patient mismatch on left ventricular mass regression following aortic valve replacement. METHODS: We evaluated 25 cases (12 males and 13 females, mean age 65.2 ± 8 years) of aortic valve replacement (17 mm SJMR in three cases and 19 mm SJMR in 22 cases). All the patients underwent at rest Doppler echocardiography before and after surgery and both basal and dobutamine stress echocardiography (DSE) at follow-up. The mean duration of follow-up was 41.3 ± 24 months. RESULTS: A significant reduction in mean and peak transaortic gradients and peak transaortic velocity over time following valve replacement has been identified. After surgery, there was a significant increase of ejection fraction. DSE significantly increased heart rate, ejection fraction, peak transaortic gradient and peak transaortic velocity. All patients passed DSE without complication. Even if a significant mismatch was present in 76% of cases, the left ventricular mass decreased significantly from preoperative value of 278.7 ± 51.1 g to 181.5 ± 52.73 g, respectively. CONCLUSION: Aortic valve replacement with 17 mm SJMR or 19 mm SJMR prostheses appear to provide satisfactory clinical and hemodynamic results at rest and under DSE, even in those patients with BSA of 1.8 ± 0.11 m(2) where it was not possible to enlarge the aortic annulus. Prosthesis-patient mismatch is not associated with lesser regression of left ventricular mass. Dobutamine stress echocardiography should be a useful and effective means for evaluating prosthesis hemodynamic aspects.

Diagnosis and definition of biventricular non-compaction associated to Ebstein's anomaly.

BACKGROUND: Non-compaction of ventricular myocardium is a rare congenital cardiomyopathy characterized by the presence of an extremely thickened endocardial layer with prominent trabeculations and deep recesses in communication with ventricular chamber and determining the typical spongeous aspect. The diagnosis of non-compaction of ventricular myocardium is possible through the identification of morphological alterations by echocardiographic evaluation. Ebstein's anomaly is a rare congenital cardiac disease, defined as the significant apical displacement of the part of the tricuspid valve causing significant tricuspid regurgitation and reduction of the functional right ventricle, right atrial and right ventricular dilatation and atrial and ventricular arrhythmias. CASE REPORT: We present a case of biventricular non-compaction and Ebstein's anomaly in a 29-year-old Italian man that was referred for chest pain. Diagnosis of Ebstein's anomaly was made during a medical control for military service through an echocardiographic evaluation which left the suspicion of myocardium non-compaction. We present the cardiac image of the 2D and 3D eco, RMN, scintigraphy and ventriculaography.

Treatment of relapsing mild-to-moderate ulcerative colitis with the probiotic VSL#3 as adjunctive to a standard pharmaceutical treatment: a double-blind, randomized, placebo-controlled study.

OBJECTIVES: VSL#3 is a high-potency probiotic mixture that has been used successfully in the treatment of pouchitis. The primary end point of the study was to assess the effects of supplementation with VSL#3 in patients affected by relapsing ulcerative colitis (UC) who are already under treatment with 5-aminosalicylic acid (ASA) and/or immunosuppressants at stable doses. METHODS: A total of 144 consecutive patients were randomly treated for 8 weeks with VSL#3 at a dose of 3,600 billion CFU/day (71 patients) or with placebo (73 patients). RESULTS: In all, 65 patients in the VSL#3 group and 66 patients in the placebo group completed the study. The decrease in ulcerative colitis disease activity index (UCDAI) scores of 50% or more was higher in the VSL#3 group than in the placebo group (63.1 vs. 40.8; per protocol (PP) P=0.010, confidence interval (CI)95(%) 0.51-0.74; intention to treat (ITT) P=0.031, CI95(%) 0.47-0.69). Significant results with VSL#3 were recorded in an improvement of three points or more in the UCDAI score (60.5% vs. 41.4%; PP P=0.017, CI95(%) 0.51-0.74; ITT P=0.046, CI95(%) 0.47-0.69) and in rectal bleeding (PP P=0.014, CI95(%) 0.46-0.70; ITT P=0.036, CI95(%) 0.41-0.65), whereas stool frequency (PP P=0.202, CI95(%) 0.39-0.63; ITT P=0.229, CI95(%) 0.35-0.57), physician's rate of disease activity (PP P=0.088, CI95(%) 0.34-0.58; ITT P=0.168, CI95(%) 0.31-0.53), and endoscopic scores (PP P=0.086, CI95(%) 0.74-0.92; ITT P=0.366, CI95(%) 0.66-0.86) did not show statistical differences. Remission was higher in the VSL#3 group than in the placebo group (47.7% vs. 32.4%; PP P=0.069, CI95(%) 0.36-0.60; ITT P=0.132, CI95(%) 0.33-0.56). Eight patients on VSL#3 (11.2%) and nine patients on placebo (12.3%) reported mild side effects. CONCLUSIONS: VSL#3 supplementation is safe and able to reduce UCDAI scores in patients affected by relapsing mild-to-moderate UC who are under treatment with 5-ASA and/or immunosuppressants. Moreover, VSL#3 improves rectal bleeding and seems to reinduce remission in relapsing UC patients after 8 weeks of treatment, although these parameters do not reach statistical significance.

Oxidative stress in young subjects with acute myocardial infarction: evaluation at the initial stage and after 12 months.

In 105 subjects (97 men and 8 women) aged <46 years (mean age 39.6 +/- 5.5 years), with recent acute myocardial infarction (T1), thiobarbituric acid reactive substances and total antioxidant status were determined; NO production was evaluated by measuring the nitrite and nitrate (NOx) concentration. The patients with acute myocardial infarction were subdivided according to the main risk factors, number of risk factors, and extent of coronary lesions. The evaluation was repeated after 12 months (T2). In these subjects, thiobarbituric acid reactive substances and NOx were significantly increased and total antioxidant status was significantly decreased at T1. In single risk factor, only NO metabolites were significantly lower in acute myocardial infarction subjects who smoke than in subjects who do not. Subdividing the subjects according to the number of risk factors and number of stenosed coronary vessels, there were no significant differences between the subgroups. At T2, thiobarbituric acid reactive substances and NOx were decreased and total antioxidant status was increased, but all parameters were still altered.

Evaluation of oxidative status in coronary heart disease at baseline and during exercise test.

Oxidative stress has probably a role in coronary heart disease (CHD), but studies focused on the behaviour of oxidative status in patients with stable CHD have obtained controversial results. On the other hand, an increased release of leukocyte elastase is considered a marker of CHD. Exercise can induce oxidative stress and leukocyte activation, so the aim of this study was to evaluate oxidative status and plasma elastase level in a group of subjects with stable coronary heart disease (CHD), at baseline and during an exercise test. We enrolled 15 patients with previous acute myocardial infarction, all treated with statins and platelet antiaggregating agents. As parameters of oxidative status we determined the thiobarbituric acid reactive substances and total antioxidant status (TAS). The exercise test was performed according to the Bruce protocol. At baseline, elastase level was higher in CHD subjects than in normal controls and during the exercise test it increased in both groups in comparison with basal values. Regarding oxidative status, only TAS was slightly lower in CHD subjects than in normal controls. In both groups, during exercise test, no parameter of oxidative status was significantly different compared to basal values. In conclusion, CHD patients showed, at rest, an abnormal neutrophil activation and a lower antioxidant status. The exercise test further activated neutrophils but did not influence oxidative status. The absence of a marked oxidative stress in our patients may be partly due to the pharmacological treatment, which apparently did not influence the abnormal leukocyte activation.

Persistence of the altered polymorphonuclear leukocyte rheological and metabolic variables after 12 months in juvenile myocardial infarction.

Acute myocardial infarction (AMI) is associated with an elevated polymorphonuclear leukocyte (PMN) count and a PMN rheological impairment. In this study we evaluated two major rheological aspects (membrane fluidity and cytosolic Ca2+ concentration) in a group of young adults with AMI. We enrolled 41 AMI patients (39 men and 2 women; mean age 41.0 +/- 4.0 years), who were examined 5-10 days after AMI (T1) and 12 months later (T2). The membrane fluidity was obtained labelling granulocytes with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH) and considering the degree of fluorescence polarization, inversely correlated to the membrane lipid fluidity. The cytosolic Ca2+ content was obtained marking PMN cells with the fluorescent probe Fura-2AM and considering the ratio between the Fura 2-Ca2+ complex and the unchelated Fura 2 fluorescence intensity. Both parameters were evaluated at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) at the concentration of 4.5 muM, prolonged for 5 and 15 minutes. At T1 the PMN membrane fluidity and cytosolic Ca2+ content in AMI patients were respectively decreased and increased in comparison with control group. At T2 the membrane fluidity was not any more different from control subjects, but there was also a further increase in cytosolic Ca2+ content. In vitro, PMN activation caused no significant variation of these parameters in the control group, while in AMI patients membrane fluidity significantly decreased and cytosolic Ca2+ content increased not only during the initial stage, but also after 12 months. The long-term functional alteration of PMN cells observed in young adults with AMI confirms the role of these cells in the inflammatory response following AMI. In the light of these data, the use of molecules able to modulate granulocyte activity, such as calcium channel blockers or pentoxifylline, should be reconsidered in myocardial infarction, together with the usual pharmacological treatment.

Plasma markers of platelet and polymorphonuclear leukocyte activation in young adults with acute myocardial infarction.

Our goal was to evaluate some plasma markers of platelet and polymorphonuclear leukocyte (PMN) activation in a group of young adults with acute myocardial infarction (AMI) at the initial stage and after three months. We enrolled 49 AMI subjects aged<45 years and examined plasmatic levels of platelet factor 4 (PF4), beta-thromboglobulin (beta-TG), elastase and myeloperoxidase (MPO) using ELISA methods. PF4 and beta-TG were increased, compared to control subjects, both at the initial stage and after 3 months. In control subjects and in AMI patients, at both times of observation, there was a significant and positive correlation between the two platelet parameters, while no correlation was present between each parameter and platelet count. In AMI patients there was an increase in elastase levels in comparison with the control group; this increase was evident at the initial stage and after 3 months. There was no difference in MPO levels between control subjects and AMI patients. In control subjects and in AMI patients there was a significant and positive correlation between elastase and MPO level, whereas no relationship was found between each marker and PMN count. Our data show that in young AMI patients the discharge treatment including antiplatelet drugs did not modify platelet activation and suggest the association of molecules able to inhibit PMN activation to the conventional therapy of these AMI patients.