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Biomedical subjects

M Gattone

Publications and source records attributed to M Gattone.

At least 19 recordsLinked to original sources
PubMed2004

Polymorphisms of the interleukin-1beta gene affect the risk of myocardial infarction and ischemic stroke at young age and the response of mononuclear cells to stimulation in vitro.

OBJECTIVE: To investigate the role of interleukin-1beta (IL-1beta) gene polymorphisms as a link between inflammation, coagulation, and risk of ischemic vascular disease at young age. METHODS AND RESULTS: A total of 406 patients with myocardial infarction (MI) at young age, frequency-matched for age, sex, and recruitment center, with 419 healthy population-based controls and 134 patients with ischemic stroke at young age, matched by age and sex, with 134 healthy population-based controls, were studied. Subjects carrying the TT genotype of the -511C/T IL-1beta polymorphism showed a decreased risk of MI (odds ratio [OR], 0.36; 95% CI, 0.20 to 0.64) and stroke (OR, 0.32; 95% CI, 0.13 to 0.81) after adjustment for conventional risk factors. In both studies, the T allele showed a codominant effect (P=0.0020 in MI; P=0.021 in stroke). Mononuclear cells from volunteers carrying the T allele showed a decreased release of IL-1beta and a decreased expression of tissue factor after stimulation with lipopolysaccharide compared with CC homozygotes. The presence of a monoclonal antibody against IL-1beta during cell stimulation resulted in a marked reduction of tissue factor activity expression. CONCLUSIONS: -511C/T IL-1beta gene polymorphism affects the risk of MI and ischemic stroke at young age and the response of mononuclear cells to inflammatory stimulation.

Adolescent↗
PubMed2001

Polymorphisms in the thrombopoietin gene are associated with risk of myocardial infarction at a young age.

Five polymorphisms in the thrombopoietin (TPO) gene were identified, one in the 5' untranslated region (UTR) (C1796T), two within intron 5 (C4830A and A4877C), and two in the 3' UTR (A5713G and A6160T). The allele frequencies were determined in a group of 450 healthy middle aged men from the UK and found to be 0.46 for 1796T, 0.38 for 4830A, 0.004 for 4877C, 0.47 for 5713G and 0.07 for 6160T. Genotypes for the three common polymorphisms were determined in a group of 176 young male Swedish survivors of a myocardial infarction (MI) and 186 age-matched controls and a group of 156 young Italian survivors of an MI and 147 age and sex matched controls. In both the Swedish and the Italian studies polymorphisms were found to be associated with increased risk of MI. In the Swedish sample the frequency of 4830A was significantly higher in controls (0.40) compared with patients (0.29) (P=0.003), with an odds ratio for AA homozygotes of 0.48 (0.25-0.92; P=0.03) compared with CC homozygotes. In the Italian sample the frequency of 5713G was significantly lower in controls (0.31) compared with cases (0.40) (P=0.03), with an odds ratio for GG homozygotes of 2.29 (1.08-4.89; P=0.03) compared with AA homozygotes. These risk associations are consistent since 4830A and 5713A show strong allelic association. After adjusting for other measured risk factors the effect on risk was still significant in the Italian sample 2.39 (1.02-5.58), but not in the Swedish sample 0.46 (0.16-1.32). The observation of frequency differences between cases and controls in two independent samples strongly suggests that the TPO gene is involved as a risk factor for developing MI at a young age, but the identified polymorphisms are probably acting as markers for an unidentified functional mutation elsewhere in the gene locus.

Adult↗
PubMed2001

Chlamydia pneumoniae and cytomegalovirus seropositivity, inflammatory markers, and the risk of myocardial infarction at a young age.

BACKGROUND: Pathogens causing chronic infections may promote atherosclerosis. The aim of our study was to evaluate the association of Chlamydia pneumoniae (Cp) and cytomegalovirus (CMV) infection and of inflammatory activation with premature myocardial infarction (MI). METHODS: Specific anti-Cp and anti-CMV immunoglobulin G (IgG), fibrinogen, white blood cells (WBC), and C-reactive protein (CRP) were measured in 120 post-MI patients </=50 years old and in 120 age-matched controls. RESULTS: Seropositivity to Cp and elevated concentrations of anti-Cp and anti-CMV IgGs were more frequent (P =.01) in patients than in control subjects, and fibrinogen, CRP, and WBC levels (P =.02) were more elevated. After adjustment for coronary risk factors and socioeconomic status, the odds ratios (95% confidence intervals) for premature MI were 2.4 (1.3-4.6) for Cp infection and 2.9 (1.5-5.8) for CMV. The risk of Cp infection was greater in smokers (3.7, 1.8-7.6). When both infections were present (35% of patients vs 8% of controls, P =.001), CRP was higher (P =.01) and the risk increased by 12 times (12.5, 4-38.9) compared with that in subjects without any infection and by 5 times (4.9, 2.2-10.9) if only one was present. CONCLUSIONS: After adjustment for confounders, seropositivity to both Cp and CMV infections is associated with the diagnosis of premature MI. The combination of both infections is associated with an enhanced inflammatory response and a markedly increased risk of premature MI.

Adult↗
PubMed2001

The E27 beta2-adrenergic receptor polymorphism reduces the risk of myocardial infarction in dyslipidemic young males.

In the present study we evaluated whether two polymorphisms of beta2-adrenergic receptors (beta2-AR) gene (R16G and Q27E) could modify the risk of myocardial infarction (MI). Using a case-control design, we analyzed the data from 125 male patients who had experienced a first episode of MI before the age of 45 years and 108 male controls matched for age. The allele frequencies for R16G and Q27E were: G16=0.56 and E27=0.36 in patients with MI and G16=0.61 and E27=0.42 in the control group. There was a trend (not statistically significant) of decreasing MI risk according to E27 or G16 alleles. Combined effect between E27 allele and history of dyslipidemia has been observed. Whereas dyslipidemia conferred a relative risk of MI of 4.8 (P<0.001) compared with normolipidemia in the entire study population, the relative risk increased to 9.0 (P<0.001) in Q27 homozygotes with dyslipidemia, and decreased to 1.8 (P=0.36) in E27 homozygotes. Our results show that the E27 allele of the beta2-adrenergic receptor has a significant protective effect on MI in dyslipidemic young male.

Adult↗
PubMed1997

Attenuation of unfavorable remodeling by exercise training in postinfarction patients with left ventricular dysfunction: results of the Exercise in Left Ventricular Dysfunction (ELVD) trial.

BACKGROUND: Exercise is currently recommended for patients after myocardial infarction; however, the effects of regular exercise on the remodeling process remain to be defined. The aim of this multicenter, randomized study was to investigate whether a long-term physical training program influences left ventricular size and function in postinfarction patients with systolic dysfunction. METHODS AND RESULTS: Consecutive patients with <40% ejection fraction after a first Q-wave myocardial infarction were randomly assigned to a 6-month exercise training program (n=39) or control group (n=38). After 6 months, a significant increase in work capacity was observed only in the training group (from 4.462+/-1.095 to 5.752+/-1.749 kilopond-meters [Kp-m], P<.01), not in the control group (from 4.375+/-1.143 to 4.388+/-1.199 Kp-m), whereas left ventricular volumes had increased in the control group (end-diastolic volume, from 94+/-26 to 99+/-27 mL/m2, P<.01; end-systolic volume, from 62+/-20 to 67+/-23 mL/m2, P<.01) but not in the training group (end-diastolic volume, from 93+/-28 to 92+/-28 mL/m2, P=NS; end-systolic volume, from 61+/-22 to 57+/-23 mL/m2, P=NS). Conversely, ejection fraction had improved in the training group (from 34+/-5% to 38+/-8%, P<.01) but not in the control group (from 34+/-5% to 33+/-7%, P=NS). CONCLUSIONS: In postinfarction patients with systolic dysfunction, long-term exercise training may attenuate the unfavorable remodeling response and even improve ventricular function over time.

Adult↗
PubMed1995

Residual exertional ischemia and unfavorable left ventricular remodeling in patients with systolic dysfunction after anterior myocardial infarction.

OBJECTIVES: This study investigated whether exercise-induced myocardial ischemia influences left ventricular remodeling after anterior myocardial infarction. BACKGROUND: The effects of acute and recurrent ischemia on ventricular function are well established. However, to our knowledge the role of exertional ischemia in the remodeling response after infarction has not been investigated. METHODS: Ninety-one patients with a first anterior Q wave myocardial infarction were studied at 5 weeks by rest echocardiography and exercise scintigraphy. The echocardiographic examination was repeated 6 months later. On the basis of the presence and extent of reversible perfusion defects on exercise scintigraphy, patients were assigned to groups with no exertional ischemia (group 1, n = 20 [22%], mild to moderate ischemia (group 2, n = 45 [49%]) and severe exertional ischemia (group 3, n = 26 [29%]). RESULTS: Initial left ventricular volumes were similar, and no differences were found among the three groups in the remodeling response over the 6-month period of the study. However, patients in groups 2 and 3 with an ejection fraction < or = 40% showed significant (p < 0.01) ventricular enlargement over time, which was similar between the two groups (end-diastolic volume [mean +/- SD] from 74 +/- 13 to 80 +/- 17 ml/m2 in group 2 and from 72 +/- 11 to 81 +/- 19 ml/m2 in group 3; regional dilation from 42 +/- 16% to 52 +/- 22% in group 2 and from 38 +/- 18% to 46 +/- 27% in group 3). In contrast, ventricular dimensions did not change in group 1 patients with an ejection fraction < or = 40% as well as in patients in all three groups with an ejection fraction > 40%. CONCLUSIONS: Exercise-induced myocardial ischemia may contribute to progressive ventricular enlargement in patients with poor left ventricular function after a large anterior myocardial infarction.

Analysis of Variance↗
PubMed1993

Long-term physical training and left ventricular remodeling after anterior myocardial infarction: results of the Exercise in Anterior Myocardial Infarction (EAMI) trial. EAMI Study Group.

OBJECTIVES: The aim of this multicenter randomized study was to investigate whether long-term physical training would influence left ventricular remodeling after anterior myocardial infarction. BACKGROUND: Exercise is currently recommended for patients after myocardial infarction; however, the effects of long-term physical training on ventricular size and remodeling still have to be defined. METHODS: Patients with no contraindications to exercise were studied 4 to 8 weeks after anterior Q wave myocardial infarction and 6 months later by echocardiography at rest and bicycle ergometric testing. After the initial study, patients were randomly allocated to a 6-month exercise training program (n = 49) or a control group (n = 46). A computerized system was used to derive echocardiographic variables of ventricular size, function and topography. RESULTS: After 6 months, a significant (p < 0.01) increase in work capacity (from 4,596 +/- 1,246 to 5,508 +/- 1,335 kp-m) was observed only in the training group, whereas global ventricular size, regional dilation and shape distortion did not change in either the control or the training group. However, compared with patients with an ejection fraction > 40%, patients with an ejection fraction < or = 40% had more significant (p < 0.001) ventricular enlargement at entry and demonstrated further (p < 0.01) global and regional dilation after 6 months, in both the control and the training group (end-diastolic volume from 77 +/- 14 to 85 +/- 17 ml/m2 in the control group and from 74 +/- 11 to 77 +/- 15 ml/m2 in the training group; regional dilation from 46 +/- 18% to 57 +/- 21% in the control group and from 42 +/- 18% to 44 +/- 26% in the training group). Ventricular size and topography did not change in patients with an ejection fraction > 40%. CONCLUSIONS: Patients with poor left ventricular function 1 to 2 months after anterior myocardial infarction are prone to further global and regional dilation. Exercise training does not appear to influence this spontaneous deterioration. Thus, postinfarction patients without clinical complications, even those with a large anterior infarction, may benefit from long-term physical training without any additional negative effect on ventricular size and topography.

Electrocardiography↗
PubMed1992

EAMI--exercise training in anterior myocardial infarction: an ongoing multicenter randomized study. Preliminary results on left ventricular function and remodeling. The EAMI Study Group.

To determine the effects of a 6-month exercise training program on left ventricular (LV) function and remodeling, 49 consecutive patients (pts) with first Q anterior myocardial infarction (51 +/- 8 years), in I-II NYHA class, were studied 4 to 8 weeks after the acute episode and 6 months later by 2D-ECHO and upright bicycle ergometric test. At entry, pts were randomly allocated to physical training (T = 25pts) or control (C = 24pts). Global endocardial surface area (ESA), LV volumes and EF, extent of abnormal wall motion (%WMA), of regional dilatation (%REG DIL), and the shape distortion (DIST) index were analyzed. After 6 months, a significant increase in work capacity (4,589 +/- 1,417 to 5,379 +/- 1,485 KPM/min, p less than 0.03) and in lactic anaerobic threshold (45 +/- 13 to 63 +/- 15 W, p less than 0.01) was observed only in T. Initial ESA, EDV, EF, %WMA, %REG DIL, and DIST index were similar and they did not change after 6 months in both groups. However, pts with less than 40%EF had greater (p less than 0.0001) EDV and %WMA with marked DIST index at entry and showed further (p less than 0.01) deterioration after 6 months both in C and in T (EDV, ml/m2: 68 +/- 12 to 77 +/- 18 in C, 71 +/- 12 to 74 +/- 18 in T; %REG DIL: 39 +/- 20 to 49 +/- 24 in C, 32 +/- 12 to 35 +/- 23 in T; DIST index: 0.16 +/- 0.07 to 0.21 +/- 0.09 in C, 0.2 +/- 0.07 to 0.22 +/- 0.1 in T). These variables did not change in pts with greater than 40%EF. Thus, from these preliminary data, pts with less than 40%EF at entry are prone to further global and regional LV deterioration. Physical training does not seem to increase this spontaneous deterioration.

Anaerobic Threshold↗
PubMed1989

The anaerobic index: uses and limitations in the assessment of heart failure.

Limitation of exercise tolerance is a hallmark of heart failure. Anaerobic threshold is a quantitative, reproducible, nonmotivational, submaximal index of exercise tolerance. The pathophysiological significance and methods of determination of anaerobic threshold are matters of debate. The principal aspects of such problems are discussed in this paper.

Exercise Test↗