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Biomedical subjects

A Muscari

Publications and source records attributed to A Muscari.

51 records · Page 3Linked to original sources
PubMed1987

[Changes in humoral immunity in ischemic cardiomyopathy].

The present study has been performed with the aim of assessing the incidence and the possible implications of the changes in humoral immunity in patients with coronary heart disease. Serial determinations of the immunoglobulins (Ig) G, A and M, of specific anti-heart antibodies and of some non-organ-specific antibodies have been carried out in the venous blood of 15 patients with acute myocardial infarction (AMI), of 30 subjects with angina pectoris (AP) and of 30 controls. The occurrence of anti-smooth muscle and anti-nuclear antibodies resulted negligible in all subjects, while anti-mitochondrial antibodies were found in a relatively high percentage of cases, which is probably due to chance. Only in 13.3% of AMI patients, and in 16.7% of AP subject, were anti-heart antibodies detectable, and their presence was not related to the occurrence of Dressler's syndrome, nor to any clinical finding. The mean IgG curve in the AMI patients showed a triphasic time-course in the first 20 days of disease. In the AP patients an inverse correlation has been found between monthly frequencies of anginal attacks and serum concentrations of IgG (r = 0.382; p less than 0.05). In the control group serum IgA were directly correlated to age (r = 0.493; p less than 0.01); furthermore, in patients with exertional or mixed angina serum IgA were often higher than those of patients with only rest angina (x2 = 3.906; p less than 0.05). These data suggest the working hypothesis that a possible link (of secondary or primary type) between serum concentrations of IgA and severity of atherosclerosis may exist.

Aged↗
PubMed1981

[Markers of necrosis and anoxia in the post-infarct heart failure: determination of infarct size (author's transl)].

28 patients with acute myocardial infarct (AMI), 10 of whom presenting left ventricular failure, have been studied. By serial determinations of alpha-hydroxybutyrate dehydrogenase (HBDH) and creatine kinase (CK), the releasing times (RT) and the total releases (TR) of the two enzymes have been calculated, according to the Shell's method modified by Norris. The RT of HBDH have resulted more prolonged in the decompensated patients (48.1 +/- 16.0 vs 37.3 +/- 9.1 h; t = 2.297; p less 0.05). Highly significant correlations have been demonstrated between the total releases of the two enzymes; r = 0.816, p less than 0.01 (with failure); r = 0.766, p less than 0.001 (without failure). For neither enzyme, instead, significant differences have been shown between the TR of the two patient groups. The following conclusions can be drawn. 1) infarct size probably is not the only factor able to induce heart failure during AMI; 2) infarct size can be equally calculated from both HBDH or CK values, though some considerations may make preferable the choice of CK; 3) the more prolonged release of HBDH during heart failure suggests the hypothesis that lactate accumulation is an important factor influencing the appearance of this compliance.

Adult↗
PubMed1981

[Relationships between the initial area of necrosis and prognosis of acute myocardial infarct].

85 patients with acute myocardial infarction (AMI) have been studied retrospectively. 25 of them died within the 40th day after admission. Serum CK release during AMI can be described by the logistic equation: (formula: see text). We have evaluated for each patient both the final infarct size (calculated at the time of maximal enzyme activity: Tmax) and the initial one (calculated at the inflection time of the curve: Tflex). The total enzyme release in 1 ml of blood has been considered as an indirect index of infarct size. Our results show a good correlation between the initial and the final infarct size. We have considered as limits between survivors and non-survivors the following values: 2.2 IU/ml and 0.6 IU/ml for total CK release at Tmax and at Tflex respectively. The percentage of mortality in those groups is very similar (69% and 75%). However only 38% of non-survivors shows higher values than both 2.2 IU/ml and 0.6 IU/ml. The calculation of infarct size at Tflex allows an early identification of the high risk patients.

Clinical Enzyme Tests↗
PubMed1980

[Prediction of the infarct size by the serum levels of creatin kinase. A new methodological method (author's transl)].

Logistic equation is proposed as a new mathematical model describing the course of the ascending branch of the serum creatine kinase curve: E(t) = K divided by 1 + ea-bt where: E(t) = CK concentration at time t (mU/ml); t = time in hours from the onset of enzyme release; e = natural logarithm base; K = horizontal asymptote of the curve (maximal enzyme activity); a, b = typical variable prameters of the curve. Prediction is based on the identification of the infection point of the ascending branch of the serum CK curve. The enzyme activity corresponding to this point is half of the maximal one. In 14 patients with acute myocardial infarction infarct size (CK-g-Eq) was calculated by the method of Shell et al. In these patients the average differences between observed and predicted parameters were respectively (X +/- SD): -0.64 +/- 2.13 h for the maximal activity time; 16.57 +/- 53.15 mU/ml for the maximal activity and 0.02 +/- 2.44 CK-g-Eq for the infarct size. In detail it can be observed that the average of the per cent differences between observed and predicted infarct size was 1.10 +/- 5.31% and the maximal per cent difference only +10.40%.

Creatine Kinase↗
PubMedDate not supplied

Creatine kinase and myoglobin determination in myocardial infarction (determination of infant size).

In order to evaluate the diagnostic and prognostic importance of serum myoglobin (Mb) determination during acute myocardial infarction (AMI) we determined the time of first rise of both CK and Mb, that is the time in hours between the onset of pain and the last normal myoglobin and enzyme determination (TFR for Mb = 2.2 +/- 1.5 h; TFR for CK = 4.0 +/- 2.5 h). We also attempted to evaluate infarct size by mathematical analysis of the serum concentrations of Mb. The average percentage difference between the infarct size calculated from the CK concentrations and Mb concentrations was 35.8 +/- 35.2%. The results show that the determination of serum myoglobin is a useful and sensitive test for the early diagnosis of AML. On the other hand, the serum myoglobin cannot be utilized to evaluate infarct size. The main limitation in the determination of infarct size from the serum Mb concentrations lies in the extreme variability of the disappearance rate (Kd), mainly resulting from the renal elimination of the substance.

Clinical Enzyme Tests↗
PubMedDate not supplied

Coronary and cerebrovascular atherosclerosis: two aspects of the same disease or two different pathologies?

Cerebrovascular and coronary disease are characterized by some common aspects. Indeed the same risk factors relate to coronary heart disease and to cerebrovascular disease. However, there may be differences in the pathogenesis of atherosclerotic lesions in coronary and cerebral arteries. In fact some populations are characterized by a high incidence of ischaemic stroke and a low incidence of myocardial infarction, while in other populations there is an opposite trend. These differences could be explained on the basis of: genetic risk factors; a different prevalence of risk factors; a different reactivity of the coronary and cerebral arteries to risk factors; anatomical differences concerning coronary and extracranial cerebral arteries with respect to intracranial cerebral arteries. Atherosclerosis is undoubtedly a systemic disorder and its genetic and environmental causal factors are only partly known. The variable incidence of cerebrovascular and coronary heart disease in the same population or in different populations as well as the different nature of atherosclerotic plaques are probably related to the different prevalence of the causal factors, even though these may not always be identified.

Journal Article↗
PubMedDate not supplied

Serum IgA antibodies to apoproteins and milk-proteins in severe atherosclerosis.

Total serum IgA and IgA antibodies to some milk antigens are often associated with severe atherosclerosis. In the present study we examined the same serum samples to evaluate the possible involvement of serum IgA antibodies to apoproteins and lipoproteins and their relationship to IgA antibodies to milk antigens. We studied 23 subjects with angiographically assessed atherosclerotic lesions (ATS group) and 20 healthy control subjects with a similar age range (59-69 years) and sex distribution. Anti-ApoB, Apo A-I, Apo A-II and anti-LDL, VLDL and HDL antibodies were measured with the ELISA method. All antibodies tested except those to anti-Apo A-I were significantly higher in the ATS group with respect to controls with a maximum significance for anti-Apo B IgA (p = 0.0018). When, for each antibody, a threshold of positivity was set to the mean + 2 SD of values in the control group, 12 ATS subjects (52%) and 1 control (5%) were found to be positive for either anti-Apo B or anti-Apo A-II IgA. Most of the correlations of anti-apoprotein and anti-lipoprotein IgA with anti-milk protein IgA and total IgA were significant. The association of these antibodies with atherosclerosis might either be specific or represent part of a polyclonal IgA response. Whether this association is a cause or an effect of atherosclerotic disease is presently unknown.

Apoproteins↗