Ettore Astorri

Fasting and post-methionine load homocyst(e)ine values are correlated with microalbuminuria and could contribute to worsening vascular damage in non-insulin-dependent diabetes mellitus patients

The study aim was to assess the relationship between homocyst(e)inemia and microalbuminuria in non-insulin-dependent diabetes mellitus (NIDDM) patients. The study was performed on 33 NIDDM patients (16 males and 17 females), and 16 healthy control subjects (seven males and nine females). Plasma fasting and post-methionine load homocyst(e)ine (tHcy), together with other parameters that could modify tHcy levels, were assessed. There were no significant differences between NIDDM patients and controls for fasting tHcy (8.12 +/- 3.17 v 7.19 +/- 2.40 micromol/L) and post-methionine load tHcy (26.51 +/- 11.50 v 25.06 +/- 10.76 micromol/L). Moreover, there was a significant correlation between urinary albumin excretion (UAE) and fasting tHcy (r = .340, P = .05) and post-methionine load tHcy (r = .502, P = .004) in NIDDM patients. Fasting tHcy was correlated both with post-methionine load tHcy (r = .429, P = .01) and with vitamin B12 (r = -.349, P = .04) in NIDDM patients. Microalbuminuric NIDDM patients had higher fasting tHcy (9.05 +/- 3.83 micromol/L) than normoalbuminurics (7.12 +/- 1.95 micromol/L). In addition, NIDDM patients with complications presented higher fasting tHcy values than the group without complications (9.61 +/- 3.34 v 6.53 +/- 2.09 micromol/L, Kolmogorov-Smirnov two-sample test for nonparametric data [KS] = 1.794, P = .003), without any other significant differences in the parameters considered. tHcy could be an important risk factor worsening the prognosis in NIDDM patients, especially microalbuminuric patients. Microalbuminuric NIDDM patients could be particularly prone to hyperhomocyst(e)inemia, probably due to endothelial or renal dysfunction with a reduction in the scavenging of tHcy.

Plasma homocysteine and folate are related to arterial blood pressure in type 2 diabetes mellitus

The aim of this study was to assess the relationship between homocysteine (tHcy), folate and vitamin B12 levels, urinary albumin excretion, and arterial blood pressure in patients with non-insulin-dependent diabetes mellitus (NIDDM). Our study was carried out in 33 NIDDM patients (16 men, 17 women) and 16 healthy volunteers as controls (seven men, nine women). Fasting and postmethionine load plasma tHcy levels were assessed, together with folate, vitamin B12, and urinary albumin excretion levels. In NIDDM patients, there were correlations between folate and mean arterial pressure (r = -0.352, P = .046), folate and systolic blood pressure (r = -0.437, P = .013), folate and vitamin B12 (r = 0.499, P = .004), tHcy and vitamin B12 (r = -0.348, P = .04), ln tHcy and ln folate (r = -0.404, P = .01), and, lastly, between tHcy, either fasting or postload, and urinary albumin excretion. Patients with elevated tHcy levels had significantly higher diastolic blood pressure (P = .04) and mean arterial pressure (P = .03). Otherwise, higher folate values were associated with lower systolic blood pressure (P = .004) and mean arterial pressure (P = .02). In addition, NIDDM patients with complications presented higher tHcy basal values than the group without complications (P = .003). A particular propensity of such patients towards endothelial dysfunction could explain the presence of correlations between these metabolic parameters and arterial blood pressure.

Left Ventricular Function in Insulin-Dependent and in Non-Insulin-Dependent Diabetic Patients: Radionuclide Assessment

The aim of this study was to compare, by gated radionuclide angiography, systolic and diastolic ventricular function in insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetic patients without overt cardiovascular disease. The study population consisted of 20 IDDM patients (15 male, 5 female; 40.7 +/- 10.3 years), 14 NIDDM patients (9 male, 5 female; 47.0 +/- 7.5 years) and 12 healthy subjects (7 male, 5 female; 41.5 +/- 6.3 years) as a control (C) group. The duration of diabetes (DD) and glycosylated hemoglobin (HbA1C) levels were significantly higher in the IDDM patients. The ventricular ejection fraction and peak ejection rate (PER) were assessed by gated radionuclide left ventriculography and were similar in three groups, while the peak filling rate (PFR) was lower in the NIDDM patients compared to the IDDM patients (p < 0.05) and controlled healthy subjects (p < 0.01, IDDM = 3.39 +/- 1.14; NIDDM = 2.65 +/- 0.83; C = 3.55 +/- 0.73), the time to PFR was significantly more prolonged in the NIDDM group than in the IDDM (p < 0.05) and C groups (p < 0.05, NIDDM = 162 +/- 26; IDDM = 140 +/- 28; C = 142 +/- 23). The PFR/PER ratio was near the normal value (approximately equal to 1) in the IDDM patients and controlled subjects, while in the NIDDM patients it was reduced (approximately equal to 0.84 +/- 0.18). Seven IDDM and 4 NIDDM patients had borderline signs of cardiovascular autonomic neuropathy, unrelated to DD, HbA1C and scintigraphic parameters. Left ventricular systolic performance was substantially normal and similar in both the IDDM and NIDDM patients. Ventricular diastolic filling was impaired in the NIDDM patients, as shown by the decrease in PFR and in particular in the PFR/PER ratio. Our radionuclide data suggest that the NIDDM patients had a prevalent abnormality of ventricular diastolic performance, with respect to the IDDM patients, although the latter patients had higher DD and HbA1C values.

Differential Structural Remodeling of the Left‐Atrial Posterior Wall in Patients Affected by Mitral Regurgitation with or Without Persistent Atrial Fibrillation: A Morphological and Molecular Study

Structural Remodeling in Atrial Fibrillation. Introduction: Atrial fibrillation (AF) in mitral regurgitation (MR) is a complex disease where multiple factors may induce left‐atrial structural remodeling (SR). We explored the differential SR of the left‐atrial posterior wall (LAPW) of patients affected by MR with or without persistent AF, and the expression of key proteins involved in its pathogenesis.

Circadian blood pressure and heart rate changes in patients in a persistent vegetative state after traumatic brain injury.

Alteration of autonomic nervous system regulation is known to be present in the persistent vegetative state after traumatic brain injury, termed the dysautonomic syndrome. This study assessed the circadian blood pressure and heart rate pattern and variability in the persistent vegetative state through noninvasive 24‐hour ambulatory blood pressure monitoring. The study was performed in 20 subjects: 10 patients (six men and four women; mean age, 29.5±9.9 years; range, 19–39 years) in a vegetative state (mean, 27.3±5.6 days after trauma) and 10 healthy subjects as controls (six men and four women; mean age, 28±5.7 years; range, 29–37 years). The patients showed a blood pressure nondipper pattern; 24‐hour, daytime, and nighttime values of blood pressure and heart rate were significantly higher in patients than in controls. The day‐night difference in heart rate and blood pressure was also significantly lower in patients. Finally, SD and variation coefficients were significantly lower in patients. The results show changes in the variability and circadian blood pressure and heart rate patterns in persistent vegetative state patients with dysautonomic syndrome, as an expression of the sympathetic‐parasympathetic activity imbalance in the control of vasomotor tone.

Heme oxygenase-1 expression in the left atrial myocardium of patients with chronic atrial fibrillation related to mitral valve disease: its regional relationship with structural remodeling.

Atrial fibrillation becomes a self-perpetuating arrhythmia as a consequence of electrophysiologic and structural remodeling involving the atrium. Oxidative stress may be a link between this rhythm disturbance and electrophysiologic remodeling. The aim of this study was to evaluate whether the heme oxygenase-1 (HO-1) marker of oxidative stress was more expressed in left atrial sites with stronger structural remodeling in patients affected by chronic atrial fibrillation (CAF) and mitral valve disease (MD). Myocardial samples were taken from the left atrial posterior wall (LAPW) and left atrial appendage (LAA) of 24 patients with CAF-MD in addition to 10 autopsy controls. The levels of HO-1 messenger RNA (mRNA) and HO-1 protein in each pathologic LAPW and LAA were quantified using reverse transcriptase polymerase chain reaction and enzyme-linked immunosorbent assay. Furthermore, light microscopy was used to morphometrically evaluate the differential myocyte and interstitial changes in the same CAF-MD LAPW and LAA samples. In controls, HO-1 protein was quantified using enzyme-linked immunosorbent assay. Unlike controls, patients with CAF-MD had higher levels of HO-1 mRNA and its protein product, expressed as LAPW/LAA ratios, in the LAPW (2.18 +/- 1.18, P < .0001, and 1.55 +/- 0.67, P < .005), and their LAPW also showed greater histologic changes in myocytolytic myocytes (15.1% +/- 3.1% versus 6.9% +/- 3.3%, P < .0001), interstitial fibrosis (8.2% +/- 2.2% versus 2.8% +/- 1.2%, P < .0001), and capillary density (816 +/- 120 number/mm(2) versus 1114 +/- 188 number/mm(2); P < .05). In addition, markers of oxidative stress were immunohistochemically studied with antinitrotyrosine and anti-iNOS antibodies. In patients with CAF-MD, the inducible enzyme HO-1 is more expressed in the left atrial areas that show greater structural remodeling. This finding strongly suggests a pathogenetic relationship between oxidative stress and the degree of histologic change.

Soluble antiapoptotic molecules and immune activation in chronic heart failure and unstable angina pectoris.

Programmed myocyte cell death and activation of the immune system have been shown to occur in patients with congestive heart failure. Besides, unstable angina episodes are likely to be associated with immune activation. Our aim was to evaluate the role of changes in circulating levels of soluble Fas (sFas), suggestive of an enhanced inhibitory response to ongoing apoptosis, and soluble IL2 receptor (sIL2-R), indicative of T-lymphocyte activation, in chronic heart failure and unstable angina pectoris. Thirty patients affected by chronic heart failure (20 idiopathic and 10 ischemic cardiomyopathy) and 13 patients with unstable angina were evaluated. Twenty healthy individuals matched for age and gender were used as controls. A complete biochemical determination of indexes of myocardial damage including cardiac troponin I (cTnI) and creatine kinase (MB/CK) was performed. The results demonstrated that mean levels of sFas and sIL2-R were significantly increased in patients affected by chronic heart failure and unstable angina and were not associated with changes in renal function or with serum levels of cTnI. Highest values of sFas were found in NYHA class IV patients (IV NYHA class = 7.39 ± 0.52 vs. controls = 1.34 ± 0.12 ng/ml; P < 0.01) and more elevated in idiopathic than in ischemic cardiomyopathy (3.64 ± 0.40 vs. 1.82 ± 0.37 ng/ml; P < 0.01). Moreover, in chronic heart failure patients sFas and ejection fraction were negatively correlated (P = 0.01), whereas sFas and sIL2-R were positively correlated (P < 0.01). In unstable angina patients too, sFas and sIL2-R appeared to be correlated (P = 0.03); whereas sFas (angina group = 3.18 ± 0.39 vs. controls = 1.34 ± 0.12 ng/ml; P < 0.01) and sIL2-R (angina group = 0.46 ± 0.11 vs. controls = 0.00 UI/ml; P < 0.01) were higher in angina group than in controls. In most of the cases, the increase of sFas was associated with comparable changes in sIL2-R serum levels, indicating that the activation of Fas system is strictly associated with autoimmune–inflammatory reactions. This phenomenon, both in chronic heart failure and in unstable angina, occurs in the absence of biochemical evidences of myocardial damage and seems to parallel the activation of T cell. Soluble Fas could have a role in sustaining inflammatory response and in prolonging the detrimental effects correlated with it in chronic heart failure and angina pectoris.

ECG mimicking acute myocardial infarction during heart involvement by lung neoplasm

Electrocardiographic abnormalities are common with tumor invasion of the heart. Pronounced lateral ST segment elevation in the absence of myocardial infarction occurred in a patient with epidermoid carcinoma of the left lung. Tomography showed the presence of tumor invasion of the heart. Prolonged ST segment elevation without Q waves seems to be a sign for tumor invasion of the heart.

Diastolic impairment in asymptomatic systemic lupus erythematosus patients.

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Myocardial indium- 111 antimyosin uptake after uncomplicated coronary artery bypass surgery

The prevalence of myocardial damage after coronary artery bypass grafting is related to the criteria of its evaluation. Indium-111 monoclonal antimyosin antibody scintigraphy has been shown to be highly sensitive and specific for even small areas of myocardial necrosis or injury like those of myocarditis or transplant rejection. Our purpose was to evaluate, by using this method, myocardial damage after uncomplicated coronary artery bypass grafting. Uptake of this radio tracer was evaluated after coronary artery bypass grafting in 14 informed and consenting consecutive patients without previous myocardial infarction, with no post-surgical complications and a favorable postoperative course, following coronary artery bypass grafting for stable angina pectoris. Monoclonal antimyosin antibody indium-111 74 MBq (Myoscint Centocor) was injected on the third postoperative day; planar images in the anterior, left anterior oblique 45 degrees and 70 degrees projections were obtained 24 and 48 h later and analyzed for myocardial uptake. Indium-111 antimyosin uptake was present in 10 out of 14 patients (71.4%); it was diffuse in 6 and localized in 4. The ratio of the maximal counts in the myocardium to the counts in the adjacent lung background was measured and found elevated: 1.94 +/- 0.23, higher than the normal values reported in the literature. Indium-111 antimyosin uptake was clear in a group of patients after uncomplicated coronary artery bypass grafting. No correlation was observed between indium-111 antimyosin uptake or heart to lung ratio and creatine kinase, creatine kinase isoenzyme MB, glutamic oxalacetic transferase levels, duration of cardiopulmonary bypass or aortic cross-clamp time, while elevated serum beta myosin heavy chain fragments (IRMA Pasteur) were observed (1378 +/- 238 microU/l). This study suggests that some degree of myocardial damage, though silent, is common after coronary artery bypass grafting.