Ochratoxin A in cereal-based baby foods: occurrence and safety evaluation.

Ochratoxin A is a typical cereal contaminant with strong nephrotoxic activity. To estimate the quantity of ochratoxin A that can be taken in by a child in the weaning period, several samples of cereal-based baby foods were analysed. Although most samples analysed contained ochratoxin A in undetectable amounts or below the Italian legal limit of 0.5 microg kg(-1), some irregular products were found. In particular, the analyses of the 119 batches (338 samples) of baby foods considered indicated that: 20 batches (16.8%) contained detectable quantities of ochratoxin A and four of these (3.4% of the total) contained ochratoxin A above the Italian permitted value. All samples coming from agricultural practices based on integrated pest management contained undetectable amounts of ochratoxin A, while approximately 5% of batches coming from conventional and organic agricultural practices were above the legal limit. On the basis of the established provisional tolerable weekly intake (PTWI), there is no significant toxicological risk for a child who occasionally consumes a formula with ochratoxin concentration slightly above the permitted level. However, stricter controls have to be applied to reject the batches containing irregular concentrations of ochratoxin A.

Aortic intramural hematoma: an increasingly recognized aortic disease.

Aortic intramural hematoma (IMH) is a rarely diagnosed pathological condition that is not well characterized to date. We diagnosed IMH in 4 of 31 patients with suspected aortic dissection admitted to our coronary care unit from 1992 to 1995. In all 4 cases, IMH was located in the ascending aorta. At the time of hospitalization, all patients showed tachycardia, hypotension and pericardial effusion. Diagnosis of IMH was made by transesophageal echocardiography and computed tomography. We performed aortography in 2 patients, but it was non-diagnostic in both of them. One patient died before surgery. Autopsy confirmed the diagnosis of IMH and showed severe pericardial effusion. In another patient, the diagnosis was confirmed during successful surgery, while the remaining 2 patients recovered after medical therapy. The 3 surviving patients are still under follow-up control 12, 16 and 20 months after the initial acute event. We briefly discuss the epidemiological, clinical, diagnostic, therapeutic and prognostic aspects of IMH.

Threshold energy dose for enzyme release after direct-current countershock.

Serial measurement of serum total creatine kinase and creatine kinase MB isoenzyme was prospectively performed by photometric assay in 82 consecutive patients (55 male and 27 female; mean age 62 +/- 11 years) after elective DC countershock for atrial flutter or fibrillation. Enzyme release is commonly observed to follow DC shock; the related energy threshold for enzyme release, however, a parameter with potential clinical usefulness, has not yet been determined. The energy dose was individually titrated but the anterolateral paddle-electrode location was used in all cases. The mean +/- S.D. (range) of shock number, peak energy level and cumulative energy dose normalized to body weight were respectively: 1.7 +/- 0.9 (1-5), 228.6 +/- 87.6 (75-400) J and 5.26 +/- 3.74 (1.0-19.7) J/kg. All these parameters had highly significant positive correlation with enzyme release (P < 0.0001), which peaked 16 h after countershock. Only creatine kinase levels changed significantly vs. baseline (P < 0.0001). As evidenced by dose vs. effect scattergram, the energy threshold value for enzyme release was around 4 J/kg for creatine kinase and 6 J/kg for creatine kinase MB isoenzyme. These energy dose figures may provide clinical usefulness to avoid unnecessary muscle damage; moreover, they may be used as a reference when enzyme elevations interfere with the diagnosis of a concomitant ischemic acute myocardial infarction.

Do inotropic drugs always induce a positive lusitropic effect? A comparison between k-strophanthidin and dobutamine in patients with coronary artery disease.

The interaction between systolic and diastolic effects of inotropic drugs is an important subject which has not yet been fully clarified in the cardiological literature. The effects of the inotropic drugs k-strophanthidin and dobutamine on left ventricular (LV) relaxation and early filling phase were compared in patients with coronary artery disease (CAD) and preserved systolic function. Twenty-two patients were randomly divided into two groups; group I was infused with 0.0035 mg.kg-1 of k-strophanthidin for 10 min and group II with dobutamine at a rate of 10 micrograms.kg-1.min-1 for 10 min. Both groups underwent simultaneous haemodynamic and echo 2D-Doppler evaluations at controlled heart rate. K-strophanthidin improved contractility indexes (peak of LV systolic pressure P < 0.001, max dP/dt + P < 0.05 and dP/dt P < 0.01) and worsened T constant and LV lowest diastolic pressure, (LVLDP) (P < 0.001 and P < 0.05 respectively) without changing early transmitral filling parameters. Dobutamine induced a significant increase in contractility in group II but at the same time significantly improved LV relaxation variables (max dP/dt - P < 0.01 and T constant P < 0.001). In addition, dobutamine reduced LVLDP (P < 0.05) and significantly increased LV early filling parameters. These results show that an acute administration of either k-strophanthidin or dobutamine enhances contractility, whereas these drugs have the opposite effect on the early diastolic phase.

Double orifice in prolapsing mitral valve.

A prolapsing mitral valve with a double orifice ('hole type') was documented by echocardiography in a 35-year-old male. His symptoms were associated to supraventricular ectopic beats and persisted unchanged during a 3-year follow-up. This malformation is usually considered benign but, as fragmentation of the atrioventricular conduction tissue was reported in some cases, a periodic observation is advisable.

Effect of dobutamine on left ventricular relaxation and filling phase in patients with ischemic heart disease and preserved systolic function.

The beneficial effects of dobutamine on left ventricular systolic and diastolic phases have been described in patients with congestive heart failure. Its influence on left ventricular diastolic phase in patients with preserved systolic function, absence of dys- or akinetic areas, and left ventricular dilatation has not yet been adequately investigated. Thus a simultaneous echo-Doppler and hemodynamic study was performed in 15 patients with ischemic heart disease and preserved systolic function in order to assess the effect of dobutamine on left ventricular relaxation and filling phase. The infusion of dobutamine at a rate of 10 micrograms/kg/min induced a marked inotropic action, as shown by the significant increase in positive dP/dt (from 1392 +/- 224 to 2192 +/- 295 mmHg/sec, p < 0.001), dP/dt/P (from 32 +/- 8.1 to 50 +/- 17 sec-1; p < 0.0001), and in peak of systolic pressure (from 143 +/- 25 to 168 +/- 36 mmHg; p < 0.005). In addition, dobutamine reduced the end-systolic volume index (from 30 +/- 16 to 26 +/- 19 ml/m2; p < 0.05), the end-systolic stress (from 222.2 +/- 65.3 to 198.4 +/- 84 g/cm2; p < 0.006), and had favorable effects on relaxation and the early filling phase.(ABSTRACT TRUNCATED AT 250 WORDS)

[Chronic treatment of dilated cardiomyopathy by beta blocking agents. Clinical and hemodynamic follow-up]. / Trattamento cronico della cardiomiopatia dilatativa con betabloccanti. Controllo clinico ed emodinamico a distanza.

symptomatic dilated cardiomyopathy were studied in order to evaluate the effect of long term sympathetic beta-blockade with metoprolol. Clinical evaluation, stress test, two-dimensional echocardiography, 24 hour ambulatory electrocardiography and hemodynamic assessment with Swan-Ganz catheter were performed before enrollment in the study. Patients were randomly assigned to the relative placebo (8 pts) or metoprolol group (12 pts) in a single-blind fashion. The placebo group received standard therapy (digitalis, diuretics, vasodilators and anticoagulants as needed), while the metoprolol group, along with standard therapy received low-dose beta-blockade, starting with 6.25 mg twice daily and then doubling every 4 days on the two daily administrations. The therapeutic end-point was 100 mg. Patients received less than 100 mg if their systolic blood pressure was less than 100 mmHg or if their resting heart rate was less than 55 beats/min. Patients were clinically assessed every month and a 24-hour electrocardiography, echocardiography and hemodynamic control was repeated after six months. In the metoprolol group there was one sudden death and two drop-outs.(ABSTRACT TRUNCATED AT 250 WORDS)

[Early changes in ventricular function in diastolic phase in the resting coronary patient]. / Precoci alterazioni della funzione ventricolare in fase diastolica nel coronaropatico a riposo.

The aim of this study is to test left ventricular diastolic function in coronary artery disease patients with preserved systolic performance. Two groups of patients (25 coronary artery disease patients with angiographic proved coronary artery stenosis, but with normal hemodynamic and angiographic indices of systolic phase, first group; and 14 normal subjects for control, second group) were tested comparing their systolic and diastolic ventricular function indices, obtained by using a Millar microtip catheter and a computerized program. Systolic ventricular function was similar in the two groups (EF: 0.61 +/- 0.05 vs 0.62 +/- 0.03, p: n.s.; Vmax:120 +/- 28 vs 112 +/- 24 sec-1, p: n.s.), while diastolic indices were significantly different (lowest diastolic pressure: 3.7 +/- 2.4 vs -1.72 +/- 1.45 mmHg, p less than 0.01; end-diastolic pressure: 11.2 +/- 4.2 vs 6.5 +/- 2.8 mmHg, p less than 0.05; T constant: 45 +/- 8 vs 35 +/- 6 mmHg, p less than 0.001; end-diastolic compliance: 2.79 +/- 0.3 X 10(-2) vs 5.68 +/- 0.4 X 10(-2) mmHg-1, p less than 0.001; Kp: 0.041 +/- 0.006 vs 0.003 +/- 0.004 p less than 0.001). In conclusion, impairment of left ventricular diastolic phase may be one of the earliest manifestations of functional alterations of ischemic ventricle.

[Effect of propafenone on the pharmacokinetics of digoxin administered orally: a study in healthy volunteers]. / Influenza del propafenone sulla farmacocinetica della digossina somministrata per via orale: studio su volontari sani.

It is well known that many cardiovascular drugs affect digoxin kinetics, but nothing is defined on propafenone-digoxin interaction. To clarify this problem, we studied digoxin kinetics in 8 healthy men, who received digoxin oral dose (0.50 mg) in the control state and again during maintenance therapy with propafenone (150 mg q.i.d.). Statistically significant changes were observed during propafenone in a number of digoxin kinetic indexes: a rise in peak serum digoxin concentration (4.30 vs 3.07 ng/ml - p less than 0.005), in area under the serum-digoxin concentration curve (4 h: 520.4 vs 368.9; 10 h: 789.6 vs 621.3 ng X min/ml - p less than 0.005; 24 h: 1187.6 vs 954.7 ng X min/ml - p less than 0.05) and urinary excretion of digoxin (277.7 vs 203.5 mcg - p less than 0.005). Renal digoxin clearance was not affected by propafenone. We conclude that propafenone interact kinetically with digoxin in healthy subjects, perhaps increasing digoxin bioavailability.