Determination of ochratoxin A in green coffee by immunoaffinity column cleanup and liquid chomatography: collaborative study.

A collaborative study was conducted to evaluate a method using immunoaffinity column cleanup with liquid chromatography (LC) for the determination of ochratoxin A (OTA) in green coffee at levels that could be included in possible future regulations of the European Union. The test portion was extracted with methanol-3% aqueous sodium hydrogen carbonate solution (50 + 50, v/v). The extract was filtered, and the filtrate was diluted with phosphate-buffered saline and applied to an immunoaffinity column containing antibodies specific for OTA. After washing, the toxin was eluted from the column with methanol and quantified by LC with fluorescence detection. Pairs of 4 homogeneous noncontaminated and naturally contaminated materials (mean levels of < 0.12, 2.44, 5.15, and 13.46 ng/g) and blank samples (< 0.12 ng/g) for spiking were sent to 20 participant laboratories from 8 countries. The materials were analyzed according to the method description and all difficulties encountered in the analysis were reported. Statistical analysis was carried out according to the Harmonized Protocol of the International Union of Pure and Applied Chemistry. The relative standard deviation for repeatability (RSDr) ranged from 7.42 to 20.94%, and the relative standard deviation for reproducibility (RSDR) ranged from 16.34 to 29.17%. The method showed acceptable within-laboratory and between-laboratories precision for green coffee materials, as evidenced by HorRat values of < or = 0.85, at the studied range, for spiked and naturally contaminated materials. The mean recovery was 92.8% for green coffee material spiked with OTA at a level of 4.82 ng/g.

[Myocardial hypertrophy and arterial hypertension]. / Ipertrofia miocardica ed ipertensione arteriosa.

Myocardial hypertrophy in different cardiac diseases is considered to be an adaptive mechanism to the increase of hemodynamic load which might restore to normal radius/wall thickness ratio and consequently to normalize wall stress. However, it has been widely demonstrated that beside the hemodynamic load, other factors contribute to the development of myocardial hypertrophy. It has been shown that in hypertensive patients, functional abnormalities (increased contribution of atrial systole to total diastolic filling, increased isovolumic relaxation period, prolonged diastolic duration, slowed ventricular filling and altered diastolic distensibility) precede the development of myocardial hypertrophy. Thus, in hypertensive patients, sign and symptoms of heart failure could be manifested in absence of myocardial hypertrophy, and might be exclusively due to diastolic dysfunction (with normal systolic function). Systolic function might be involved and compromised late when focal myocardial cell death and fibrosis occur and consequently ¿adequate¿ hypertrophy is shifted to ¿inadequate¿. This evolution is accompanied by morphological and functional changes of the myocardium similar to those encountered in dilated cardiomyopathy. Impairment of systolic function in ¿inadequate¿ hypertrophy is also due to structural changes; altered ratio between sarcomers and mitochondria, increased intercapillary distance, sarcoplasmatic reticulum dysfunction, increase of collagene component with a consequent increment of wall rigidity, hypertrophy of arterial tunica media, which alters coronary flow and coronary reserve. The progression of these morpho-functional abnormalities is a very slow process, in which adaptive mechanism mediated by several enzymes and contractile protein, contribute to maintain myocardial viability. However, over the long course, disseminated focal myocardial cell necrosis and fibrosis, which is an evolving process, is considered to be the main responsible factor for the irreversible myocardial damage and systolic dysfunction in advanced myocardial inadequate hypertrophy.

[Elements conditioning the severity of myocardial infarction damage]. / Elementi condizionanti la gravità del danno miocardico infartuale.

The severity of myocardial damage following acute myocardial infarction (AMI) is essentially influenced by the duration of coronary flow interruption during the acute episode. Furthermore the duration and severity of "culprit" lesion before AMI, as well as the presence of adequate collaterals to the culprit vessel represent important factors able to influence the severity of myocardial dysfunction after AMI. Left ventricular damage might evolve progressively depending on the infarct size, the presence of diffuse and severe coronary artery disease and concomitant systemic disease, such as diabetes and systemic hypertension. From a therapeutic point of view, in the presence of irreversible myocardial damage (scar tissue) following AMI medical therapy must be addressed to reduce myocardial consumption and to prevent ventricular dilatation. However myocardial dysfunction following AMI might be reversible (hibernated myocardium). It is of remarkable value the recognition of the hibernated but viable tissue because restoration of normal blood flow, which is the gold standard therapy in these patients, improves myocardial function and clinical outcome in AMI patients. In the presence of hibernated tissue following AMI, pharmacological therapy might temporarily protect the hibernated areas; however, when restoration of normal blood flow (myocardial revascularization) is not performed early, myocardial dysfunction might worsen and progressively evolve becoming irreversible event with restoration of normal coronary flow.

[Mechanisms of transluminal mechanical coronary recanalization]. / I meccanismi della ricanalizzazione coronarica meccanica transluminale.

Coronary angioplasty (PTCA) represents one of the most diffuse technique for myocardial revascularization in coronary artery disease patients. The principal mechanisms, responsible for the luminal increment after successful balloon dilatation are stretching of the vessel wall and splitting of the plaque and its rearrangement in an increased cross section of the vessel. Soon after balloon deflation elastic recoil of the vessel wall might occur at different grades which result in a partial loss of the result achieved by balloon PTCA. This phenomenon seems to be one of the major factors influencing the acute and long-term results of PTCA. Balloon inflation is also followed by endothelial denudation and intramural hemorrhage and intramural thrombus apposition. Then, a proliferative process takes place which is characterised by intimal and smooth muscle proliferation and migration. This process, beside the elastic recoil of the vessel wall, might also contribute to restenosis following balloon PTCA. Other devices for myocardial revascularization were introduced in the clinical practice based on different mechanisms from that of conventional PTCA. Transluminal atherectomy (directional, rotational and rotational-ablation) is based on the removal of plaque material from the vessel, increasing the lumen and creating a smooth surface. By this mechanism of action, plaque splitting and vessel wall stretching might be avoided, thus acute and long-term results are supposed to be improved as compared to balloon angioplasty. Another device for the removal of plaque material is represented by laser angioplasty which utilizes laser energy for the evaporation of the atherosclerotic material and the increase of vessel lumen without vessel wall stretching and plaque splitting.(ABSTRACT TRUNCATED AT 250 WORDS)

[Prevention of reinfarction: a global strategy]. / Prevenzione del reinfarto: strategia globale.

Reinfarction occurs in approximately 10-20% of patients with acute myocardial infarction with an year incidence of about 3% for males and 9% for females. The reinfarction induces a worsen prognosis by producing arrhythmias and a new ventricular "remodelling" with an increase in sudden death and cardiogenic shock. The new event may occur, early or later, in regions either adjacent to or remote from the initial myocardial infarction. Among all the patients admitted to our coronary care unit (1181) during the last 6 years, the overall reinfarction rate was 11.4%; among these, 46% were in the same side (SSMI), while 54% in the distant side (DSMI). The SSMI occurred more often during early months after infarction, while the DSMI occurred significantly later. Cigarettes smoking has been shown to be a common and often the only risk factor in patients with early reinfarction; while arterial hypertension, mostly associated with diabetes and hypercholesterolemia, was found the most important risk factor in later reinfarctions. SSMI was strongly related to one coronary vessel disease or to a double vessel disease (especially with interventricular artery and right coronary artery); while DSMI occurred in presence of triple coronary vessel disease involving secondary branches. The later SSMI is related to serious impairment of left ventricular function in 30% of patients, with cardiogenic shock and death evolution in 25%. The clinical trials for prevention of reinfarction showed that the correction of risk factors and the use of anticoagulation and/or antiaggregation therapy, beta-blockers or Ca(++)-antagonist drugs, must be chosen in relation to the myocardial damage related to previous infarct. In all the patients follow-up during the acute, subacute and chronic phases, must be performed by clinical and instrumental controls able to evidence the developing new cardiovascular events in order to decision making.