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M Triggiani

Publications and source records attributed to M Triggiani.

At least 55 records · Page 3Linked to original sources
PubMed1996

[Emergency surgical revascularization in acute myocardial infarct. The preliminary results of a prospective study].

In this paper we describe 1-year experience with a perspective operative protocol of emergency myocardial revascularization in extensive acute myocardial infarction (AMI). Entry criteria were: age < 75 years; anterior AMI with ST segment elevation > 4 leads, infero-postero-lateral or inferior and right ventricular AMI, within 6 hours from symptom onset. After coronary arteriography, an emergency staff, composed by cardiologists and cardiac surgeons, addresses the patients to coronary artery bypass grafting (CABG) or to percutaneous transluminal coronary angioplasty (PTCA). From November 1994 to November 1995, 35 patients were enrolled: 19 (mean age 54.3 +/- 9.7 years) underwent CABG and 16 were treated with PTCA. Myocardial protection was such as to restore energetic substrates and to prevent reperfusion injury: surgical technique consisted of antegrade-retrograde substrate-enriched blood cardioplegic solution delivery, early cardioplegic delivery on the infarcting area via a saphenous graft, retrograde controlled reperfusion before aortic unclamping and then prolonged reperfusion of the infarcted myocardium. In 8 patients (mean age 50.9 +/- 8.6 years), with anterior AMI and stable hemodynamics, a left internal thoracic artery graft was used, performing the prolonged controlled reperfusion retrogradely before aortic unclamping. In hospital death occurred in 1/19 (5.3%) patients because of cerebral hemorrhage. At a mean follow-up of 5.1 +/- 3.7 months 17 patients (94.4%) were in NYHA functional class I-II and 1 patient (5.6%) complained of effort angina, that was well controlled with medical therapy. Left ventricular ejection fraction calculated by echocardiography preoperatively, before discharge and at follow-up was respectively 39.3 +/- 12.7, 43.1 +/- 8.9 and 43.4 +/- 9.0%. In the last 8 consecutive patients thermodilution and transesophageal echocardiography monitoring were performed preoperatively and 12 hours after CABG: in all cases ejection fraction and cardiac index increased after CABG, from 42.2 +/- 13.5 to 48.6 +/- 14.3% (p = 0.01) and from 2.8 +/- 0.5 to 3.4 +/- 0.6 l/min/m2 (p = 0.005), respectively. The preliminary results show the effectiveness of this perspective protocol in the management of critically ill patients with extensive AMI.

Clinical Protocols↗
PubMed1995

Migration of human inflammatory cells into the lung results in the remodeling of arachidonic acid into a triglyceride pool.

Increasing evidence suggests that the metabolism of arachidonic acid (AA) may be different in inflammatory cells isolated from blood or migrating into tissues. To explore the possibility that changes in AA metabolism between blood and tissue inflammatory cells could be due in part to a different content or distribution of AA in glycerolipid classes, we studied these parameters in six human inflammatory cells isolated from blood (eosinophils, monocytes, neutrophils, and platelets) or from the lung tissue (mast cells and macrophages). Lung cells generally had a higher total cellular content of AA than that found in the blood cells. In addition, both mast cells and macrophages had a large endogenous pool of AA associated with triglycerides (TG), containing 45 and 22% of their total cellular AA, respectively. To address the hypothesis that cells migrating into the lung had a higher cellular level of AA and a larger AA pool in TG, we studied neutrophils isolated from the bronchoalveolar lavage (BAL) of patients with adult respiratory distress syndrome. BAL neutrophils had a fourfold increase in cellular AA as compared with blood neutrophils and contained 25% of their AA in TG versus 3% in blood neutrophils. BAL neutrophils also had a higher number of cytoplasmic lipid bodies (8 +/- 3/cell) relative to blood neutrophils (2 +/- 1/cell). High concentrations of free AA were also found in the cell-free BAL fluid of adult respiratory distress syndrome patients. To explore whether changes in BAL neutrophils may be due to the exposure of the cells to high concentrations of exogenous AA found in BAL, we incubated blood neutrophils in culture with AA (10-100 microM) for 24 h. Neutrophils supplemented with AA had a 10-fold increase in the amount of AA associated with TG and a sixfold increase in the number of lipid bodies. In addition, supplementation with AA induced a dose-dependent formation of hypodense cells. Taken together, these data indicate that human inflammatory cells undergo a fundamental and consistent remodeling of AA pools as they mature or enter the lung from the blood. These biochemical and morphological changes can be mimicked in vitro by exposing the cells to high levels of AA. This mechanism may be responsible for the changes in AA mobilization and eicosanoid metabolism observed in tissue inflammatory cells.

Adult↗
PubMed1995

Clinical advances in mastocytosis.

Mastocytosis is a disease characterized by an abnormal proliferation of tissue mast cells. The events primarily responsible for mast cell proliferation in mastocytosis are largely unknown, but a derangement of the network involving c-kit receptor and its natural ligand (stem cell factor, which promotes mast cell growth and differentiation in man) is likely to have a primary role in this disease. Mastocytosis comprises a wide spectrum of clinical conditions determined by the degree of mast cell proliferation, the organ systems involved, the age at onset and the association with hematologic diseases. Mastocytosis can occur in a pediatric or an adult form. In both groups of patients, the disease may be limited to the skin (cutaneous mastocytosis) or be systemic, involving predominantly the bone marrow and the gastrointestinal tract. The symptoms in patients with mastocytosis are generally related to the increased release of mast-cell-derived mediators, such as histamine, prostaglandin D2, peptide leukotrienes, platelet-activating factor, heparin and proteolytic enzymes. The measurement of these chemical mediators (histamine, tryptase and prostaglandin D2 and their metabolites) in body fluids is useful for the diagnosis and the laboratory evaluation of patients with systemic mastocytosis. As little is known about the pathogenesis of the different forms of mastocytosis, the treatment of the majority of these patients is largely symptomatic.

Humans↗
PubMed1995

Oxidative structural modifications of low density lipoprotein in homozygous familial hypercholesterolemia.

Patients with homozygous familial hypercholesterolemia (FH), as a result of the increased levels and prolonged residence time of low density lipoprotein (LDL) in plasma, have a strong tendency toward accumulation of LDL-cholesterol in the arterial wall, causing premature atherosclerosis. This phenomenon may enhance per se the physiological degradation of both protein and lipid component of LDL, which be more susceptible to oxidative damage induced by oxygen radicals. It is well known that LDL may undergo oxidative modification before being taken up by macrophages which are then transformed into foam cells. It has been suggested that platelet-activating factor (PAF) may play an important role in atherogenesis and PAF catabolism is known to be mediated by serum acetylhydrolase, an enzyme that is normally associated with LDL. Thus, the present study was designed to investigate the structural properties of LDL, including acetylhydrolase activity, in homozygous FH as compared to normolipidemic subjects before and after xanthine/xanthine oxidase-mediated oxidation. We studied 8 homozygous FH patients matched with 8 normolipidemic volunteers. Lipids of LDL fraction were extracted and verified by thin layer chromatography (TLC) analysis. Fatty acids were methylated and injected into a gas chromatograph/mass spectrometer. Vitamin E in LDL was determined by high performance liquid chromatography (HPLC). As an index of susceptibility of LDL to oxidative modifications, the formation of lipid-conjugated dienes was continuously monitored at 234 nm. Lipid peroxidation was also evaluated from the amount of both lipid peroxides (LPO) and malonyldialdehyde (MDA) content. Apolipoprotein (apo) B-100 on LDL was carried on polyacrylamide and agarose gel electrophoresis. In the homozygous FH patients, the relative content of cholesteryl ester was slightly increased. Interestingly, the relative amount of arachidonic acid (20:4) was constantly increased in each lipid fraction in homozygous FH patients. The amount of vitamin E was not significantly different in the patient group from that in the control group. However, LDL from patients carried lower levels of vitamin E (nmol/mg LDL) than controls (2.7 +/- 0.4 vs. 2.9 +/- 0.3 P = NS). The results shows that lag time (min) was decreased (82 +/- 19 vs. 111 +/- 21; P < 0.05) and the maximal rate of diene production and total diene production was increased in homozygous FH patients. Mean levels of MDA were similar in both groups before oxidation, but levels after initiation of oxidation were significantly higher in the patient group. In contrast, mean levels of LPO were already higher in patients before oxidation (58 vs. 27 nmol/mg of protein; P < 0.05), and after initiation of oxidation were also significantly higher at each time points. When oxidized LDL was run on a polyacrylamide gel, an extensive apo B-100 fragmentation replaced by lower molecular mass fragments ranging from 45,000 to 205,000 m.wt., was observed only in LDL from homozygotes. Relative LDL agarose gel mobility shows that LDL from patients migrated higher than LDL of controls. Finally acetylhydrolase activity associated with LDL in patients was significantly reduced as compared to controls. Thus, in homozygous FH patients, LDL appeared more susceptible to oxidation in vitro; the indices for LDL oxidizability were all significantly different from those of controls. This phenomenon might be due to prolonged residence time of LDL in these patients, as suggested from high basal LPO levels and lower vitamin E levels carried by LDL. This hypothesis may explain together with the high content of arachidonic acid, the enhanced susceptibility of LDL from homozygous FH patients to oxidative damage.

Apolipoprotein B-100↗
PubMed1995

Warm heart surgery in cold haemagglutinin disease.

Continuous warm retrograde blood cardioplegia and systemic normothermia are a promising method for heart surgery in patients with cold autoimmune disorders in order to avoid the adverse effects of both systemic and coronary hypothermia during cardiac arrest and cardiopulmonary bypass. A 59-year-old white man with cold haemagglutinin disease who underwent coronary surgery using continuous retrograde normothermic blood cardioplegia and systemic normothermia is reported.

Anemia, Hemolytic, Autoimmune↗
PubMed1995

Advantages of delayed sternal closure in cardiac-compromised adult patients.

Severe hemodynamic dysfunction may follow closure of the median sternotomy in patients with myocardial edema, cardiac dilatation, postcardiotomy shock, or raised end-expiratory alveolar pressure. Open sternotomy and delayed sternal closure (DSC) is a well described adjunct in complicated cardiac operations, which is more widely applied in neonates. In this article we report our results in using open sternotomy in eight adult patients from January 1994 to February 1995 (excluding patients who needed ventricular assistance devices [VADs]). Three patients died in hospital: 1 case of multiorgan failure; 1 cases of refractory low cardiac output syndrome; and 1 case of respiratory distress syndrome. Our experience confirms that DSC is an effective means of dealing with postoperative hemodynamic impairment. Furthermore, this technique may represent an intermediate step between intraaortic balloon counterpulsation and VADs and should be given a role in the prophylaxis of low postoperative cardiac output and multiorgan failure, particularly when contraindications to VAD exist.

Aged↗
PubMed1994

Differential roles for triglyceride and phospholipid pools of arachidonic acid in human lung macrophages.

Arachidonic acid (AA) incorporation into and release from cellular glycerolipids are thought to be crucial events for the regulation of eicosanoid biosynthesis in inflammatory cells. The goal of our study was to determine the distribution of AA in the lipid pools of human lung macrophages (HLM) isolated from human lung parenchyma and to define the changes in AA pools occurring during cell activation. Mass spectrometry analysis indicated that the major pools of AA in HLM were located in phosphatidylethanolamine (PE), phosphatidylcholine (PC), and triglycerides (TG), and, to a lesser extent, in phosphatidylinositol/phosphatidylserine (PI/PS) and in a phospholipid similar to bis-(monoacylglyceryl)-phosphate (BMP). Exogenous AA was initially incorporated into TG and subsequently distributed within phospholipids. After 24 h of labeling, the distribution of exogenous AA in glycerolipid classes closely mimicked that of endogenous AA. Under these equilibrium conditions, HLM released 18.7 and 20.2% of cellular AA when stimulated with TPA or A23187, respectively. Free AA was the major product released by TPA- or A23187-stimulated HLM. However, A23187 but not TPA also induced the formation of leukotriene B4 and 5-HETE. AA was released from PC > PI/PS > or = PE > BMP. In contrast to phospholipids, the amount of AA in TG increased 15 to 90 min after cell activation and returned to prestimulation levels after 180 min. These data indicate that AA is stored in several glycerolipid pools of HLM. Among these pools, BMP is unique of macrophages and TG are particularly enriched in AA in HLM. During the early stage of cell activation, phospholipids act as a source of AA, whereas TG function as a reacylation pool for AA released from phospholipids. These data indicate that TG and phospholipid pools have a differential role in the control of free AA levels generated during HLM activation.

Arachidonic Acid↗
PubMed1994

Oxygen radicals inhibit human plasma acetylhydrolase, the enzyme that catabolizes platelet-activating factor.

Platelet-activating factor (PAF) can exert profound inflammatory effects at very low concentrations. In plasma, PAF is hydrolyzed to lyso-PAF by acetylhydrolase, an enzyme that circulates bound to LDL. Previous studies suggest that oxygen radicals may act synergistically with PAF to potentiate tissue injury. However, mechanisms underlying this interaction have not been elucidated. In this study we investigated whether oxygen radicals may inactivate PAF acetylhydrolase. PAF acetylhydrolase activity was measured in human plasma and purified LDL before and after exposure to radicals (10-20 nmol/min per ml) generated by xanthine/xanthine oxidase. Oxygen radicals induced > 50% loss of PAF acetylhydrolase activity within 60 s and almost complete inactivation by 10 min. This phenomenon was irreversible and independent of oxidative modification of LDL. Inactivation occurred without changes in the affinity constant of the enzyme (Km was 17.9 microM under control conditions and 15.1 microM after exposure to oxygen radicals). Inactivation was prevented by the scavengers superoxide dismutase or dimethylthiourea or by the iron chelator deferoxamine. Thus, superoxide-mediated, iron-catalyzed formation of hydroxyl radicals can rapidly and irreversibly inactivate PAF acetylhydrolase. Since concomitant production of PAF and oxygen radicals can occur in various forms of tissue injury, inactivation of acetylhydrolase might represent one mechanism by which oxygen radicals may potentiate and prolong the proinflammatory effects of PAF.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1994

Assisted circulation in postcardiotomy heart failure: experience with the Bio-Medicus centrifugal pump in ten patients.

Between January 1990 and September 1992, ten patients required assisted circulation for postcardiotomy heart failure which was unresponsive to inotropic drugs and aortic counterpulsation. All patients were supported by a Bio-Medicus centrifugal pump (biventricular assist in five, left ventricular in three, right ventricular in two); six had ischaemic heart disease, two a congenital ventricular septal defect, one an acute mitral valve incompetence and one an aortic type 'A' dissection. The mean duration of circulatory support was 5.1 days (range 2 hours to 8 days). Six patients were weaned from the device and four were discharged; the perioperative deaths among the patients weaned from support were the result of cerebral haemorrhage and multiorgan failure respectively. No late deaths occurred at a mean follow-up of 15 months. Common complications were bleeding (40%), acute renal failure (30%) and sepsis (30%). All patients who developed renal failure died. The high incidence of haemorrhagic complications makes the use of pre-heparinized circuits desirable as these patients do not then require additional anticoagulation.

Acute Kidney Injury↗
PubMed1994

Measurement of cardiac troponin T and myosin to detect perioperative myocardial damage during coronary surgery.

This study evaluated the use of monitoring blood levels of the isoenzyme of creatine phosphokinase, troponin T (tnT) and myosin in the detection of perioperative myocardial damage after coronary artery surgery. Serial blood samples were collected in 24 patients undergoing myocardial revascularization. The patients were retrospectively divided into three groups: group A with no changes in their electrocardiogram; group B showing non-specific signs of perioperative myocardial infarction such as deep and permanent T wave inversion; and group C with definite electrocardiographic signs of perioperative myocardial infarction (new persistent Q-waves and loss of R-waves). Group A (n = 17) demonstrated a mean(s.d.) troponin T peak blood level of 0.64(0.35) ng/ml at 12-24 h after surgery, a myosin peak of 1030(670) mu units/l at 3-6 days afterwards, and a creatine phosphokinase isoenzyme peak of 25.8(10.6) units/l. In group B (n = 5), mean(s.d.) troponin T levels were elevated to a peak of 4.8(3.9) ng/ml 24 h after intervention, while myosin rose to 2074(340) mu units/l 3-6 days after surgery and creatine phosphokinase isoenzyme reached 57.8(38) units/l. Group C (n = 2) had a mean(s.d.) troponin T peak of 4.8(2.6) ng/ml, a myosin peak of 2404(392) mu unit/l and a creatine phosphokinase isoenzyme peak of 88.5(20) units/l. Peak values of troponin T and myosin in groups B and C were statistically different from those in group A (P < 0.001). These results suggest that troponin T and myosin are reliable indicators of perioperative myocardial damage. In particular, troponin T may allow the differentiation of reversible from irreversible myocardial injury.

Biomarkers↗
PubMed1994

Rest and exercise hemodynamics of stentless porcine bioprostheses in aortic position.

Mechanical and conventional stented bioprostheses, because of need for anticoagulants, hemodynamic characteristics and long-term durability, do not represent the optimal heart valve replacement device. In this study we compared the hemodynamic function of a stented aortic bioprosthesis (St Jude Bioimplant), implanted in 10 patients, with a stentless porcine aortic bioprosthesis (Biocor) implanted in 7 patients, by means of Doppler echocardiography early postoperative at rest (T1) and 6 months later at rest (T2a) and during exercise (T2b). Mean and peak systolic gradients across stentless porcine prostheses were significantly lower than across stented bioprostheses (T1 p = 0.008 and p = 0.004; T2a p < 0.0001 and p < 0.0001; T2b p < 0.0001 and p < 0.0001, respectively). Our results show that systolic and diastolic mechanical stress on biological components of a glutaraldehyde-fixed stentless porcine aortic bioprosthesis is much lesser than on stented bioprostheses. This feature has appeared evident at rest and much more after exercise testing. The reduction of systolic and diastolic stress is expected to determine lower calcification degree and longer durability of stentless porcine aortic bioprostheses. Moreover, aortic valve replacement by means of stentless bioprostheses allows the implantation of a 1 size (2 mm) larger device, appearing favourable especially in small aortic annulus. On the basis of these promising results we suggest that stentless bioprostheses are a valid alternative to stented bioprostheses for aortic valve replacement. However, patient population is too small and the follow-up is too short to draw a definite statement about long-term hemodynamic performance of this device.

Aged↗
PubMed1994

[Myocardial revascularization in patients with impaired left ventricular function].

From March 1988 to May 1993, 1,125 patients with coronary artery disease (CAD) underwent coronary surgery at our Institute. In the same period 74 patients (mean age 59 +/- 7 years; range 36-73) with left ventricular dysfunction (LVD) were referred for surgical decision making. All patients underwent [99mTc]MIBI/SPET to assess perfusion at rest and [99mTc]MIBI first pass radionuclide angiography to assess the ejection fraction (EF). In 44/74 patients we performed [18F]FDG/PET in fasting conditions and pharmacologic wash-out, in order to identify viable myocardium. We divided patients with LVD into 3 groups: Group A (30 patients) operated on without preoperative [18F]FDG/PET, Group B (37 patients) operated on with FDG uptake in segments with wall motion abnormalities, and Group C (7 patients) with no FDG uptake, who were excluded from coronary surgery; there was no significant difference among the 3 groups with respect to age, sex, CAD, risk factors and EF (Group A: 29.1% +/- 6.6%, range 16-39%; Group B: 30.8 +/- 5.6%, range 20-40%; Group C: 26.5 +/- 6.8%, range 18-37%). The study of perfusion and EF was repeated 6 months postoperatively in Group A and B. Left ventricular end-dyastolic pressure at cardiac catheterization was 19.9 +/- 5.1 mmHg, 20.4 +/- 4.7 mmHg and 26.8 +/- 9.2 mmHg in Group A, B and C, respectively. Myocardial protection was achieved according to the Buckberg protocol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗