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Biomedical subjects

F Pileggi

Publications and source records attributed to F Pileggi.

At least 19 recordsLinked to original sources
PubMed2000

Hormonal and cardiovascular reflex assessment in a female patient with pure autonomic failure.

We report the case of a 72-year-old female with pure autonomic failure, a rare entity, whose diagnosis of autonomic dysfunction was determined with a series of complementary tests. For approximately 2 years, the patient has been experiencing dizziness and a tendency to fall, a significant weight loss, generalized weakness, dysphagia, intestinal constipation, blurred vision, dry mouth, and changes in her voice. She underwent clinical assessment and laboratory tests (biochemical tests, chest X-ray, digestive endoscopy, colonoscopy, chest computed tomography, abdomen and pelvis computed tomography, abdominal ultrasound, and ambulatory blood pressure monitoring). Measurements of catecholamine and plasmatic renin activity were performed at rest and after physical exercise. Finally the patient underwent physiological and pharmacological autonomic tests that better diagnosed dysautonomia.

Aged↗
PubMed1999

The effect of red wine on experimental atherosclerosis: lipid-independent protection.

To assess the effect of red wine on atherosclerosis, New Zealand rabbits were given 1% cholesterol diet for 12 weeks and compared to animals that received the diet plus either red wine or nonalcoholic wine products (NAWP). Diet induced marked increases in total and LDL cholesterol; yet no significant changes in HDL and triglyceride concentrations occurred. In the control group, plaque area was 69 +/- 9% of the aortic surface, while in the wine and NAWP groups it was only 38 +/- 9 and 47 +/- 12%, respectively (P < 0.0001). The average intima/media thickness ratio was 0.60 +/- 0.2 in control animals, 0.14 +/- 0.09 in the wine group, and 0.39 +/- 0.19 in the NAWP group (P < 0.0001). No significant differences were noted in LDL oxidizability among treatments. Thus, both red wine and NAWP can prevent plaque formation in hypercholesterolemic rabbits despite significant increases in LDL. We speculate that anti-platelet effect, blockade of expression of endothelial cell adhesion molecules, and/or NO stimulation by red wine flavonoids are possible explanations.

Animals↗
PubMed1999

Coronary artery bypass graft surgery in patients with ischemic cardiomyopathy and severe left ventricular dysfunction: short and long-term results.

BACKGROUND: We evaluated the prognostic value of preoperative parameters, surgical risk, functional benefits and long-term survival after myocardial revascularization in patients with established ischemic cardiomyopathy. METHODS: Seventy-one patients with ischemic cardiomyopathy, severe left ventricular dysfunction (left ventricular ejection fraction < 30%), and myocardial perfusion evaluated by Thallium-201 scintigraphy, were studied before and after myocardial revascularization, during hospitalization and throughout 48 months (average) of late follow-up. RESULTS: The early postoperative mortality was 2.8% and the five-year survival rate was 62.8%. When the survival rate was studied, there was no correlation with 1) the presence of Q-waves on preoperative cardiogram, 2) the presence of ischemia on Tl-201 scintigraphy, 3) the degree of left ventricular ejection fraction, or 4) the presence of angina. There was a statistically significant difference for survivors and non-survivors in the following parameters: 1) functional class IV of CHF, and 2) the presence of left bundle-branch block (LBBB). CONCLUSIONS: Our surgical results confirm that myocardial revascularization is a safe procedure, and that it increases late survival and improves the quality of life in patients with ischemic cardiomyopathy and severe left ventricular dysfunction. We also observed that due to heterogeneous coronary and myocardial patterns of ischemic cardiomyopathy, preoperative prognostic parameters are difficult to establish. Preoperative functional class IV congestive heart failure, and LBBB were the main predictors of poor outcome following surgical revascularization for ischemic cardiomyopathy.

Aged↗
PubMed1998

Oxidized thiols markedly amplify the vascular response to balloon injury in rabbits through a redox active metal-dependent pathway.

OBJECTIVE: Our aim was to assess whether exposure to oxidized thiols--a known usual consequence of oxidant stress--has the potential to affect the vascular repair response to angioplasty-induced injury. In addition, we also assessed the role of redox active metals in disulfide effects. METHODS: In 82 rabbits submitted to overdistention of iliac arteries, the following variables were analyzed: neointimal thickening, immunoreactivity to Proliferating Cell Nuclear Antigen, and cellular and collagen densities. RESULTS: A single intraarterial challenge of oxidized glutathione (GSSG, 6.5 mumol/kg) during and immediately after injury triggered a marked increase of the vascular repair reaction, as follows: (A) at day 7 after injury, there was a 2.7-fold increase in proliferation (p < 0.001 vs. control); (B) at day 14, there was increase of intimal/medial area ratio to 1.35 +/- 0.14, vs. 0.56 +/- 0.08 in controls. Proliferating cells increased to 5.5 +/- 0.8 cells/mm2, vs. 2.2 +/- 0.5 in controls (p < 0.002 for both variables). Overall cellularity was enhanced 2.2-fold; (C) at day 28, there was ongoing vessel wall proliferation, contrarily to controls. All GSSG effects were completely prevented by co-infusion of reduced glutathione (GSH) and were mimicked by cystine (6.5 mumol/kg). The uninjured artery showed no response to disulfides. To assess the role of redox active metals in GSSG action, the effects of 1,10-phenanthroline or N-CBZ-Pro-Leu-Gly hydroxamic acid (HXA), metal chelators with metalloproteinase inhibitor properties, were evaluated. Both compounds totally blocked the GSSG-induced amplification of vascular responses. In rabbits not exposed to GSSG, HXA decreased neointimal thickening by 50% (p < 0.05). CONCLUSIONS: Exposure to excess disulfide levels early after vascular balloon injury markedly amplified the late cellular response through interaction with redox active metals. These pathways can potentially mediate noxious effects of oxidative stress in vessels.

Animals↗
PubMed1998

Histological patterns of atherosclerotic plaques in unstable angina patients vary according to clinical presentation.

BACKGROUND: Unstable angina is a heterogeneous clinical syndrome. The diverse clinical presentations of unstable angina may reflect different pathogenic mechanisms within the plaque. OBJECTIVE: To investigate the cellular constituents of culprit coronary atheromatous plaques in patients with stable angina pectoris and patients with diverse clinical presentations of unstable angina. METHODS: 48 patients who underwent coronary atherectomy for management of ischaemic heart disease: 23 had stable angina and 25 had unstable angina. Of the latter, 11 patients were classified as Braunwald's IIB and 14 as Braunwald's IIIB unstable angina. The presence of thrombus, cholesterol clefts, and smooth muscle cell proliferation was assessed in atherectomy samples using standard histological techniques. Monoclonal antibodies were used to identify smooth muscle cells and macrophages within atherosclerotic plaque fragments. RESULTS: Fresh thrombus was more frequently found in patients with Braunwald's IIIB unstable angina (64%) than in patients with stable angina (22%) or IIB unstable angina (27%) (p < 0.0006). A pattern of smooth muscle cell proliferation ("accelerated progression pattern") was observed which was also associated with coronary thrombus. This pattern was present in 30% of patients with stable angina, 64% of patients with IIIB unstable angina, and in all patients (100%) with IIB unstable angina. Atherosclerotic plaques with thrombus, cholesterol clefts, and macrophages were more common in patients with unstable angina than in stable angina patients. CONCLUSION: The presence of a specific smooth muscle cell proliferation (accelerated progression) pattern in patients with unstable angina, particularly in those with Braunwald's IIB unstable angina, suggests that episodic plaque disruption and subsequent healing may be an important mechanism underlying angina symptoms in these patients.

Adult↗
PubMed1998

Higher incidence of malignant neoplasms after heart transplantation for treatment of chronic Chagas' heart disease.

BACKGROUND: Heart transplantation is a new therapeutic procedure to treat heart failure resulting from Chagas' disease. Experimental studies have demonstrated neoplastic effects of benznidazole, which is used for treatment of Trypanosoma cruzi infection. We compared the incidence and characteristics of neoplasia after heart transplantation for treatment of chronic Chagas' disease with those of other diseases. METHODS: Sixteen patients with Chagas' disease and 75 patients with other diseases underwent heart transplantation. Benznidazole was administered to 14 patients with Chagas's disease either for prophylaxis (4 patients) or for treatment of Chagas' disease reactivation (10 patients). RESULTS: The survival rate of patients in the nonchagasic group was 90% at 1 year and 82.4% at 2 years, and the survival rate in the chagasic group was 63% at 1 year and 57% at 2 years. Six of 16 patients (37.5%) with Chagas' disease had malignant tumors after a mean follow-up time of 25.3+/-2.1 months in contrast to 2 of 75 patients (2.7%) in the nonchagasic group after 34.6+/-3.6 months of follow-up. In the chagasic group, lymphoproliferative disorder was diagnosed in three patients, Kaposi's sarcoma in two, and squamous cell carcinoma in one patient. Reactivation of T. cruzi infection was diagnosed in all patients who had lymphoproliferative disorder. One patient without Chagas' disease had lymphoproliferative disorder in the lung, and another had malignant schwannoma affecting the skin. CONCLUSIONS: We found a higher incidence of malignant neoplasia after heart transplantation for treatment of chronic Chagas' disease. It is likely that the neoplasia is the result of chronic infection with an immunomodulator protozoan, immunosuppression, reactivation of the T. cruzi infection, or the toxicity of therapeutic intervention with benznidazole.

Adult↗
PubMed1998

[Stenting in a recently implanted stent in a saphenous vein graft for optimizing angiographic results].

A 60 year-old woman with progressive angina who had been submitted to saphenous bypass-graft to right coronary artery and a left mammary artery graft to anterior descending artery eight years previously, underwent implantation of a Gianturco Roubin II stent in the proximal third of the saphenous vein graft. The result was suboptimal by persistence of a residual stenosis probably due to prolapse of atherosclerotic material through the coil spaces. Another stent (Palmaz-Schatz biliar stent) was implanted at the previously stented site with no residual stenosis. Another Palmaz-Schatz biliar stent was successfully implanted in the distal body of the graft to treat another lesion (passing through the previously stents without difficulty). Stenting a stent, in selected situations, is a useful tool to optimize the angiographic result of stent implantation.

Catheterization↗
PubMed1997

Short-term anti-ischemic effect of 17beta-estradiol in postmenopausal women with coronary artery disease.

BACKGROUND: Short-term administration of 17beta-estradiol improves effort-induced myocardial ischemia in female patients with coronary artery disease. 17Beta-estradiol also has direct and indirect coronary vascular smooth muscle relaxing properties. The aim of the present study was to evaluate the effect of short-term administration of 17beta-estradiol on pacing-induced myocardial ischemia by means of continuous monitoring of coronary sinus pH in 16 postmenopausal female patients with coronary artery disease. METHODS AND RESULTS: Patients underwent incremental atrial pacing starting at a rate of 100 bpm and increments of 20 bpm every 2 minutes up to 160 bpm before and 20 minutes after either 17beta-estradiol (1 mg sublingual, 9 patients) or placebo (sublingual, 7 patients). The time to the onset of myocardial ischemia during pacing was significantly increased by 17beta-estradiol (mean+/-SD, 254+/-36 versus 298+/-23 seconds; P<.02) but not by placebo (262+/-45 versus 256+/-34 seconds; P=NS) The pH shift was significantly reduced by 17beta-estradiol but not by placebo at every step of the pacing protocol. The maximum pH shift at peak pacing was significantly reduced by the administration of 17beta-estradiol by 0.022 pH units (95% CI, 0.001, 0.043; P<.04) but not by sublingual placebo (-0.002 pH units; 95% CI, -0.0073, 0.0021; P=NS). The maximum pH shift at maximum comparable pacing was also reduced by 17beta-estradiol by 0.015 pH units (95% CI, 0.012, 0.017; P<.001) but not by placebo (-0.0022 pH units; 95% CI, -0.006, 0.0015; P=NS). CONCLUSIONS: 17Beta-estradiol reduces the degree of pacing-induced myocardial ischemia in postmenopausal patients with coronary artery disease. The reduction of pacing-induced coronary sinus pH shift is consistent with an anti-ischemic effect of the hormone and is not due to preconditioning, as evidenced by the absence of improvement after placebo.

Cardiac Pacing, Artificial↗
PubMed1997

Clinical outcome after left ventricular surgical remodeling in patients with idiopathic dilated cardiomyopathy referred for heart transplantation: short-term results.

BACKGROUND: Left ventricular partial ventriculectomy (LVPV), an unconventional operation to reverse some aspects of the cardiac remodeling, has been proposed for treatment of congestive heart failure. METHODS AND RESULTS: Twenty-four patients (age 46+/-9 years) referred to heart transplantation underwent isolated LVPV or LVPV associated to valve annuloplasty. Patients were in New York Heart Association functional class IV (15) or III (9) due to idiopathic dilated cardiomyopathy. Functional class, left and right ventricular ejection fraction (radionuclide), left ventricular end-diastolic and end-systolic diameter, and fractional shortening (by echocardiography), and hemodynamic variables were determined. The mean follow-up was 474+/-174 days. Survival at 30, 180, and 365 days was 92+/-6%, 67+/-10%, and 63+/-10%, respectively. Nine patients died, and the cause was associated with arrhythmias in 4 patients. The left ventricular end-diastolic diameters before and at 23+/-14 days, 188+/-27, and 365+/-14.8 days of follow-up were 82.6+/-9.8, 68.9+/-7.8, 69.9+/-6.9, and 70+/-5.3 mm, respectively (P=0.0001). The left ventricular end-systolic diameters were 73.5+/-7.4, 55.9+/-7.5, 57.4+/-7.8, and 55+/-5.5 mm (P=.0001). Fractional shortenings were 13+/-3, 19+/-4, 18+/-5, and 22+/-2%, respectively (P=.0001). The left ventricular ejection fractions before and 18+/-14, 188+/-26, and 369+/-3.6 days after the surgery were 17.2+/-4.7, 24.5+/-8.3, 24.5+/-7.4, and 23.7+/-6.1%, respectively (P=.004). The right ventricular ejection fractions were 20.5+/-6.2, 27.9+/-8.4, 28.2+/-10.1, and 27.4+/-7.3% (P=0.02). Pressures were unchanged. There was improvement in cardiac index from 2.11+/-0.52 to 2.53+/-0.64 L/min (P=.0037). Norepinephrine blood levels reduced from 702+/-258 to 439+/-307 pg/mL (P=.001). Most surviving patients presented improvement in functional class. Sustained ventricular tachycardias were observed in 9 patients (38%). CONCLUSIONS: The left ventricular partial ventriculectomy may improve the left and right ventricular function, functional class, and cardiac output. These initial results were associated to high prevalence of sustained ventricular tachycardia. The ventriculectomy introduces the concept that reduction of left ventricular chamber diameter may improve cardiac function in heart failure. Further progress is necessary to improve the results and evaluate its proper role in the management of heart failure.

Adult↗
PubMed1997

Normal high energy phosphate ratios in "stunned" human myocardium.

OBJECTIVES: We sought to investigate whether alterations in cardiac high energy phosphates occur in postischemic "stunned" human myocardium. BACKGROUND: Transient postischemic myocardial dysfunction is a common phenomenon that occurs in a variety of clinical settings in the absence of necrosis, and its pathogenesis is still unclear. Cardiac high energy phosphates are reduced during ischemia, and persistently altered myocardial high energy phosphate metabolism has been suggested as a mechanism contributing to stunning. METHODS: We studied 29 patients with a first anterior myocardial infarction (MI) who underwent successful reperfusion within 6 h of the onset of chest pain. These patients underwent 31P magnetic resonance spectroscopy (MRS) a mean of 4 days after MI for measurement of left ventricular contractility and relative high energy phosphate metabolites. Twenty-one patients underwent a second 31P MRS study a mean of 39 days after MI. Eight volunteers served as control subjects. RESULTS: Global and infarct area wall motion scores improved significantly between the early and late studies. No difference was found between early cardiac phosphocreatine (PCr)/beta-adenosine triphosphate (beta-ATP) ratios in patients and control subjects ([mean +/- SD] 1.51 +/- 0.17 vs. 1.61 +/- 0.18, respectively, p = 0.17) or between early and late study results in patients (1.51 +/- 0.17 vs. 1.53 +/- 0.17, respectively, p = 0.6). For alpha of 0.05, the study had a 90% power to detect a 9% difference. CONCLUSIONS: The results of this study demonstrate normal myocardial PCr/ATP ratios in patients with myocardial stunning after reperfusion and suggest that relative cardiac high energy phosphates are not depleted in stunned human myocardium.

Adenosine Triphosphate↗
PubMed1997

Usefulness of ST-segment depression in non-infarct-related electrocardiographic leads in predicting prognosis after thrombolytic therapy for acute myocardial infarction.

This study investigated both the in-hospital and long-term prognostic significance of ST-segment depression in non-infarct-related leads in patients who received thrombolytic therapy after acute myocardial infarction (AMI). We evaluated 221 consecutive patients who were admitted with their first AMI and underwent thrombolysis. Patients were followed for an average of 31 months and were classified into 3 groups: group 1 included 51 patients with persistent ST-segment depression, group 2 had 97 patients with transient ST-segment depression, and group 3 consisted of 73 patients without ST-segment depression (absent). Group 1 had significantly worse long-term survival during follow up by Kaplan-Meier analysis (55%) versus group 2 (81%) and group 3 (94%) (p = 0.0004) and higher event rates. This prognostic significance seemed to be maintained in both the anterior and inferior wall AMI groups. Multivariate analysis, using the Cox model, showed that Killip class, in-hospital left ventricular ejection fraction, and the persistence of ST-segment depression on the predischarge electrocardiogram (group 1) were independent predictors of survival. ST-segment depression in non-infarct-related leads on the predischarge electrocardiogram is an independent risk factor for worse long-term survival after anterior as well as inferior AMI treated with thrombolytic therapy.

Disease-Free Survival↗
PubMed1997

An in situ quantitative immunohistochemical study of cytokines and IL-2R+ in chronic human chagasic myocarditis: correlation with the presence of myocardial Trypanosoma cruzi antigens.

Inflammatory cells positive for the cytokines IL-2, IL-4, IL-6, TNF-alpha, and IFN-gamma and for IL-2R, as well as CD8+ and CD4+ T cells and B cells were quantified using an immunoperoxidase technique in 25 fresh myocardial fragments from patients presenting with chronic chagasic cardiomyopathy. The presence of Trypanosoma cruzi antigens (Ags) in the myocardium was also investigated. The cases were grouped into group A (no Ag), group B (scarce extramyocardial fiber Ags), and group C (intramyocardial pseudocysts and extramyocardial fiber Ags). IL-2 was detected in very few cells (0.30 +/- 0.40 positive cells/hpf), suggesting immunological imbalance in chronic chagasic patients. IFN-gamma+ was the cytokine most frequently demonstrated (7.52 +/- 5.87 positive cells/hpf) and there was a good correlation between the number of IFN-gamma+ cells and CD8+ T cells in group A. IL-4+ cells were present in higher numbers in group C (2.78 +/- 1.49 positive cells/hpf). TNF-alpha+ (1.59 +/- 1.68 positive cells/hpf) and IL-6+ (2.76 +/- 2.32 positive cells/hpf) cells were present in moderate numbers. Fewer B cells were present, not related with the intensity of T. cruzi Ags. These results suggest that cytokines, as they occur in other infectious diseases, play a fundamental role in the control of T. cruzi in chronic human chagasic disease. A fatal outcome seems to be associated with the increased production of cytokines derived from the Th2 subpopulation of the CD4+ T cells.

Animals↗
PubMed1997

Plasma kinetic behavior in hyperlipidemic subjects of a lipidic microemulsion that binds to low density lipoprotein receptors.

It was previously reported that a protein-free microemulsion (LDE) with structure roughly resembling that of the lipid portion of low density lipoprotein (LDL) was presumably taken up by LDL receptors when injected into the bloodstream. In contact with plasma, LDE acquires apolipoproteins (apo) including apo E that would be the ligand for receptor binding. Currently, apo were associated to LDE by incubation with high density lipoprotein (HDL). LDE-apo uptake by mononuclear cells showed a saturation kinetics, with an apparent K(m) of 13.1 ng protein/mL. LDE-apo is able to displace LDL uptake by mononuclear cells with a Ki of 11.5 ng protein/mL. LDE without apo is, however, unable to displace LDL. The uptake of 14C-HDL is not dislocated by increasing amounts of LDE-apo, indicating that HDL and LDE-apo do not bind to the same receptor sites. In human hyperlipidemias, LDE labeled with 14C-cholesteryl ester behaved kinetically as expected for native LDL. LDE plasma disappearance curve obtained from eight hypercholesterolemic patients was markedly slower than that from 10 control normolipidemic subjects [fractional clearance rate (FCR) = 0.02 +/- 0.01 and 0.12 +/- 0.04 h-1, respectively; P < 0.0001]. On the other hand, in four severely hypertriglyceridemic patients, LDE FCR was not significantly different from the controls (0.07 +/- 0.03 h-1). These results suggest that LDE can be a useful device to study lipoprotein metabolism.

Adult↗
PubMed1997

Nitric oxide inhalation reduces pulmonary tidal volume during exercise in severe chronic heart failure.

Multiple mechanisms have been proposed to explain the hyperventilation and the limited exercise capacity in congestive heart failure (CHF) including increased intrapulmonary pressures, total pulmonary resistance, and airway abnormalities. We investigated the hypothesis that inhalation of nitric oxide could influence the maximum exercise capacity and excessive ventilatory response to exercise in CHF. Fifteen patients in CHF (mean age 48 +/- 12 years) underwent a control and a nitric oxide inhalation progressive treadmill exercise test with 30 ppm. We determined the maximum oxygen consumptiom (peak VO2), CO2 production (VCO2), minute pulmonary ventilation (VE), respiratory rate, tidal volume (VT), ventilatory equivalent for oxygen (VE/VO2), ventilatory equivalent for carbon dioxide (VE/VCO2), estimated physiologic dead space/tidal volume ratio (VD/VT), VE/VCO2 slope, heart rate, systemic arterial pressure, VE/exercise time slope, and VT/exercise time slope during every incremental exercise. Mean maximum exercise values of heart rate, systolic systemic arterial pressure, diastolic systemic arterial pressure, VD/VT, respiratory rate, peak VO2, VO2/heart rate, VE/CO2, and maximum exercise time were unchanged by inhalation of nitric oxide. There was a strong trend toward reduction of VE/VO2 from 53 +/- 15 to 47 +/- 12 (p = 0.051) and in maximum VE from 58 +/- 21 to 48 +/- 17 L x min(-1) (p = 0.059). Maximum VT decreased from 1639 +/- 556 to 1406 +/- 479 ml (p = 0.04). The VE/VCO2 slope was reduced from 43 +/- 12 to 35 +/- 8 (p = 0.018). Two patients had signs of pulmonary congestion during peak exercise or the recovery period with inhalation of nitric oxide. The VE/exercise time slope and VT/exercise time slope during incremental exercise were reduced by inhalation of nitric oxide, demonstrating a statistically significant minor increase in VE and VT. Inhalation of nitric oxide attenuated the excessive increase in VT response to exercise in CHF. The L-arginine-nitric oxide pathway may be involved in mechanisms contributing to hyperventilation during exercise in CHF.

Administration, Inhalation↗
PubMed1997

Coronary angioplasty results in leukocyte and platelet activation with adhesion molecule expression. Evidence of inflammatory responses in coronary angioplasty.

OBJECTIVES: This study sought to characterize leukocyte and platelet activation and adhesion molecule expression after coronary angioplasty. BACKGROUND: Coronary angioplasty can be regarded as a clinical model of postischemic inflammation because this intervention leads to the release of inflammatory mediators as a result of plaque rupture and endothelial injury. METHODS: In 13 patients with stable angina (mean [ +/- SEM] age 56.0 +/- 2.4 years, range 44 to 79), blood samples were drawn from the aorta and coronary sinus immediately before and immediately and 15 min after coronary angioplasty. Subsequently, leukocyte and platelet functions were determined. Eleven control patients (57.5 +/- 2.3 years, range 52 to 78) underwent coronary arteriography. RESULTS: Coronary arteriography and angioplasty showed no difference in number of leukocytes between the coronary sinus and the aorta. However, 15 min after coronary angioplasty, there was an increase in neutrophil CD18 and CD11b, monocyte CD14 and platelet glycoprotein IIb/IIIa expression and a decrease in neutrophil L-selectin expression (189 +/- 25%, 163 +/- 27%, 158 +/- 35%, 141 +/- 22% and 31 +/- 10%, respectively, p < 0.01). In the control subjects, no change in adhesion molecule expression occurred. Superoxide production and aggregation in ex vivo-stimulated neutrophils collected from the coronary sinus 15 min after coronary angioplasty was significantly decreased compared with that after coronary arteriography (54 +/- 12% vs. 106 +/- 30% and 58 +/- 11% vs. 102 +/- 29%, respectively, p < 0.01). The reduced responses to phorbol ester stimulation may be explained by previous in vivo activation of neutrophils during coronary angioplasty. CONCLUSIONS: Coronary angioplasty increases neutrophil, monocyte and platelet adhesion molecule expression and induces a significant decrease in ex vivo-stimulated neutrophil superoxide generation and aggregation. These findings suggest that coronary angioplasty triggers cellular activation with an inflammatory response that could contribute to restenosis.

Angioplasty, Balloon, Coronary↗
PubMed1997

[Early luminal diameter reduction after coronary angioplasty and its relation to the restenosis phenomenon].

PURPOSE: To evaluate the early luminal diameter loss in the first 15 min after percutaneous transluminal coronary angioplasty (PTCA) and its influence on coronary restenosis. METHODS: In a prospective study, we evaluated 86 patients. The patients were divided in two groups based on the presence or absence of coronary restenosis. Thirty one lesions developed restenosis and 55 lesions did not. RESULTS: Univariate analysis showed that balloon/artery ratio was lower in the group of restenosis (0.92 +/- 0.01 vs 1.00 +/- 0.11, P = .003). Absolute and relative elastic recoil at 1 min was greater in the group that developed restenosis (0.79 +/- 0.54 vs 0.68 +/- 0.59 mm; P = .007 and 32.04 +/- 14.27 vs 22.15 +/- 16.65%; P = .006). Similarly, absolute and relative elastic recoil at 15 min were greater in the group with restenosis (1.25 +/- 0.59 vs 0.90 +/- 0.65 mm, P = .017 e 46.75 +/- 15.69 vs 29.18 +/- 17.84%, P < .00001). Minimal luminal diameter (MLD) at 1 min was lower in the group with restenosis (2.15 +/- 0.42 vs 2.43 +/- 0.58 mm; P = .022). The very early loss was greater in the group with restenosis (0.46 +/- 0.34 vs 0.22 +/- 0.35 mm, P = .004). MLD at 15 min was lower in the group of restenosis than in the group without restenosis (1.69 +/- 0.48 vs 2.20 +/- 0.61; P = .0001). Multivariate analysis revealed balloon/artery ratio and MLD at 15 min as independent correlates of the late outcome. CONCLUSION: The late outcome of PTCA is influenced by elastic recoil and the early MLD loss after PTCA. However, the strongest and most important predictors of late outcome by multivariate analysis were balloon/artery ratio and MLD at 15 min.

Angioplasty, Balloon, Coronary↗
PubMed1997

Early elevation of lipoprotein(a) levels in chronic renal insufficiency.

Serum lipoprotein(a) [Lp(a)] concentrations in chronic renal failure patients were investigated in relation to the degree of renal insufficiency, treatment by maintenance hemodialysis, and correction of uremia by renal transplantation with or without cyclosporin immunosuppression. Fast serum levels of Lp(a) (mg/100 mL) were determined in 34 chronic renal failure patients not in need of maintenance dialysis (16 with serum creatinine 2.0-4.0 mg/100 mL; 18 with serum creatinine higher than 4.0 mg/100 mL), 40 patients treated by hemodialysis, 55 successful renal transplant recipients (28 under cyclosporin treatment and 27 receiving no cyclosporin), and 34 healthy controls. Age and sex distributions were similar among groups. Pregnant women; non-White individuals; subjects with obesity, diabetes, nephrotic syndrome, and hepatic and thyroid diseases; and those treated with oral contraceptives or lipid-lowering drugs were excluded from the study. Compared to controls, median Lp(a) was increased in nondialyzed renal failure patients (11 vs. 47.5 p < 0.001) and this was the only lipid abnormally observed in the group. There was no significant difference in Lp(a) levels between nondialized renal failure patients with serum creatinine 2.0-4.0 and > 4.0 mg/100 mL (47 vs. 49, NS). Moreover, Pearson correlation coefficient (r = 0.01, NS) showed that Lp(a) values were not related to serum creatinine in nondialyzed patients, In hemodialysis subjects Lp(a) concentrations (median = 29) were intermediate between those observed in nondialyzed patients and controls but the differences were not significant. Lp(a) levels in renal transplant patients treated with cyclosporin (median = 6) and not receiving cyclosporin (median = 13) were similar and did not differ from controls. Serum Lp(a) increases and attains maximum levels with mild/moderate reduction in renal function, and does not seem to change through late renal failure stages or in relation to the introduction of maintenance hemodialysis treatment. Correction of uremia by successful renal transplant caused normalization of Lp(a) levels regardless of the use of cyclosporin. Increased Lp(a) levels may be the earliest and more consistent lipid alteration seen in predialysis renal failure.

Adult↗