Monoclonal gammopathies with a high MC elicit altered phenotypic and genotypic features.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to C Greco.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Nitroglycerin (NTG) is known to increase the blood supply to the myocardium, and would thus increase the delivery of a perfusional tracer such as sestamibi (MIBI) to the tissue. The latter, in turn, would take up and concentrate the tracer to a greater extent than in basal conditions only if energy-dependent mechanisms were still available-that is, only if the cells were still viable. METHODS: We evaluated the changes that intravenous administration of NTG induced on the uptake of MIBI by akinetic myocardial areas, using tomographic perfusional imaging in 23 patients with previously ascertained anterior myocardial infarction who were undergoing myocardial revascularization procedures. Changes in uptake were compared with echocardiographic and perfusional changes occurring after operation. RESULTS: The improvement of MIBI uptake after NTG correctly identified 12 of the 16 patients (75%) showing postoperative wall motion improvement; they comprised 12 of the 14 (86%) patients with NTG-induced increase in MIBI uptake who showed improved wall motion after operation. A close correlation (r = 0.88, P < 0.001) was found between the increase in myocardial MIBI uptake induced by NTG infusion and that induced by revascularization. The presence of collaterals to the akinetic area was associated with a significantly (P < 0.01) greater increase in MIBI uptake both during NTG infusion and after operation. CONCLUSIONS: The results of this study suggest that MIBI perfusional myocardial scintigraphy during infusion of NTG is capable of detecting viable but chronically hypoperfused myocardium, predicting postoperative wall motion and perfusional improvement, and reflecting the postoperative pattern of perfusion. The best results were achieved in patients with evidence of collateral circulation supplying the infarcted area.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Encapsulated cell grafting is one approach for the delivery of neurotransmitters and/or neurotrophic factors to the brain. Baby hamster kidney (BHK) cells were genetically modified to secrete high levels of human nerve growth factor (hNGF). Following polymer encapsulation, these cells were implanted into the left lateral ventricle or the left striatum 1.5 mm away from striatally cografted unencapsulated adrenal medullary chromaffin cells in hemiparkinsonian rats. Although the animals receiving adrenal medulla alone or adrenal medulla with intraventricular hNGF-secreting cell grafting did not show recovery of apomorphine-induced rotational behavior, the animals receiving adrenal medulla with intrastriatal hNGF-secreting cell implants showed a significant recovery of rotational behavior 2 and 4 weeks after transplantation. Histological analysis revealed that in animals receiving adrenal medulla with intraventricular hNGF-secreting cell grafting, the number of tyrosine hydroxylase-immunoreactive (TH-IR) surviving chromaffin cells tended to be higher (approximately five to six times) than in animals receiving adrenal medulla alone; however, this increase did not reach statistical significance. In contrast, in animals receiving adrenal medullary cells together with intrastriatal hNGF-secreting cells, the number of TH-IR surviving chromaffin cells was more than 20 times higher than that in animals receiving adrenal medullary cells alone. Analysis of retrieved capsules revealed that hNGF continued to be released by encapsulated BHK-hNGF cells after 4 weeks in vivo. Moreover, histological analysis confirmed the presence of numerous viable encapsulated BHK-hNGF cells. These results indicate the potential use of intrastriatal implantation of encapsulated hNGF-secreting cells for augmenting the survival of cografted chromaffin cells as well as promoting the functional recovery of hemiparkinsonian rats. These data indicate that this approach may have potential application for treating Parkinson's disease.
BACKGROUND: On the basis of extensive studies concerning the prognostic value of Holter monitoring in patients with angina, we evaluated the clinical outcome of patients with transient ischemic episodes soon after myocardial infarction. METHODS: The incidence and clinical significance of myocardial ischemia, detected in the acute phase of myocardial infarction, were evaluated in 87 patients. Twenty-four-hour Holter recordings were obtained on the 2nd, 4th, 6th, and 12th hospital day. RESULTS: Myocardial ischemia was detected during at least one of the four recording periods in 28 patients (32%). A total of 157 ischemic episodes were documented. The proportion of recordings that showed transient myocardial ischemia progressively declined from 20% on the 2nd day to 5% on the 12th post-infarction day. Of the 157 ischemic episodes, 132 (84%) were silent and 25 (16%) were symptomatic. Transient ST-segment elevation was present in 99 of the 157 episodes (63%), while transient ST-segment depression occurred in the remaining 58 of the 157 cases (37%). One or more in-hospital cardiac events (reinfarction, acute pulmonary edema, ventricular tachycardia or fibrillation, cardiac death) were more frequent in patients with (group I) than in those without (group II) transient myocardial ischemia [nine out of 28 (32%) versus six out of 59 (10%); P < 0.03]. At follow-up (mean 11.5 +/- 2 months) the incidence of cardiac events (angina, reinfarction, heart failure, ventricular tachycardia or fibrillation, revascularization procedures, cardiac death, sudden death) was comparable in the two groups [four out of 24 (17%) versus 10 out of 49 (20%); NS]. Predischarge exercise testing, performed in 64 patients (74%), showed myocardial ischemia in 50%; the percentage did not vary significantly between group I and group II patients. Moreover, a positive exercise test was not predictive of major cardiac events at follow-up. CONCLUSION: Transient myocardial ischemia, frequently silent, is not uncommon in the acute phase of myocardial infarction and progressively decreases during the in-hospital stay. Its recognition in the subacute phase of myocardial infarction may lead to the identification of a subset of patients at the highest risk of early major complications, who may benefit from aggressive diagnostic and therapeutic strategies.
We prospectively evaluated 50 patients with mitral stenosis (43 women and 7 men; mean age 45 years) to assess the results of surgical reconstruction of the mitral valve. All patients underwent a complete echocardiographic examination before and after operation. Surgical reconstruction was extensive, and included commissurotomy, thinning of the valvular leaflets, calcification removal, splitting of subvalvular apparatus, and posterior annuloplasty. Surgical reconstruction resulted in increasing mitral functional area from 0.89 +/- 0.23 to 2.07 +/- 0.42 cm2. NYHA functional class decreased from 2.76 +/- 0.55 to 1.52 +/- 0.71. Before discharging, 10% of patients had moderate mitral insufficiency. All patients were followed at 6-month intervals in our clinic. Mean follow-up was 37 +/- 18 months. During follow-up 5 patients (10%) developed severe mitral incompetence, which required mitral valve replacement. Chi-square and Student t-test were used to analyze the correlation between variables and outcome. The occurrence of severe mitral incompetence was correlated with: the degree of enlarged left atrium; chronic atrial fibrillation; postoperative more than mild mitral regurgitation. No correlation was found with anatomical parameters detected by echocardiography, or intraoperative anatomy. In conclusion, surgical reconstruction of mitral stenosis provides satisfactory short-term results. We believe that the low mortality rate and the low incidence of complications justify an effort to save the native mitral valve before considering prosthetic replacement. More attention to the development of residual mitral incompetence with intraoperative control may improve long-term results.
The resumption of contractility of asynergic segments in survivors after acute myocardial infarction (AMI) may be detected in viable myocardial areas. We have correlated the detection of viable myocardium, assessed with low dose dobutamine testing, with coronary angiography and clinical outcome in 66 consecutive survivors of AMI using the echocardiographic evidence of left ventricular wall motion abnormalities. The test enabled the identification of two groups: group A, comprising 32 patients (pts) demonstrating wall motion recovery at dobutamine infusion and group B, comprising 34 pts without wall motion recovery. The mean basal asynergy score index was 5.8 +/- 4.2 in group A and 6.0 +/- 4.2 in group B (p = ns). With dobutamine testing the score decreased to 2.8 +/- 3.6 in group A (p < 0.001 with respect to basal value), while it did not change significantly in group B. Left ventricular end diastolic volume (ml) was similar in the two groups (114 +/- 35 vs 107 +/- 79, p = NS). The infarct related artery (IRA) patency rate was 87.5% in group A, vs 26.5% in group B (p < 0.001). After a mean follow-up of 11 +/- 5 months, group A pts had basal asynergy score improvement (2.6 +/- 3.1, p < 0.001) and mild left ventricular end diastolic volume (ml) reduction, (108 +/- 32, p = NS), while group B pts had left ventricle end diastolic volume enlargement (130 +/- 38, p < 0.05), without score asynergy modification. Moreover all pts who experienced heart failure at follow-up were in group B.(ABSTRACT TRUNCATED AT 250 WORDS)
Serum levels of various immunochemical markers of clinical interest, as interleukin-6 (IL-6), C-reactive protein (CRP) and beta 2-microglobulin (beta 2M), were measured in sera from 98 subjects affected with monoclonal gammopathy of undetermined significance (MGUS; 80% of which bearing cancer too) and from 39 patients with multiple myeloma (MM). In addition, the ratio between serum IgG/IgA amounts (GAR) was also calculated in monoclonal gammopathies of IgG type. Consistent with our previous investigations, we found that tumor presence significantly influenced the serum levels of the various markers (except GAR) in MGUS patients; in fact, only when comparing MGUS without tumor and MM patients, was a clear difference observed for all markers considered. The data presented discourage the use of IL-6, CRP and beta 2M as discriminant indices between MGUS and MM patients, unless a careful selection of MGUS subjects is performed. Further investigations on these potential markers are therefore needed for a more rational clinical application.
To test the affinity of a new F(ab')2 monoclonal antibody (TRF1) against human fragment D dimer of cross-linked fibrin for atherosclerotic plaques free of detectable thrombi, 6 atherosclerotic segments of carotid and femoral artery, and as a control 5 segments of atherosclerosis-free internal mammary artery, were drawn from 11 male patients undergoing bypass surgery. All segments were carefully washed in order to remove possible endoluminal thrombi, and cut to obtain pairs of intimal fragments of similar weight, containing either plaques (n = 16), or fatty streaks (n = 12), or normal endothelium (n = 20). Each fragment underwent a direct binding test to TRF1, or to a non-specific antibody, both labeled with 125I. The activity in each fragment was measured after 3 h of incubation at 37 degrees C, and after washing the fragments every hour for 3 h. TRF1 binding (as percentage of initial activity) was significantly higher (P < 0.001) in atherosclerotic than in normal fragments (26% +/- 11.5%, vs. 9.2% +/- 3.9% in fatty streaks, and 1.9% +/- 0.6% in normal endothelium), and indirect immunofluorescence confirmed TRF1 uptake within the plaque wall. By contrast, the non-specific antibody did not show any significant binding. These preliminary results demonstrate the high specific affinity of TRF1 for atherosclerotic plaques, probably due to the hemorheologic phenomena that activate platelets and provoke the formation of fragment D dimers of cross-linked fibrin on the plaque surface.
Two patients with the permanent form of junctional reciprocating tachycardia successfully treated with the radiofrequency catheter ablation technique are described. In both patients a reentrant tachycardia utilizing a concealed slow conducting posterior septal accessory pathway for retrograde conduction was demonstrated. Radiofrequency current was delivered below the coronary sinus orifice. The procedure resulted in ablation of the accessory pathway conduction in both patients. During the follow-up, both patients remained free from tachycardia on no medication. This report demonstrates that the arrhythmogenic substrate of the permanent junctional reciprocating tachycardia can be easily suppressed by means of the radiofrequency catheter technique.
Noninvasive detection of atherosclerotic plaques remains a major challenge for clinical diagnosis, therapy and prognosis. Several approaches have been explored as a tool for thrombus imaging, using platelets, antiplatelet antibodies and fibronectin or as a direct metabolic marker as low density lipoproteins or photophrine II. We tested the affinity of a new F(ab')2 monoclonal antibody (TRF1) against human fragment D-dimer of cross-linked fibrin, for atherosclerotic plaques free of detectable thrombi on their surface. Six atherosclerotic segments of carotid and femoral arteries, and (as a control) 5 segments of atherosclerosis-free internal mammary artery, were drawn from 11 male patients undergoing bypass surgery. All segments were carefully washed in order to dissolve and remove possible endoluminal thrombi, and were subsequently cut to obtain couples of fragments of intima of similar weight, containing atherosclerotic plaques (n 16), or fatty streaks (n 12), or normal endothelium (n 20). Each fragment was separately put into a radioimmunoassay vial, and underwent a direct binding test to TRF1, or to an aspecific antibody, which both were labelled with 125I. The activity present in each fragment was measured with a gamma-counter after 3 h of incubation at 37 degrees C, and every hour after washing the fragments in order to remove the unbound antibody. No significant binding difference (expressed as per cent final activity in comparison with initial one) of the aspecific antibody between normal and atherosclerotic fragments was found. By contrast, TRF1 binding was significantly higher (p < 0.001) in atherosclerotic than in normal fragments (26.0 +/- 11.5% in atherosclerotic plaques, versus 9.23 +/- 9% in fatty streaks, versus 1.9 +/- 0.6% in normal endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)
During the past decade, a variety of innovative procedures and devices for non-pharmacological treatment of tachyarrhythmias have been proposed. Recent improvements in the implantable cardioverter/defibrillators and transcatheter ablative techniques have resulted in a revolution of the therapeutic approach in ventricular and supraventricular tachyarrhythmias, respectively, providing a valuable alternative to conventional antiarrhythmic surgery. Indeed, the selection criteria for surgery for tachyarrhythmias have been revised, and this therapeutic option is considered appropriate only for selected patients with postinfarction ventricular tachycardia. Ther implantable cardioverter/defibrillator has proved effective in conversion of life-threatening tachyarrhythmias, leading a dramatic decrease in the incidence of sudden death in high risk subjects. Thus, with further refinements, a wide use of this therapeutic modality can be anticipated. Transcatheter ablation has become the first-line option in the most common forms of supraventricular tachycardias, such as accessory pathway-mediated tachycardia and AV nodal reentry. More recently, encouraging results of this technique in common atrial flutter and ectopic atrial tachycardia have been reported, although confirmation with larger series and longer follow-up is needed. In general, results of catheter ablation in ventricular tachycardia have been disappointing, with the exception of bundle branch reentry and idiopathic ventricular tachycardia, in which a high success rate is reported. An increasingly important role of these therapeutic modalities is expected. In the meanwhile, due to their evolutional character and the specific competence required for their use, such procedures should be performed exclusively in well trained centers.
To assess the safety and diagnostic value of dobutamine stress-echocardiography (DSE), we studied 109 patients with ischemic heart disease: 78 patients with recent myocardial infarction, 31 patients with chest pain (14 patients without and 17 patients with previous myocardial infarction). Echocardiograms were recorded during dobutamine infusion in 5-minute stages to a maximum dose of 40 mcg/kg/min. The test was considered positive when dobutamine infusion induced a new wall motion abnormality. In 95 pts with recent or previous myocardial infarction new asynergies were classified as being within the infarct zone or outside the infarct zone based on the relation with vascular zones at coronary angiography. All patients underwent exercise stress test (EST) according to the Bruce protocol, and coronary angiography within one week from the test: significant coronary artery disease was defined as > or = 50% diameter stenosis for left main artery and > or = 70% for the other vessels. Five patients (4.6%) had ventricular arrhythmias and 3 patients (2.7%) had systolic blood pressure increase > or = 200 mm Hg in the first stage of DSE, without new wall motion abnormalities, and were excluded from diagnostic value analysis. DSE had a sensitivity of 86% vs 56% of EST (p < 0.001); both had specificity of 94% and positive prognostic value of 98%; diagnostic accuracy of DSE was 87% vs 62% of EST (p < 0.001); negative predictive value was not statistically different. Sensitivity of DSE in single vessel disease (78%) was significantly lower (p < 0.05) than sensitivity in multivessel disease (95%). Sensitivity of DSE in detecting multivessel disease in patients with myocardial infarction was 80% vs 55% of EST (p < 0.05); specificity 96% vs 63% (p < 0.001); diagnostic accuracy 90% vs 60% (p < 0.001); positive predictive value 93% vs 48% (p < 0.001); negative predictive value 89% vs 70% (p < 0.05). At the ischemic threshold, EST caused the achievement of higher heart rate and rate-pressure product; in patients with single vessel disease heart rate was higher than in multivessel disease (141 +/- 19 vs 117 +/- 21, p < 0.001). No differences were detected during DSE in heart rate, blood pressure, rate-pressure product; the dose of dobutamine infused at the ischemic threshold in patients with multivessel disease was significantly lower than in those with single vessel disease (15.2 +/- 5.4 vs 19.4 +/- 6 mcg/kg/min, p < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)