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Biomedical subjects

A Azzarelli

Publications and source records attributed to A Azzarelli.

At least 19 recordsLinked to original sources
PubMed2000

Low grade fibromyxoid sarcoma. a further low-grade soft tissue malignancy characterized by a ring chromosome.

Supernumerary rings in the context of a simple karyotype characterize several low-grade malignant tumors of soft tissue and bone. Low-grade fibromyxoid sarcoma is an uncommon low-grade sarcoma, the cytogenetics of which has not yet been reported. Here we describe the first molecular-cytogenetic characterization of a pulmonary metastasis of low-grade fibromyxoid sarcoma. The histology of the primary and recurrent tumors was consistent with the diagnosis of low-grade fibromyxoid sarcoma of the usual type, whereas the pulmonary metastasis was of the "giant rosettes" variant. Cytogenetic analysis revealed a ring chromosome. Because gain of material of chromosomes 7 and 16 was detected by CGH, the ring chromosome is assumed to be composed of material from these respective chromosomes.

Adult↗
PubMed2000

A novel zinc finger gene is fused to EWS in small round cell tumor.

Ewing sarcoma family of tumors share recurrent translocations that fuse EWS from 22q12 to five different members of transcription factors namely FLI-1, ERG, ETV1, E1AF and FEV. Different classes of DNA binding proteins, ATF1, WT1 and CHOP are fused to EWS generating distinct tumor phenotypes: clear cell sarcoma, desmoplastic small round cell tumor, and myxoid liposarcoma, respectively. We have cloned a novel gene located at 22q12 fused to EWS by a submicroscopic inversion of 22q in a small round cell sarcoma showing a translocation (t(1;22)(p36.1;q12). The gene, designated ZSG (Zinc finger Sarcoma Gene), is a putative Cys2-His2 zinc finger protein which contains a POZ transcriptional repressor-like domain at the N-terminus. The rearrangement involves intron 8 of EWS and exon 1 of ZSG creating a chimeric sequence containing the transactivation domain of EWS fused to zinc finger domain of ZSG. This product lacks the transcriptional repressor domain at the N-terminus of ZSG. A rearrangement of the second ZSG allele was also found in tumor cells. This is the first example of an intra-chromosomal rearrangement of chromosome 22, undetectable by cytogenetics, activating EWS in soft tissue sarcoma.

Adolescent↗
PubMed2000

The expression of MDM2/CDK4 gene product in the differential diagnosis of well differentiated liposarcoma and large deep-seated lipoma.

Ordinary lipomas are cytogenetically characterized by a variety of balanced rearrangements involving chromosome segment 12q13-15, whereas well differentiated liposarcomas (WDL) show supernumerary ring and giant marker chromosomes, known to contain amplified 12q sequences. The tight correlation between the presence of ring chromosomes and both amplification and overexpression of MDM2 and CDK4 genes suggests the exploration of the possibility that immunocytochemistry (ICC) might assist in the differential diagnosis of lipoma-like well differentiated liposarcomas (LL-WDL) and large deep-seated lipomas (LDSL). For this purpose, 21 cases of the former and 19 cases of the latter tumours were analysed by ICC and, according to the availability of material, by molecular and cytogenetic approaches. All lipomas displayed a null MDM2/CDK4 phenotype, whereas all LL-WDL showed MDM2/CDK4 or CDK4 phenotypes. Southern blot analysis performed on 16 suitable cases, complemented by fluorescence in situ hybridization and classical cytogenetic analysis in 11 cases, was consistent with, and further supported the immunophenotyping data. In conclusion, MDM2/CDK4 product-based immunophenotyping appears to represent a valuable method for the categorization of arguable LDSL.

Adult↗
PubMed2000

[The evaluation of the appropriateness of instrumental exams in cardiology. The case of echocardiography].

BACKGROUND: The aim of this study was to evaluate the appropriateness and utility rates of echocardiograms performed in 309 patients in an outpatient clinical setting. METHODS: Data were collected by means of a questionnaire filled in by the cardiologists who performed the examinations. Appropriateness was evaluated according to international guidelines and scored as class I: appropriate, class II: doubtful appropriateness, class III: inappropriate; the exam was deemed useful if it was able to influence the clinical decision-making; normalcy rate was also checked. The relationship between both the referring physicians and motivation of the exam and its appropriateness, and the relationship between appropriateness and both the normalcy rate and utility of the exam were assessed. RESULTS: An echocardiogram was requested by the cardiologist in 46% of patients; the more common reasons for the exam were arterial hypertension (26%), cardiac murmur (18%), palpitations (15%), and known coronary artery disease (10%). The echocardiogram was appropriate (class I) in 25% of patients, doubtfully appropriate (class II) in 39% of patients and inappropriate (class III) in 36% of patients. The appropriateness rate between the cardiologists was similar to that of other prescribing clinicians (p = NS). The highest class III rate was found in patients with hypertension, while the highest class I rate was found in patients with a cardiac murmur (p < 0.01). Normalcy rate was lower in class I than in class II and III exams (p < 0.001). The utility rate was higher in class I (76%) than in class II (13%) and III (< 1%) exams (p < 0.01). CONCLUSIONS: International guidelines can be used effectively and safely to identify (not to prescribe) the useless echocardiograms.

Chi-Square Distribution↗
PubMed1999

Soft tissue limb sarcomas: Italian clinical trials with hyperthermic antiblastic perfusion.

BACKGROUND: Of the different options for limb-sparing treatment for patients with soft tissue limb sarcomas (STLS), hyperthermic antiblastic perfusion (HAP) combined with surgery might be the most effective in terms of tumor resectability, local control, and aesthetic and functional results. The aim of this study was to identify the most safe, active, and effective perfusional regimen in order to improve multidisciplinary treatment for patients with advanced STLS. METHODS: The first trial undertaken (which involved 18 patients) was a Phase I study to assess the maximum tolerable dose of doxorubicin, the second (with 29 patients) was a Phase II study of HAP with doxorubicin, and the third (with 20 patients) was a Phase I-II study to assess the maximum tolerable dose and tumor response to doxorubicin combined with tumor necrosis factor (TNF). Statistical tests were performed on the whole series to evaluate the factors influencing local toxicity, tumor response, and local disease free and overall survival. RESULTS: Grade IV systemic toxicity was observed in only 2 cases (TNF >1 mg). Muscle temperature (>41.5 degrees C) was the limiting factor for locoregional toxicity. Limb-sparing surgery was feasible for 60 patients (92.3%). The highest tumor response was observed in the third trial, with complete histologic necrosis in 26.3% of cases. Muscle and tumor temperature (>41.5 degrees C) and the type of trial had a statistically significant influence on response. The local recurrence rate was influenced by tumor site, type of trial, maximum tumor temperature, and local toxicity, whereas the overall survival was influenced by the presence of metastasis, tumor grade, and response to treatment. CONCLUSIONS: These findings show that HAP with doxorubicin and TNF (< or =1 mg) at a muscle temperature of < or =41.5 degrees C is a safe, active, and effective perfusional regimen for the multidisciplinary treatment of patients with advanced STLS.

Adult↗
PubMed1999

Hyperthermic antiblastic perfusion with alpha tumor necrosis factor and doxorubicin for the treatment of soft tissue limb sarcoma in candidates for amputation: results of a phase I study.

To improve the therapeutic effectiveness of hyperthermic antiblastic perfusion (HAP), the association of recombinant tumor necrosis factor alpha (rTNF alpha), doxorubicin, and true hyperthermia (41 degrees C) was employed for the treatment of soft tissue limb sarcoma. A dose-escalation study according to Fibonacci's modified scheme was conducted, starting with a rTNF alpha dose of 0.5-3.3 mg. The doxorubicin doses (0.7 and 1.4 mg for the upper and lower limbs, respectively) and temperature level (41 degrees C) remained unchanged. Eighteen patients have been treated thus far: 9 males and 9 females of a mean age of 33 years (range: 24-71 years). The tumor was located in the upper limb in one patient and in the lower limbs in seventeen. Only 16 patients were evaluable, as 2 refused further treatment after the perfusion. In terms of local toxicity, a grade I limb reaction was observed in 3 patients, a grade II or III in 10 patients, and a grade IV in 5 patients, showing a strict correlation between the TNF dose and the grade of limb reaction. In fact, a grade III-IV limb reaction was observed in 66.6% of the patients treated with > 1 mg of rTNF alpha. The maximum tolerable dose in association with doxorubicin and true hyperthermia (41 degrees C) was 2.4 mg. Eleven patients showed a good pathological response (> 75%) and five patients showed a partial response (> 25%-< 75%). In no case was stable or progressive disease observed. The postperfusional tumor shrinkage permitted limb-sparing surgery in 75% of the patients, all of whom were candidates for amputation before HAP. No recurrences have been observed thus far. Two patients developed regional disease: one presented with a skip femur metastasis that disappeared after radiotherapy and systemic chemotherapy; the second developed regional node involvement, requiring a radical node dissection. Another patient had pulmonary metastases, 2 months after the HAP, which were resected. At a median follow-up of 12 months, all the patients are living without disease. The results of this phase I study suggest that the association of rTNF alpha, doxorubicin, and true HAP (41 degrees C) by regional perfusion is feasible and safe at a maximum tolerable rTNF alpha dose of 2.4 mg. However, because no correlation was found between the amount of rTNF alpha and the tumor response, 1 mg is recommended as the dose able to provide a high tumor necrosis rate and low local and systemic toxicity. This association appears to play an important role in the neoadjuvant treatment of soft tissue limb sarcoma.

Adult↗
PubMed1999

[Variation in the evoked ventricular potentials after the implantation of an endocardiac catheter; the correlation with stimulation thresholds].

BACKGROUND: The drop in T wave amplitude of the ventricular pace-evoked response (VER) is a well-recognized and reliable mean of detecting localized conditions of myocardial hypoxia. In patients who undergo pacemaker implantation, the post-implant change at the electrode-tissue interface consists of an early inflammatory reaction. The aim of this study was to establish whether the extent of the inflammatory reaction following an endocardial lead can be assessed by the changes in the T wave amplitude of VER. METHODS: Modifications in VER amplitude and the correlation between these changes and pacing threshold time-course were evaluated in 30 patients receiving an endocardial catheter. Telemetered endocardial recordings of T wave amplitude and pacing thresholds were measured at the time of implant and after 1, 2, 3, 7, 14 and 30 days. RESULTS: A biphasic time-course was observed for T wave, characterized by reduction in amplitude of 48% (p < 0.005) from baseline at day 3 and subsequent increment up to 84% (p = ns) of the baseline value at day 30. By using a linear regression analysis, a significant correlation between T wave changes and increment in pacing threshold was found (r = 0.81; p < 0.002). A higher pacing threshold increment was observed in patients having a decrease in VER amplitude > or = 1 mV at 3rd in comparison with patients with a decrease in VER amplitude < 1 mV (1.1 +/- 0.4 vs 0.2 +/- 0.2 V; p < 0.001). CONCLUSIONS: VER recordings during the first days after endocardial lead implantation may be a valuable means of assessing the extent of the inflammatory reaction developing at the electrode-tissue interface. This method may be useful for early identification of patients at risk of increases in pacing threshold and for evaluation of the biocompatibility of different leads.

Aged↗
PubMed1998

Molecular abnormalities in liposarcoma: role of MDM2 and CDK4-containing amplicons at 12q13-22.

It has recently been shown that mdm2 overexpression with stabilization of p53 represents a characteristic of retroperitoneal well-differentiated-dedifferentiated, here renamed evolved (WD-E), liposarcomas at the immunocytochemical, molecular, and cytogenetic level. This make-up appears to be confined to half the cases in non-retroperitoneal well-differentiated liposarcomas. Since in different tumours MDM2 amplification involves amplicons encompassing flanking genes, such as CDK4, the possibility was investigated that in these tumours, CDK4 could act as an alternative or additional gene involved in the transformation mechanism. Forty-one retroperitoneal (R)/non-retroperitoneal (NR) well-differentiated-dedifferentiated (WD-DD) and 33 myxoid/round cell liposarcomas were reanalysed by immunocytochemical, molecular (nine cases) and fluorescence in situ hybridization (FISH) (one case) techniques. The results showed that all but one R WD-E cases carried the mdm2+, p53+, cdk4+ immunophenotype. In NR-WD liposarcomas, this immunophenotype was shared in five cases and the remainder showed mdm2+, p53-, cdk4+ in four and mdm2-, p53-, cdk4+ in one case, showing ring chromosomes by FISH analysis. TP53 mutations are confirmed to be closely correlated with NR-DD liposarcomas and no CDK4 involvement was found in the myxoid/round cell liposarcoma group. As well as confirming the synergistic effect of MDM2 and CDK4, these results are consistent with the concept that amplicon(s) excluding MDM2 may contribute to transformation and support a role of CDK4 in opposing p53 function, particularly in NR WD liposarcoma.

Blotting, Southern↗
PubMed1998

A novel EWS-ERG rearrangement generating two hybrid mRNAs in a peripheral primitive neuroectodermal tumour (pPNET) with a t(15;22) translocation.

The occurrence of a t(15;22) translocation in a peripheral primitive neuroectodermal tumour (pPNET) has been previously reported. Molecular examination revealed the presence in tumour mRNA of two hybrid transcripts containing the 5' portion of the EWS gene fused to the 3' portion of the ERG gene. Sequence analyses indicated that both aberrant mRNAs most likely originated from the same rearrangement, which produced different hybrid isoforms due to the presence of an alternatively spliced exon in the ERG gene. To the authors' knowledge, this is the first report of the detection of two hybrid EWS-ERG mRNAs within the same tumour.

Adult↗
PubMed1998

Mutations of adenomatous polyposis coli (APC) gene are uncommon in sporadic desmoid tumours.

Desmoids are locally aggressive, non-metastasizing soft-tissue tumours, whose aetiology is still unclear. In patients affected with familial adenomatous polyposis (FAP), the incidence of desmoids is much higher than in the general population. The APC gene, which is responsible for FAP, is involved in the development of desmoids associated with this syndrome. In this study 16 sporadic and four FAP-related desmoids were analysed in order to investigate the possible involvement of APC in non-syndromic cases also. The 5' end (exons 1-11) and the coding portion of exon 15 of APC were screened using the in vitro synthesized-protein assay (IVSP). Exons 5, 6, 8-14, and a region of exon 15 spanning codons 1036-1634 were investigated by single-strand conformation polymorphism (SSCP) analysis. APC germline mutations were identified in all FAP patients, but not in sporadic cases. Somatic mutations were found in three FAP-associated desmoids (75%) and two sporadic tumours (12.5%). In one of the latter cases, both alleles were affected. These findings indicate a limited role of the gene in the development of desmoid tumours outside FAP.

Adenomatous Polyposis Coli↗
PubMed1998

Left ventricular size and function in patients with noninsulin-dependent diabetes and postinfarction total or subtotal coronary occlusions.

The aim of this study was to establish the effects of postinfarction total or subtotal coronary occlusion on left ventricular remodeling in patients with noninsulin-dependent diabetes (NIDD) compared with the effects in postinfarct nondiabetic patients. The authors selected 100 patients submitted to coronary angiography between 1 and 5 weeks after acute myocardial infarction (T0: 20.5+/-15.4 days) and classified into three groups: G1: NIDD with coronary occlusion/subocclusion (n=24), G2: controls with coronary occlusion/subocclusion (n=43), G3: controls without coronary occlusion/subocclusion (n=33). At time zero (T0) the following parameters were evaluated: end-systolic and end-diastolic volume indexes (ESVi, EDVi), ejection fraction (EF), echocardiographic wall motion score index (WMI), presence of left ventricular aneurysm, and triple-vessel coronary disease. The frequencies of major cardiovascular events were recorded during follow-up. Significantly greater ESVi and EDVi were noted in G2 compared with G3 (P<0.0001), while no significant differences were observed between NIDD patients and controls. Although left ventricular global and segmental dysfunctions were increased in diabetics, controls with coronary occlusion/subocclusion presented more pronounced EF reduction (P<0.0001 G2 vs G3) and higher elevation in WMI (P<0.005 G2 vs G3). Cardiac events during follow-up were elevated in G1 and G2, particularly as regards the occurrence of congestive heart failure. The authors conclude that NIDD seems to influence in a positive way left ventricular remodeling associated with postinfarct total or subtotal coronary occlusion.

Coronary Angiography↗
PubMed1997

Distinct mdm2/p53 expression patterns in liposarcoma subgroups: implications for different pathogenetic mechanisms.

Recent findings have indicated that TP53 inactivation in sarcomas may result from mutation and/or deletion of the TP53 gene or, alternatively, from binding to the MDM2 gene products. To investigate further a possible role of the two genes in sarcomas, 24 large and deep-seated lipomas and 74 liposarcomas of various subtypes were analysed for mdm2 and p53 overexpression by immunocytochemistry. Nineteen cases of the same series were also molecularly analysed for both MDM2 gene amplification and TP53 mutations, and a further ten cases for non-random chromosomal abnormalities. In the retroperitoneal well-differentiated-dedifferentiated (WD-DD) group, 15/16 WD and 8/8 DD liposarcomas displayed the mdm2+/p53+ phenotype, consistent with MDM2 gene amplification in the absence of TP53 mutations. In the non-retroperitoneal WD-DD group, 5/11 WD liposarcomas also retained the mdm2+/p53+ phenotype whereas all DD liposarcomas showed an immunophenotype and, when assessed, a genotype consistent with mutant TP53. Null mdm2 immunophenotype, coupled with evidence of a specific chromosome translocation t(12;16), was constantly observed in both the usual and the cellular subtypes of myxoid liposarcoma, three cases of which also showed TP53 alterations at the genetic or protein level. Neither mdm2 nor p53 overexpression was observed in the lipomas. The results show the existence of three main pathogenetically distinct groups of liposarcoma. The first retroperitoneal WD-DD group, which represents a novel class of tumours within a single histological category of sarcoma, where MDM2-mediated inactivation of p53 could be related to the pathogenetic mechanism. The second is the non-retroperitoneal WD-DD group, where the TP53 mutations appear to correlate with the dedifferentiation process. The third is the myxoid group, which is characterized by its own unique cytogenetic profile and never shows any involvement of TP53 or MDM2 genes. As for diagnostic significance, the absence of mdm2 and p53 reactivity in lipomas seems to represent a useful marker for differential diagnosis from lipoma-like WD liposarcomas.

Adolescent↗
PubMed1997

Relevance of cytogenetic and fluorescent in situ hybridization analyses in the clinical assessment of soft tissue sarcoma.

Soft tissue sarcomas are a heterogeneous group of malignant tumors displaying a wide range of clinical presentations, morphological features, and biological behaviors. These characteristics and the recent development of differentiated treatment regimens for the different types of soft tissue sarcomas call for refined histological classification using additional ancillary approaches such as cytogenetic and molecular genetic analyses. We coupled classical cytogenetics and fluorescent in situ hybridization (FISH) on both metaphases and interphase nuclei to show the feasibility of this approach to characterize tumor type-specific chromosome rearrangements in soft tissue sarcomas of different histotype. In 35 cases analyzed, we detected the presence of specific chromosome rearrangements such as t(X;18) in synovial sarcoma (SS), t(12;16) in myxoid liposarcoma (MLS), t(11;22) in peripheral primitive neuroectodermal tumors (pPNET), t(2;13) in alveolar rhabdomyosarcoma (ARMS) and ring chromosomes in dermatofibrosarcoma protuberans (DFSP). In several cases, the presence of these cytogenetic rearrangements was of help for a differential diagnosis. The FISH analysis using painting probes not only confirmed the cytogenetic results but also allowed the identification of tumor-specific chromosome changes in those cases presenting low mitotic index or with poor quality chromosomes. Moreover, in the absence of analysable metaphases, FISH was successfully performed on interphase nuclei. Taken together, these results indicate both the diagnostic and clinical relevance of a molecular cytogenetic analysis in the study of soft tissue sarcomas.

Biomarkers, Tumor↗
PubMed1996

Variant translocation t(6;10)(p21;q22) in pulmonary chondroid hamartoma.

Banding cytogenetics and fluorescence in situ hybridization analysis of a pulmonary chondroid hamartoma (PHC) showed the presence of a t(6;10)(p21;q22). A cytogenetically identical translocation has previously been found in another case of PHC, suggesting that it could represent a variant form of the standard t(6;14)(p21;q24).

Chromosome Banding↗
PubMed1996

Prior myocardial infarction and prognostic outcome in patients with unstable angina in a postdischarge follow-up.

The authors investigated how a previous myocardial infarction (MI) affects the prognosis of unstable angina pectoris in patients with maintained or slightly reduced left ventricular performance. From January 1991 to August 1993, 131 patients hospitalized with the diagnosis of Braunwald's class II-III unstable angina and ejection fraction > 40% were included. The enrolled patients were divided into two groups: (1) group I: unstable angina with prior MI (n = 70, 49 men, 21 women, aged between fifty-one and eighty years, mean: 65.7 +/- 8.5 years, Braunwald's class III: 71.4%), (2) group II: unstable angina with previous infarction (n = 61, 31 men, 30 women, aged between forty-nine and eighty, mean: 66.3 +/- 7.9 years, Braunwald's class III: 83.6%). The follow-up varied between six and twenty-four months. The frequency of major cardiovascular events (deaths, MI, reinfarction, heart failure, and recurrent unstable angina) and the number of revascularization procedures (percutaneous transluminal coronary angioplasty [PTCA] and coronary artery bypass grafting [CABG]) established during follow-up were evaluated. Hospitalization was 10.1 +/- 2.9 days in group I and 8.6 +/- 2.6 days in group II (P < 0.01). The duration of the follow-up was comparable between the two groups. Based upon predischarge noninvasive evaluation, patients in both groups were selected to undergo coronary and ventricular angiography: 38 of 70 (55.7%) in group I and 39 of 61 (62.3%) in group II; among them, 52.9% in group I and 24.6% in group II (P < 0.05) were submitted to coronary revascularization, while the others received medical treatments: 33 of 70 in group I and 46 of 61 in group II (P < 0.05). In the subset of patients submitted to angiography, the severity of coronary disease did not differ between the groups, and group I showed a statistically lower ejection fraction than group II (P < 0.005). The frequency of major cardiovascular events demonstrated a mortality rate of 2.9% in group I and 1.6% in group II. Acute MI/reinfarction accounted for 2.9% of the cases in group I and 3.3% in group II. Heart failure was present in 2.9% of group I. Recurrence of unstable angina was diagnosed in 11.4% of group I and 6.5% of group II. CABG and PTCA were performed, respectively in 7.1% and 5.7% in group I and in 6.6% and 4.9% in group II. During follow-up 75.7% of patients in group I and 80.3% in group II were asymptomatic. No significant differences in the frequency of cardiovascular events were reported between the two groups. As result of more aggressive therapeutic approaches following the detection of residual ischemia in patients with prior infarction, the authors conclude that the prognosis of unstable angina in the group with previous infarction does not seem to differ from that of unstable angina in the absence of prior necrosis in patients whose left ventricular function is maintained or slightly decreased.

Aged↗
PubMed1995

Involvement of chromosomes 17 and 22 in dermatofibrosarcoma protuberans.

Literature on the cytogenetics of dermatofibrosarcoma protuberans (DFSP) is limited; only 10 cases with chromosome aberrations have been reported. They are karyotypically characterized by the presence of supernumerary ring(s), either as the sole cytogenetic abnormality or together with a few additional structural or numerical changes. We report the cytogenetic and fluorescence in situ hybridization (FISH) analysis of three new DFSP, one primary and two recurrent tumors. In two cases we found a supernumerary ring as the sole change, whereas the third had two copies of a marker chromosome and monosomy of chromosome 22. Sequences of chromosomes 17 and 22 were identified by FISH in the supernumerary rings and in the markers. The fluorescence pattern suggested that additional sequences were present in the two rings, but showed that the marker chromosomes were entirely painted by chromosome 17 and 22 probes. The findings indicate that juxtaposition and/or amplification of chromosome 17 and 22 sequences could be crucial in the pathogenesis of DFSP.

Adult↗
PubMed1995

NIDDM as unfavorable factor to the postinfarctual ventricular function in the elderly: echocardiography study.

BACKGROUND: Aging and diabetes mellitus have been recognized as strong predictors of heart failure in patients with acute myocardial infarction. The aim of this study was to assess, by echocardiography, the influence of aging and non-insulin-dependent diabetes mellitus on the changes of left ventricular parietal kinesis in patients with acute myocardial infarction over the 6 months after hospitalization. METHODS: The study population consisted of 82 patients (42 male, 40 female) aged 70 years, consecutively admitted to coronary care unit with acute myocardial infarction from January 1991 to May 1993. They were divided into two groups: group 1 comprised 36 patients with non-insulin-dependent diabetes mellitus, aged 78.8 +/- 6.02 years, 17 men and 19 women; group 2 comprised 46 patients without diabetes aged 78.7 +/- 6.9 years, 25 men and 21 women. Echocardiography was performed at admission to the unit (T0), at discharge (T1), and after 6 months of follow-up (T2). The echocardiographic wall motion score index was calculated by considering the number of akinetic and dyskinetic left ventricular wall segments. Fatal and non-fatal incidents of heart failure were also considered and a multivariate analysis was applied to identify the clinical and instrumental parameters that were independent predictors of wall motion score index changes and heart failure events. RESULTS: At T1 the two groups were comparable in localization of acute myocardial infarction, previous myocardial infarction, creatinine kinase serum peak, ECG score and wall motion score index. A statistically significant reduction in akinesia (P < 0.001) was observed in group 2 at T1 and T2, but was not seen in group 1. At T2 the difference in wall motion score index between the groups became significant (P < 0.05). The occurrence of heart failure was significantly higher in group 1 than in group 2 either during hospitalization (P < 0.03) or during follow-up (P < 0.004). The multivariate analysis identified non-insulin-dependent diabetes mellitus as an independent predictor of lacking recovery in LV kinesis (P < 0.01) and of heart failure development (P < 0.001). CONCLUSION: In elderly patients with non-insulin-dependent diabetes mellitus lack of recovery in wall motion score index after acute myocardial infarction seems to be an important factor, with a higher heart failure prevalence adversely affecting the in-hospital and long-term outcome. Non-insulin-dependent diabetes mellitus appears to be an important factor related to this unfavorable outcome.

Aged↗