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Attilio Maseri

Publications and source records attributed to Attilio Maseri.

At least 19 recordsLinked to original sources
PubMed2006

Myocardial infarction complicating the initial phase of an ovarian stimulation protocol.

Two previous reports have reported myocardial infarction during ovarian hyperstimulation syndrome, a complication of controlled ovarian stimulation characterized by ascites, pleural effusion, hemoconcentration and an increased thromboembolic risk, but no association with the initial phase (before treatment with human chorionic gonadotropin) of a normal ovarian stimulation protocol for infertility has ever been described. We report the first case, to our knowledge, of acute myocardial infarction occurring during the initial phase of an otherwise uncomplicated ovarian stimulation protocol. A young woman with infertility associated to polycystic ovary syndrome was treated with leuprolide acetate and recombinant follicle stimulating hormone to induce ovarian stimulation for in vitro fertilization and embryo transfer. After 12 days the patient presented a non-ST elevation myocardial infarction, which was treated with aspirin, clopidogrel, enoxaparin, intravenous nitrates and beta blockers. Cardiac catheterization showed angiographically normal coronary arteries. Echocardiography showed a circumscribed akinesis of the inferior apical segment of the left ventricle and right ventricular apex, which was confirmed by cardiac magnetic resonance. A screening for thrombophilic diathesis was negative. The patient was discharged and remained asymptomatic at 1 and 3 months follow up. Further ovarian stimulations were excluded and a trial of oocyte retrieval on spontaneous cycle was planned. Myocardial infarction can complicate ovarian stimulation protocols for infertility even in their early phase without any sign of ovarian hyperstimulation syndrome.

Adult↗
PubMed2006

Smooth muscle cells in human atherosclerotic plaques secrete and proliferate in response to high mobility group box 1 protein.

High mobility group box 1 protein (HMGB1) is a chromatin component leaked out by necrotic cells and actively secreted by activated myeloid cells. The extracellular protein is a potent mediator of tissue remodeling. We show here that human atherosclerotic plaques, but not normal arteries, produce extracellular HMGB1. Secreted HMGB1 originates from endothelial cells, by neointimal foam cells, and also smooth muscle cells (SMCs). SMCs are an unexpected source for secreted HMGB1, since they normally express much lower amounts of HMGB1 than other cells types, and they do not secrete it. However, cultured SMCs actively secrete HMGB1 after cholesterol loading. In turn, in response to HMGB1, SMCs proliferate, migrate, and secrete more HMGB1. Thus, SMCs are both a source and a target of HMGB1; blocking HMGB1 secretion by SMCs can be an important strategy for treatment of atherosclerotic disease and in particular restenosis.

Atherosclerosis↗
PubMed2006

Differential gene expression profiling in genetic and multifactorial cardiovascular diseases.

Gene expression profiling by microarray technologies has been successfully applied to study the transcriptional changes that occur in tissues such as heart, vessels and blood cells in different cardiovascular disorders. Such studies have been performed in human cardiovascular syndromes and in animal models with the aim of unraveling the complex molecular pictures underlying human pathophysiology. As already observed in cancer research, gene expression studies in humans may provide a finer molecular classification of patients with cardiovascular diseases and indicate new markers useful for prognostic and therapeutic strategies. In this paper, we present the findings obtained with microarray platforms to explore transcriptome alterations in cardiovascular diseases. To describe the potential of global expression profiling approach in this field, we have chosen to review the genomic findings obtained in some classic heart diseases with genetic transmission such as hyperthrophic cardiomyopathy and Fabry disease, together with findings obtained in common multifactorial cardiovascular disorders such as heart failure, atherosclerosis and infarction. Wherever feasible, we present the results obtained in patients together with those obtained in the corresponding animal and cellular models.

Animals↗
PubMed2006

Current clinical features, diagnostic assessment and prognostic determinants of patients with variant angina.

BACKGROUND: Clinical characteristics and outcome of patients with variant angina were assessed in the 1970-1980s of the past Century. The recent progress in prevention, diagnosis and treatment of coronary artery disease may have significantly modified clinical characteristics and prognosis of these patients. METHODS: From January 1991 to December 2002, 202 patients (57.1+/-12 years; 166 men) were diagnosed to have variant angina at our Institute. Detailed clinical findings and clinical events were prospectively collected for each patient. RESULTS: The median time from the first angina attack to diagnosis was 2 months (range 1-276), with diagnosis requiring >6 months in 31.7% of patients. Coronary angiography (n=183) showed normal coronary arteries in 42.1% of patients and significant coronary stenoses (>50%) in 44.3%, with multi-vessel disease in 8.7%. Diagnosis of variant angina was done during coronary angiography in 3% of cases during the first half of the study period, but in 42% of patients in the second half of the study period. Major cardiac events (MCE, i.e., death, resuscitation from cardiac arrest, myocardial infarction) occurred in 41 patients (20.3%), with 43.9% of events occurring within 1 month of symptom onset. The only variable significantly associated with MCE was the detection during angina of ST segment elevation in both anterior and inferior ECG leads (odds ratio 3.24; 95% confidence interval 1.43-7.36; P=0.005). CONCLUSION: Our data suggest that variant angina is still a frequently overlooked diagnosis, and a timely diagnosis would be crucial to prevent early life-threatening events. Patients with diffuse ST segment elevation on ECG are those at the highest risk of MCE, independently of angiographic findings.

Adult↗
PubMed2006

Relation of heart rate variability to serum levels of C-reactive protein in patients with unstable angina pectoris.

Heart rate variability (HRV) and systemic markers of inflammation have prognostic value in patients with unstable angina pectoris (UAP). However, it is unknown whether any relation exists between HRV parameters and indexes of inflammation in this clinical context. We assessed HRV on 24-hour electrocardiographic Holter recordings, performed within 24 hours of admission, and measured C-reactive protein (CRP) serum levels by a high-sensitivity assay on admission, in 531 patients with UAP (65+/-10 years of age; 347 men) who were enrolled in the prospective multicenter study Stratificazione Prognostica dell'Angina Instabile (SPAI). A significant inverse correlation was found between CRP levels and all HRV parameters, with the highest r coefficient shown with SD of all RR intervals (r= -0.23; p<0.001) in the time domain and with very low-frequency amplitude (r= -0.22; p<0.001) in the frequency domain. When patients were categorized into 4 groups according to CRP quartile levels, statistically significant lower HRV values were observed in the upper CRP quartile. On separate multiple regression analyses, including the most important clinical and laboratory variables, SD of all RR intervals and very low-frequency amplitude were the most significant predictors of increasing CRP levels (p<0.001 for the 2 comparisons). In contrast, in models with SD of all RR intervals and very low-frequency amplitude as dependent variables, CRP was a strong predictor of impaired cardiac autonomic function (p<0.001 for the 2 comparisons). Thus, our data show that, in patients with UAP, high levels of serum CRP levels are significantly associated with decreased HRV, suggesting a possible pathophysiologic link between cardiac autonomic dysfunction and inflammatory activity.

Adult↗
PubMed2006

Delayed gadolinium-enhanced cardiac magnetic resonance in patients with chronic myocarditis presenting with heart failure or recurrent arrhythmias.

OBJECTIVES: We evaluated the effectiveness of contrast-enhanced cardiac magnetic resonance (CE-CMR) in detecting chronic myocarditis (CM). BACKGROUND: Chronic myocarditis represents a common evolution of acute myocarditis. Although CE-CMR has been revealed to be effective in identifying areas of myocardial damage in acute myocarditis, its role in the diagnosis of chronic myocardial inflammation has not yet been investigated. METHODS: Twenty-three patients with CM underwent CE-CMR and endomyocardial biopsy (EMB). Chronic myocarditis was defined by the presence of: 1) chronic (>6 months) heart failure symptoms and/or repetitive ventricular arrhythmias; 2) no history of recent flu-like symptoms or infections; and 3) histologic evidence of active myocarditis (AM) or borderline myocarditis (BM) according to Dallas criteria. Contrast-enhanced cardiac magnetic resonance included black-blood T2-weighted (BBT2w) images without and with fat saturation and delayed three-dimensional T1 turbo field-echo inversion-recovery sequences obtained 15 min after gadolinium injection. RESULTS: Histology showed AM in 14 patients and BM in 9 patients. FatSat BBT2w revealed the presence of edema in five (36%) patients with AM but not in BM patients. Areas of late enhancement (LE) were observed in 12 (84%) subjects with AM and in 4 (44%) cases with BM. A mid-wall LE pattern was the most frequent finding in both groups while a subepicardial distribution of LE was observed only in patients with AM. CONCLUSIONS: Contrast-enhanced cardiac magnetic resonance identified areas of myocardial inflammation in up to 70% of patients with biopsy-proven CM. We suggest that CE-CMR may be a useful non-invasive diagnostic tool in patients with CM, and it may indicate and even guide the execution of left ventricular EMB with relevant prognostic and therapeutic implications.

Adult↗
PubMed2006

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Biomedical Research↗
PubMed2006

Assessment of resting perfusion defects in patients with acute myocardial infarction: comparison of myocardial contrast echocardiography, combined first-pass/delayed contrast-enhanced magnetic resonance imaging and 99mTC-sestamibi SPECT.

BACKGROUND: Information on the accuracy of both magnetic resonance imaging (MRI) and myocardial contrast echocardiography (MCE) for the identification of perfusion defects in patients with acute myocardial infarction is limited. We evaluated the accuracy of MRI and MCE, using Single Photon Emission Computed Tomography (SPECT) imaging as reference technique. METHODS: Fourteen consecutive patients underwent MCE, MRI and 99mTc-MIBI SPECT after acute myocardial infarction to assess myocardial perfusion. MCE was performed by Harmonic Power Angio Mode, with end-systolic triggering 1:4, using i.v. injection of Levovist. First-pass and delayed enhancement MRI was obtained after i.v administration of Gadolinium-DTPA. At MCE, homogeneous perfusion was considered as normal and absent or "patchy" perfusion as abnormal. At MRI, homogenous contrast enhancement was defined as normal whereas hypoenhancement at first-pass followed by hyperenhancement or persisting hypoenhancement in delayed images was defined as abnormal. RESULTS: At MCE 153 (68%) of segments were suitable for analysis compared to 220 (98%) segments at MRI (p<0.001). Sensitivity, specificity and accuracy of MCE for segmental perfusion defects in these 153 segments were 83, 73 and 77%, respectively. Sensitivity, specificity and accuracy of MRI were 63, 82, and 77%, respectively. MCE and MRI showed a moderate agreement with SPECT (k: 0.52 and 0.46, respectively). The agreement between MCE and MRI was better (k: 0.67) that the one of each technique with SPECT. CONCLUSION: MCE and MRI may be clinically useful in the assessment of perfusion defects in patients with acute myocardial infarction, even thought MCE imaging may be difficult to obtain in a considerable proportion of segments when the Intermittent Harmonic Angio Mode is used.

Contrast Media↗
PubMed2006

Elderly manifestation of non-compaction of the ventricular myocardium.

Non-compaction of the ventricular myocardium (NCVM) is a rare disorder of myocardial morphogenesis usually diagnosed in paediatric age associated with high mortality rates. Among reported cases, NCVM has been described in only six patients > or = 70 years. We describe the case of a 74-year-old male with NCVM involving the left ventricle, representing one of the oldest patients ever reported in the literature. Of note, this case was characterized by late appearance of NCVM and rapid deterioration of clinical conditions. The wide age range of symptom onset from prenatal to geriatric age supports the hypothesis that NCVM is a multifactorial rather than a simple congenital disorder.

Age of Onset↗
PubMed2005

Abnormal pH-sensing of platelet Na+/H+ exchanger in patients with cardiac syndrome X.

An enhanced activity of Na(+)/Li(+) countertransport, studied as a surrogate of Na(+)/H(+) exchanger, has been described in red blood cells of patients with cardiac syndrome X. In this study we investigated whether abnormalities in the activity of platelet Na(+)/H(+) exchanger (NHE) also existed in syndrome X patients and whether such abnormality was associated with platelet activation. Platelet NHE activity was evaluated in 21 syndrome X patients and 18 controls by measuring the pH recovery in platelets after acid loading and/or thrombin stimulation. The linear correlation existing between the initial intracytoplasmic pH (pH(i)) values and the maximal velocity of pH recovery allowed to calculate the values of slope and intercept at pH(i)=6.6 (I(pH6.6)) for each individual. Urinary excretion of the major TXB(2) metabolite, 11-dehydro-TXB(2) was measured in 15 syndrome X patients and 15 controls. The acidification-induced NHE activity resulted significantly higher in syndrome X patients compared to controls. Indeed, slope values were 0.75+/-0.29 and 0.5+/-0.23 min(-1) in patients and controls, respectively (P=0.01), while I(pH6.6) values were 0.24+/-0.1 and 0.17+/-0.1 DeltapH/min (P=0.04). The thrombin-stimulated NHE activity, however, was not different in the two groups and no significant difference in the urinary excretion of 11-dehydro-TXB(2) between patients and controls (median 920 vs. 765 pg/mg creatinine, respectively) (P=0.32) was also found. Thus our data demonstrate an alkaline shift in pH-dependence of platelet NHE of syndrome X patients. This abnormality does not seem to be associated with increased platelet activation.

Female↗
PubMed2005

Persistent systemic inflammation in unstable angina is largely unrelated to the atherothrombotic burden.

OBJECTIVES: The aim of this study was to assess the relationship between systemic inflammation, atherosclerosis, and thrombosis in two distinct clinical models of atherothrombosis. BACKGROUND: Persistent unstable angina (UA) is commonly associated with coronary thrombosis and persistent systemic inflammation. METHODS: We assessed circulating markers of activation of the thrombotic and fibrinolytic cascades and systemic soluble and cellular markers of inflammation on admission in 40 patients with persisting UA (Braunwald class IIIB; group 1) and 30 patients with Leriche-Fontaine stage IIB-III peripheral artery disease awaiting revascularization (group 2). RESULTS: The extent of atherosclerosis (p < 0.01) and activation of the coagulation system were greater in group 2, which had higher thrombin-antithrombin III complexes and D-dimer levels (2.7 and 24.4 microg/l, respectively), than in group 1 (2.0 microg/l and 12.9 microg/l, p = 0.02 and p = 0.0001, respectively). In contrast, C-reactive protein and interleukin-6 levels were higher in group 1 (7.6 pg/ml and 7.8 pg/ml, respectively) than in group 2 (4.5 pg/ml and 3.0 pg/ml, p < 0.01 and p = 0.03, respectively). Moreover, neutrophil activation was only found in group 1 (neutrophil myeloperoxidase content -4.0 arbitrary units vs. +3.4 arbitrary units in group 2, p < 0.0001). These differences persisted during the initial three days of hospitalization. CONCLUSIONS: Such a large, consistent discrepancy between atherothrombotic burden and systemic inflammation suggests that atherothrombosis, by itself, is an unlikely cause of persisting, recurring UA. An understanding of the primary inflammatory mechanisms of persistent and recurrent coronary instability could open the way to novel therapeutic strategies.

Aged↗
PubMed2005

Laser microdissection in clinical cardiovascular research.

Laser microdissection (LMD) is an accurate and fast method to procure pure populations of cells from complex, heterogeneous tissues under direct microscopic visualization. It can be applied to a wide range of cell preparation, including paraffin-embedded material. The morphology of the captured cells is retained, and DNA, RNA, and proteins can be extracted for molecular analysis. The potential applications of LMD to human cardiovascular research are multiple, including viral/autoimmune myocarditis and arteritis, atherosclerotic lesions, and myocardial and vascular cell proliferation and death. Molecular and genetic analysis of LMD-procured cells in cardiac and vascular tissues may provide a better understanding of several cardiac diseases.

Biopsy↗
PubMed2004

Intramyocyte detection of Epstein-Barr virus genome by laser capture microdissection in patients with inflammatory cardiomyopathy.

BACKGROUND: The causal role of Epstein-Barr virus (EBV) in inflammatory cardiomyopathy (IC) is still unclear, because this virus is present in latently infected circulating B lymphocytes in 90% of adults. Laser capture microdissection (LCM) has been applied on endomyocardial biopsy samples from patients with IC to assess the presence of EBV genome in separately dissected lymphocytes and myocytes. METHODS AND RESULTS: Among 142 patients with cardiac dilation and dysfunction and a histological and immunohistochemical diagnosis of myocarditis, 44 had a myocardial viral infection detected by polymerase chain reaction on frozen endomyocardial biopsy samples. In 9 of them, the virus detected was EBV. LCM was performed on 5-microm-thick paraffin sections of EBV-infected hearts. Lymphocytes and myocytes were microdissected and analyzed separately by polymerase chain reaction analysis on DNA extracted from the collected cells. Blood and myocardial samples from patients with positive and negative serology for EBV were used as controls. EBV genome was detected in myocytes but not in infiltrating lymphocytes of patients, nor in myocardial samples from controls. Despite full conventional antifailure therapy, a progressive cardiac dilation and dysfunction was documented in patients with EBV-related IC at a mean of 31+/-14 months of follow-up. CONCLUSIONS: Intramyocyte detection of EBV can be obtained by LCM in up to 6.3% of patients with IC. This supports a cytopathic EBV role and suggests the opportunity for an antiviral/immunomodulatory therapy.

Adult↗
PubMed2004

Prevalence of Fabry disease in female patients with late-onset hypertrophic cardiomyopathy.

BACKGROUND: Fabry disease (FD) has been recognized as the cause of left ventricular hypertrophy in 6% of men with late-onset hypertrophic cardiomyopathy (HCM). Although FD is considered a recessive X-linked disorder, affected women are increasingly reported. The aim of our study was to determine the prevalence of FD in female patients with HCM. METHODS AND RESULTS: Thirty-four consecutive women (mean age, 50+/-13.6 years) who received an ECG and echocardiographic diagnosis of HCM were submitted to an invasive cardiac study that included a biventricular endomyocardial biopsy. Tissue samples were analyzed for histology and electron microscopy. Peripheral blood activity of alpha-galactosidase (alpha-Gal) A was assessed in all patients. None of them had a family history of FD. Histology and electron microscopy showed in 4 patients (12%; mean age, 51.5+/-3.9 years) the presence of cell vacuoles characterized by the accumulation of glycolipid material organized in concentric lamellar structures, diagnostic for FD. In the remaining patients, histology was consistent with HCM. In all the female carriers, the heart was the only organ clinically involved in the disease, showing concentric hypertrophy in 2 patients, asymmetric hypertrophy in 1, and apical hypertrophy in 1. The alpha-Gal A enzymatic activity was 44+/-14% of control values. Genetic analysis showed the presence of alpha-Gal A gene mutation in all 4 cases. CONCLUSIONS: FD may account for up to 12% of females with late-onset HCM. Those heterozygous for FD with left ventricular hypertrophy are potential candidates for enzyme enhancement/replacement therapy.

Adult↗