Biomedical subjects
Publications and source records attributed to Giuseppe Di Pasquale.
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UNLABELLED: The aims of this study were to: (1) retrospectively investigate the birth length and weight of our patients with congenital adrenal hyperplasia (CAH); (2) compare these parameters with standards for birth length and weight recently assessed in an Italian control population; (3) evaluate whether neonatal auxological data may change depending on the different clinical forms of CAH. Birth length and weight were retrospectively evaluated in 101 children with different clinical forms of CAH and compared with standards for birth length and weight assessed in an Italian control population. In both sexes the average birth length of patients with classical CAH was greater than the mean birth length of the controls, and both length and weight were greater in children with classical CAH than in those with the non-classical form. Among the patients with classical CAH, those with the salt-wasting form were longer but also weighed less than those with the simple-virilizing form. CONCLUSIONS: (1) fetal length velocity in patients with CAH may be increased only in those infants with classical forms of the syndrome, while it is unaffected in those with the non-classical form; (2) the greater the enzymatic activity impairment, the longer the birth length of newborns with CAH.
BACKGROUND: The possibility of preventing atrial fibrillation recurrence with anti-arrhythmic agents is very limited, given the discouraging results obtained with current drugs in many patients. Data from experimental studies suggest that angiotensin II AT1-receptor blockers can influence atrial remodelling, a key factor in atrial fibrillation initiation and maintenance. Moreover, some preliminary clinical data show that angiotensin II AT1 -receptor blockers can prevent atrial fibrillation episodes. The GISSI-Atrial Fibrillation (AF) trial is a randomized, prospective, parallel group, placebo-controlled, multicentre study designed to test whether angiotensin II AT1-receptor blockers can reduce atrial fibrillation recurrence. OBJECTIVES AND METHODS: The primary objective of the study is to demonstrate that, in patients with a history of recent atrial fibrillation who are treated with the best recommended therapies, the addition of the angiotensin II AT1-receptor blocker valsartan (titrated up to 320 mg) is superior to placebo in reducing atrial fibrillation recurrence. A substudy will analyse the effect of valsartan on left atrial dimensions and on neurohormones. The study population consists of patients with symptomatic atrial fibrillation (at least two electrocardiogram documented atrial fibrillation episodes in the previous 6 months or successful cardioversion in the last 2 weeks) with underlying cardiovascular diseases or comorbidities. With approximately 100 centres participating in Italy, a total of 1402 patients are randomized in a 1 : 1 ratio to receive valsartan or placebo. The enrolment period will last 12 months and the patients will be followed for 12 months from study entry. CONCLUSIONS: The GISSI-AF is the largest trial aimed at assessing the role of angiotensin receptor blockade in reducing the recurrence of atrial fibrillation and its possible mechanisms of action in terms of its effects on atrium remodelling and neurohormones.
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Heart diseases are the leading cause of death and morbidity in western countries and among them acute coronary artery diseases result to be the major contributor. During the last few decades a lot of energy has been mostly applied to the acute phase of non-ST-elevation acute coronary syndromes (ACS), where cardiac events concentrate. In fact a timely risk stratification along with an early aggressive invasive strategy and very powerful antithrombotic treatment have profoundly improved the in-hospital prognosis of such patients. Such a strong emphasis on the acute phase of ACS could have limited the interest in the equally important post-discharge therapies. However, several studies have demonstrated that different preventive treatments (aspirin, beta-blockers, angiotensin-converting enzyme inhibitors, statins and clopidogrel) could substantially reduce the long-term mortality and morbidity of such patients. Therefore, current guidelines emphasize the role of aggressive secondary preventive treatments after ACS. However, a strong discrepancy between the indications of the guidelines and their application in the real world arises day by day. Such a discrepancy could be due to errors of omission or therapeutic paradoxes. Since patients with ACS are a subgroup of subjects where secondary preventive measures could be useful and cost-effective, cardiologists should not limit their attention to the acute phase of the disease but should eagerly concentrate their efforts on an aggressive secondary preventive treatment as well. Pursuing such a task could extend and magnify the benefits obtained with acute treatment of ACS and significantly improve the outcomes of such patients. Therefore, the role of the Scientific Societies is to improve the application of guidelines and the utilization of all evidence-based treatments even in such post-discharge phase.
Atrial fibrillation and severe carotid artery stenosis are the most common causes of stroke. However, several patients recognize unusual cause for their cerebral ischemia. At the beginning of the last decade after the introduction of transesophageal echocardiography (TEE) and other imaging techniques, atheromatosis of the thoracic aorta has been recognized as an important source of stroke or systemic embolism. Formerly in the pre-TEE era, this entity was included into cryptogenic strokes. Notably, aortic atheromas are found in about one quarter of patients presenting with embolic events and their grading by TEE correlates with the risk of future embolism, especially if mobile lesions or superimposed thrombi are present. Unfortunately, the diagnosis of aortic atheroma is mostly established when an embolic event has already occurred. The aim of this paper is to review the current evidence for aortic atheroma as an important independent risk factor for stroke, and to discuss the potential therapeutic options. Unfortunately, randomized studies addressing the treatment of patients with severe aortic atheroma are not yet completed. Furthermore, although warfarin and statins look promising in several retrospective series, their results are by most controversial so far. In conclusion, although the diagnostic criteria and the negative prognostic significance of aortic atheroma are almost defined, its therapeutic options are far to be clear. Therefore, clinical trials addressing this relevant pathologic condition are urgently needed.
BACKGROUND: To evaluate 10-year cardiovascular risk, the risk chart and the individual risk score from the CUORE Project were recently introduced in Italy. These tools differ as for age range and some risk factors. Therefore, the aim of this study is to evaluate the difference between the global absolute risk assessed by the risk chart and the individual risk score using the data collected through the Osservatorio Epidemiologico Cardiovascolare (OEC). METHODS: From the Osservatorio Epidemiologico Cardiovascolare sample, 6508 people aged 40-69 years without clinical manifestations of atherosclerosis were selected. Cardiovascular risk was assessed using risk chart and individual risk score and the 10-year risk was categorized in six classes (< 5%, 5-9%, 10-14%, 15-19%, 20-29%, > or = 30%). As coefficient of agreement between risk chart and individual risk score, Cohen kappa statistic was computed using the Cicchetti-Allison weights (k(w)). RESULTS: From contingency tables of the two methods distribution, k(w) was 0.71 (p < 0.0001 and 95% confidence interval 0.70-0.72). Using the 20% risk threshold reported in Nota 13 of Agenzia Italiana del Farmaco and excluding persons who were treated for hyperlipemia refunded regardless of their chart or individual score estimation of cardiovascular risk, the differences between the two tools classification resulted in the 2.6% of the sample (1.4% were assessed as at non-high risk [< 20%] using the risk chart and at high risk using the individual risk score, and the opposite for 1.2%). CONCLUSIONS: Classification difference between risk charts and the individual risk score is quite small. Updating of predictive functions of two tools could improve their concordance also for individual evaluation, including older people and better reflecting current Italian lifestyle.
Aging is associated to a progressive establishing of a chronic inflammatory state linked to a continuous long exposure to antigens. Since IL-15 stimulates the proliferation of memory T cells and the immunosenescence is characterized by accumulation of memory T cells and exhaustion of naive T cells, we analyzed IL-15 levels in sera from 30 ultralongeval subjects with respect to those from young and old adults. IL-15 levels were assayed by immunoenzymatic methods. Ultralongeval subjects displayed significantly higher IL-15 levels with respect to both young and old controls. No statistical difference was found between old and young controls. These findings may explain, at least in part, the characteristic increase of memory cells in immunosenescence and the capacity of the immune system of centenarians to defend itself from infections through immune-inflammatory responses.
Cytostatic anticancer drugs are known as carcinogenic, mutagenic, and teratogenic risk factors for health care workers occupationally exposed. It has been demonstrated that the administration of interleukin-15 in rat models of colon carcinoma protects against chemotherapy-induced gastrointestinal toxicities. We found that occupational exposure to chemotherapeutic antiblastic agents in vivo modified circulating levels of interleukin-15 in 17 health care workers exposed to antineoplastic drugs in relation to their jobs and in as many healthy age- and sex-matched subjects. Health care workers displayed significantly higher circulating interleukin-15 levels compared to their age-matched controls. If this increase representing an anticancer response remains to be established, these findings strengthen the idea of a therapeutic use of interleukin-15 in the field of cancer.
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BACKGROUND: While the effect of psychological stress and depression on the course of heart disease is commonly recognized, the relationship between recent life events, major depression, depressive symptomatology and the onset of acute coronary heart disease (CHD) has been less considered. The aim of this study was to investigate the presence of stressful life events, major and minor depression, recurrent depression and demoralization in the year preceding the occurrence of a first acute myocardial infarction (AMI) and/or a first episode of instable angina and to compare stressful life events, also related with mood disorders, in patients and healthy controls. METHODS: 97 consecutive patients with a first episode of CHD (91 with AMI and 6 with instable angina) and 97 healthy subjects matched for sociodemographic variables were included. All patients were interviewed with Paykel's Interview for Recent Life Events, a semistructured interview for determining the psychiatric diagnosis of mood disorders (DSM-IV), a semistructured interview for demoralization (DCPR). Patients were assessed while on remission from the acute phase. The time period considered was the year preceding the first episode of CHD and the year before the interview for controls. RESULTS: Patients with acute CHD reported significantly more life events than control subjects (p < 0.001). All categories of events (except entrance events) were significantly more frequent. 30% of patients were identified as suffering from a major depressive disorder; 9% of patients were suffering from minor depression, 20% from demoralization. Even though there was an overlap between major depression and demoralization (12%), 17% of patients with major depression were not classified as demoralized and 7% of patients with demoralization did not satisfy the criteria for major depression. Independently of mood disorders, patients had a higher (p < 0.001) mean number of life events than controls. With regard to life events, the same significant difference (p < 0.001) compared to controls applied to patients with and without mood disorders. CONCLUSIONS: Our findings emphasize, by means of reliable methodology, the relationship between life events and AMI. These data, together with those regarding traditional cardiac risk factors, may have clinical and prognostic implications to be verified in longitudinal studies.
BACKGROUND: Several studies outlined the role of stressful life events in the pathogenesis of coronary heart disease. It has recently been emphasized the role of depression, both clinical and subclinical, in the course of myocardial infarction. The relationship between recent life events, major depression, depressive symptomatology and onset of acute coronary heart disease has been less considered. METHODS: Ninety-seven consecutive patients with first episode of coronary heart disease and 97 healthy subjects matched for sociodemographic variables were included. All patients were interviewed by Paykel's interview for recent life events, a semistructured interview for determining the psychiatric diagnosis of mood disorders, a semistructured interview for demoralization. Patients were assessed while on remission from the acute phase. The time period considered was the year preceding the first episode of coronary heart disease, and the year before interview for controls. RESULTS: Patients with acute coronary heart disease reported significantly more life events than control subjects (p < 0.001). All categories of events (except entrance events) were significantly more frequent. Thirty percent of patients were identified as suffering from a major depressive disorder; 9% of patients were suffering from minor depression, and 20% from demoralization. Even though there was an overlap between major depression and demoralization (12%), 17% of patients with major depression were not classified as demoralized and 7 % of patients with demoralization did not satisfy the criteria for major depression. Independently of mood disorders, patients have a higher (p < 0.001) mean number of life events than controls. With regard to life events, the same significant difference (p < 0.001) compared to controls applied to patients with and without mood disorders. CONCLUSIONS: Our findings emphasize the relationship between life events and acute coronary heart disease. These data, together with those regarding traditional cardiac risk factors, may have clinical and prognostic implications to be verified in longitudinal studies.
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Atrial fibrillation is a benign arrhythmia but it is associated with an elevated thromboembolic risk. The treatment of choice is oral anticoagulation. However not all the patients can benefit from oral anticoagulation, due to bleeding risk or other contraindications. Considering that the most common embolic source in patients with atrial fibrillation is the left atrial appendage, different surgical techniques have been suggested for its closure. For patients at high risk, since August 2001 a device is available for percutaneous occlusion of the left atrial appendage (PLAATO). The PLAATO device consists of a self-expandable nitinol cage with small anchors on its surface to avoid systemic migration. The implantation procedure is performed with local anesthesia. It requires transseptal puncture and the device is delivered to the appendage through a specially designed sheath. The maneuver is performed under transesophageal and fluoroscopic guidance. At present more than 250 patients have been implanted, and the results, as far as the safety and the effectiveness are concerned, are really promising. We report 2 cases of recently successfully implanted at our Center.
During the last decades, the prognosis of non-ST-elevation acute coronary syndromes has greatly improved. This improvement mainly depends on a better understanding of their pathophysiological background that allowed a remarkable evolution of their diagnostic and therapeutic management. Likewise, invasive strategies have evolved accordingly. Initially, patients with non-ST-elevation acute coronary syndromes had a very conservative approach and coronary revascularization was strongly discouraged during the acute phase. Afterward, as pharmacological therapies and revascularization techniques improved, interventional strategies gradually switched to a careful "delayed invasive approach". Recently, several studies, taking full advantage from the most effective treatments, have demonstrated that an early aggressive strategy (coronary revascularization within 48 hours of symptom onset) could reduce the incidence of cardiac events in patients with non-ST-elevation acute coronary syndromes at medium-to-high risk. These findings made this "early aggressive" strategy very attractive. However, in the real world such a strategy is rarely an option due to several logistical constraints and very often the selection of the therapeutic strategy depends more on resource availability than on patients' risk profile. Therefore, Italian cardiologists should pursue integrated healthcare models in order to overcome such limitations. They should develop critical pathways able to target adequately the patient risk and improve interventional networks where even subjects admitted to peripheral hospitals could benefit from a timely revascularization procedure according to their risk profile. This could reduce treatment disparities and could counteract the vicious circle that tends to privilege interventions in low-risk subjects instead of high-risk patients, like the elderly, women or diabetics.
Vasopressin (AVP), an antidiuretic hormone, is known to induce hypervolemia and to regulate the renal expression of aquaporin-2 (AQP2) water channels, but it is not yet known whether the latter are involved in the pathogenesis of essential hypertension. The aim of the present study was therefore to make a comparative study of blood pressure (BP), urinary volume (UV), urinary osmolarity (uOsm), urinary AQP2 (uAQP2), and plasma AVP levels (PAVP) in male spontaneously hypertensive rats (SHR; n = 30) at 3, 7, and 12 weeks of age and in male Wistar-Kyoto rats (WKY, n = 30), also after the subcutaneous administration of OPC-31260 (OPC), a human AVP V(2) receptor antagonist. At 3 weeks, SHR had markedly higher uOsm and lower UV levels than WKY. At 7 weeks, SHR were hypertensive, showing increased uAQP2, PAVP, and uOsm levels and a decreased UV. At 12 weeks, no significant changes were observed in this condition. At 7 and 12 weeks of age, OPC-treated WKY rats showed significant reduction in BP and uOsm and increase in UV with respect to untreated animals. From 3 weeks of age, OPC-treated SHR presented significantly lower BP levels, higher UV levels, and lower uOsm than untreated animals. In treated WKY and SHR, uAQP2 levels were lower than in untreated animals. The PAVP appeared to be higher in OPC-treated rats from both strains. These findings suggest that AVP and the AQP2 are involved in the pathogenesis of hypertension in SHR.
Moderate-severe depression (MSD) is linked to overexpression of proinflammatory cytokines and chemokines. Fractalkine (FKN) and macrophage inflammatory protein-1 alpha (MIP-1alpha) are, respectively, members of CX3C and C-C chemokines, and both are involved in recruiting and activating mononuclear phagocytes in the central nervous system. We analysed the presence of FKN and MIP-1alpha in sera of untreated MSD patients and healthy donors. High FKN levels were observed in all MSD patients as compared with values only detectable in 26% of healthy donors. MIP-1alpha was measurable in 20% of patients, while no healthy donors showed detectable chemokine levels. In conclusion, we describe a previously unknown involvement of FKN in the pathogenesis of MSD, suggesting that FKN may represent a target for a specific immune therapy of this disease.