1,721,017 research outputs found

    Esiste e cos'è il "cuore senile"?

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    The study of the aging heart raised for a long time difficulties in distinguishing the age-related physiological processes from the associated pathological changes. In recent years, however, several obscure or controversial items have been clarified through a wide use of imaging techniques such as echocardiography, positron emission tomography, and of molecular biology. The general notion of remodeling has been extended to include the arterial capacitance vessels, and the emerging concept of "ventricular-arterial coupling" has yielded a rational explanation for some structural and functional changes of the aging heart. Particular attention has been paid to the left ventricular diastolic dysfunction, while the new data have generally confirmed the old ones regarding the preserved systolic performance at rest. The aging of the heart should anyhow be considered in the context of the "cardiopulmonary unit" and by the light of the new acquisitions on the loss of skeletal muscle mass and strength (sarcopenia)

    Treatment of acute attacks of hereditary angioedema with C1-inhibitor concentrate

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    Attacks of laryngeal edema in patients with hereditary angioedema (HAE) have been successfully treated with the infusion of C1-inhibitor (C1-INH) concentrate. No side effects were observed

    Idiopathic nonhistaminergic angioedema

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    PURPOSE: We sought to describe the characteristics of a group of patients with idiopathic nonhistaminergic angioedema and their response to prophylactic treatment with tranexamic acid. METHODS: We identified 25 patients (15 men and 10 women; age at diagnosis 16 to 77 years) who had idiopathic nonurticarial angioedema that was not prevented by histamine-1 (H1) blockers. Known causes of angioedema were excluded by clinical history, physical examination, and diagnostic tests. RESULTS: The median age at the onset of symptoms was 35 years (range 8 to 66). The frequency of attacks was > 12 per year for 16 patients, six to 11 per year for 6 patients, and one to five per year for 3 patients. All patients had cutaneous attacks, 13 (52%) reported swellings of the pharynx or larynx, and 5 (20%) had symptoms consistent with bowel angioedema. Because of the similarities between these patients and patients who are deficient in C1 inhibitor, the 15 patients with severe and frequent attacks were started on prophylactic treatment with the antifibrinolytic agent tranexamic acid, 1 g three times a day orally for 3 months, tapered according to its effectiveness. The symptoms of 11 patients decreased to less than one attack per year, and the remaining 4 patients had partial remissions (less than 4 attacks per year). Fourteen patients are still being treated with tranexamic acid. CONCLUSION: Patients with idiopathic nonhistaminergic angioedema appear to have similar clinical features and response to treatment with tranexamic acid as those who are deficient in C1 inhibitor. This suggests that those two forms of angioedema might have, at least in part, a similar pathogenesis

    Angioedema associated with angiotensin-converting enzyme inhibitor use : outcome after switching to a different treatment

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    Background: Angiotensin-converting enzyme (ACE) inhibitors are associated with angioederna episodes that are potentially life-threatening. Few data are available on the outcome of patients reporting this adverse effect when they are switched to another drug. Scattered reports of angioedema associated with angiotensin 11 receptor blocker (ARB) use question the safety of using these drugs in patients with ACE inhibitor-related angioedema. We describe 64 consecutive patients with ACE inhibitor-related angioedema, the outcome after discontinuing this treatment, and the safety of using ARBs. Methods: Retrospective analysis of 64 consecutive patients (January 1993 to June 2002) presenting with angioedema onset while receiving treatment with an ACE inhibitor. Results: Patients were recommended to stop ACE inhibitor use, substituting it upon advice of the physician. Fifty-four patients were available for follow-up (median follow-up, 11 months; range, 1-80 months): 26 had switched to an ARB, 14 to a calcium antagonist, and 14 to other antihypertensive drugs. Angioedema disappeared or drastically reduced upon withdrawal of the ACE inhibitor in 46 patients (85%). For the remaining 8 patients, angioedema was due to a cause other than ACE inhibitor use in 2; angioedema persisted independent of the treatment and without apparent cause (idiopathic angioedema) in 4; angioedema persisted after switching to an ARB and disappeared upon its withdrawal in 2. Conclusions: Stopping ACE inhibitor use without further assessments is a successful measure in the large majority of patients developing angioedema while taking this drug. Only a small percentage of patients with ACE inhibitor-related angioedema continue with this symptom when switched to an ARB
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