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Query: UMLS:C0019079 (hemoptysis)
6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevation of pulmonary arterial pressure may be secondary to many diseases of the lungs, chest wall, and heart. From a pathophysiologic viewpoint, pulmonary hypertension is secondary to vascular obstruction, vasoactivity, increased circulation, and passive forces. Clinically, the entities that result in secondary pulmonary hypertension present with a picture that identifies the primary disease. Patients with primary pulmonary hypertension may be difficult to identify. Pulmonary hypertension may present early with dyspnea and fatigue, while syncope and hemoptysis are late symptoms. In many instances, pulmonary hypertension can be diagnosed utilizing physical examination and noninvasive tests. Eventually, right heart catheterization is necessary to confirm the diagnosis and to monitor trials of therapy with vasodilators. Treatment may be specific (closure of a septal defect, thromboendarterectomy) or generic (vasodilators). These have been used recently for both secondary and primary pulmonary hypertension in an effort to reduce pulmonary vascular resistance, thereby decreasing right ventricular afterload and improving cardiac output and oxygen delivery. The success of these treatments has not been demonstrated.
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PMID:Pulmonary hypertension: etiology and clinical evaluation. 333 61

The objective of this study was to determine the long-term survival pattern and variables affecting long-term survival and complications occurring during follow-up of patients with Eisenmenger syndrome. A retrospective study of patients diagnosed with Eisenmenger syndrome were followed up. A tertiary care centre was used and it provided superspeciality services in various disciplines. The subjects included 201 patients with Eisenmenger syndrome--diagnosed by a combination of echocardiography and a peripheral arterial oxygen saturation study and/or cardiac catheterisation with or without angiocardiography--worked up and followed up for variable duration over a period of 16 years from 1976 to 1992. One hundred nine patients were females and 92 were males--age of presentation varied from 3 months to 62 years (mean +/- standard deviation 19.23 +/- 12.62 years). A total of 12 different anatomic lesions were seen--the most common three being ventricular septal defect (33.33%), aterial septal defect (29.85%), and patent ductus arteriosus (14.23%). History, physical examination, chest skiagram and electrocardiogram established only the presence of pulmonary arterial hypertension except where differential cyanosis indicating ductus was discernible or the degree of splitting of second heart sound provided some clue to the level of shunt. Contrast echocardiography, completed in 25.4% established the level of shunt in all patients. In others the diagnosis was confirmed by cardiac catheterisation. Twenty patients died during a mean follow-up period of 54.6 +/- 54.47 months. Sudden cardiac deaths (30%), congestive heart failure (25%) and haemoptysis (15%) were the most predominant causes of death. Only one patient died during puerperium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognosis for patients with Eisenmenger syndrome of various aetiology. 796 Feb 65

A retrospective study of adults with Eisenmenger syndrome assessed at a tertiary referral center was performed to identify clinical characteristics and establish prognostic determinants. Mortality and cause of death are reported with baseline clinical data correlated with mortality to identify predictors of death. Clinical events during follow-up, including heart failure, atrial arrhythmia, hemoptysis, and syncope were also reviewed. A total of 109 adults with Eisenmenger syndrome (mean +/- SD age 29 +/- 11 years, 43% men) were followed for a median of 6.3 years. Sixty-six patients (61%) had simple cardiac anatomy (13 atrial septal defect, 43 ventricular septal defect, 10 patent ductus arteriosus). The remainder (43 patients) had complex cardiac anatomy (including atrioventricular septal defect, truncus arteriosus, univentricular heart, and transposition of the great arteries). There were 33 deaths and 9 transplantations during follow-up. Median survival was 53 years. Multivariate Cox regression analysis identified age at presentation (hazard ratio [HR] 0.90), supraventricular arrhythmia (HR 3.44), precordial electrocardiogram voltage (HR 1.61/mV increase), and poor New York Heart Association functional class (HR 2.60) as independent predictors of mortality. There is a large variation in the life expectancy for adults with Eisenmenger syndrome. Baseline characteristics associated with increased mortality include younger age at presentation (associated with complex anatomy), functional class, supraventricular arrhythmia, and an electrocardiogram index for right ventricular hypertrophy.
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PMID:Determinants of survival and length of survival in adults with Eisenmenger syndrome. 1049 38