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With the availability of better treatment and prophylactic regimens for the infectious complications of human immunodeficiency virus (HIV), the non-infectious complications are gaining greater attention. HIV-related pulmonary arterial hypertension (HIV-PAH) is one of these. The incidence of HIV-PAH is estimated at 0.5% of HIV-infected individuals. The pathogenesis remains unclear. Patients present with symptoms as diverse as progressive shortness of breath, pedal edema, dry cough, fatigue, syncope, as well as chest pain. Chest X-ray always shows cardiomegaly and prominent pulmonary artery, and evidence of right ventricular hypertrophy can be seen from the electrocardiogram. The pulmonary arterial systolic pressure, diastolic pressure and pulmonary vascular resistance from right heart catheterization are increased. There are a few small studies showing the benefit of prostacyclin analog (epoprostenol and iloprost) and bosentan. The role of antiretrovirals remains controversial, as do those of other agents such as calcium channel blockers and anticoagulants. The prognosis of HIV-PAH is grave. Two thirds of HIV-PAH related mortality is usually secondary to consequences of pulmonary hypertension, with the worst survival noted in New York Heart Association (NYHA) functional class III-IV. The probability of survival in one series was 73%, 60% and 47% at one, two and three years, respectively.
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PMID:HIV-related pulmonary hypertension. 1719 95

Respiratory failure results from the incompetence of the respiratory system to eliminate the CO2 produced by the metabolism and to extract the O2 from the atmosphere. Manifestations of the chronic form are: dyspnea, fatigue, headaches, oedema, polyglobulia, and also anxiety, denutrition, social isolation. If neglected, it will lead to pulmonary hypertension and rapidly fatal chronic cor pulmonale. At home mechanical ventilation and oxygen-therapy are the basis of treatment. Major goals of chronic treatment are: control of dyspnea and anxiety, maintenance of a regular physical activity and a sufficient alimentation. These goals can only be achieved by a network of professionals taking charge of these complex patients, with their periodic inclusion in a pulmonary rehabilitation program.
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PMID:[Respiratory insufficiency]. 1742 97

Clinicians should be cognizant of the symptoms and risk factors associated with pulmonary hypertension (PH). While known PH poses significant therapeutic challenges, occult PH carries the added potential for unanticipated complications when treating concurrent medical illnesses. PH may occur with underlying medical conditions and risk factors or may occur de novo as idiopathic pulmonary arterial hypertension (IPAH). Symptoms of PH are frequently attributed to more common conditions, and their nonspecific nature and insidious onset may lead to delay in presentation, evaluation, and diagnosis. Initial symptoms are dyspnea, fatigue, chest pain, and palpitations. Lower extremity edema, presyncope, and syncope are symptoms of more advanced disease. Thorough evaluation of symptoms and identification of patients with risk factors for PH are critical in making a timely diagnosis. History and physical examination can identify patients with suspected PH. Further testing is necessary for definitive diagnosis, classification, assessment of severity, and guiding therapeutic decisions.
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PMID:Clinical presentation, differential diagnosis, and vasodilator testing of pulmonary hypertension. 1753 15

This case involved a 38-year-old man who was referred to our hospital with general fatigue, appetite loss, weight loss, cough and exertional dyspnea. Within a couple of days, he was admitted due to advanced dyspnea and general fatigue. Severe hypoxemia was identified and acute right heart failure developed on admission. Treatment was initiated using oxygen, antibiotics and heparin sodium, but the patient died of sudden cardiopulmonary arrest 30 h after admission. Autopsy revealed advanced gastric cancer and widespread tumor embolism together with fibrocellular intimal proliferation and thrombus formation in the small arteries. Pulmonary tumor thrombotic microangiopathy (PTTM) with gastric cancer was diagnosed. PTTM is characterized by widespread fibrocellular intimal proliferation of the small pulmonary arteries and arterioles in patients with metastatic carcinoma. Microscopic pulmonary tumor emboli frequently occur in patients with malignant tumors, but very few cases of PTTM have been reported. PTTM should be considered in the differential diagnosis of acute dyspnea or pulmonary hypertension. In cases of acute cor pulmonal, the existence of malignant cells can be examined using pulmonary arterial wedge aspiration cytology where feasible, in addition to positron emission tomography with F-2-deoxy-2-fluoro-D-glucose, which can be used to investigate certain primary tumors and associated metastatic disease. The suitability of gastroendoscopy to screen for malignancies should be examined.
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PMID:[Pulmonary tumor thrombotic microangiopathy caused by signet ring cell carcinoma in gastric cancer]. 1768 68

This study deals with clinical features, course and results of an eleven year follow-up of 22 patients with myxoma of the heart, 16 females and 6 males, mean age 48 years. Left atrial myxoma was found in 18 patients (82%) and right atrial myxoma in 4. The most frequent clinical features were fatigue in 64%, shortness of breath in 82%, systemic pulmonary embolism in 50% and prolonged fever in 27% of patients. On auscultation of the heart diastolic murmur was found in the mitral area in 36% and in tricuspid area in 14% of patients. The most helpful diagnostic noninvasive procedure was echocardiography which showed myxoma of the heart in all 22 patients. Left and right heart catheterisation studies were performed in 11 patients; in all patients with left atrial myxoma various degrees of pulmonary hypertension were found. Twenty one patients underwent open heart surgery; in twenty removal of myxoma was performed and in one concomitant mitral valve replacement was done. The mean follow-up of this group of patients was 6.2 years. All patients were asymptomatic and without clinical or echocardiographic signs of reccurrence.
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PMID:[Myxoma of the heart--clinical features, course and long term follow-up]. 1797 99

Pulmonary hypertension (PH) is a hemodynamic state characterized by elevation in the mean pulmonary arterial pressure and pulmonary vascular resistance leading to right ventricular failure and premature death. PH can be the result of a variety of diseases of different etiologies. Pulmonary arterial hypertension (PAH) should be distinctly differentiated from pulmonary venous hypertension (PVH) as a result of left heart disease. PAH is commonly caused by or associated with an underlying pulmonary, cardiac, or systemic disease (APAH). In the absence of an identifiable etiology or associated underlying disease, PAH is referred to as idiopathic (IPAH). IPAH, formerly known as primary pulmonary hypertension (PPH), is a rare disease most commonly seen in women of childbearing age. Presenting symptoms and signs are nonspecific and include dyspnea on exertion, fatigue, and a loud pulmonary component of the second heart sound. Transthoracic Doppler echocardiography is an excellent noninvasive test to detect the presence of pulmonary hypertension, although every patient should receive a right heart catheterization to confirm the diagnosis. A detailed work up, including laboratory tests and imaging studies, is also indicated to rule out known causes of pulmonary hypertension. Several targeted treatment options have become available in recent years and include parenteral and inhaled prostanoids, oral endothelin receptor antagonists, and oral phosphodiesterase type-5 inhibitors. As a result of their complex care, patients should be referred to centers with expertise in pulmonary hypertension.
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PMID:Pulmonary hypertension: evaluation and management. 1800 30

Pulmonary hypertension is a serious disease with a poor prognosis. Pulmonary hypertension is defined by a mean pulmonary arterial pressure over 25 mm Hg at rest or over 30 mm Hg during activity. According to the recent WHO classification from 2003 pulmonary hypertension can be categorized as pulmonary arterial hypertension, pulmonary venous hypertension, hypoxic pulmonary hypertension, chronic thromboembolic pulmonary hypertension and pulmonary hypertension from other causes. Pulmonary arterial hypertension is characterized histopathologically by vasoconstriction, vascular proliferation, in situ thrombosis, and remodeling of all 3 levels of the vascular walls. These pathologic changes result in progressive increases in the mean pulmonary artery pressure and pulmonary vascular resistance, which, if untreated leads to right-ventricular failure and death. Early in the disease process, the signs and symptoms of PAH are often nonspecific, making diagnosis challenging. Patients often present with progressively worsening dyspnea and fatigue. Patients with severe pulmonary arterial hypertension die of right heart failure. The diagnostic procedures include clinical history and physical examination, a standard chest radiography, electrocardiography, transthoracic Doppler echocardiography, pulmonary function tests, arterial blood gas analysis, ventilation and perfusion lung scan, high-resolution computed tomography of the lungs, contrast-enhanced spiral computed tomography of the lungs and pulmonary angiography, blood tests and immunology, abdominal ultrasound scan, exercise capacity assessment, and hemodynamic evaluation. Invasive and non-invasive markers of disease severity, either biomarkers or physiological parameter and tests that can be widely applied, have been proposed to reliably monitor the clinical course. Pulmonary biopsy is rarely indicated. Transthoracic echocardiography is a key screening tool in the diagnostic algorithm. Because transthoracic echocardiography is an inexpensive, easy, and reproducible method, it is the most commonly used noninvasive diagnostic tool to determine pulmonary arterial pressure. But it not only provides an estimate of pulmonary pressure at rest and during exercise, but it may also help to exclude any secondary causes of pulmonary hypertension, predict the prognosis, monitor the efficacy of specific therapeutic interventions, and detect the preclinical stage of the disease. In addition, the measurement of serum markers, such as brain natriuretic peptide (BNP), are diagnostically useful and of prognostic significance. Once the diagnosis and etiology of pulmonary hypertension have been established, several parameters can predict outcome in these patients: functional class, right ventricular function, pulmonary hemodynamics, and certain laboratory parameters. Also, exercise parameters such as walking distance, peak oxygen uptake or peak systolic blood pressure can reliable predict prognosis in these patients.
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PMID:Diagnostics in pulmonary hypertension. 1820 73

Pulmonary hypertension (PH) is a serious form of pulmonary complication that occurs less frequently in lupus than in other connective tissue diseases like scleroderma; however, it is likely that it is under-recognized in lupus. The symptoms of PH in lupus are non-specific (dyspnea, fatigue, impaired exercise tolerance) and can also be caused by other factors such as pleural or pericardial effusions, interstitial lung disease and many more, making it possible to miss the diagnosis. There are several potential causes of PH in lupus including thromboembolic disease, pulmonary vasculitis, and hypoxia and fibrosis from interstitial lung disease. Endothelin-1 is elevated in lupus and may be associated with PAH. In some studies, pulmonary arterial hypertension (PAH) has been found to be a major cause of mortality in lupus patients. Echocardiograms are a screening tool, but may yield false positives, and a right heart catheterization must be performed to confirm PAH. Early identification is important and can alter the natural history of this dangerous complication of lupus. Treatment of PAH associated with lupus includes standard PAH treatment as well as immunosuppression.
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PMID:An update in pulmonary hypertension in systemic lupus erythematosus - do we need to know about it? 1907 76

Congenital unilateral absence of a pulmonary artery is a rare anomaly most frequently accompanied by other cardiovascular anomalies. We report a 10-year-old girl presenting with fatigue and recurrent hemoptysis who was initially misdiagnosed with idiopathic pulmonary hemosiderosis. Her symptoms did not resolve despite treatment so she was referred to our center for further evaluation. We carried out an angiography which revealed the absence of the right pulmonary artery and multiple collaterals originating from the right subclavian and right internal mammary arteries supplying the right lung. During the follow-up the patient developed a severe episode of pulmonary infection and pulmonary hypertension which responded well to medical treatment. Physicians should be aware of the congenital absence of the right pulmonary artery especially in patients presenting with recurrent respiratory symptoms. Although this condition is generally considered to have a good prognosis, close observation is mandatory in order to prevent further complications and comorbidities.
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PMID:A case of congenital agenesis of the right pulmonary artery presenting with hemoptysis and mimicking pulmonary hemosiderosis. 1847 62

Mild-to-moderate pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD); such a complication is associated with increased risks of exacerbation and decreased survival. Pulmonary hypertension usually worsens during exercise, sleep and exacerbation. Pulmonary vascular remodelling in COPD is the main cause of increase in pulmonary artery pressure and is thought to result from the combined effects of hypoxia, inflammation and loss of capillaries in severe emphysema. A small proportion of COPD patients may present with "out-of-proportion" pulmonary hypertension, defined by a mean pulmonary artery pressure >35-40 mmHg (normal is no more than 20 mmHg) and a relatively preserved lung function (with low to normal arterial carbon dioxide tension) that cannot explain prominent dyspnoea and fatigue. The prevalence of out-of-proportion pulmonary hypertension in COPD is estimated to be very close to the prevalence of idiopathic pulmonary arterial hypertension. Cor pulmonale, defined as right ventricular hypertrophy and dilatation secondary to pulmonary hypertension caused by respiratory disorders, is common. More studies are needed to define the contribution of cor pulmonale to decreased exercise capacity in COPD. These studies should include improved imaging techniques and biomarkers, such as the B-type natriuretic peptide and exercise testing protocols with gas exchange measurements. The effects of drugs used in pulmonary arterial hypertension should be tested in chronic obstructive pulmonary disease patients with severe pulmonary hypertension. In the meantime, the treatment of cor pulmonale in chronic obstructive pulmonary disease continues to rest on supplemental oxygen and a variety of measures aimed at the relief of airway obstruction.
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PMID:Pulmonary hypertension in COPD. 1897 37


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