Cases reported "Hypertension, Pulmonary"

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1/57. Right ventricular myocardial bridge in a patient with pulmonary hypertension--a case report.

    Myocardial bridge is a not uncommon finding in routine diagnostic coronary angiography or pathological examination of the heart. It is almost always confined to the left ventricle and the left anterior descending coronary artery. This report describes a patient with chronic lung disease, severe left ventricular dysfunction, and pulmonary hypertension in whom coronary angiography revealed bridging of the right ventricular branch of the right coronary artery.
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ranking = 1
keywords = ventricular dysfunction, left ventricular dysfunction, dysfunction
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2/57. Transient left ventricular failure following bilateral lung transplantation for pulmonary hypertension.

    BACKGROUND: Bilateral lung transplantation is an established therapy for end-stage pulmonary hypertension. Its early postoperative outcome may be biased by various complications resulting in unexpected deterioration of the patient in terms of hemodynamics and blood gases. methods: We have reviewed the early postoperative course of patients who underwent bilateral lung transplantation for pulmonary hypertension at our institution and analyzed all available data, especially hemodynamic measurements, echocardiographic documentation and therapeutical strategies, in those cases where cardiac dysfunction was found to be responsible for clinical deterioration. RESULTS: Three out of 20 lung transplant recipients operated for pulmonary hypertension experienced severe respiratory insufficiency accompanied by hemodynamic decompensation during the first days after surgery. Clinical and laboratory findings together with results of echocardiography and pulmonary artery catheterism helped establish the diagnosis of left ventricular failure. This proved to be transitory, but the response to therapy (inotropic drugs, afterload reduction and eventually prostaglandins) was very variable. Adequately treated, this complication did not preclude the outcome of transplantation by itself. CONCLUSION: Left ventricular failure is a possible complication after lung transplantation for pulmonary hypertension. echocardiography and pulmonary artery catheterism may be useful adjuvant diagnostic tools, beside routine physical examination, chest X-ray, and laboratory analysis. Therapy of this complication must be adapted individually and may be complex.
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ranking = 0.0042634521518782
keywords = dysfunction
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3/57. Pulmonary hypertension caused by Graves' thyrotoxicosis: normal pulmonary hemodynamics restored by (131)I treatment.

    We describe a case of pulmonary hypertension, initially thought to be idiopathic, which resolved after treatment of Graves' hyperthyroidism. Results of pulmonary artery catheterization before and after treatment are reported, and the effects of thyrotoxicosis on hemodynamics and pulmonary function are briefly reviewed. Possible mechanisms for development of pulmonary hypertension caused by hyperthyroidism include pulmonary vascular endothelial dysfunction or damage because of autoimmunity or the high cardiac output state, or increased metabolism of intrinsic pulmonary vasodilators.
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ranking = 0.0042634521518782
keywords = dysfunction
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4/57. Inhaled nitric oxide ameliorates postoperative acute graft dysfunction after living-donor lobar lung transplantation.

    Inhaled nitric oxide, a selective pulmonary vasodilator, decreases mean pulmonary artery pressure and pulmonary vascular resistance and improves oxygenation in previously unobtainable ways without significant changes in systemic hemodynamics. We report successful treatment of a patient with acute graft dysfunction after living-donor lobar lung transplantation using nitric oxide inhalation.
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ranking = 0.021317260759391
keywords = dysfunction
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5/57. Aerosolized iloprost for severe pulmonary hypertension as a bridge to heart transplantation.

    Preexisting pulmonary hypertension in pediatric patients is associated with poor outcome after cardiac transplantation because of donor right ventricular dysfunction. To avoid a combined heart-lung transplantation in a 17-year-old patient, we used an intensified pretreatment with intravenous prostacyclin and dobutamine combined with an inhalative therapy with the aerosolized prostacyclin-analog iloprost. With this regimen, the patient was hemodynamically stabilized for the waiting period of 21 days after which an uneventful cardiac transplantation was performed.
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ranking = 0.89579370840183
keywords = ventricular dysfunction, dysfunction
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6/57. Stenting to reverse left ventricular ischemia due to left main coronary artery compression in primary pulmonary hypertension.

    Angina is a common symptom of severe pulmonary hypertension. Although many theories for the source of this pain have been proposed, right ventricular ischemia is the one most commonly accepted as the cause. We report on two patients with primary pulmonary hypertension who had angina with normal activity or on provocation. One patient had severe left ventricular dysfunction. Both were found to have severe ostial stenosis of the left main coronary artery as a result of compression from a dilated pulmonary artery. Both patients underwent stenting of the left main coronary artery with excellent angiographic results, and complete resolution of the signs and symptoms of angina and left ventricular ischemia. Left ventricular ischemia due to compression of the left main coronary artery may be a much more common mechanism of angina and left ventricular dysfunction in patients with pulmonary hypertension than previously acknowledged. Stenting of the coronary artery can be done safely with the resolution of these symptoms.
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ranking = 2
keywords = ventricular dysfunction, left ventricular dysfunction, dysfunction
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7/57. Regression of hiv-associated pulmonary arterial hypertension and long-term survival during antiretroviral therapy.

    In a 37-year-old patient hiv infection was diagnosed in June 1986. Eight years later the patient complained of increasing shortness of breath and occasional syncopes on exertion. He developed peripheral oedema and ascites. echocardiography revealed severe pulmonary hypertension. Right ventricular systolic pressure (RVSP) was 77 mm Hg. There was no evidence of left ventricular dysfunction, valvular heart disease, thromboembolic disease or obstructive or restrictive lung disease, nor were there other known causes or risk factors of pulmonary hypertension. hiv-associated pulmonary arterial hypertension was diagnosed. Oral anticoagulation and zidovudine were begun, but RVSP rose to 96 mm Hg. After the introduction of lamivudine, and later stavudine and nelfinavir, hiv-rna copies decreased from 133 400 to below 50 copies per mL. Six years after the diagnosis of hiv-associated pulmonary arterial hypertension RVSP had continually fallen to 49 mm Hg and the grossly enlarged right heart dimensions had nearly normalised without vasodilator treatment. The patient remains in excellent health and his sole complaint is of mild dyspnoea on exertion.
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ranking = 0.0042634521518782
keywords = dysfunction
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8/57. Staged fontan procedure for mitral atresia associated with severe tricuspid regurgitation, pulmonary hypertension, and pulmonary artery distortion.

    Optimal initial palliation and a subsequent staged approach is mandatory for high-risk Fontan candidates. We describe the case of mitral atresia with severe tricuspid regurgitation and pulmonary hypertension successfully managed by repeated palliation from the neonatal period and 2-stage Fontan surgery. A 1-month-old boy diagnosed with mitral atresia and double-outlet right ventricle underwent pulmonary artery banding at 1 month of age, followed by repeated pulmonary artery banding accompanied by tricuspid annuloplasty and atrial septal defect enlargement at 6 months. Because of the presence of pulmonary artery distortion, right ventricular dysfunction, and borderline pulmonary vascular resistance, a hemi-fontan procedure was conducted with extended pulmonary artery plasty when the boy was 3 years and 8 months old. cardiac catheterization done 3 months after showed improvement in risk factors, and the final Fontan operation (total cavopulmonary connection) was successfully done in conjunction with repeated tricuspid annuloplasty when the boy was 4 years and 5 months old. The patient remains in excellent clinical condition at the last follow-up 5 years after the final fontan procedure with sinus rhythm and good ventricular function.
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ranking = 0.89579370840183
keywords = ventricular dysfunction, dysfunction
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9/57. Misalignment of lung vessels: diagnostic role of conventional histology and immunohistochemistry.

    Misalignment of lung vessels represents a rare congenital anomaly that may cause respiratory failure in the newborn. It is characterized by abnormal position of pulmonary veins and venules that lie adjacent to arteries and bronchi, and it is usually associated with a decreased number of alveolar capillaries (i.e., alveolar capillary dysplasia), although these two conditions have been separately described. awareness of this anomaly is required by pathologists because it can be easily overlooked on lung biopsy or autopsy, and because definite diagnosis relies on histology. We report the case of a newborn male baby who developed respiratory distress 18 h after an uncomplicated delivery. The patient died on the 7th day, after high frequency oscillatory ventilation, nitric oxide inhalation and extracorporeal membrane oxygenation were unsuccessful. On autopsy, histology and immunohistochemistry demonstrated diffuse changes, fulfilling diagnostic criteria of misalignment of lung vessels and of alveolar capillary dysplasia in both lungs, with muscularization of very peripheral pulmonary arteries and a prominent interstitial and periadventitial fibrosis. Diffuse distribution of vessel misalignment could explain the rapid onset of respiratory failure, and the presence of diffuse fibrosis might have contributed to irreversible respiratory dysfunction by impairment of lung parenchyma extensibility.
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ranking = 0.0042634521518782
keywords = dysfunction
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10/57. A 25-year clinical history of portopulmonary hypertension associated with latent myeloproliferative disorder.

    Pulmonary hypertension associated with increased pulmonary vascular resistance occurring in the setting of portal hypertension, referred to as "portopulmonary hypertension", is a complication of chronic liver disease, and occurs in 2% to 3% of patients with portal hypertension. Portal hypertension is a relatively common finding in patients with chronic myeloproliferative disorder (CMPD). Pulmonary hypertension is also an occasional finding in CMPD patients. Latent myeloproliferative disorder, on the other hand does not fulfill the diagnostic criteria of classical CMPD and is characterized by younger age of onset, slow disease progression, a high risk of thrombosis, platelet dysfunction, and normal or increased platelet count in spite of the presence of splenomegaly. We report findings in a 50-year-old woman with portal hypertension for which there were three major etiological findings-increased splenic blood flow, infiltration of hematopoietic cells in the liver, and thrombosis in the portal or hepatic vein-over a 25-year clinical course, during which there was also reversible stenosis of the portal vein. Twenty-three years after her first admission, her condition was diagnosed as latent myeloproliferative disorder, and she developed pulmonary hypertension. Her clinical history and data indicated that the portopulmonary hypertension was due to the latent myeloproliferative disorder.
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ranking = 0.0042634521518782
keywords = dysfunction
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