Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether a better understanding of primary pulmonary hypertension has affected its clinical presentation, natural history, and prognosis, we retrospectively compared patients with primary pulmonary hypertension presenting to our institution during two different periods: 1962 to 1978 (group 1, n = 38) and 1979 to 1989 (group 2, n = 33). Demographic characteristics were similar in both groups. Dyspnea on exertion was the most frequent presenting symptom in both groups. Fatigue, cough, dizziness, right heart failure, and cyanosis were more frequent in group 1. The electrocardiographic, radiographic, and echocardiographic findings did not differ between groups. Hemodynamic measurements revealed severe pulmonary hypertension and a normal pulmonary capillary wedge pressure and cardiac index; these measurements were similar in both groups. Complications related to cardiac catheterization were more frequent in group 1 (32%) than in group 2 (3%). Causes of death were comparable in both groups, the most frequent being progressive right heart failure, sudden death, and death of unknown cause. Patients from both groups received standard treatment with digitalis, diuretics, and vasodilators; however, group 2 had a higher probability of survival than group 1. We conclude that patients with pulmonary hypertension seen in more recent years tend to present at earlier stages of disease, have fewer complications during cardiac catheterization, and probably survive longer than those seen several decades ago. A clear cause for the longer survival could not be identified, although it may be partly related to earlier presentation in the course of disease.
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PMID:Primary pulmonary hypertension, then and now: 28 years of experience. 152 74

A 56-year-old woman with aortic arch syndrome and finally right pulmonary artery obstruction secondary to Takayasu's aortitis was presented. She had had a history of visual disturbance and dizziness when she looked upward since 1983. On admission in July, 1984, aortography showed obstruction of the right innominate artery and of the left subclavian artery. Pulmonary arterial pressure, pulmonary perfusion and ventilation images seemed to be normal at that time. After discharge from our hospital, she began in 1987, to be aware of dyspnea on effort. Because of this symptom, she was admitted again in March, 1988. The pulmonary perfusion images showed complete lack of perfusion in the right lung, and arterial blood gas showed hypoxia with 62 mmHg in PaO2, 39 mmHg in PaCO2. Cardiac catheterization confirmed pulmonary hypertension with pulmonary artery pressure of 56/18 mmHg. In conclusion, pulmonary perfusion and ventilation scintigraphy proved to be the best way to clarify the nature of a lesion of the pulmonary artery in aortitis syndrome.
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PMID:[Right pulmonary artery obstruction and pulmonary hypertension secondary to aortitis syndrome]. 223 68

A clinical syndrome identical to the chronic mountain sickness of the Andes occurs commonly in Lhasa, Tibet. It affects, almost exclusively, the immigrant Han population and develops after an average of 15 years' residence at high altitude. The early symptoms are attributable to polycythaemia--headache, dizziness, loss of memory and fatigue being prominent. In the later stages of the disease, dyspnoea and peripheral oedema develop. Haemodynamic investigations show pulmonary hypertension with a normal cardiac output and dilatation of the right ventricle in the long-established case. Respiratory gas studies provide evidence of alveolar underventilation and ventilation: perfusion inhomogeneity. Both clinical and investigatory data suggest that the earlier stages of the disease are dominated by polycythaemia, while cardiopulmonary involvement increases with the duration of the disease. The disease is rare in women and uncommon in Tibetans. Cigarette smoking appears to be a contributory factor.
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PMID:Chronic mountain sickness in Tibet. 251 94

Urapidil is a postsynaptic alpha 1-adrenoceptor antagonist with a pharmacodynamic profile similar to prazosin. Unlike prazosin, however, urapidil also has some central activity which may explain the apparent improved tolerability of urapidil, including the absence of first-dose syncope. In clinical trials urapidil therapy resulted in significant reductions in blood pressure in patients with mild to severe essential hypertension, with little influence on heart rate. It is an effective antihypertensive when administered as monotherapy or in combination with beta-blockers and thiazide diuretics. In the few patients with cardiac dysfunction who have been studied to date, urapidil has improved myocardial oxygen consumption, systemic vascular resistance, left ventricular function, cardiac output and pulmonary capillary wedge pressure; however, further study is needed to assess the full therapeutic potential of urapidil in these patients. Urapidil has also been used successfully in the treatment of hypertensive emergencies, including eclampsia and pre-eclampsia, hypertensive crisis and hypertension occurring during general and cardiac surgery, rapidly lowering blood pressure without altering heart rate. Urapidil does not affect lipid or glucose metabolism, nor does it impair renal function. In addition, urapidil may be beneficial to patients with pulmonary hypertension, in whom it dilates pulmonary vascular beds to a greater extent than systemic vasculature, although therapeutic trials have not examined this effect. The most common adverse effects associated with urapidil therapy are dizziness, nausea, headache, fatigue and palpitations; however, these tend to be mild and transient and usually do not require discontinuation of treatment. Thus, urapidil offers a useful alternative to currently available drugs for the treatment of mild to severe hypertension, either as monotherapy or in combination with other antihypertensive drugs.
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PMID:Urapidil. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in the treatment of hypertension. 269 46

Two autopsy cases of pulmonary hypertension (PH) associated with liver cirrhosis are presented. Both patients were hepatitis B (HB) virus carriers and suffered from type B cirrhosis during the clinical course. The first patient was a 52-year-old male with type B cirrhosis. He died of hepatic encephalopathy but did not have any specific symptoms for PH except abnormal laboratory findings. Chest roentgenograms displayed prominence of the central pulmonary artery. Cardiac catheterization indicated marked increment of pulmonary arterial pressure. Autopsy revealed dilatation and sclerosis of the main pulmonary artery and right ventricular hypertrophy. Microscopically, the pulmonary arteries showed intimal fibrosis, medial hypertrophy, and plexiform lesions throughout the lungs. The second patient, a 15-year-old boy, had PH with juvenile liver cirrhosis which had existed for 8 years prior to the onset of PH. He complained of severe dyspnea and dizziness before death. Electrocardiogram indicated right ventricular hypertrophy. Autopsy disclosed cardiomegaly, type B cirrhosis and sclerotic pulmonary arteries. Grade VI pulmonary plexogenic arteriopathy including plexiform lesions and necrotizing arteritis was observed. HBsAg was detected in both the hepatocytes and the pulmonary arterial walls. We discuss the possible relationship between persistent HB viral infection and PH with liver cirrhosis.
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PMID:Pulmonary hypertension in hepatitis B virus carriers. 344 51

A case of progressive systemic scleroderma in a 33 year-old woman who was referred to our Arrhythmia Unit due to daily palpitations and dizziness is presented. The 24-hour Holter recording showed monomorphic ventricular tachycardia which lasted several minutes. Hemodynamic study showed dilated right chambers and right ventricular dysfunction, without pulmonary hypertension. Left ventricular angiography and coronary arteries were normal. During programmed electrical stimulation, two different ventricular tachycardia were induced and ablated with radiofrequency on the right ventricle. The patient remains free of recurrence of tachycardia after (10 months of follow up). Patients with progressive systemic scleroderma may present several different cardiac arrhythmias. Involvement of the right ventricle is particularly frequent as is the origin of ventricular tachycardia in this ventricle. Radiofrequency catheter ablation is safe and effective in the management of these patients.
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PMID:[Radiofrequency ablation of recurrent monomorphic ventricular tachycardia in a patient with severe systemic scleroderma]. 1126 81

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

We report 2 patients with recurrent syncope and dizziness, later noted to have single coronary arteries. Both had right heart strain, one having pulmonary hypertension and the other having right ventricular outflow obstruction, which resulted in sinus node dysfunction. Patients were refractory to medical therapy and improved after pacemaker implantation.
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PMID:Single coronary artery and sick sinus syndrome. 1204 27

Pulmonary hypertension is a disorder characterized by an increase in mean pulmonary arterial pressure (mPAP > 25 mmHg), which is responsible for the transport of blood from the heart to the lungs. Increased pressure leads to decreased flow of blood through the lungs and decreased oxygen deliverance throughout the body. The disorder causes right ventricular hypertrophy and can quickly lead to death, especially with the severe forms of pulmonary hypertension. Symptoms include fatigue, shortness of breath, dizziness and peripheral edema in the lower extremities. Symptoms are usually delayed in appearance and progress slowly, which leads to a late diagnosis and often a poor prognosis. Despite large advances in the last 10 years, there is still about a 15% annual mortality for diagnosed patients. Despite the number of medications available, there are still no cures for this fatal disease. Current therapies include endothelin receptor antagonists, prostacyclin agonists and cGMP-specific 3',5'-cyclic phosphodiesterase (PDE5) inhibitors or combinations. Recent strategies have shown promise in animal models to prevent the onset of pulmonary hypertension when it is induced. However, few of them show a sustained benefit in clinical trials. Strategies for the cure of this debilitating disease should be the focus of future research.
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PMID:Current and future treatment of pulmonary hypertension. 2238 53

Glycogen storage diseases (GSDs) comprise a large, heterogeneous group of disorders characterized by abnormal glycogen deposition. Multiple cases in the literature have demonstrated an association between GSD type I and pulmonary arterial hypertension (PAH). We now also report on two patients with GSD type III and PAH, a novel association. The first patient was a 16-year-old girl of Nicaraguan descent with a history of hepatomegaly and growth retardation. Molecular testing identified a homozygous 17delAG mutation in AGL consistent with GSD type IIIb. At the age of 16, she was found to have PAH and was started on medical therapy. Two years later, she developed acute chest pain and died shortly thereafter. The second patient is a 13-year-old girl of Colombian descent homozygous for the c.3911dupA mutation consistent with GSD IIIa. An echocardiogram at age 2 showed left ventricular hypertrophy, which resolved following the institution of a high protein, moderate carbohydrate diet during the day and continuous gastric-tube feeding overnight. At the age of 12, she was found to have pulmonary hypertension. She was started on sildenafil, and her clinical status has shown marked improvement including normalization of her elevated transaminases. PAH may be a rare association in patients with GSD IIIa and IIIb and should be evaluated with screening echocardiograms for cardiac hypertrophy or if they present with symptoms of right-sided heart failure such as shortness of breath, chest pain, cyanosis, fatigue, dizziness, syncope, or edema. Early diagnosis of PAH is important as increasingly effective treatments are now available.
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PMID:Two Cases of Pulmonary Hypertension Associated with Type III Glycogen Storage Disease. 2343 Aug 32


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