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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mitral Valve Prolapse (MVP) is a common cardiac disorder in our community. It is estimated that 4% to 15% of the general population have the anatomical defect of prolapsed mitral valve leaflets during ventricular systole. Patients with MVP that suffer from chest pain, dyspnea, fatigue, dizziness, syncope, palpitations, cardiac arrhythmias, anxiety, and panic attacks are diagnosed as having Mitral Valve Prolapse Syndrome. There is much controversy in the medical literature as to the causes of MVPS symptomatology. Some scientists believe that autonomic dysfunction, adrenergic, and vagal responsiveness are factors which appropriately explain the symptoms of MVPS. Pharmacological therapy, depending on the severity of the symptoms, is one option for treatment. Education on the etiology of their symptoms, instruction on lifestyle modifications, and reassurance from their physician are appropriate methods for the management of MVPS patients.
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PMID:Mitral valve prolapse. 186 Oct 97

Clinical symptoms were studied in 69 consecutive patients below the age of 40 years who were attending the emergency unit because of unexplained chest pain. In a structured interview a few weeks after the emergency visit, only one-third of the patients reported that they believed in the doctor's diagnosis; they believed in a psychological or cardiac origin of the pain more often than the doctors. The chest pain was most often described as oppressive and/or stabbing. In 95% of cases it was central or left-sided. Associated symptoms were commonly reported, breathlessness being most commonly reported by two-thirds of the patients, followed by dizziness, palpitation and numbness/tingling. Mental symptoms such as tiredness, anxiety and tension were frequently reported. On the basis of the background literature the aetiology is discussed. We conclude that immediate symptom analysis, including psychosomatic symptoms, particularly breathing problems, is of central importance.
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PMID:Clinical symptoms in young adults with atypical chest pain attending the emergency department. 189 50

The associations between exercise capacity, symptoms and specific aspects of quality of life were examined in subjects participating in a trial of the treatment of heart failure. Patients were assessed on entry and after three months treatment. The principle symptoms were fatigue, breathlessness and chest pain. These limited the extent and speed of physical activities, restricted social, leisure and family life and were associated with emotional distress. There were associations between baseline exercise capacity and measures of quality of life. Change in exercise capacity during three months treatment was correlated with changes in measures of symptoms, limitation of activity and quality of life. The findings confirm the value of change in exercise capacity as a measure of functional status and suggest that it should be supported by a limited number of specific measures of quality of life.
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PMID:Cardiac failure: symptoms and functional status. 192 Jan 71

We present 3 cases of apical hypertrophic cardiomyopathy. The presenting symptoms were dyspnea on exertion in 2 of 3 patients, typical anginal pain in 1 patient, atypical chest pain in 1 patient, and fatigue in 1 patient. One patient was asymptomatic with an abnormal electrocardiogram. Sustained apical impulse was noted in all patients, Grade 1/6 systolic murmur was audible in 2 patients. Electrocardiogram showed T wave inversion in the left precordial leads in all patients with amplitudes of 1.4, 0.8 and 2.0 mV, respectively. Isolated apical hypertrophy was noted in all patients. Two-dimensional echocardiogram and the left ventriculogram revealed a "spade-shaped" configuration of the left ventricular cavity at endo-diastole in only one patient. Left ventricular end diastolic pressures were elevated and coronary angiograms were normal in all 3 cases. We conclude that this disease entity should be considered in patients whose electrocardiogram shows a large inverted T wave in the left precordial leads, either accompanied by symptoms such as dyspnea on exertion or chest pain, or even when asymptomatic. Echocardiogram is the most useful screening tool in the diagnosis of apical hypertrophic cardiomyopathy.
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PMID:Apical hypertrophic cardiomyopathy: clinical, echocardiographic and angiographic features in 3 Chinese patients. 197 49

To determine the clinical, laboratory and hemodynamic profile in patients with primary pulmonary hypertension and associated portal hypertension, 7 new cases and 71 previously reported cases were analyzed. There was no gender predilection and the average age at diagnosis was 41 years. Liver cirrhosis was the most frequent cause of hypertension (82%) and a surgical portosystemic shunt was present in 29%. Almost invariably, portal hypertension either preceded or was diagnosed concurrently with pulmonary hypertension, favoring the hypothesis that in portal hypertension, the pulmonary vasculature may be exposed to vasoactive substances normally metabolized or produced by the diseased liver, possibly inducing vasoconstriction or direct toxic damage to the pulmonary arteries. Clinically, exertional dyspnea was the most frequent presenting symptom (81%); other symptoms, such as syncope, chest pain and fatigue, were present in less than 33%. An accentuated pulmonary component of the second heart sound (82%) and a systolic murmur (69%) were the most common physical findings. At least 75% of these patients had evidence of pulmonary hypertension on electrocardiography (right ventricular hypertrophy) or roentgenography (cardiomegaly or dilated main pulmonary arteries, or both). Hemodynamic findings included severe pulmonary hypertension (mean pulmonary artery pressure 59 +/- 19 mm Hg) with normal pulmonary capillary wedge pressure and cardiac output. Treatment was basically palliative and the mean and median survival times were 15 and 6 months, respectively. In brief, on the basis of clinical presentation and laboratory features, patients with combined primary pulmonary hypertension and portal hypertension seldom represent a diagnostic challenge. Further research is needed on treatment, which remains palliative. The survival rate is poor and worse than that seen in isolated primary pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association between primary pulmonary hypertension and portal hypertension: analysis of its pathophysiology and clinical, laboratory and hemodynamic manifestations. 199 8

The effects of a 12-week aerobic exercise training protocol on 32 symptomatic women with mitral valve prolapse were studied. Subjects were randomly assigned to control or exercise groups. Exercise subjects completed a 12-week (3 times per week) exercise training program based on guidelines established by the American Heart Association for phase II cardiac rehabilitation programs; control group subjects maintained normal activities. Before and after training, subjects underwent maximal multistage treadmill testing, and measurements were obtained for plasma catecholamine levels at rest and during peak exercise; they completed the State Trait Anxiety Inventory and General Well-Being Schedule. Weekly symptom frequency of chest pain, arm pain, palpitations, shortness of breath, fatigue, headache, mood swings, dizziness and syncope were monitored for the 12-week period. Data were analyzed using multivariate analysis of variance, multivariate analysis of covariance, and analysis of covariance with repeated measures. Compared with control subjects, the exercise group showed a significant (p less than 0.05) decrease in State Trait Anxiety Inventory scores, an increase in General Well-Being scores, an increase in functional capacity and a decline in the frequency of chest pain, fatigue, dizziness and mood swings. No statistically significant differences were noted in catecholamine levels at rest or during peak exercise. These findings support the use of aerobic exercise in the management of symptomatic women with mitral valve prolapse.
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PMID:Effects of aerobic exercise training on symptomatic women with mitral valve prolapse. 201 86

In a double-blind study comparing two active treatments (digoxin and xamoterol) and placebo in patients with heart failure, improvements in exercise capacity and quality of life were observed in all three groups, with no significant differences. The substantial benefits seen in the placebo group were probably the result of increased attention from the medical and research staff and suggest the therapeutic value of special heart failure clinics. The relationship between exercise and symptomatic/functional status has been unclear. We developed quantitative measures of quality-of-life variables and examined their relationship with exercise capacity. There were significant relationships between change in exercise duration and changes in breathlessness, tiredness, chest pain, walking difficulty, rate of walking, difficulty with daily tasks, speed of daily tasks, mood, and sleeping. This study confirms the validity of measuring change in exercise capacity and demonstrates that specific measurements of quality of life make an important contribution to the evaluation of the treatment of heart failure.
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PMID:Exercise capacity and quality of life in the treatment of heart failure. 214 3

Primary pulmonary hypertension is an enigmatic disease found predominantly in young women, but it also affects a significant number of middle-aged and elderly males and females. Its onset, characterized by progressively worsening dyspnea, fatigue, and chest pain, is insidious. Three distinct histopathologic subtypes have been identified, and the natural history of the disease process has been well-defined. Pharmacologic treatment options have, in general, been disappointing, and it appears that heart-lung transplantation will be applied only to a small minority of young patients with primary pulmonary hypertension in the near future. We review the histopathology, evaluation, treatment, and prognosis of primary pulmonary hypertension.
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PMID:Primary pulmonary hypertension in adults. 218 65

Squash is a moderate- to high-intensity intermittent exercise. Players are active 50 to 70% of the playing time. 80% of the time, the ball is in play 10 seconds or less. The rest intervals fit a normal distribution with an average duration of 8 seconds. Heart rate increases rapidly in the first minutes of play and remains stable at approximately 160 beats/min for the whole match no matter what levels the players are. The energy expenditure for medium-skilled players is approximately 2850 kJ/h and over 3000 kJ/h for A grade players. The thermal and metabolic response to squash is similar to that of moderate intensity running. Hyperglycaemia, elevated free fatty acids and growth hormone levels, and low serum insulin values are the common metabolic changes. Blood lactate levels are understandably low due to the very short work to rest pattern of play. Injuries are not frequent in squash but they can occur. Serious eye injuries have been documented and as a result protective equipment is highly recommended. To reduce the possibility of sudden death on the court or after the game, older players that present some risk factors for cardiovascular disease should be warned against smoking after the game and informed of the serious implications of the development of chest pain, or undue tiredness before, during or after squash.
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PMID:Applied physiology of squash. 219 98

Although most patients with coccidioidomycosis are asymptomatic, up to 40 percent develop fatigue, cough, chest pain and fever. Erythema nodosum is often present. Chest radiographs may be normal or may show hilar adenopathy, infiltrates, pulmonary nodules or thin-walled cavities. The spherulin skin test is usually positive within three weeks of infection. Specific IgM [corrected] antibodies may be detected early in the course; IgG [corrected] antibodies develop after two to three months. In most patients, the disease has a self-limited course and requires no specific therapy. A few patients develop progressive pulmonary or disseminated disease. Extrapulmonary sites of disease include the skin, the skeleton and, rarely, the nervous system. Amphotericin B and ketoconazole are used to treat disseminated disease. Because coccidioidomycosis is caused by a fungus that is endemic in the Southwest, a travel history should be elicited from patients with persistent pulmonary symptoms.
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PMID:Coccidioidomycosis: office diagnosis and treatment. 233 27


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