Cases reported "Hypertension"

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11/22. Ocular ichemia syndrome - a malignant course of giant cell arteritis.

    PURPOSE: To call attention to a malignant course of ocular ischemic syndrome in patients with giant cell arteritis (GCA). methods/PATIENT: A 84-year-old woman developed severe headache for about 3 (1/2) months prior to myocardial infarction and visual disturbances. RESULTS: An anterior ischemic optic neuropathy (AION) in the right eye with a distinct reduction in visual acuity was found. The retina revealed several cotton-wool spots in both eyes. Serologic examinations showed inflammatory signs. Despite treatment with prednisolone, eye pressure decreased to 2 mm Hg in the right eye and 4 mm Hg in the left eye in a few days. An ischemic iritis developed in the right eye. visual acuity worsened to detection of hand motions in the right eye and to 0.1 in the left eye. Approximately 8 (1/2) months after her initial headache, a biopsy was carried out. The patient was treated continuously with corticosteroids. histology of the superficial temporal artery indicated inflammatory cells in the vessel wall. - The patients daughter developed symptoms of GCA at the age of 54 years. CONCLUSION: An ocular ischemic syndrome points to a malignant course of the disease. A cardiac infarction can develop in GCA. A biopsy of the temporal artery can reveal inflammatory changes even after 8 (1/2) months.
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12/22. Increased mitral regurgitation during the valsalva maneuver in a patient with pheochromocytoma, uncontrolled hypertension, cardiac hypertrophy, and dynamic outflow tract obstruction.

    Dynamic left ventricular outflow tract obstruction is a common feature of hypertrophic cardiomyopathy, but it can also be demonstrated in other conditions that result in increased thickness of the left ventricular septal wall. Severe uncontrolled hypertension may lead to severe hypertrophy of the left ventricle and produce systolic anterior motion of the mitral valve and an outflow gradient. We report a case of pheochromocytoma with echocardiographic demonstration of markedly increased mitral regurgitation during the valsalva maneuver in a patient with left ventricular hypertrophy and a dynamic outflow tract obstruction.
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13/22. posture- and emotion-induced severe hypertensive paroxysms with baroreceptor dysfunction.

    In a patient followed up for 30 years, severe but brief posture- or emotion-induced hypertensive paroxysms with flushing were associated with an increased cardiac output [inconsistently accompanied by increased plasma catecholamines (CA)] and a decreased blood pressure reactivity to norepinephrine with decreased reflex bradycardia. sodium depletion further accentuated the latter abnormality and reproducibly reversed orthostatic hypertension to orthostatic hypotension. Abnormal responses in the Valsalva manoeuvre in an upright position suggested a defect in baroreceptor sensitivity, but may also have been due to an impaired venous return. The indices of the efferent portion of the reflex and central nervous system responses to stimuli were normal or exaggerated. The abnormality was probably due to a hypothalamic dysfunction and/or an abnormal central baroreceptor integration in the nucleus tractus solitarii. The absence of left ventricular hypertrophy and other target lesions, despite spectacular rises in blood pressure, suggests an excellent cardiovascular tolerance of hypertensive episodes if they are short-lived.
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14/22. Psychological symptoms and intermittent hypertension following acute microwave exposure.

    Two men who were accidentally, acutely irradiated with X-band microwave radiation have been followed up clinically for 12 months. Both men developed similar psychological symptoms, which included emotional lability, irritability, headaches, and insomnia. Several months after the incidents, hypertension was diagnosed in both patients. No organic basis for the psychological problems could be found nor could any secondary cause for the hypertension. A similar syndrome following microwave exposure has been described by the East Europeans. The two cases we report, with comparable subjective symptoms and hypertension following a common exposure, provide further strong, circumstantial evidence of cause and effect. A greater knowledge of the mechanisms involved in bioeffects which may be induced by radiofrequency and microwave radiation is definitely needed.
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15/22. Exacerbation of rheumatoid arthritis after removal of adrenal adenoma in Cushing's syndrome.

    A 46-year-old woman with rheumatoid arthritis had been on non-steroidal antiinflammatory agents for eighteen years until she developed cushingoid features and hypertension resistant to antihypertensive drugs. She had high plasma cortisol and 24 h urinary 17-hydroxycorticosteroids (17HCS) which were not suppressed by 8 mg dexamethasone per day for two days. The circadian rhythm of plasma cortisol was absent and plasma ACTH concentrations were suppressed before and after intravenous administration of CRH. Abdominal computed tomography demonstrated a tumor (3.0 x 3.0 x 2.3 cm) in the right adrenal gland and a 131I-6 beta-19-nor-methylcholesterol scan revealed marked uptake on the same side. The patient underwent a right adrenalectomy and the diagnosis of a cortisol secreting benign adenoma was histologically confirmed. blood pressure declined and cushingoid features regressed, but three months after the operation and while the patient was on replacement, she complained of pain on motion, marked tenderness and swelling of fingers, wrists, elbows, knees and foot joints, and had very high rheumatoid factors. Treatment with immunosuppressive drugs and oral and intraarticular administration of glucocorticoids were necessary to relieve the clinical symptoms of rheumatoid arthritis. In summary, we report a patient with rheumatoid arthritis and Cushing's syndrome due to an adrenal adenoma, in whom rheumatoid arthritis was exacerbated after curing the Cushing's syndrome. This suggests that it is imperative to follow the development and/or course of autoimmune diseases after the treatment of Cushing's syndrome.
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16/22. Aortic regurgitation due to non-traumatic rupture of the aortic valve commissures: report of two cases.

    Two cases of severe aortic regurgitation due to non-traumatic rupture of the aortic valve commissures are reported. The cause of rupture was hypertension in one patient, but it could not be identified in the other, where microscopic examinations of the aortic wall and the aortic cusps showed no particular pathologic changes. M-mode echocardiography revealed enlargement of the left ventricle, diastolic flutter of the anterior mitral leaflet and diastolic separation of the closure line of the aortic cusps in both patients. Two-dimensional echocardiography showed a downward displacement of the prolapsing motion of the aortic valve cusp during diastole toward the left ventricular outflow tract in one patient, and eccentricity of the coaptation point of the aortic valve without thickening of the cusps in the other. In addition to clinical features of progressive heart failure and characteristic cardiac murmur, echocardiographic studies provided correct diagnosis of aortic valve prolapse resulting from rupture of the aortic valve commissures. Both patients underwent aortic valve replacement successfully.
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17/22. A model of psychosomatic illness.

    An attempt is made to provide a general theoretical framework for psychosomatic disease. It is suggested that the convergence of a number of factors is necessary for the production of the illness. These factors include an individual's control or repression of emotional discharge over a long period. In addition, the affected person may show personality characteristics consistent with such control, and may live in a situation of unresolved conflict. The choice of illness might be determined by organ "weakness". The persistence of symptoms after resolution of the conflict is explained in terms of conditioning.
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18/22. Improved hypertension control after disclosure of decades-old trauma.

    This report presents the case of a 49-year-old woman who had been treated unsuccessfully for 6 years for longstanding severe and refractory essential hypertension. Although she reported no extraordinary stress or distress, her disclosure of a 3-decade-old rape and the experiencing of previously repressed and unconfided emotions related to it were followed by a dramatic and sustained improvement in her blood pressure. This case suggests that repressed emotions, which patients cannot report, may contribute substantially to the development of essential hypertension, even when they are related to decades-old events. More attention to repressed emotions, and better means of studying them, are needed before the mystery of the links between psychological factors and essential hypertension is unraveled.
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19/22. A case of hypertensive-diabetic cardiomyopathy demonstrating left ventricular wall motion abnormality.

    We report a case of hypertensive-diabetic cardiomyopathy demonstrating left ventricular regional wall motion abnormality, with a normal coronary artery documented on coronary arteriography. dipyridamole-infusion 201Tl scintigraphy demonstrated transient perfusion defects in the infero-posterior wall of the left ventricle, where reduced wall motion was demonstrated on contrast left ventriculography. Myocardial SPECT (single photon emission tomography) imaging with [123I] beta-methyliodophenylpentadecanoic acid (BMIPP) and 201Tl demonstrated reduced [123I]BMIPP uptake compared with 201Tl uptake in the infero-posterior wall of left ventricle. These results suggest that the impairment of myocardial free fatty acid metabolism is an etiologic or contributory factor for regional wall motion abnormality, together with small-vessel coronary artery disease, in this patient.
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20/22. Unusual left ventricular wall motion and a loud added sound during the isovolumic relaxation period in a patient with hypertensive heart disease.

    A 69 year old woman with hypertensive heart disease had a loud added sound which coincided with a sudden interruption of the early diastolic motion of the left ventricular posterior wall, as visualised by M mode echocardiography, and came just before early diastolic transmitral flow, as measured by a pulsed Doppler echocardiogram. Early diastolic motion velocity from the base to the middle of the posterior wall, assessed by pulsed Doppler tissue imaging, was markedly high and sharp, and its peak coincided with the sound. A notch, similar to that in the posterior wall motion, occurred in the left ventricular pressure curve during early diastole. No intraventricular flow signal was detected during the isovolumic relaxation period, as measured by pulsed and colour Doppler imaging. The added sound was probably produced by impact between the dilated heart, with a relaxation abnormality, and the extracardiac structures during the isovolumic relaxation period.
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