Cases reported "Hypertension"

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1/22. role of angiotensin and its inhibition in hypertension, ischemic heart disease, and heart failure.

    This is a personal historical account relating the events that led to the first application of angiotensin inhibition (either by ACE inhibitors or by angiotensin receptor blockade) to the investigation of the pathogenesis and treatment of hypertension, ischemic heart disease, and heart failure. Included are animal experiments, clinical observations, and the earliest clinical experimental studies that helped define some of the detrimental effects of angiotensin ii and the beneficial hemodynamic results of its inhibition, which have been subsequently corroborated and amplified by large randomized outcome trials.
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2/22. phenytoin/isradipine interaction causing severe neurologic toxicity.

    OBJECTIVE: To report a young man on phenytoin who developed acute neurologic symptoms after isradipine was introduced to his treatment regimen and discuss the possible causes of this drug interaction. CASE SUMMARY: A 21-year-old white man, with propionic acidemia and seizures treated with phenytoin and carbamazepine, was started on isradipine for essential hypertension. Soon thereafter, he developed acute and severe lethargy, ataxia, dysarthria, and weakness that resolved once isradipine was withheld. phenytoin concentrations were within normal limits or elevated, despite sequential reductions of phenytoin dosage, during concomitant isradipine administration. DISCUSSION: isradipine is a known inhibitor of the CYP450 isoenzyme family. Although the daily dose of phenytoin was decreased significantly, phenytoin blood concentrations remained high, suggesting a pharmacokinetic interaction. Previously, the patient had never had neurologic symptoms associated with increased phenytoin concentrations. This also indicates a likely pharmacodynamic interaction between phenytoin and the calcium-channel blocker. Both phenytoin and isradipine have been shown to bind to calcium channels and to inhibit calcium entry into the cells. Binding of isradipine to the brain has been described in humans and animals, and calcium-channel blockers have been shown to cause potentiation of anticonvulsant action of phenytoin. CONCLUSIONS: Acute pharmacokinetic and pharmacodynamic interactions between phenytoin and isradipine were probably responsible for the lethargy, dysarthria, ataxia, and weakness our patient developed. The combination of phenytoin and calcium-channel blockers should be used with caution.
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3/22. sirolimus-induced thrombotic microangiopathy in a renal transplant recipient.

    A rare but well-documented serious adverse reaction to the administration of the calcineurin inhibitors tacrolimus and cyclosporine in renal transplant recipients is the development of medication-induced thrombotic microangiopathy. The recently introduced immunosuppressive medication sirolimus has a very similar molecular structure to tacrolimus and also binds to the same intracellular proteins. Despite these similarities with tacrolimus, sirolimus has a different side-effect profile and reportedly lacks documented specific renal toxicity. This is a case report of the isolated administration of sirolimus without a concomitant calcineurin inhibitor being associated with the development of renal transplant biopsy-proven thrombotic microangiopathy. The patient is a 47-year-old African-American woman whose primary cause of renal failure was not thrombotic micrangiopathy, and she received a 5-antigen mismatched cadaveric renal transplant. Because of preexisting nephrosclerosis in the renal transplant, this patient was never administered a calcineurin inhibitor but was always maintained on sirolimus. With recent animal data showing that sirolmus can be nephrotoxic in a renal ischemic-reperfusion model (similar to what happens with a renal transplant), the authors speculate on a mechanism for this adverse reaction.
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4/22. Irukandji-like syndrome in South florida divers.

    Irukandji syndrome is a constellation of delayed severe local and systemic symptoms occurring after a Carukia barnesi box jellyfish sting involving any exposed skin. These cases are limited to australia, the habitat of that animal. Numerous other cases of an Irukandji-like syndrome after other small Carybdeid genus envenomations have been reported elsewhere in the world. There have yet been no reports of Irukandji-like syndrome occurring in continental US coastal waters. We describe 3 cases of marine envenomation causing such a symptom complex in US military combat divers off Key West, FL. It is unclear what species caused the injuries, but a member of the Carybdeid genus seems most likely.
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5/22. Novel representation of astasia associated with posterior cingulate infarction.

    BACKGROUND AND PURPOSE: The representation elicited in the cingulate motor area has been demonstrated in animals, but remains unclear in humans. In particular, the representation and pathogenic mechanisms of the posterior cingulate cortex are poorly understood, especially in humans. We describe a case of posterior cingulate infarction associated with contralateral astasia. CASE DESCRIPTION: A 67-year-old right-handed man with a 10-year history of hypertension suddenly presented with right-sided pulsion on attempting to stand or sit. On the following day, he could not maintain a sitting position. The patient immediately fell to the floor because of instability, characterized by marked right-sided pulsion despite no muscle weakness, sensorial deficits, or cerebellar ataxia. Magnetic resolution imaging of the brain showed abnormal intensity in the posterior parts of the cingulate, with no other clinically significant lesions. CONCLUSIONS: Because the cingulate motor area is connected to the vestibulocerebellar system through the thalamic nuclei, disruption of this connection by posterior cingulate infarction may result in astasia.
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6/22. Foetal kidney maldevelopment in maternal use of angiotensin ii type I receptor antagonists.

    We report renal lesions observed in a foetus exposed throughout pregnancy to angiotensin ii type I (AT 1) receptor antagonists. The mother suffered from essential hypertension and was treated with Cozaar (losartan 50 mg). autopsy examination of the foetus revealed severe renal lesions, including tubular dysgenesis, hypertrophy of the endothelial and medial cells lining the arterial and arteriolar walls, hyperplasia of the juxtaglomerular apparatus and poorly developed vasa recta. Similar lesions have already been observed in foetuses of women treated with angiotensin-converting enzyme antagonists and also in foetuses and neonates of animals undergoing experimental blockade of the renin-angiotensin system. The purpose of this report is to describe structural lesions observed in the kidneys, and, particularly, vascular lesions. Our results suggest that the use of AT 1 receptor antagonists during pregnancy may have a severe deleterious effect on kidney development in the foetus.
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7/22. Hypothalamic-midbrain dysregulation syndrome: hypertension, hyperthermia, hyperventilation, and decerebration.

    Certain decerebrate lesions of brain stem or hypothalamus induce pharmacologically reversible hypertension and hyperthermia in animals. We observed three young patients with episodic decerebration, hyperthermia, hypertension, and hyperventilation during recovery from comas of different etiologies. The shared pathology on neurologic examinations and computed tomographic scans was hypothalamic-mesencephalic dysfunction, suggesting a diencephalic-brain-stem disconnection syndrome or brain-stem release mechanism. propranolol was the most effective drug tested, but only two patients responded, one dramatically. This novel clinical syndrome may have localizing and therapeutic significance in pediatric coma that needs to be further defined in future studies.
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8/22. Effects of a lack of aortic "Windkessel" properties on the left ventricle.

    After the long bypass grafting between ascending and abdominal aorta with exclusion of the aortic arch using conventional synthetic vascular graft, a considerably remarkable hemodynamic change and progressive hypertrophy of the left ventricle occurred until stabilized. In the clinical cases and animal experiments, systolic hypertension, diastolic pressure decrease and consequent pulse pressure widening were observed. Furthermore, the phase difference between flow and pressure waves approximated to zero. Elevation of the afterload due to systolic hypertension and widening of pulse pressure may result in energy loss in vascular pulsation, not maintaining forward flow but increasing the left ventricular external work. Furthermore, as the peak flow approximates the peak pressure and its point situated relatively early in systole, external work and wall stress of the left ventricle are markedly elevated. All those factors mentioned above lead concentric hypertrophy of the left ventricle to normalize the wall stress. Fall in the diastolic pressure at the aortic root may decrease coronary flow to lead ischemia of the hypertrophied left ventricle. This can occasionally lead to fatal heart failure after a long postoperative period. It may be concluded that these new findings are produced by a loss of compliance (Windkessel properties) in aortic root which occurred as consequence of using conventional synthetic vascular graft with exclusion of aortic arch.
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9/22. The sympathetic nervous system in clinical and experimental hypertension.

    In summary, many lines of evidence indicate that the sympathetic nervous system, via the renal nerves, plays an important role in the pathogenesis of renovascular hypertension in humans and laboratory animals. patients with established renovascular hypertension have increased sympathetic nervous system activity, as evidenced by increased plasma and urinary norepinephrine levels, elevated excretion of catecholamine metabolites, and an exaggerated depressor response to centrally acting sympatholytic agents. The observation that converting enzyme inhibitors can cause both blood pressure and urinary norepinephrine excretion to return to normal in patients with renovascular hypertension is consistent with the interpretation that activation of the sympathetic nervous system in these subjects is, at least in part, angiotensin-induced. The sympathetic nervous system, via the efferent renal nerves, plays a role in the pathogenesis of hypertension in a number of experimental models. In the spontaneously hypertensive rat of the Okamoto strain (SHR) and in the DOCA/NaCl hypertensive model, increased renal efferent nerve activity contributes to the development of hypertension by causing increased renal sodium retention. In both of these experimental models, renal denervation delays the development and blunts the severity of hypertension. This delay is associated with increased urinary sodium excretion, suggesting a renal efferent mechanism. In contrast to the predominantly efferent renal nerve mechanisms observed in the DOCA-NaCl and SHR models, studies of the effects of renal denervation in one-kidney, one-clip and two-kidney, one-clip Goldblatt hypertensive rats suggest that renal afferent nerves are important in these models of hypertension. Total renal denervation in rats with established 1K, 1C and 2K, 1C hypertension attenuates the severity of the hypertension without altering sodium intake or excretion, renin activity, water intake, or renal function. Thus, efferent renal nerve activity does not appear to be involved in the development of maintenance of 1K, 1C or 2K, 1C hypertension. In contrast with the findings in SHR and DOCA-NaCl rats, these studies provide indirect evidence that the renal afferent nerves play a role in the pathogenesis of this form of experimental hypertension. The major effect of renal denervation in these models appears to be an interruption of renal afferent nerve activity, which by a direct feedback mechanism attenuates systemic sympathetic tone, thereby lowering blood pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
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10/22. Paroxysmal hypertension due to sinoaortic baroreceptor denervation in humans.

    A 41-year-old man with a remote history of neck and mediastinal radiation was seen with severe paroxysms of hypertension, headache, and cutaneous flushing after bilateral carotid bypass surgery. Investigation revealed marked parallel fluctuations in blood pressure and heart rate and elevation of plasma norepinephrine to 1164 pg/ml during a paroxysm. We systematically evaluated his arterial and cardiopulmonary baroreceptor reflex function by assessing changes in heart rate, arterial pressure, and efferent muscle sympathetic nerve activity, which was measured directly by the microneurographic technique. Elevating resting arterial pressure from 130/88 to 164/100 mm Hg with phenylephrine or lowering it to 88/56 mm Hg with nitroprusside produced no reflex changes in heart rate or efferent sympathetic nerve activity. In contrast, decreases in cardiac filling pressures with lower body negative pressure produced a marked increase in sympathetic nerve activity. These findings indicate complete loss of the afferent limb of the arterial baroreceptor reflex but preservation of the cardiopulmonary baroreceptor reflex. They suggest that both carotid and aortic baroreceptors were impaired by the previous radiation and surgery. Despite the loss of arterial baroreceptor function, the patient did not have sustained hypertension. The paroxysms of hypertension appear to be due to spontaneous fluctuations in central sympathetic drive not buffered by arterial baroreceptors in a manner similar to that seen in sinoaortic-denervated animals.
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