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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although splenectomy is the most effective treatment for chronic idiopathic thrombocytopenic purpura (ITP), many post-splenectomy patients have recurrent thrombocytopenia refractory to multiple medical therapies. Three consecutive patients with relapsed ITP after splenectomy and who were refractory to multiple medical therapies were treated with low dose cyclosporin A (CsA). In all 3 patients, the platelet count increased dramatically within 1 month from the onset of CsA therapy. The only detectable toxicity was hypomagnesemia and mild hypertension in 1 patient. CsA may be efficacious in treating patients with chronic ITP, which is refractory to all medical and surgical therapies currently being used.
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PMID:Low-dose cyclosporin A therapy in children with refractory immune thrombocytopenic purpura. 1002 20

We report a rare case of idiopathic thrombocytopenic purpura (ITP) associated with acute myocardial infarction (AMI). A 72-year-old woman with hypertension and hemorrhoids was admitted because of chest pain, severe anemia (RBC 340 x 10(4)/microliter, Hb 5.4 g/dl, Ht 21.7%) and thrombocytopenia (0.2 x 10(4)/microliter). AMI was diagnosed by electrocardiogram (ST elevation and negative T in V2-5), echocardiogram (hypokinesis in anteroseptal wall) and laboratory (CPK 470 U/l) findings and was treated with only blood transfusion. Chest pain disappeared the day after admission, and neither heart failure nor arrhythmia occurred. Based on bone marrow findings (hyperplasia of erythroblast and megakaryocyte), endoscopic (internal hemorrhoids) and laboratory (antiplatelet antibody positive, platelet associated IgG 257.8 ng/10(7) cells) findings, iron deficiency anemia and ITP were diagnosed. Anemia improved after blood transfusion, but thrombocytopenia (< 1.0 x 10(4)/microliter) without active bleeding continued after steroid and gamma-globulin therapy. At discharge, electrocardiogram showed a negative T in I, aVL and V2-5, and T1 and BMIPP myocardial scintigram showed defects in the anteroseptal and apical wall.
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PMID:[An elderly case of idiopathic thrombocytopenic purpura associated with acute myocardial infarction]. 1061 30

The regulation of arterial pressure in early vertebrate embryos and larvae with non-innervated hearts is poorly understood. We used nanoliter intravascular injections in anaesthetized Xenopus laevis larvae (stage 49-51) to assess their ability to maintain arterial pressure in the face of a volume load. Injections of saline and hetastarch (a volume expander) were made into the ventricle. Arterial pressure, end-diastolic ventricular volume, end-systolic ventricular volume and heart rate were measured. Injection of 800 nl caused a rapid rise in arterial pressure and stroke volume. There were no changes in heart rate, indicating the absence of an arterial baroreflex. Blood pressure in saline-injected animals recovered quickly (within 5 min), whereas hetastarch injections caused hypertension to be maintained for much longer, for over 40 min in the most extreme case. We surmise that Starling forces at the capillary play an important role in pressure regulation but are not adequate to explain the entire response. Finally, there was ample evidence for a Frank-Starling relationship in the ventricle.
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PMID:Blood pressure control in a larval amphibian, Xenopus laevis. 1085 Nov 21

Elderly individuals experience a disproportionate burden from cardiovascular disease. Global changes in aging will have a significant impact on the future of medical practice. However, most physicians have little formal training in geriatric medicine and sometimes fail to distinguish disease states from normal aging. Increasingly, it is recognised that a sedentary lifestyle may be responsible for a large fraction of the so-called 'age-related' changes in the cardiovascular system. Nonetheless, well characterised changes do occur in most individuals with aging. Loss of myocytes with subsequent hypertrophy of the remaining cells is usually observed. Calcification involving the conduction and valvular apparatus is seen in most elderly individuals and may predispose to the common arrhythmias of old age. Age-related loss of arterial compliance contributes to isolated systolic hypertension and left ventricular hypertrophy. Despite these changes, for the majority of healthy older adults, cardiac output is well maintained in the basal state through use of the Frank-Starling principle, in the setting of reduced early diastolic filling. Myocardial relaxation is slowed in part due to age-related changes in the sarcoplasmic reticulum Ca2+ ATPase pump. Elevated blood levels of catecholamines contribute to desensitisation to noradrenergic stimulation and this is associated with an age-related decline in maximum achievable heart rate. Changes in the baroreceptor reflex function and decreased sodium conservation may predispose some individuals to orthostatic and postprandial hypotension. The aetiology of cardiovascular aging is under intense study. The most likely mechanisms involve the result of cumulative damage mediated through a variety of insults. Oxidative stress, non-enzymatic glycation, inflammation and changes in cardiovascular gene expression all seem to influence cardiovascular aging. The benefits of exercise continue to be discovered. Endurance-type training has been shown to have a dramatic impact on parameters of cardiovascular aging. Favourable effects are seen in maximum oxygen consumption, diastolic filling, relaxation and arterial stiffness. Some changes such as the maximum heart rate response do not appear to change with conditioning. Pharmacotherapy may afford the opportunity to influence the aging process. Drugs that can reduce age-associated arterial stiffness, cardiac fibrosis and ventricular hypertrophy should prove useful. Antioxidants continue to be a topic of great interest and require more study. Despite some well described changes with aging, most elderly individuals maintain the opportunity for improved cardiovascular function through conditioning. Early recognition and treatment of diseases that are distinguishable from normal aging, including hypertension and atherosclerosis, together with preventive efforts, should reduce the predicted trends in cardiovascular morbidity and mortality among the aged.
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PMID:Clinical implications of physiological changes in the aging heart. 1134 74

We present two cases of the May-Hegglin anomaly discovered in a patient and one of her two sons. The female patient was known to have proteinuria from the age of 14 and was hospitalized in 1980, at the age of 25 years, because of hypertension and proteinuria (1.5 g/day). Thrombocytopenia was found with an abundance of megakaryocytes in the bone marrow. Both steroid treatment and splenectomy failed to ameliorate the thrombocytopenia, thought to be due to idiopathic thrombocytopenic purpura. Progressive renal failure, secondary hyperparathyroidism and uremic osteodystrophy were diagnosed in 1995. In January 1996, when she was hospitalized because of high-grade fever, we saw giant platelets and prominent blue inclusion bodies in almost all granulocytes in the peripheral blood smear. Electron microscopy confirmed the diagnosis of May-Hegglin anomaly in this patient and one of her sons, who at that time showed thrombocytopenia but no renal disease. Three years later, however, at the age of 15, the affected son was found to develop proteinuria. Coexpression of the May-Hegglin anomaly and renal disease, reported previously in a few other patients, may in fact represent a new subentity.
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PMID:Familial occurrence of the May-Hegglin anomaly: is the accompanying renal failure part of a new subentity? 1147 53

Prompt active postural manoeuvres induce an immediate arterial pressure variation followed by a period of regulation. For the squatting manoeuvre, initial hypertension was explained by a rise of cardiac filling pressure due to "squeezing blood out of the veins of the legs", leading to an increase in stroke output by Frank-Starling mechanism. For a minor part, it was also explained by "kinking" of the femoral arteries. O'Donnel and Mc Ilroy observed an increase in central blood volume and accepted the idea of a rise of cardiac filling. However, they did not observe so consistent circulatory variations when postural changes were realized in a water tank. Therefore, they concluded that kinking of the arteries and veins of the legs could not be very important. Moreover, the immediate pressure variations, most often appearing in the first beat succeeding the postural manoeuvres cannot be easily explained by the previously invoked modifications of cardiac filling pressures. When Hoffman et al lifted dogs until they stood erect, the right ventricular stroke volume usually fell in the first beat after the postural change, but the left ventricular stroke volume did not fall for another 1-3 beats. When the dogs were rapidly lowered to standing on four legs again, a delay of 2-3 beats was also observed. Thus, another interpretation of immediate hypotension must be added. It should especially take into account the natural gravitational fluid mechanics phenomena imposed to the arterial blood. Besides, to allow the investigation of the orthostatic regulation of arterial blood pressure, it would be necessary to separate the cardiovascular regulation component of the arterial pressure time course from the pressure evolution that would naturally appear in the network without physiological contribution. It is the aim of this study.
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PMID:Isolation of the physiological regulation component of the arterial pressure time variation after postural stresses in by a model of the gravitational and arterial kinking effects. 1153 20

It is now clear that diastolic heart failure (DHF) is an important, perhaps even dominant form of heart failure in older Americans. However, our knowledge base regarding the epidemiology, pathophysiology, natural history, and therapy of this relatively recently recognized disorder is limited. A number of normal age related changes in the heart and vascular system may predispose to or lower the threshold for expression of DHF. Recent reports from large population-based observational studies indicate that over 50% of persons 65 years and older who have heart failure have normal LV systolic function (presumed DHF). Among these, 45% have no other confounding variables (coronary, valvular, or pulmonary disease) and meet the criteria for isolated DHF. DHF is substantially more common in older women than men. A history of systemic hypertension and left ventricular hypertrophy are almost invariably present. Mortality rates are about 50% lower in DHF than in systolic heart failure (SHF) when stable outpatients are considered. However, in hospitalized and very elderly patients, the mortality rate appears similar in DHF and SHF. Furthermore, due to its higher prevalence, the total mortality in the older population attributable to DHF exceeds that of SHF. Morbidity in DHF is substantial and approaches that of SHF. In the chronic setting, DHF patients can have severe exercise intolerance related to failure of the Frank-Starling mechanism with reduced peak cardiac output, heart rate, and stroke volume and increased LV filling pressure. DHF patients also appear to have increased vascular stiffness, accelerated systolic blood pressure response to exercise, neuroendocrine activation, and reduced quality of life. Acute exacerbations (pulmonary edema) frequently occur and are associated with severe hypertension, sodium indiscretion, and medication non-compliance. Surprisingly, overt myocardial ischemia appears to infrequently play a role in these acute exacerbations. Therapy is currently empiric and multicenter, randomized, controlled trials are urgently needed. Anecdotally, control of blood pressure appears to improve symptoms and reduce the frequency of acute exacerbations. In addition, non-pharmacologic intervention, including multi-disciplinary case management is useful.
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PMID:Diastolic heart failure in the elderly. 1179 Sep 20

The management of idiopathic thrombocytopenic purpura (ITP) during pregnancy, especially with ongoing bleeding diathesis, has not been highlighted sufficiently in the literature. Aortocaval compression and reduction in uteroplacental circulation resulting in foetal hypoxia and acidosis, Mendelson's syndrome due to gravid uterus, trauma to airway with resultant haemorrhage and aspiration into lungs, compromised airway due to short neck, anasarca and heavy breast, limitation in using invasive monitoring and regional anaesthesia and uncontrolled bleeding leading to placental hypoperfusion and foetal hypoxia are some of the important risks. In the present case report, anaesthetic management for splenectomy during pregnancy complicated with pregnancy induced hypertension and bleeding diathesis secondary to ITP is described with reference to above risks.
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PMID:Anaesthetic management of splenectomy in Evan's syndrome during pregnancy with pregnancy induced hypertension. 1183 24

A 68-year-old woman with idiopathic thrombocytopenic purpura (ITP) was admitted to our hospital with acute myocardial infarction on 7 February 1999. She had been treated since 1991 for mitral stenosis and regurgitation, atrial fibrillation due to mitralism, diabetes mellitus, hypertension, hyperlipidemia. Chest radiograph on admission showed cardiomegaly with congestion and cardiothoracic ratio was 63%. The platelet count on admission was 22,000/microliter, but she did not have petechia or purpura. Urgent coronary angiography revealed total occlusion in segment 7, and 13 and 75% stenosis in segment 4PD, 9 and 10. Subsequently, direct percutaneous transluminal coronary angioplasty (PTCA) was performed in segment 7. Dissection occurred during the intervention, and a coronary stent was implanted, we started heparin infusion and medication with ticlopidine hydrochloride as post-stenting therapy after the intervention, and there was no bleeding tendency.
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PMID:[A case of intracoronary stent implanted for acute myocardial infarction in an elderly patient with idiopathic thrombocytopenic purpura]. 1185 81

Endothelin-1 is involved in mechanical load-induced cardiac growth processes; it also has effects on contractility. The interaction of endothelin-1 and the Frank-Starling response is unknown. The present study aimed to characterize the role of endothelin-1 in the regulation of the Frank-Starling response, one of the major mechanisms regulating cardiac contractile force, in both normal and hypertrophied hearts. Nontransgenic rat hearts and hypertrophic hearts of hypertensive double transgenic rats harboring human angiotensinogen and renin genes were studied in a Langendorff isolated heart setup with a liquid-filled balloon inside the left ventricle used to measure contractile parameters. The rats were studied at compensated phase, before showing any signs of heart failure. Compensated hypertrophy in double transgenic rat hearts resulted in improved contractility at a given level of preload when compared with nontransgenic rat hearts. Hearts of both rat lines showed preserved Frank-Starling responses, that is, increased contractile function in response to increased end-diastolic pressure. The mixed endothelin A/B receptor antagonist bosentan attenuated the Frank-Starling response by 53% (P<0.01) in the double transgenic hearts but not in nontransgenic hearts. The diastolic parameters remained unaffected. The left ventricles of the double transgenic rat hearts showed an 82% higher level of endothelin type A receptor mRNA and a 25% higher level of immunoreactive endothelin-1 compared with nontransgenic rat hearts. The type 1 angiotensin II receptor antagonist CV-11974 had no significant effect on contractile function in response to load in either strain. These results show that endogenous endothelin-1 contributes to the Frank-Starling response in hypertrophied rat hearts by affecting systolic performance.
Hypertension 2003 Jan
PMID:Endothelin-1 contributes to the Frank-Starling response in hypertrophic rat hearts. 1251 36


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