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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To differentiate the functional changes from the organic changes in malignant hypertension, the author studied the changes in the blood vessel of ocular fundus by ophthalmoscopical and histopathological methods using malignant strain of stroke-prone spontaneously hypertensive rat (M-SHRSP; Okamoto, K et al., 1986), an animal model of human juvenile malignant hypertension, in which the systolic blood pressure elevates rapidly with age and death appeared by the 15th month of life, if they are untreated. Fundus changes progressed with age and duration of hypertension and they altered from functional changes to organic ones. In M-SHRSPs with age of 8 weeks, systolic blood pressure was 220mmHg or more and retinal arterioles showed generalised narrowing but no dye leakage was recognized by fluorescein angiography (FAG). Dye leakage was observed on the 9th week of age. Death of M-SHRSP appeared, after the 13th week of age, coincidentally with appearance of wide retinal edema. Papilledema appeared often in this period. Little histological change was found in the retinal arterioles in spite of severe and marked ophthalmoscopic changes. No feature of angionecrosis was observed in the retina while it was recognized in choroidal arteriole with thrombosis. The fundus changes in M-SHRSP were ophthalmoscopically classified by using scores as following. Grade 0: normal fundi, Grade I (score 1): slight generalized narrowing, caliber irregularity and tortuosity of the retinal arterioles, slight retinal edema and choroidal changes. Grade II (score 2): moderate generalised narrowing, caliber irregularity, tortuosity of the retinal arterioles, moderate retinal edema and choroidal ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ophthalmological study on the M-strain of stroke-prone spontaneously hypertensive rat (M-SHRSP) (1). Classification of hypertensive fundus changes in M-SHRSP]. 204 25

Angiotensin(Ang) contents in the adrenal gland of stroke-prone spontaneously hypertensive rats(SHRSP) and age-matched Wistar Kyoto rats(WKY) were determined using reverse phase high performance liquid chromatography combined with a specific radioimmunoassay. In normotensive 5 wk-old SHRSP, the adrenal renin activity was about 3 times higher than that of age-matched WKY while the adrenal Ang I and Ang II concentrations did not differ from those of WKY. In the severely hypertensive 25 wk-old SHRSP, the adrenal Ang II and Ang I, and plasma aldosterone concentrations were about 5-fold, 2-fold and 4-fold, respectively, increased compared with levels in the WKY. In the 25 wk-old SHRSP 24 h after bilateral nephrectomy, the adrenal Ang II and plasma aldosterone levels were not decreased and were 10 and 3 times, respectively, higher than those of nephrectomized control WKY. Thus, the enhanced local generation of Ang II in the adrenal gland may contribute to the increased release of aldosterone in SHRSP with malignant hypertension.
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PMID:Increased production of angiotensin II in the adrenal gland of stroke-prone spontaneously hypertensive rats with malignant hypertension. 206 54

Antihypertensive management reduces the incidence of congestive heart failure, malignant hypertension and stroke; however, the overall incidence of events due to ischemic heart disease was not influenced by antihypertensive treatment. One of the possible explanations might be some negative metabolic effects of antihypertensive drugs. Hypokalemia develops in 20 to 50% patients who receive a thiazide diuretic. An association between hypokalemia and malignant arrhythmias (including ventricular fibrillation), in acute myocardial infarction, has been observed. 24-hour ambulatory electrocardiographic monitoring demonstrated a higher frequency of ventricular ectopic beats in hypertensive patients taking thiazides. There is, however, no convincing evidence of a simple causative relation between ventricular extrasystoles and low concentrations of serum potassium. Hypertensives with left ventricular hypertrophy (ECG criteria) had significantly more premature ventricular contractions than patients with established hypertension without left ventricular hypertrophy or normotensive subjects. These data could provide an electrophysiologic substrate for the epidemiologic findings of increased morbidity and mortality in patients with left ventricular hypertrophy.
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PMID:The heart in hypertension and arrhythmias. 213 16

Some old icons of hypertension warrant questioning in view of new insights. Lowering of blood pressure is no criterion of efficacy in prevention of cardiovascular morbidity, mortality and sudden death. The drugs used in early studies - diuretics, vasodilators and reserpine - greatly improved mortality from malignant hypertension, apoplectic stroke and congestive heart failure, but had little or no effect in persons with milder degrees of elevated blood pressure, who constitute the vast majority of hypertensives. The failure of diuretics and vasodilators to influence cardiovascular disease favorably appears due not to their known adverse effects on risk factors, such as lipids, as some have held, but to a failure - in conjunction with some sympathetic blocking agents - to cause effective regression of left ventricular hypertrophy, the keystone of successful therapy. A study of 674 hypertensive persons surveyed in the United States and eastern Canada, personally examined during their visit to a Florida health resort, has shown striking changes in prescribing practice during the period surveyed (1985-88), notably with increased use of angiotensin converting enzyme (ACE) inhibitors and, to a lesser degree, increased use of calcium channel blockers. Both of these cause regression of left ventricular hypertrophy, and will hopefully show long term benefit in decreasing hypertension mortality. Left ventricular hypertrophy is detected most sensitively echocardiographically, and is worthwhile not only for estimation of prognosis, but also for guiding therapy. Left atrial hypertrophy is a mirror of left ventricular hypertrophy and may be detected echocardiographically and in the electrocardiogram.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The heart (ventricle and atrium) is the heart of hypertension, not blood pressure. 214 1

The effective treatment of hypertension is a major factor in the declining incidence of stroke in North America. There are subsets of patients, however, in which antihypertensive therapy may actually cause cerebral ischemia and infarction. Elderly patients and those with malignant hypertension, acute stroke, and occlusive cerebrovascular disease appear to be the populations at greatest risk of iatrogenic stroke. This article reviews the effect of beta-blockers, angiotensin-converting enzyme inhibitors, direct vasodilators, and calcium-channel blockers on cerebral blood flow in various populations. Although many investigations have been performed, it remains difficult to predict the risk of cerebral hypoperfusion due to antihypertensive medication in an individual patient. It is best for practitioners to be aware of the patient populations at risk and treat high blood pressure cautiously in these patients.
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PMID:Risk of cerebral hypoperfusion with antihypertensive therapy. 269 Apr 72

In chronic hypertension, the lower limit of autoregulation of cerebral blood flow (CBF) is shifted towards high blood pressure with a consequent impairment of the tolerance to acute hypotension. Despite this, antihypertensive treatment in the great majority of patients prevents stroke and the risk for treatment-induced cerebral ischemia is only real in a limited number of clinical settings such as malignant hypertension, hypertension in the elderly, and hypertension associated with acute stroke. During long-term treatment adaptive hypertensive changes in CBF autoregulation may be reversible, especially in young patients. Drugs used for emergency lowering of blood pressure may be classified into four groups according to their effect on CBF and intracranial pressure: (1) drugs with no pharmacological action in the cerebral circulation; (2) cerebral vasodilators; (3) alpha-adrenergic and ganglionic blockers; and (4) angiotensin-converting enzyme (ACE) inhibitors. Oxygen saturation in the jugular venous blood is of the order of 60% to 70% and is considerably higher than in the coronary sinus. It is hypothesized that this oxygen reserve enables the brain better than the heart to take hemodynamic advantage of pressure lowering without risking tissue ischemia. This may explain why antihypertensive treatment prevents stroke but not myocardial infarction. Acute hypertensive encephalopathy is probably caused by failure of autoregulatory vasoconstriction with focal or generalized dilatation of small arteries and arterioles. This is associated with a high CBF, dysfunction of the blood-brain barrier, and the formation of brain edema that is thought to cause the clinical symptoms.
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PMID:Cerebral blood flow and its pathophysiology in hypertension. 275 6

The benefits of antihypertensive treatment are well-known. In malignant hypertension antihypertensive therapy has markedly improved prognosis and increased 5-year survival from 0% to 75%. In addition, the incidence of this severe form of hypertension has been shown to decrease significantly in some centers. In nonmalignant hypertension prognosis is also markedly improved thanks to antihypertensive therapy, with substantial reductions in the incidence of stroke and congestive heart failure, whereas the beneficial effects against coronary heart disease are less obvious. In addition, during recent years there has been some discussion about the J-curve phenomenon. There are several conceivable explanations behind the less than optimal outcome of antihypertensive therapy. Some of these will be discussed here, e.g. the fact that hypertension-induced pathology is only partially reversible. Moreover, in several intervention studies strict normotensive blood pressures have not been obtained during treatment. In addition, some of the antihypertensive drugs used may cause potentially negative effects, e.g. by increasing serum lipoproteins. Finally, the pathophysiology behind stroke and myocardial infarcts differ in several respects, and this may contribute to the less favourable effects of antihypertensive treatment on coronary artery disease-morbidity as compared to stroke-morbidity.
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PMID:Analysis of treatment outcomes. Why is benefit not larger? 279 27

The benefits of the treatment of hypertension currently consist of a substantially reduced incidence of premature stroke, left ventricular failure and malignant hypertension. The benefits for the individual are most clearcut in those who have already had severe or symptomatic hypertension. Older subjects who have a higher risk of stroke and heart failure also show more immediate benefits in terms of stroke and heart failure reduction. However, in the community as a whole, mild hypertensives account for over half the cardiovascular deaths attributable to high blood pressure. In such patients a more systematic approach to the use of non-pharmacological measures for both control of blood pressure and coronary heart disease, coupled where necessary with the judicious use of existing and new antihypertensive and lipid lowering drugs, offers the prospect for a new era of prevention in relation to hypertensive cardiovascular disease.
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PMID:Value of non-drug treatment and drug treatment in hypertension. 307 10

Hypertension can directly damage blood vessels, and leads to renal failure, intracranial bleeds, and lacunar infarctions. Of equal importance is the effect of hypertension on the development of atherosclerosis. Specific changes in both the microvasculature and macrovasculature vary depending on the degree and rapidity of blood pressure elevation. Changes in the intima and media can lead to significant narrowing of vessels and ischemia in various tissues. In addition, changes in small-resistance vessels contribute to changes in peripheral-vasculature resistance and thus affect blood pressure regulation. Treatment of moderate to severe elevation in blood pressure clearly results in a decrease in the incidence of stroke. However, evidence that treating mild hypertension reduces coronary events is less convincing. Antihypertensive therapy may result in partial regression of vascular changes, especially fibrinoid necrosis seen in malignant hypertension, but more work needs to be done to clearly define the roles of specific drugs in preventing or regressing hypertensive vascular disease.
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PMID:Vascular changes in hypertension. 330 5

Calcium antagonism of nifedipine, nitrendipine or nisoldipine prevented salt-induced hypertension, renovascular damage and mortality in Dahl salt-sensitive (S) rats. The calcium agonist BAY K 8644 accelerated the development of salt-induced hypertension in S rats. In some S rats on a low-salt diet BAY K 8644 induced renovascular damage without sustained hypertension. In stroke-prone spontaneously hypertensive rats (SHRSP) on a normal diet the natural appearance of stroke was correlated with an increased calcium content in brain and kidney tissue. Nimodipine prevented stroke and the increase in brain calcium content without affecting the high blood pressure. A similar protective effect without substantial influence on high blood pressure was achieved by bilateral parathyroidectomy. Hypertension-associated vascular damage does not necessarily depend on the systemic intravascular pressure. In malignant hypertension the deleterious calcium overload in tissues may be activated or inhibited independently of the regulation of arterial blood pressure.
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PMID:Calcium antagonism and protection of tissues from calcium damage. 348 33


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