Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four-hour noninvasive ambulatory blood pressure (ABP) was performed in 131 consecutive elderly subjects (61 with isolated systolic hypertension, ISH; 19 with mixed/diastolic hypertension, MDH; 29 with borderline hypertension, BLH; 23 in the normotensive group, NT). It was found that in ISH blood pressure rised during awaking period and fell during sleeping period (P < 0.05); the circadian systolic blood pressure rhythm was similar to ones in MDH, BLH and NT. However, the circadian diastolic blood pressure rhythm was attenuated in ISH. We conclude that circadian blood pressure rhythm alters in ISH, which may be related to the ischemia in organs, especially cerebral ischemia.
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PMID:[Circadian blood pressure rhythm and its characterization in isolated systolic hypertension (ISH)]. 130 16

Hypertension is a major contributor to cardiovascular morbidity and mortality, increasing risk threefold. It predisposes to every clinical manifestation of coronary heart disease, now the most common and lethal outcome. It is as relevant a risk factor in the elderly as in the young. Risk is proportional to the degree of blood pressure elevation without a discernible critical value. Cardiovascular sequelae do not derive chiefly from the diastolic component, and isolated systolic hypertension confers increased risk at all ages. Hypertension tends to cluster with other cardiovascular risk factors, which must be taken into account in evaluating the risk and in choosing treatment. The excess cardiovascular risk in hypertension is concentrated in those with an increased total/high density lipoprotein cholesterol ratio, glucose intolerance, cigarette smoking, elevated fibrinogen, and electrocardiogram abnormalities. Left ventricular hypertrophy (LVH) is a common feature of hypertension and an ominous harbinger of cardiovascular sequellae. Electrocardiographic evidence of LVH, when manifested by repolarization abnormalities and voltage elevations, is particularly hazardous, reflecting not only anatomical hypertrophy but also ischemia. Electrocardiogram-LVH adds to cardiovascular risk associated with X ray or echocardiographic evidence of anatomical LVH. Because of a tendency to ventricular ectopy, LVH is associated with increased risk of sudden death. Electrocardiogram-LVH can be corrected or avoided by control of hypertension and weight reduction. The efficacy of correcting LVH remains to be demonstrated but benefits seem likely.
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PMID:Hypertension, hypertrophy, and the occurrence of cardiovascular disease. 183 77

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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PMID:Effects of a lack of aortic "Windkessel" properties on the left ventricle. 285 95

Clinical events following cerebral angiography were prospectively evaluated in 1,002 procedures. The ischemic event rate between 0 and 24 hours was 1.3% (0.1% permanent). This incidence was higher (2.5%) in patients investigated for cerebrovascular disease, but the difference was not significant. In addition, 1.8% of the patients suffered ischemia (0.3% permanent) between 24 and 72 hours after angiography. Cerebral ischemic events occurred as a recurrence or worsening of a preexisting phenomenon. twice as often as de novo. All permanent ischemia was a worsening of a preexisting phenomenon. There was a significant increase in the incidence of neurologic events between 0 and 24 hours when the procedure lasted longer than 60 minutes and when there was systolic hypertension. Trends toward higher incidence were noted with the use of increased volume of contrast, with increased serum creatinine, when transient ischemic attacks or stroke were the indications, and when 3 or more catheters were used. The incidence of neurologic events between 24 and 72 hours increased significantly with the increase in the amount of contrast used, with age, and with diabetes. The occurrence of nonneurologic events (mostly hematomas) was significantly increased by multiple factors. This study shows that events can and do occur beyond the usual observation period of 24 hours but confirms the low risk of cerebral angiography when performed judiciously.
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PMID:Clinical events following neuroangiography: a prospective study. 368 97

We evaluated ischemia-induced cellular electrophysiologic abnormalities in chronic pressure overload ventricular myocardium in vitro. Left ventricular systolic hypertension was induced in cats via partial supracoronary aortic constriction (overload); at 1 1/2-3 months, resulting pressure overload was accompanied by ventricular hypertrophy (25-35% by weight) and patchy endocardial fibrosis. Two hours of subsequent acute myocardial ischemia (ischemia) was imposed on overload (ischemia/overload) via total occlusion of distal branches of the left coronary artery system. Spontaneous premature depolarizations in vitro were increased in ischemia/overload compared to control, ischemia or overload alone; bursts of spontaneous, repetitive depolarizations were also unique to these preparations. Multiple site recordings of endocardial transmembrane action potentials overlying the borders (interface) of fibrotic areas in ischemia/overload demonstrated numerous electrophysiologic abnormalities, including several not observed in control, ischemia or overload. Unique to the border areas of ischemia/overload preparations was the presence of maintained but depressed resting potential without action potentials; also, the incidence of depolarizations at the onset of the plateau phase was highest in these preparations. In non-fibrotic areas, electrophysiologic properties including resting potential and action potential amplitude and rate of rise were diminished in ischemia/overload compared to ischemia or overload preparations. These data demonstrate that acute myocardial ischemia in the setting of chronic pressure overload leads to additional cellular electrophysiologic abnormalities compared to ischemia or overload alone.
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PMID:Cellular electrophysiology of coronary artery ligation in chronic pressure overload. 381 32

To test the hypothesis that left ventricular hypertrophy (LVH) may predispose the subendocardium to ischemia, we studied regional myocardial blood flow in dogs with the fibrous ring form of subvalvular aortic stenosis and concentric LVH. Radioactive microspheres, 9 +/- 1 mu in diameter, were used. Eleven dogs with LVH (left ventricular body weight ratio of 6.35 +/- 0.46 gm/kg [mean +/- SEM] and peak left ventricular outflow gradient of 51 +/- 7 mm Hg) were compared to 12 normal dogs (left ventricular/body weight ratio of 3.41 +/- 0.12 gm/kg and peak left ventricular outflow gradient of 6 +/- 3 mm Hg). The two groups of dogs were subjected to comparable experimental interventions including (1) tachycardia produced by atrial pacing (221 +/- 4 beats/min), (2) ascending aortic constriction producing systolic hypertension (212 +/- 5 mm Hg), and (3) creation of an aortic-right atrial fistula lowering diastolic blood pressure (38 +/- 3 mm Hg). Basal regional myocardial blood flow was distributed similarly for LVH and normal dogs (endocardial/epicardial ratio = 0.90 +/- 0.05 and 0.94 +/- 0.03, respectively). During experimental interventions, regional blood flow remained equal to all myocardial layers in normal dogs; however, the endocardial/epicardial ratio diminished in LVH dogs during atrial tachycardia to 0.61 +/- 0.08, during systolic hypertension to 0.68 +/- 0.06, and during diastolic hypotension to 0.50 +/- 0.09. When the diastolic/systolic pressure time index ratio (DPTI/SPTI) was less than 0.8, subendocardial ischemia occurred in dogs with LVH (endocardial/epicardial ratio = 0.66 +/- 0.04) but not in normal dogs (endocardial/epicardial ratio = 0.92 +/- 0.03) (p less than 0.0001). Animals with infracoronary obstruction and LVH demonstrate greater susceptibility to development of subendocardial ischemia for identical hemodynamic interventions than do normal animals.
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PMID:Regional myocardial blood flow in left ventricular hypertrophy. An experimental investigation in Newfoundland dogs with congenital subaortic stenosis. 621 74

With acutely increasing right ventricular (RV) hypertension, failure eventually occurs because of RV ischemia. This study examines the effects of RV hypertension on the diastolic right coronary circulation. Conscious dogs instrumented to measure right coronary artery pressure and blood flow were studied after maximal coronary vasodilation with chromonar. Diastolic coronary pressure-flow relations, described by slope (conductance) and zero-flow, pressure axis intercept (Pf = 0), were generated before and during RV hypertension. Diastolic Pf = 0 increased from 11.8 +/- 6.5 to 17.1 +/- 7.1 (means +/- SD, P < 0.01) Torr, with no change in conductance. During RV hypertension, RV diastolic pressure increased. To examine possible mechanisms for the increase in Pf = 0, pressure-flow relations were generated before and after volume loading, without systolic hypertension. Diastolic Pf = 0 increased from 15.5 +/- 3.1 to 20.8 +/- 4.1 Torr, suggesting that changes in Pf = 0 with RV hypertension were mediated by increased filling pressures. Pressure flow relations were derived from mean right coronary flow and RV driving pressure before and during RV hypertension. Under these conditions, Pf = 0 is close to zero; the use of RV driving pressure provides a method for calculating maximal right coronary conductance.
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PMID:Maximal vascular conductance in right ventricular myocardial circulation. 818 14

We surveyed 1,545 subjects--recruited into the UK Medical Research Council elderly hypertension treatment trial between 1982 and 1987--to detect incident cases of dementia, identifying 50 cases of dementia, including 31 cases of probable or possible Alzheimer's disease (AD). These we compared with 223 unimpaired, unmatched controls from the same population for exposure to familial, cardiovascular, educational, and geographic risk factors for dementia. Our study confirms the association of family history of dementia with dementia (odds ratio [OR] = 4.36) and AD (OR = 4.69), and of advanced age with dementia (OR = 2.81). Rural residence exerted a protective effect for dementia (OR = 0.21) and AD (OR = 0.28). We report near-significant associations between AD and dementia and several cardiovascular risk factors (ECG ischemia, systolic hypertension, and smoking) among subjects lacking a family history of dementia. We postulate the existence of a nonfamilial form of dementia transcending traditional categories of multi-infarct dementia and AD, more common among urban residents, and mediated through vascular pathology. Risk factors reported elsewhere but not confirmed in this study were advanced maternal age and winter season of birth.
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PMID:Risk factors for Alzheimer's disease and dementia: a case-control study based on the MRC elderly hypertension trial. 829 99

AGE-RELATED CARDIOVASCULAR CHANGES: Age-related changes in vascular structure and function may contribute to isolated systolic hypertension and target-organ damage. These include cardiac hypertrophy, systolic as well as diastolic dysfunction, congestive heart failure, coronary artery disease, cardiac arrhythmias, cerebrovascular diseases, peripheral vascular diseases and renal insufficiency. POTENTIAL ADVANTAGES OF CALCIUM ANTAGONISTS IN THE ELDERLY: Dihydropyridine calcium anatagonists have been advocated as first choice agents for the treatment of hypertension in the elderly on the grounds that (1) they may be more active in lowering blood pressure because of the predominantly low renin status in elderly hypertensives, (2) they may be better tolerated because side effects related to the activation of the sympathetic system may be less frequent because of attenuation of baroflexes during ageing and (3) they may have beneficial effects on a variety of concomitant cardiovascular diseases which are frequently present in the elderly. These assumptions, however are not always proven in clinical practice. ADVANTAGES OF NICARDIPINE: Additional to its potent vasodilatator action, nicardipine has anti-ischemic effects in both the coronary and the cerebral circulation, including antiplatelet and hemorrheological effects, and protection at ther cellular level against calcium overload and ischemia. The results of a large number of studies in cerebrovascular insufficiency suggest that nicardipine, may favourably affect the cerebral circulation and may improve the patient's cognitive function. Nicardipine may decrease left ventricular mass by about 4-12% and may reduce both the frequency and the severity of arrhythmias. The anti-anginal effects of nicardipine are well established. The drug is also able to decrease the progression of new atherosclerotic lesions in coronary arteries and is consequently potentially beneficial in elderly hypertensives with coronary artery disease. Nicardipine has no clinically significant negative inotropic effect. Nevertheless, in congestive heart failure, the use of calcium antagonists is usually not recommended because of the lack of clinical benefit and of possible harmful effects, including sympathetic and renin-angiotensin system stimulation. Although kidney protection may be provided by a strict and long-term control of blood pressure, the effects of nicardipine on long-term protection of renal function are not clear at present. RECENT CONTROVERSY CONCERNING SHORT-ACTING CALCIUM ANTAGONISTS: Much-debated recent case-control studies suggest that hypertensive patients treated with short-acting calcium antagonists may have an increased incidence of myocardial infarction and possibly of cardiovascular and total mortality. However, only well designed prospective comparative trials can answer this question.
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PMID:Concomitant diseases in elderly hypertensives: the position of nicardipine. 912 Jun 65

Several trials performed in elderly patients have demonstrated that antihypertensive drugs are effective in both systo-diastolic and isolated systolic hypertension, reducing the incidence of fatal and nonfatal cardiovascular events. However because of technical and design problems, the studies carried out to date have involved highly selected patients, almost always without any target organ damage, independent, cognitively normal and with low comorbidity. Therefore, trial results may be transferred to clinical practice only with some caution. Therapeutic behavior could be different in the presence of diseases associated with hypertension: a) in case of associated specific cardiovascular complications and/or diseases, such as diabetes or dyslipidemia, which could increase cardiovascular risk, treatment must be more aggressive; b) in case of associated diseases with fatal prognosis, treatment is aimed at preventing hypertensive emergencies; c) in case of associated diseases, which are not life-threatening but require chronic pharmacological intervention, drug interaction must be carefully considered. Finally, sudden and significant blood pressure drops due both to overdosage of antihypertensive drugs and/or to intercurrent illnesses must be prevented, because the reduction of blood flow may induce severe target organ ischemia.
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PMID:Treatment of hypertension in the elderly. 1038 46


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