Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High-risk strategies represent important preventive measures that focus on individuals with a defined high risk of suffering a chronic disease. They are valuable in addition to measures of prevention within the general population. One example for a high-risk approach for stroke prevention is the treatment of hypertension in individuals that have previously suffered a transient ischemic attack (TIA). Data from the Klosterneuburg Stroke Data Bank and other sources enable an estimate of 2000 TIAs occurring in Austria each year, half of them being hypertensives that are mostly not treated or not sufficiently treated for their hypertension. A high-risk programme that implies forced and effective treatment of hypertension would prevent some 400 strokes or 3% of 16,000 first-ever strokes per year. Costs for preventing one stroke by means of Betablocker agents would amount to ATS 3500 and by ACE-inhibitor agents ATS 11,500, respectively. In addition to general preventive measures, such a programme would have an important impact on stroke incidence and public health.
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PMID:[Stroke prevention with a high risk strategy of treating hypertension in patients after a transient ischemic attack]. 913 69

The number of patients who needs for dialysis therapy is increasing rapidly among the older population. Although control of hypertension can delay or arrest the progression of renal failure, there are lacking of studies about antihypertensive treatment of chronic renal failure in the elderly. We have studied the effects of treating hypertension with a calcium antagonist, benidipine, on renal function and blood pressure in 58 patients (mean age: 71 +/- 9) with hypertension and chronic renal insufficiency (the levels of creatinine ranging from 1.5 to 4.0 mg/dl). The underlying disease included glomerulopathies (in 33), diabetic nephropathy (in 15), and other causes (in 10). Forty two patients who had been treated with other antihypertensive drugs other than angiotensin converting enzyme (ACE) inhibitors, antihypertensive drugs were withdrawn 2 weeks before the entry. At the entry, patients should have sitting systolic blood pressure (SBP) of above 160 mmHg and diastolic blood pressure (DBP) of above 90 mmHg. In total, both SBP and DBP decreased from 169/95+/-12.5/8.9 to 148/81+/-16.1/8.0 mmHg (p<0.001) with remaining the serum creatinine levels from 2.2+/-0.8 vs 2.4+/-1.3 mg/dl (P>0.05). Retrospective analysis revealed that in 4 of 4 patients treated with benidipine and 2 of 3 patients with benidipine and ACE inhibitors with systolic blood pressure more than 160 mmHg at the end of the study, the levels of serum creatinine increased from 2.5+/-0.3 to 2.8+/-0.4 with significance (P<0.05). If systolic blood pressure was reduced less than 159 mmHg, 38 of 48 patients did not show any deterioration of renal function. Compared to the significance of SBP in preserving renal function, DBP did not associate with the changes in renal function. No patients died during the study. One patient had transient ischemic attack and one patient had stroke in benidipine treated group. One patient had angina pectoris in benidipine-ACE inhibitors treated group. The results of our trial seem to give some support for the idea that long-acting calcium antagonists such as benidipine are renoprotective through reduction of SBP in the elderly people with hypertension and chronic renal insufficiency. However, if systolic blood pressure was not reduced below 160 mmHg throughout a year, the substantial declines in renal function would be expected.
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PMID:Effects of calcium antagonist, benidipine, on the progression of chronic renal failure in the elderly: a 1-year follow-up. 1133 86

PROGRESS ("Perindopril pROtection aGainst REcurrent Stroke Study") demonstrated that blood-pressure lowering treatment with perindopril, an angiotensin converting enzyme inhibitor (combined with the diuretic agent indapamide when necessary), reduces the risk of stroke by 28% (95% CI: 17-38, p < 0.0001) among patients with a history of stroke or transient ischaemic attack. This protective effect was observed among both hypertensive and non-hypertensive individuals. It was more marked in the patients receiving combined perindopril + indapamide treatment (-43%; 95% CI 30-54) who were those who showed the greatest reduction in arterial blood pressure (-12/5 mm Hg). According to these observations, the authors concluded that treatment with these two agents should now be considered routinely for patients with a history of stroke or transient ischaemic attack, irrespective of their blood pressure.
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PMID:[Clinical study of the month. Secondary prevention of cerebrovascular accident with perindopril: the PROGRESS study]. 1178 95

Last year, in 2001, the results of several major clinical trials have been published, concerning hypertensive patients with type 2 diabetes (IRMA, RENAAL and IDNT studies) and patients with previous strokes. Angiotensin II antagonists (irbesartan and losartan) are able to reduce the rate of progression of diabetic nephropathy in hypertensive patients with type 2 diabetes. This preventive effect occurs independently of the stage of renal dysfunction (early stage in IRMA, patent nephropathy in RENAAL and advanced nephropathy in IDNT). The PROGRESS study shows that the decrease in blood pressure, in response to an ACE inhibitor/diuretic bitherapy (perindopril/indapamide), in patients with previous minor stroke or transient ischaemic attack, reduces significantly the risk of recurrent stroke.
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PMID:[The best of 2001. Arterial hypertension]. 1190 4

Stroke is a major cause of morbidity and mortality. Full assessment of stroke or transient ischaemic attack (TIA) patients is required to identify all risk factors and apply appropriate secondary preventative strategies. Antiplatelet therapies are effective in the secondary prevention of ischaemic stroke and can be justified despite adverse effects such as gastrointestinal haemorrhage. Aspirin (acetylsalicylic acid), aspirin plus dipyridamole, ticlopidine and clopidogrel are all of value but their adverse effect profiles vary significantly. Combinations of antiplatelet agents may offer additional benefit but not all combinations have been studied in stroke patients. Anticoagulation with agents such as warfarin is effective with coexisting atrial fibrillation and other conditions predisposing to cardioembolic stroke. Antihypertensive agents have been extensively studied in the primary prevention of stroke; however, relatively few trials of antihypertensive agents in the secondary prevention of stroke are available. The incidence of adverse effects of antihypertensive agents is relatively low and the benefit-risk profile would tend to favour their use in the secondary prevention of stroke. Recent studies of ACE inhibitors have identified an important role for these agents in the secondary prevention of stroke even in those who are normotensive and in those who have had a haemorrhagic stroke. The incidence of serious adverse effects with ACE inhibitors appears relatively low. Lipid-lowering agents may have a role to play in certain groups of patients with stroke. The incidence of adverse effects is relatively low with HMG-CoA reductase inhibitors. Cigarette smoking is an important risk factor for stroke and evidence is available that smoking cessation does reduce the individual's risk of stroke. Pharmacological agents are available to help smoking cessation. In patients with diabetes mellitus, intensive regimens with insulin and oral hypoglycaemic agents have so far not definitively been shown to reduce the incidence of macrovascular complications such as stroke. Tight glycaemic control has been shown to improve microvascular complications such as retinopathy, nephropathy and neuropathy and hence this is reason enough to advocate the use of these agents. Future developments in the treatment of diabetes may help. Secondary prevention of stroke has improved greatly over the past decade and hopefully will continue to improve. The use of pharmacological agents available currently and in the future will be clarified and refined as further clinical trials report.
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PMID:A benefit-risk assessment of agents used in the secondary prevention of stroke. 1238 Dec 15

The fact that transient ischaemic attacks are a harbinger for the possible development of ischaemic stroke has been recognised for several decades. However, within the past decade, our concepts regarding transient ischaemic attacks as a distinct entity from stroke and the prognosis for transient ischaemic attack patients have been challenged. In addition, clinical trials have clarified that modern transient ischaemic attack management is more complex than in the past, with the addition of newer pharmacological options to the stroke prevention armamentarium. Recent information regarding newer antiplatelet agents is reviewed in this article, along with results of clinical trials pertaining to warfarin in stroke prevention. The evolving role of statins, ACE inhibitors and estrogen replacement is reviewed. Finally, the appropriate use of surgery following transient ischaemic attacks is outlined. Recent studies have shown that many patients will benefit from a multimodal pharmacological approach following transient cerebral ischaemia, and the potential for combination therapy is highlighted.
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PMID:Transient ischaemic attacks : new approaches to management. 1266 89

Hypertension is the most important risk factor for stroke and vascular dementia. Antihypertensive treatment reduces stroke risk by 40%. Most probably all antihypertensive drugs are equally effective with the exception of alpha-blockers. Blood pressure is increased in many patients with acute stroke. In this phase sudden drops in blood pressure should be avoided. The combination of an ACE-inhibitor and a diuretic reduced strokes by 28% after TIA or a first stroke. Whether this is a drug specific effect or due to lowering blood pressure per se is investigated at the moment.
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PMID:[Sequelae of hypertension on end-organs of the brain]. 1463 75

Diabetes mellitus, arterial hypertension, smoking are major stroke risk factors. The role of hypercholesterolemia in stroke has not been established yet. In patients with type 2 diabetes mellitus there is evidence that intensive glucose lowering therapy diminishes the risk of microvascular complications. In all patients with stroke or transient ischemic attack (TIA), blood pressure should be lowered irrespectively of the baseline level with either diuretics, angiotensin converting enzyme (ACE) inhibitors, beta-blockers, or calcium antagonists. The role of angiotensin II (AT2) receptor blockers has not been established so far. In general terms a global approach to management of patients with vascular risk factors should be developed. An extended follow-up of randomised trials on preventive therapy should be completed. Controlled trials comparing angiotensin receptor blockers with ACE inhibitors should be started. Further research may focus on the new lipid lowering agents, and on the comparison of single lipid lowering agent vs. combinations in stroke prevention. These efforts should help in finding the best vasoprotective strategy in stroke prevention.
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PMID:Antihypertensive and lipid lowering treatment in stroke prevention: current state and future. 1607 57

High blood pressure (BP) is the most important modifiable risk factor for stroke and other vascular diseases. Evidence from randomized controlled trials supports the use of antihypertensive drugs to lower blood pressure for stroke prevention. There is some evidence that specific classes of antihypertensive drugs have different effects and/or their pharmacological actions differ in patient subgroups. This review evaluates the development of antihypertensive therapies and the latest studies of arterial hypertension and stroke prevention: HOPE trial (ramipril versus placebo), ALLHAT trial (CCB or/ and Angiotensin-Conventing enzyme Inhibitors (ACE-Is) versus diuretic), LIFE trial (losartan versus atenolol), and PROGRESS trial (perindopril or/and indapamide versus placebo). Despite the results of these relevant clinical trails, some aspects still remain unresolved. Future clinical trials on hypertension and stroke prevention should answer the following questions: Does lowering BP reduce stroke risk due to specific drug effect or class effect? Are angiotensin II receptor blockers (ARBs) better than ACE-Is? Should ACE-Is and ARBs be considered routinely for either high-risk stroke patients or patients with history of stroke or transient ischemic attack, irrespective of blood pressure? What is the role of lifestyle in BP control?
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PMID:Arterial hypertension and stroke prevention: an update. 1683 41

Hypertension is the major risk factor for ischaemic and haemorrhagic clinical strokes as well as for silent brain infarcts with a continuous association between both systolic and diastolic blood pressures. Epidemiological data highlight the increasing burden to come over the next decades. Without any doubt, antihypertensive treatment is the most important therapy to reduce the risk of stroke by approximately 30-40%. International guidelines recommend antihypertensive treatment for primary prevention with evidence level A. Recurrent strokes or transient ischaemic attack (TIA) are an important practical, clinical and economic problem, and have a major impact on the development of vascular dementia. All stroke patients and patients with TIA have to be regarded as very high-risk patients. Hypertension increases the risk of recurrent strokes. Only limited data directly address the role of blood pressure treatment among individuals with stroke or TIA. There is a general lack of definitive data regarding when to start antihypertensive treatment in the initial phase, and treatment of hypertension in the acute period after stroke is still under debate. Experimental and clinical data suggest that reducing the activity of the renin-angiotensin aldosterone system (RAAS) may have beneficial effects beyond the lowering of blood pressure. There is increasing evidence of cerebroprotective effects for medication influencing the RAAS, such as angiotensin receptor antagonists or ACE inhibitors. The MOSES study showed for the first time superiority of an angiotensin receptor antagonist compared with a calcium channel antagonist in antihypertensive treatment for secondary stroke prevention. Optimal blood pressure range in secondary prevention seems to be 120-140/80-90 mm Hg, but questions about a J- or U-shaped curve are still not answered sufficiently. The effects of additional antihypertensive treatment in the evening for stroke patients with 'non-dipping' blood pressure need to be investigated.Currently, the most important goal in primary and secondary prevention of stroke is a strict normotensive blood pressure control. Antihypertensive treatment is recommended for both prevention of recurrent stroke and prevention of other vascular events in individuals who have had an ischaemic stroke or TIA (class I, level of evidence A). Many open questions remain and funding of stroke research needs to be increased in the near future.
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PMID:Drug therapy for the secondary prevention of stroke in hypertensive patients: current issues and options. 1748 41


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