Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension should be detected and treated early in diabetic patients. It markedly affects the morbidity and mortality of diabetic individuals as a result of both atherosclerosis and microvascular disease. Antihypertensive treatment is an effective tool in slowing the progression of early and advanced diabetic nephropathy. No prospective studies have addressed the effects of antihypertensive regimens on the incidence of congestive heart failure, stroke, and coronary artery disease in large groups of diabetic patients. Such studies are urgently needed. Special consideration should be given to the effects of antihypertensive drugs on glycemic control and the lipid profile of the diabetic patient. Because hyperinsulinemia (and insulin resistance) have been advocated as hypertensive and atherosclerotic risk factors, the effects of antihypertensive drugs on insulin action and plasma insulin levels may become an important element in the selection an antihypertensive agent. More information, however, is needed in these areas. ACE inhibitors, calcium channel blockers, and alpha-adrenergic blockers probably offer a more favorable metabolic profile as compared with diuretics and beta-blockers. The former agents should be used as initial drugs in most clinical settings.
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PMID:Management of hypertension in diabetes. 161 71

The aim in treatment of hypertension is normalization of blood pressure. The impact of treatment of hypertension on the development of IHD depends not only on the treatment of hypertension but also on influencing other basic risk factors, i.e. hyperlipoproteinaemia and smoking. Treatment of hypertension can be and should be individual and depends on a) age, b) the level of hypertension, c) complications of hypertension and d) the presence of other diseases, in particular hyperlipoproteinaemia and diabetes mellitus. The treatment of choice in hyperlipoproteinaemia are calcium antagonists, prazosin, ACE inhibitors and beta-blockers with ISA. There is experimental evidence suggesting that calcium antagonists (in particular isradipine) but also beta-blockers suppress the progression of atherosclerosis and AGE inhibitors prevent the development of cardiac and vascular hypertrophy. Effective treatment leads to a decline in the mortality from cerebrovascular attacks--in the USA in the course of 20 years a decline by 60%--in Czechoslovakia so far the mortality from cerebrovascular disease did not change which indicates unfortunately a very poor control of hypertension in the population.
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PMID:[Treatment of hypertension and cardiovascular complications]. 182 87

Since hypertension is an important risk factor for atherosclerosis, it is logical to assume that treatment to lower blood pressure will prevent atherosclerosis. However, the relationship between hypertension and atherosclerosis is indirect and complex. Drugs that lower pressure will prevent heart failure and arteriolar complications such as renal failure or strokes caused by lacunar infarction or brain haemorrhage due to rupture of microaneurysms. However, there is little evidence that atherosclerotic complications can be reduced by lowering pressure. It is important to understand the pathogenesis of atherosclerosis and its complications, which are related to lipoproteins and arterial flow disturbances, in order to develop an approach to selecting those antihypertensive drugs which may prevent atherosclerotic complications related not only to initiation and progression of atherosclerotic plaques, but to the embolisation of platelet clumps or atherosclerotic debris, or events such as intraplaque haemorrhages, that lead to myocardial or cerebral infarction. Antihypertensive drugs have different effects on lipoproteins and on arterial flow disturbances that may have important implications for prevention. Alpha-blockers and drugs with beta 2 agonist activity have beneficial effects on lipoprotein profiles, ACE inhibitors and calcium channel antagonists have some anti-atherosclerotic effects in animal models, while beta-blockers have beneficial effects on flow disturbances and are anti-atherosclerotic in animal models and man. Future studies to determine how to prevent atherosclerotic complications in hypertensive patients will require methods for noninvasive measurement of atherosclerosis.
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PMID:Pathogenesis of atherosclerosis and its complications: effects of antihypertensive drugs. 269 95

The use of ACE-inhibitors has increased greatly during the last years. They were first used in treating hypertension, but nowadays cardiac diseases, mainly cardiac failure, are common indications. This means that the drugs are used in the treatment of more elderly patients who often have generalised atherosclerosis. This means that the patients must be controlled more often after initiation of treatment, especially concerning kidney function, since treatment with ACE-inhibitors can cause pronounced changes in renal haemodynamics and kidney function. This review focuses on the effects of ACE-inhibitors on renal haemodynamics and kidney function, which may be positive, with preservation of kidney function in diabetic and other chronic nephropathy, or negative, for example in cases with atherosclerotic stenosis of large or small renal arteries. It is concluded, that in cases of diabetic nephropathy an ACE-inhibitor is the "drug of choice" for treatment of hypertension. Furthermore the ACE-inhibitors seem to reduce the rate of deterioration of renal function and proteinuria in other kidney diseases. It is emphasized, that during treatment with ACE-inhibitors kidney function must be controlled before and following one to two weeks of treatment, if the dose is changed and in all cases following two to three months of treatment. Special attention should be given to patients with atherosclerotic manifestations e.g. angina.
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PMID:[Renal function during treatment with angiotensin converting enzyme inhibitors]. 748 49

The effect on kidney function fo treatment of cardiac failure with ACE-inhibitors was examined retrospectively in a material of 87 consecutive patients. Furthermore, it was evaluated whether concomitant treatment with diuretics or existing generalised atherosclerosis as indicated by ongoing treatment with nitrates could be a risk factor concerning reduction of kidney function. In 11.9% of the patients an increase in S-creatinine of > 30% was observed during the first weeks of treatment. It was only necessary to stop treatment in two of these patients. In the remainder S-creatinine decreased again during ongoing treatment. In another 10.7% of patients an increase of 20-30% in S-creatinine was observed. Seventy-two point six percent of the patients had unchanged kidney function during treatment with an ACE-inhibitor. Ongoing treatment with diuretics did not seem to be a risk factor for developing reduced kidney function, whereas significantly more patients on treatment with nitrates, indicating generalised atherosclerosis, developed reduced kidney function during treatment with ACE-inhibitors. It is recommended to control kidney function before, one to two weeks and two to three months following initiation of treatment with ACE-inhibitors and to pay special attention to patients with generalised atherosclerosis.
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PMID:[Renal function during treatment of chronic renal failure with angiotensin converting enzyme inhibitors]. 748 50

Cardiac transplant atherosclerosis is thought to result from immune-mediated vessel wall injury. The present experiments were designed to test whether CsA alone or in combination with the ACE-inhibitor cilazapril has any effect on graft atherosclerosis in a rat cardiac transplant model. Cardiac grafts were transplanted heterotopically into either syngeneic or allogeneic recipients and followed by daily palpation; long-surviving grafts were removed after 100 days and the extent and degree of atherosclerosis was assessed using computerized morphometry. Atherosclerosis was more extensive in grafts removed from untreated allogeneic recipients compared with syngeneic recipients; CsA treatment increased the extent of atherosclerosis in syngeneic transplants. The extent and degree of vascular occlusion in allogeneic grafts from recipients treated with 15 mg/kg of CsA every other day was not different from that in grafts removed from recipients that received initially higher CsA doses. Cilazapril had no effect on the extent of graft atherosclerosis but decreased the degree of luminal narrowing in grafts from CsA-treated recipients significantly. Some grafts showed neovascularization in the subendocardial region adjacent to organized intraventricular clots, suggesting the release of angiogenic factors from such clots; such growth factors may contribute to the atherosclerotic vessel wall reaction in this model. We conclude that CsA promotes the development of graft atherosclerosis in heterotopically transplanted syngeneic cardiac grafts in the rat. We furthermore found that cilazapril has a beneficial effect on the degree of atherosclerosis in CsA-treated recipients.
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PMID:Cardiac allograft atherosclerosis in the rat. The effect of histocompatibility factors, cyclosporine, and an angiotensin-converting enzyme inhibitor. 751 77

Aim of recent experimental and clinical studies has been to evaluate the important role of the renin-angiotensin system in the development of cardiac hypertrophy, of vascular hypertrophy and of left ventricular fibrosis and remodelling in essential hypertension and ischemic heart disease. It has been suggested that ACE-inhibitors are the class of antihypertensive drugs more effective in reducing left ventricular hypertrophy (LVH) in hypertensive patients. The possible mechanisms are, beyond the decrease in blood pressure, the possibility of interfering not only with the renin-angiotensin system activity, but also with the sympathetic nervous system activity as well as with aortic distensibility, all factors that can influence the development of LVH. Vascular changes in essential hypertension are complex and depend not only on the severity of blood pressure levels, but are related to diameter and structure of the vessels and to the presence of other atherosclerosis risk factors. ACE-inhibitors are effective in inducing the regression of structural changes in resistance arterioles and furthermore can increase arterial compliance in large arteries; new studies are undergoing in order to assess the effects of these drugs on atherosclerotic plaque progression/regression. The results of large clinical trials have shown the efficacy of ACE-inhibitors in the treatment of heart failure, in addition, after it has been demonstrated that ACE-inhibitors can influence the structural remodelling process after myocardial infarction, their use has been extended to patients with ischaemic heart disease.
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PMID:[ACE-inhibitors and cardiovascular protection]. 763 57

From pharmacological investigations and clinical studies, it is known that ACE inhibitors exhibit additional local actions that are not related to hemodynamic changes and that cannot be explained only by interference with the renin-angiotensin system by means of an inhibition of ANG II formation. Because ACE is identical to kininase II, which inactivates the nonapeptide BK and related kinins, potentiation of kinins might be responsible for these additional effects of ACE inhibitors. ACE inhibition, concentration, and time dependently increased the formation of NO and PGI2 in cultured endothelial cells of different origin and from different species, including humans. The specific B2 kinin receptor antagonist, icatibant, suppressed the ACE inhibitor-induced increase in endothelial cyclic GMP accumulation index for NO-formation and, in parallel, attenuated the increase in PGI2 release. In renovascular models of hypertension associated with a stimulated renin-angiotensin system (two-kidney, one-clip), blood pressure reduction by ACE inhibitors was attenuated by icatibant, whereas in rats with genetic hypertension with normal to low plasma renin, blood pressure reduction through ACE inhibitors was not affected. In experimental atherosclerosis in rabbits, ACE inhibitors were able to preserve endothelial function and vascular reactivity and to reduce surface involvement. In the balloon denudation model of carotid arteries in rats, it was found that ACE inhibition markedly reduced neointima formation. However, when the ACE inhibitor was given together with icatibant, its effect was significantly blunted. Perfusion with ACE inhibitors induced a reduction of the incidence, as well as of the duration, of ventricular fibrillation and improved cardiodynamics and myocardial metabolism. BK perfusion induced comparable cardioprotective effects. In addition, perfusion with ACE inhibitors markedly increased the outflow of BK and related kinins from isolated rat hearts. The antiischemic effect of ACE inhibitors and BK were abolished by the addition of L-NNA (1 x 10(-6) mol/l) or icatibant (1 x 10(-9) mol/l). Similar results were found in dogs and rabbits with myocardial infarction. BK and related kinins also seem to be involved in preconditioning and remodeling. The effect of ACE inhibition in LVH was investigated in rats made hypertensive by aortic banding. ACE inhibition with ramipril, in the antihypertensive dose of 1 mg/kg/day for 6 weeks, prevented the increase in blood pressure and the development of LVH. A lower, nonantihypertensive dose of the ACE inhibitor (10 micrograms/kg/day for 6 weeks) had no effect on the increase in blood pressure or on plasma ACE activity, but also prevented LVH after aortic banding.4+ off
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PMID:Contribution of kinins to the cardiovascular actions of angiotensin-converting enzyme inhibitors. 778 79

The ACE gene has recently been shown to be associated with myocardial infarction, especially in subjects considered at low risk for coronary heart disease (CHD) according to common classification criteria. The possible relationship between deletion polymorphism in this gene and CHD risk factors, as well as asymptomatic extracoronary atherosclerosis, has been investigated in the present study. One hundred and seventy-four subjects, enrolled in a cardiovascular disease prevention study, underwent clinical and biochemical examination and ACE-I/D polymorphism determination. Subjects > 45 years of age (n = 107) also received echo-Doppler examination of the carotid arteries. Based on the results of ACE-I/D polymorphism, subjects were divided into three groups: homozygous for deletion (D/D), homozygous for insertion (I/I) and heterozygous (I/D). The prevalence of CHD risk factors as well as of extracoronary atherosclerosis was similar in the three genotype groups. Similarly, there was no association between the presence of atherosclerotic lesions and genotype in subjects at low and high CHD risk. Ten subjects with diabetes mellitus had ACE-D/D genotype. Among these subjects seven had hypertension. Eight subjects with diabetes mellitus had ACE-I/D genotype and only one of these was hypertensive. None of the ACE-I/I subjects was diabetic. ACE-I/D polymorphism seems to play a role in the development of hypertension, at least in diabetic subjects. Its determination may help to identify and monitor diabetic subjects prone to hypertension.
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PMID:Association between ACE-D/D polymorphism and hypertension in type II diabetic subjects. 780 99

Lipoprotein(a) [Lp(a)] consists like the low-density-lipoprotein (LDL) in the structure protein apolipoprotein B, but is additionally connected with apolipoprotein(a), which is highly homologous to plasminogen. The physiological function of Lp(a) is yet not entirely clear. Lp(a) is established to be an independent factor in the genesis of atherosclerosis however. With occurrence of high Lp(a) Lp(a) plasma levels and other atherogenous risk factors at the same time a potentiation of their effects on genesis of atherosclerosis is observed. Unfortunately the therapeutic possibilities of counteracting the high atherogenicity of Lp(a) are still limited, because LDL apheresis as the only known effective technique today cannot be applied in all cases. In several studies it has been shown, that Lp(a) concentrations can be reduced mainly by long term treatment with lipid-lowering sustained-release bezafibrate, ACE-inhibitor fosinopril, alpha-tocopheryl-nicotinate and N-acetylcysteine. Because of the synergistic effects of atherogenous risk factors patients with high Lp(a) concentrations should avoid additional risk factors such as hypertension, smoking, diet increasing LDL, etc.
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PMID:[The significance of lipoprotein(a) in assessment of risk for atherosclerosis]. 783 88


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