Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Recent guidelines recommend initiation of antihypertensive therapy with fixed-dose combinations in high-risk patients because such patients usually need two or more blood pressure (BP)-lowering agents in order to normalize their BP. Agents that block the renin-angiotensin system (ACE inhibitors or angiotensin II receptor antagonists [angiotensin receptor blockers; ARBs]) are preferred for the management of hypertension in most patients exhibiting subclinical target organ damage, or established cardiovascular or renal diseases. Unless contraindicated they should be one of the components of fixed-dose combinations, whereas the other component may be either a calcium channel antagonist or a thiazide diuretic. Fixed-dose combinations containing an ACE inhibitor or ARB plus a calcium channel antagonist appear particularly effective in preventing complications of coronary heart disease.
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PMID:Fixed-dose combinations as initial therapy for hypertension: a review of approved agents and a guide to patient selection. 1971 32

There is little prevalence data for chronic kidney disease (CKD) in Ireland and it has been suggested that rates of diagnosis of CKD in primary care are low. The aim of this cross sectional study was to examine the prevalence, diagnosis and standards of care for CKD. All patient records in three general practices in the West of Ireland were reviewed. In 2602 patients > 50 years in the community, 435 (16.7%) had chronic kidney disease defined as eGFR <60 ml/min/1.73 m2. Of these 435 individuals, only 58 (13.3%) had a diagnosis of CKD documented in their patient record. Among all patients with an eGFR <60 ml/min/1.73 m2, those with a documented diagnosis of CKD were significantly more likely to be prescribed an ACE/ARB and a lipid-lowering agent and were more likely to have had an ACR/PCR checked in the previous twelve months. Blood pressure was being appropriately monitored in the majority of patients but irrespective of eGFR level or a documented diagnosis of CKD, less than a fifth of patients had achieved a target of <130/80 mmHg. CKD is common in primary care but remains largely undiagnosed and blood pressure control remains suboptimal. A key step in improving care appears to be documenting the diagnosis which in turn appears to lead to improved standards of care and risk factor management.
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PMID:Chronic kidney disease in general practice: prevalence, diagnosis, and standards of care. 1990 46

The inhibition of renin-angiotensin system (RAS) has an effect beyond reducing blood pressure in the treatment of cardiovascular diseases; it also reduces mortality and morbidity. Although the classic RAS blockage is effective, due to blockage of negative feedback inhibition, it increases plasma renin activity and as a result generates a residual cardiovascular risk. Different from ACE-i and ARB treatments, aliskiren, a direct renin inhibitor, is the only pharmacologic agent that noticeably reduces the plasma renin activity, an independent cardiovascular risk factor. This creates a new option in RAS blockage. The efficacy and safety of aliskiren in the treatment of hypertension has been well established. The effect of aliskiren on cardiovascular mortality and morbidity is being researched. At this point there are many experimental and clinical studies to answer questions on this subject.
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PMID:[Renin and the heart]. 2001 73

Diabetes mellitus is highly prevalent in older adults in the industrialized world. These patients are at high risk of complications from diabetes, including diabetic kidney disease. ACE inhibitors and their newer cousins, angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), are powerful medications for the prevention of progression of diabetic renal disease. Unfortunately, among the elderly, these medications have been underutilized. The reasons for this include physician concerns regarding patient age and limited life expectancy and potential complications of ACE inhibitor or ARB use, specifically an increase in creatinine levels and hyperkalaemia. As discussed in this article, there have been several studies that show that the effects of inhibition of the renin-angiotensin system can be beneficial for the treatment of cardiovascular disease and renal disease among elderly patients with diabetes and that the potential risks mentioned above are no greater in this group than in the general population. For these reasons, several professional societies recommend that elderly patients with diabetes and hypertension (systolic blood pressure >or=140 mmHg or diastolic blood pressure >or=90 mmHg) be treated with an ACE inhibitor or ARB (as is recommended for younger diabetics). Use of ACE inhibitors or ARBs is also recommended for those with cardiovascular disease or those who are at risk of cardiovascular disease. Furthermore, in the management of diabetic kidney disease in elderly patients, treatment with ACE inhibitors or ARBs is also recommended to reduce the risk or slow the progression of nephropathy. Renal function and potassium levels should be monitored within the first 12 weeks of initiation of these medications, with each dose increase, and on a yearly basis thereafter. This article summarizes the current guidelines on the use of ACE inhibitors and ARBs in older adults with diabetes, reviews the evidence for their use in the elderly population, and suggests potential reasons for the observed underuse of these powerful drugs in this vulnerable population.
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PMID:ACE inhibitor and angiotensin II type 1 receptor antagonist therapies in elderly patients with diabetes mellitus: are they underutilized? 2010 36

Most patients with hypertension require two or more agents from different classes to achieve BP control. Several fixed-dose combinations are available, often combining agents that target the renin angiotensin system (angiotensin-converting enzyme [ACE] inhibitors or an angiotensin receptor blockers [ARBs]) plus either thiazide diuretics or calcium channel blockers (CCBs). At low doses, these combinations may have greater efficacy and better tolerability than the respective high dose monotherapies. Combining an ARB (instead of an ACE inhibitor) with the CCB amlodipine offers efficacy with improved tolerability. This review aims to highlight the simplicity, tolerability, and convenience of fixed-dose combinations targeting the renin-angiotensin system, which can lead to improved compliance and more patients achieving BP goals.
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PMID:The role of fixed-dose combination therapy with drugs that target the renin-angiotensin system in the hypertension paradigm. 2014 71

Acute coronary syndrome (ACS) is often associated with formation and development of atherosclerotic plaque, coronary artery vasoconstriction, rupture of vulnerable atherosclerotic plaque, coronary thrombus formation, and abrupt limitation of blood flow, leading to adverse outcomes. It is known that activation of the renin-angiotensin-aldosterone system(RAAS) contributes to aggravation of the condition. Thus, the RAAS inhibition is one of the therapeutic strategies of ACS. Considering the former evidence, ACE inhibitors and ARB are effective for prevention of ACS, respectively whereas ACE inhibitors would be slightly superior to ARB.
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PMID:[RAAS inhibitors]. 2038 65

The cardiovascular and cardiorenal disease continuum comprises the transition from cardiovascular risk factors to endothelial dysfunction and atherosclerosis, to clinical complications such as myocardial infarction (MI) and stroke, to the development of persistent target-organ damage and, ultimately, to chronic congestive heart failure (CHF), end-stage renal disease or premature death. The renin-angiotensin-aldosterone system (RAAS) is involved in all steps along this pathway, and RAAS blockade with ACE inhibitors or angiotensin AT(1)-receptor antagonists (angiotensin receptor blockers; ARBs) has turned out to be beneficial for patient outcomes throughout the disease continuum. Both ACE inhibitors and ARBs can prevent or reverse endothelial dysfunction and atherosclerosis, thereby reducing the risk of cardiovascular events. These drugs have further been shown to reduce end-organ damage in the heart, kidneys and brain. Aldosterone antagonists such as spironolactone and eplerenone are increasingly recognized as a third class of RAAS inhibitor with potent risk-reducing properties, especially but not solely with respect to the inhibition of cardiac remodelling and the possible prevention of heart failure. In secondary prevention, head-to-head comparisons of ACE inhibitors and ARBs, such as the recent ONTARGET study, provided evidence that, in addition to better tolerability, ARBs are non-inferior to ACE inhibitors in the prevention of clinical endpoints such as MI and stroke in cardiovascular high-risk patients. However, the combination of both ramipril and telmisartan at the maximally tolerated dosage achieved no further benefits and was associated with more adverse events such as symptomatic hypotension and renal dysfunction. In acute MI complicated by heart failure, the VALIANT trial has shown similar effects of ACE inhibition with captopril and ARB treatment with valsartan, but dual RAAS blockade did not further reduce events. In CHF, meta-analyses of RESOLVD, ValHeFT and CHARM-ADDED have shown that combined RAAS inhibition with an ACE inhibitor and ARB significantly reduced the morbidity endpoint in certain patient subgroups compared with standard therapy. However, in clinical practice, dual RAAS blockade is rarely employed, as seen, for instance, in the CORONA trial. The RALES and EPHESUS trials, investigating the effects of aldosterone blockade on cardiovascular outcomes in CHF patients, revealed that the addition of an aldosterone antagonist to standard heart failure therapy conferred powerful relative risk reductions for both morbidity and mortality. Future studies will elucidate whether this also holds true for patients who are asymptomatic or who have heart failure with preserved ejection fraction. In selected patients with renal disease, several studies have suggested that combined RAAS blockade brings about additional renoprotective antiproteinuric effects independent of blood pressure reduction, and large trials with robust endpoints are underway. In summary, combined therapy with several RAAS inhibitors is not recommended for all patients along the cardiorenovascular continuum. Patients with CHF with incomplete neuroendocrine blockade, as indicated, for example, by repetitive cardiac decompensation or refractory symptoms, might benefit from dual therapy as long as safety issues are well controlled. Finally, novel pharmacological agents such as the direct renin inhibitor aliskiren may provide additional therapeutic tools, but their role has yet to be established.
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PMID:Optimal antagonism of the Renin-Angiotensin-aldosterone system: do we need dual or triple therapy? 2056 30

Aldosterone production occurs in the adrenal cortex, and is regulated primarily by angiotensin II (Ang II), potassium and adrenocorticotropin (ACTH). In the presence of the aldosterone stimulators, steroidogenesis is further governed by local autocrine and/or paracrine factors in the adrenal cortex. We reported the presence of functional bone morphogenetic protein (BMP) system in the adrenal cortex and also demonstrated that BMP-6 increases Ang II-induced aldosterone production, which could be involved in the "aldosterone breakthrough" phenomenon. Aldosterone breakthrough is the phenomenon by which circulating aldosterone concentrations increase above pre-treatment levels after long-term therapy with ACE inhibitors or Ang II type 1 receptor antagonists (ARB). This phenomenon may lead to important clinical consequences since increased aldosterone in a high-salt state facilitates cardiovascular and renal damage in hypertensive patients. We found that long-term ARB treatment reverses the reduction of aldosterone synthesis by adrenocortical cells, thereby causing "cellular aldosterone breakthrough". The availability of BMP-6 in the adrenal cortex may be at least partly involved in the occurrence of cellular escape from aldosterone suppression under chronic treatment with ARB.
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PMID:Roles of bone morphogenetic protein-6 in aldosterone regulation by adrenocortical cells. 2080 37

A 76 year-old woman with a history of coronary artery bypass grafting and prior myocardial infarction was transferred to the emergency room with loss of consciousness due to marked bradycardia caused by hyperkalemia. The concentration of serum potassium was high, and normal sinus rhythm was restored after correction of the serum potassium level. The cause of hyperkalemia was considered to be several doses of spiranolactone, an aldosterone antagonist, in addition to the long-term intake of ramipril, an ACE inhibitor. This case is a good example of electrolyte imbalance causing acute life-threatening cardiac events. Clinicians should be alert to the possibility of hyperkalemia, especially in elderly patients using ACE/ARB in combination with potassium sparing agents and who have mild renal disturbance.
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PMID:Syncope caused by hyperkalemia during use of a combined therapy with the angiotensin-converting enzyme inhibitor and spironolactone. 2085 99

Medical management of systolic heart failure is standardized and based on international guidelines. They promote the use of combination therapy based on neurohormonal blockade targeting both the renin-angiotensin system (with ACE inhibitors or ARB) and sympathetic nervous system (i.e., beta blockers). Drugs have to be titrated at the maximum tolerated level. In symptomatic patients, loop diuretics remain the treatment of choice with dosage adaptation according to symptoms and fluid management. Aldosterone antagonists are indicated in patients with severe heart failure (i.e., NYHA class 3 or 4) and creatinine clearance above 30 ml/min. Their combination with RAS blockers warrants strict biological follow up.
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PMID:[Medical management of chronic systolic heart failure]. 2103 91


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