UMLS:C0007222 - FACTA Search

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Query: UMLS:C0007222 (cardiovascular disease)
65,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension is a well documented risk factor for cardiovascular disease (CVD) and substantially contributes to the global burden of disease. Different drug options exist for combination therapy as part of an overall control of risk factors in order to decrease the absolute risk of CVD. Several guidelines in recent years have tried to set up recommendations to increase the proportion of subjects in acceptable BP control from high-risk groups. Some conventional drugs are still very important in modern hypertension treatment, e.g. low-dose thiazide diuretics. However, newer compounds have added to the list of useful agents to be used as monotherapy or in combination therapy for improved target organ protection, e.g. the calcium channel antagonists and ACE inhibitors. The role of beta-adrenoceptor antagonists (beta-blockers) has changed somewhat as a result of critical comments from recent meta-analyses. Currently, therefore, beta-blockers are recommended less often for primary prevention and monotherapy, but should still be used for secondary prevention, combination therapy, and for symptom relief. Finally, the new angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]) are still rather expensive, but have been increasingly documented in clinical trials for patients with essential hypertension. One controversial aspect is whether ARBs are better, worse, or equal to standard therapy with an ACE inhibitor for cardiovascular protection. BP remains poorly controlled in a large number of hypertensive patients and there is a greater need to control all relevant CVD risk factors in such patients. Therefore, different drugs are needed in order to be used in evidence-based synergistic and cost-effective drug combinations.
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PMID:Optimizing the pharmacologic treatment of hypertension: BP control and target organ protection. 1708 63

Cardiovascular disease (CVD) has been the primary cause of death in women for almost a century, and more women than men have died of CVD every year since 1984. Although CVD incidence can be reduced by adherence to a heart-healthy lifestyle and detection and treatment of major risk factors, preventive recommendations have not been consistently or optimally applied to women. The American Heart Association guidelines for CVD prevention in women provide physicians with a clear plan for assessment and treatment of CVD risk and personalization of treatment recommendations. The emphasis of preventive efforts has shifted away from treatment of individual CVD risk factors in isolation toward assessment of a woman's overall or "global" CVD risk. In addition to accounting for the presence or absence of preexisting coronary heart disease or its equivalents (e.g., diabetes, chronic kidney disease), cardiovascular risk can be further calculated with the Framingham risk score, which is based on age, sex, smoking history, and lipid and blood pressure levels. Intervention intensity and treatment goals are tailored to overall risk, with those at highest risk receiving the most intense risk-lowering interventions. Women at high risk for CVD and without contraindications should receive aspirin, beta blockers, and an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker in addition to pharmacologic therapy for hyperlipidemia, hypertension, and diabetes. Women who already are at optimal or low risk for CVD should be encouraged to maintain or further improve their healthy lifestyle practices. Optimal application of these preventive practices significantly reduces the burden of death and disability caused by heart attack and stroke in women.
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PMID:Preventing cardiovascular disease in women. 1708 23

Heart failure is thought to be more common and of greater severity in African-Americans (AAs). Potential mechanisms remain uncertain. The importance of micronutrient deficiencies in the pathophysiologic expression of congestive heart failure (CHF) in AAs remains to be explored, including hypovitaminosis D, which can promote secondary hyperparathyroidism (SHPT), together with hypozincemia and hyposelenemia, the 2 most crucial trace minerals integral to diverse biologic functions. Serum parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), Zn, and Se were monitored in 30 AAs hospitalized during June through December 2005, with decompensated failure and reduced ejection fraction (EF) (<35%) of predominantly nonischemic origin treated with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB), furosemide, and spironolactone. Based on their symptomatic status before hospitalization, 15 patients were stratified as having protracted (>or=4 weeks) CHF, whereas 15 patients had short-term (1-2 weeks) CHF. These hospitalized patients were compared with 10 AA outpatients with stable, similarly treated compensated failure and comparable EF, and 9 AA normal volunteers without cardiovascular disease. Serum PTH was elevated in all patients with protracted CHF and in 60% of patients with short-term CHF, but not in compensated patients or normal volunteers. However, serum 25(OH)D was reduced in all patients with >or=4 weeks and 80% with either 1-2 weeks CHF or compensated failure compared with volunteers. Serum Zn was below normal in 11 of 15 patients with protracted CHF, in 8 of 15 patients with shorter duration CHF, and in 5 of 10 patients with compensated failure. Serum Se was reduced in all patients with >or=4 weeks, 60% with short-term CHF, and 90% of compensated patients. Concomitant to hypovitaminosis D, hypozincemia, and hyposelenemia, SHPT is a covariant of CHF in housebound AAs.
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PMID:Micronutrients in African-Americans with decompensated and compensated heart failure. 1716 51

Metabolic syndrome is a constellation of interrelated abnormalities that increase the risk for the development of cardiovascular disease and type 2 diabetes. Together with obesity and dyslipidaemia, hypertension is one of the basic elements of the metabolic syndrome. Current guidelines do not provide specific recommendation for pharmacological management of the hypertensive patients with metabolic syndrome. Recent trials have consistently shown that therapy involving beta-blockers and diuretics may have some negative impact on metabolic and haemodynamic disorders present in metabolic syndrome. Several lines of evidence support the use of angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers as the appropriate first-line therapy and calcium channel blockers, as the second, in the patients with metabolic syndrome.
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PMID:[Metabolic syndrome in patients with hypertension]. 1721 93

An increase or decrease in urinary albumin excretion (UAE) is associated with, respectively, a higher or lower risk for renal and cardiovascular disease, independent of widely known cardiovascular risk factors. This study aimed to identify factors that are associated with changes in UAE in the nondiabetic population using data of the Prevention of Renal and Vascular End stage Disease (PREVEND) Study, a community-based prospective cohort study. Data of the 6647 nondiabetic participants who completed the first (1997 through 2001) and second (2001 through 2003) screening were used. Change in UAE was categorized as regression (n = 650), stable (n = 5240), or progression (n = 757) on the basis of change in class during follow-up, with classes being a UAE <15, 15 to 30, 30 to 300, and >300 mg/24 h. With the use of stepwise forward multinomial regression analysis changes in BP, fasting glucose concentration, and start of antihypertensive drugs were found to be the most important modifiable variables associated with the risk for progression and regression (P < 0.01 for likelihood ratio test). The odds ratios to develop regression or progression of UAE during follow-up were 0.64 (95% confidence interval [CI] 0.57 to 0.73) and 1.91 (95% CI 1.72 to 2.12), respectively, per 10-mmHg increase in BP during follow-up, 0.89 (95% CI 0.80 to 0.98) and 1.09 (95% CI 1.01 to 1.17), respectively, per 1-mmol/L increase of fasting glucose levels during follow-up, and 1.57 (95% CI 1.21 to 2.06) and 0.70 (95% CI 0.51 to 0.95), respectively, for start of antihypertensive drugs during follow-up. These associations were independent of baseline BP, glucose, body mass index, estimated GFR, and UAE and changes in high-sensitivity C-reactive protein during follow-up. In conclusion, changes in glucose concentration and BP and start of antihypertensive drugs (angiotensin-converting enzyme inhibitors/angiotensin receptor blockers in >50% of cases) are associated with progression and regression of UAE in the nondiabetic population. Although associations do not necessarily suggest causality, it is hypothesized that in the general population, the most important ways to reduce UAE are by lowering glucose concentration and BP (including start of antihypertensive medication), even in normotensive, nondiabetic individuals.
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PMID:What predicts progression and regression of urinary albumin excretion in the nondiabetic population? 1721 42

The renin-angiotensin-aldosterone system (RAAS) is now known to play a key role in the pathogenesis of hypertension and a range of other cardiovascular diseases. Two groups of drugs, the ACE inhibitors and angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]) have been developed with the aim of improving clinical outcomes by regulating the RAAS in patients with cardiovascular disease. Initial assumptions were that these two drug types might be interchangeable, but ongoing research has revealed differences between them in terms of pharmacology and outcomes in clinical trials. Although both groups of drugs lower blood pressure, studies of the ACE inhibitor perindopril have revealed preservation of beneficial vascular and endothelial effects mediated by bradykinin and nitric oxide. The selective blockade exerted by ARBs is not associated with these effects. Furthermore, examination of clinical endpoints in major clinical trials has provoked discussion about outcomes comparing ACE inhibitors and ARBs, with recent debate focusing on the incidence of myocardial infarction (MI) in patients receiving these agents. Whether there is an actual difference in protection from MI remains unresolved, although available data confirm the benefit and safety of ACE inhibitors, in particular perindopril, for myocardial protection.
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PMID:Perindopril versus angiotensin II receptor blockade in hypertension and coronary artery disease: implications of clinical trials. 1730 12

Type 2 diabetes often occurs in association with hypertension and cardiovascular disease, and markedly increases cardiovascular risk. Strategies to reduce the incidence of diabetes in patients with cardiovascular disease or at high risk for such disease are therefore important. Certain classes of antihypertensive agents, namely the thiazide diuretics and beta-blockers, have an adverse impact on the metabolic profile and increase the risk for new-onset diabetes in hypertensive subjects. In contrast, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), which are blockers of the renin-angiotensin system (RAS), have been shown to increase insulin sensitivity. They may also reduce the risk of diabetes in patients with hypertension or cardiovascular disorders. Some of the evidence in favour of ACE inhibitors and ARBs has come from studies with active comparators that have potential adverse metabolic effects. However, the Candesartan in Heart failure-Assessment of Reduction in Mortality and morbidity (CHARM) programme demonstrated that the ARB candesartan reduced the incidence of diabetes in heart failure patients in comparison to placebo. The mechanisms responsible for the beneficial effects of RAS blockade remain to be established. Nevertheless, a treatment that can control hypertension and reduce the risk of onset of type 2 diabetes at the same time is certainly desirable.
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PMID:Renin-angiotensin-system blockade in the prevention of diabetes. 1732 Sep 99

Premature coronary artery disease (CAD) in subjects with type 1 diabetes dramatically affects quality of life and morbidity and leads to premature death, but there is still little known about the mechanisms and predictors of this complication. In the present study, we explored the role of genetic variants of angiotensinogen (AGT, M235T), ACE (I/D), and angiotensin type 1 receptor (ATR1, A1166C) as predictors of rapid progression of subclinical coronary atherosclerosis. Five-hundred eighty-five type 1 diabetic patients and 592 similar age and sex control subjects were evaluated for progression of coronary artery calcification (CAC), a marker of subclinical CAD, before and after a 2.5-year follow-up. In logistic regression analysis, CAC progression was dramatically more likely in type 1 diabetic subjects not treated with ACE inhibitor/angiotensin receptor blocker who had the TT-ID-AA/AC genotype combination than in those with other genotypes (odds ratio 11.6 [95%CI 4.5-29.6], P < 0.0001) and was even stronger when adjusted for cardiovascular disease risk factors and the mean A1C (37.5 [3.6-388], P = 0.002). In conclusion, a combination of genotype variants of the renin-angiotensin system genes is a powerful determinant of subclinical progression of coronary artery atherosclerosis in type 1 diabetic patients and may partially explain accelerated CAD in type 1 diabetes.
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PMID:Polymorphisms of the renin-angiotensin system genes predict progression of subclinical coronary atherosclerosis. 1759 5

Nowadays the endothelium is considered a key determinant of vascular health. NO is the principal mediator of all endothelial protective effects, due to its antiinflammatory, antiproliferative, immunomodulatory and vasorelaxant properties. On the contrary, a growing body of evidence suggests that endothelial dysfunction is associated with cardiovascular events. Emerging data suggest that acute coronary syndromes (ACS) may involve a complex interplay between endothelial dysfunction, inflammation and thrombosis. Despite the success in reducing the mortality from acute cardiovascular events, the incidence of cardiovascular disease and its complication continues to increase. New insights into mechanisms of endothelial dysfunction, such as a better understanding of the regulation of vascular sources of oxygen radicals, may lead to novel therapeutic strategies with the potential to improve prognosis. The key pharmacological agents that improve clinical outcome in high-risk patients are statins, ACE-inhibitors or angiotensin receptor antagonists. Compelling scientific evidence suggests that these medications are effective in improving endothelial function. The present review focuses on the potential importance of benefits on endothelium of these medicaments in the management of acute coronary syndromes.
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PMID:Restoring the dysfunctional endothelium. 1743 Jan 68

The issue of drug-drug interactions is particularly relevant for geriatric patients with epilepsy because they are often treated with multiple medications for concurrent diseases such as cardiovascular disease and psychiatric disorders (e.g., dementia and depression). The antidepressants with the least potential for altering antiepileptic drug (AED) metabolism are citalopram, escitalopram, venlafaxine, duloxetine, and mirtazapine. The use of established AEDs with enzyme-inducing properties, such as carbamazepine, phenytoin, and phenobarbital, may be associated with reductions in the levels of drugs such as donepezil, galantamine, and particularly warfarin. Carbamazepine, phenytoin, and phenobarbital have been reported to decrease prothrombin time in patients taking oral anticoagulants, although with phenytoin, an increase in prothrombin time has also been reported. Drugs associated with increased risk of bleeding in patients taking oral anticoagulants include selective serotonin reuptake inhibitors (especially fluoxetine), gemfibrozil, fluvastatin, and lovastatin. Other drugs affected by enzyme inducers include cytochrome P450 3A4 substrates, such as calcium channel blockers (e.g., nimodipine, nilvadipine, nisoldipine, and felodipine) and the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors atorvastatin, lovastatin, and simvastatin. Although there have been no reports of AEDs altering ticlopidine metabolism, ticlopidine coadministration can result in carbamazepine and phenytoin toxicity. Also, there is a significant risk of elevated levels of carbamazepine when diltiazem and verapamil are administered. In addition, there are case reports of phenytoin toxicity when administered with diltiazem. Drugs with a lower potential for metabolic drug interactions include (1) cholinesterase inhibitors (although the theoretical possibility of a reduction in donepezil and galantamine levels by enzyme-inducing AEDs should be considered) and the N-methyl-D-aspartate receptor antagonist memantine and (2) antihypertensives such as angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, hydrophilic beta-blockers, and thiazide diuretics. There is a moderate risk that enzyme-inducing AEDs will decrease levels of lipophilic beta-blockers. Newer AEDs have a lower potential for drug interactions. In particular, levetiracetam and gabapentin have not been reported to alter enzyme activity. In summary, there is a significant potential for drug interactions between AEDs and drugs commonly prescribed in geriatric patients with epilepsy.
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PMID:Risk and predictability of drug interactions in the elderly. 1743 28

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