Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In addition to its role as an energy storage depot, adipose tissue is now recognized as a complex endocrine organ. Adipose tissue releases a variety of factors, termed adipokines, that regulate energy metabolism, cardiovascular function, reproductive status, and immune function. Some of the better-studied adipokines include leptin, adiponectin, and components of the renin-angiotensin system such as angiotensinogen. The function of more recently discovered adipokines such as resistin are under intense scrutiny. Abnormal production or regulation of adipokines occurs in obese individuals and is implicated in the development of a variety of associated co-morbidities including metabolic syndrome, type 2 diabetes, atherosclerosis, heart disease, and cancer in people, although evaluation in domestic species is just beginning. Adipokines are now being examined as potential biomarkers for risk assessment for development of complications related to obesity. This article summarizes the function and regulation of some better-characterized adipokines. It also reviews the current information on the characterization of adipokines in some domestic species in which rates of obesity and obesity-related disorders are increasing, such as the dog, cat, and horse.
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PMID:Adipokines: a review of biological and analytical principles and an update in dogs, cats, and horses. 1939 60

The hormonal derivative of vitamin D, 1,25-dihydroxyvitamin D (1,25[OH](2)D) or calcitriol, has been implicated in many physiologic processes beyond calcium and phosphorus homeostasis, and likely plays a role in several chronic disease states, in particular, cardiovascular disease. Experimental data suggest that 1,25(OH)(2)D affects cardiac muscle directly, controls parathyroid hormone secretion, regulates the renin-angiotensin-aldosterone system, and modulates the immune system. Because of these biologic effects, vitamin D deficiency has been associated with hypertension, several types of vascular diseases, and heart failure. We conducted a MEDLINE search of the English-language literature (1950-2008) to identify studies that examined these relationships; additional citations were obtained from the articles retrieved from the literature search. Treatment with vitamin D lowered blood pressure in patients with hypertension and modified the cytokine profile in patients with heart failure. Measurement of serum 25-hydroxyvitamin D concentration usually provides the best assessment of an individual's vitamin D status. Serum levels below 20 ng/ml represent vitamin D deficiency, and levels above 30 ng/ml are considered optimal. Although the observational data linking vitamin D status to cardiovascular disease appear robust, vitamin D supplementation is not recommended as routine treatment for heart disease until definitive prospective, randomized trials can be carried out to assess its effects. However, such supplementation is often appropriate for other reasons and may be beneficial to cardiovascular health in certain patients.
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PMID:Vitamin D and cardiovascular disease. 1947 21

High blood pressure (BP) is a major risk factor for heart disease, stroke, congestive heart failure, and kidney disease. Inverse associations between dairy product consumption and systolic blood pressure (SBP) and diastolic blood pressure (DBP) have been observed in cross-sectional studies; some studies, however, have reported an inverse association with only one BP parameter, predominantly SBP. Randomized clinical trials examining the effect of calcium and the combination of calcium, potassium and magnesium provide evidence for causality. In these studies, reductions in BP were generally modest (-1.27 to -4.6 mmHg for SBP, and -0.24 to -3.8 mmHg for DBP). Dairy nutrients, most notably calcium, potassium and magnesium, have been shown to have a blood pressure lowering effect. A low calcium intake increases intracellular calcium concentrations which increases 1,25-dihydroxyvitamin D(3) and parathyroid hormone (PTH), causing calcium influx into vascular smooth muscle cells, resulting in greater vascular resistance. New research indicates that dairy peptides may act as angiotensin converting enzyme (ACE) inhibitors, thereby inhibiting the renin angiotensin system with consequent vasodilation. A growing evidence base shows that dairy product consumption is involved in the regulation of BP. Consequently, inclusion of dairy products in a heart healthy diet is an important focal point to attain BP benefits.
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PMID:Milk products, dietary patterns and blood pressure management. 1957 Nov 68

The purpose of this study was to investigate whether the ideal control of atrial fibrillation (AF) associated with hypertensive patients depends on the usage of renin-angiotensin system (RAS) inhibitors or whether it occurs regardless of the kind of antihypertensive agents used. The control of AF was compared in 112 outpatients between 1) those with or without the administration of RAS inhibitors, and 2) those with an ideal or poor control of the blood pressure (BP) regardless of the kind of antihypertensive therapy used. The therapies with or without RAS inhibitors did not yield any significant difference in the AF control states, even though RAS inhibitors had been administered to the patient group with a high proportion of organic heart disease. The ideal BP control group exhibited a significantly better AF control in comparison to the poor BP control group. The former group had a significantly smaller left atrial diameter determined by ultrasonic echocardiography. BP control itself may essentially be important for preventing AF in the general patient population. Poor BP control seemed to have an affect on worsening AF possibly via left ventricular diastolic dysfunction, followed by left atrial overload.
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PMID:Blood pressure control and the reduction of left atrial overload is essential for controlling atrial fibrillation. 1960 49

Microalbuminuria-increased urinary albumin excretion undetectable by traditional urinary dipstick-has been associated with insulin resistance, diabetes mellitus, obesity, and hypertension. It is also a powerful predictor for heart disease and all-cause mortality. In diabetic patients, microalbuminuria has been correlated with the progression of diabetic nephropathy and the development of renal insufficiency. Furthermore, its correlation with markers of inflammation such as C-reactive protein suggests that microalbuminuria may indicate generalized endothelial dysfunction rather than isolated nephropathy. Drugs that block the renin-angiotensin system, such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have been shown to reduce albuminuria, resulting in renal protection. Recently, dualaction beta-adrenergic blockers such as carvedilol have been shown to exert favorable effects on albuminuria in diabetic patients with hypertension. Insulin resistance reflects a predictable risk for diabetes, and there appears to be a good correlation between insulin resistance, albuminuria, and progression of renal disease in diabetes with or without hypertension. As in microalbuminuria, ACE inhibitors, ARBs, and dual-action beta-blockers help improve insulin sensitivity.
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PMID:Microalbuminuria, insulin resistance, diabetes, hypertension, and kidney function: the latest concepts in pathology and pharmacologic treatment. 1966 9

Renin-angiotensin system blockade retards the progression of diabetic and non-diabetic chronic kidney disease of the native kidneys. Though most patients suffer from a significant renal insufficiency (chronic kidney disease stage III) and a concomitant heart disease after renal transplantation, there is up to now no evidence supporting the use of inhibitors of the renin-angiotensin system in these patients. We wish to summarize the available evidence on the use of inhibitors of the renin-angiotensin system after renal transplantation. We specifically discuss potential beneficial as well as adverse effects of a renin-angiotensin system blockade. In addition, we review their influence on morphologic and biochemical markers as well as on renal function, graft and patient survival after renal transplantation.
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PMID:Angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor blockers after renal transplantation. 1993 Mar 14

Atrial fibrillation (AF) is the most common chronic cardiac arrhythmia and a major public health problem, leading to high rates of morbidity and mortality. The most prevalent cause of AF in the western world is hypertensive heart disease. Blood pressure increase leads to hemodynamic modifications which usually have direct effects on left ventricular and atrial structure and function. The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating blood volume and systemic vascular resistance. Furthermore, recent studies showed that RAAS plays a key role in left atrial and ventricle structural and functional remodeling. Experimental studies and clinical trials have shown that angiotensin-II converting enzyme (ACE) inhibitors and angiotensin-II receptor blockers are effective in preventing atrial fibrillation in patients with arterial hypertension or several forms of heart disease. In our study, we showed that ramipril is effective in preventing AF relapses in patients with lone AF (LAF: i.e AF in the absence of clinical and echocardiographic evidence of cardiovascular, pulmonary, or endocrine disease), independently of any sizeable effect on cardiac echocardiographic anatomy when compared with baseline data. In this paper, we briefly discuss: 1) the role of ACE inhibitor ramipril in preventing AF relapses in LAF patients; 2) the underlying mechanisms by which it can potentially act; 3) the possibility of considering the occurrence of LAF as a marker of subclinical organ damage in subjects with blood pressure values in the 130 to 139 mm Hg range, that is in the pre-hypertension classification according to the JNC-7 Report, of high normal blood pressure levels according to the 2007 ESC/ESH guidelines.
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PMID:[Role of ACE-inhibitors in preventing atrial fibrillation relapses in normotensive patients]. 2006 82

Life-threatening ventricular arrhythmias such as sustained ventricular tachycardia and ventricular fibrillation are responsible for two thirds of sudden cardiac deaths annually in the United States. Implantable cardioverter-defibrillator (ICD) therapy prevents mortality from arrhythmic death but is expensive and has some associated morbidity from proarrhythmia and mechanical malfunction. Furthermore, ICDs treat ventricular arrhythmias but do not prevent them. Antiarrhythmic drugs (AADs) can be used for acute or chronic therapy to prevent ventricular arrhythmias and sudden cardiac deaths. AADS are often used in patients with an ICD who have recurrent ICD shocks resulting from ventricular arrhythmias. Class I AADs are contraindicated in patients with structural heart disease. Other than amiodarone, all Class III drugs have either a neutral or deleterious effect on mortality. Dronedarone, a new Class III drug, may reduce mortality, but more information is needed to be sure. A class of drugs that do not qualify as an AAD can modify cardiovascular remodeling processes and have a delayed and indirect antiarrhythmic effect. These so-called "nonantiarrhythmic drugs" such as drugs acting on the renin-angiotensin-aldosterone system, fish oil, and statins can reduce the likelihood of future ventricular tachycardia/ventricular fibrillation in patients with coronary artery disease or congestive heart failure. The role of AADs for chronic therapy for primary and secondary prevention of sudden cardiac death is problematic because of proarrhythmia and adverse side effects. Because these nonantiarrhythmic drugs are well tolerated and have no proarrhythmic actions, their benefits should outweigh risks.
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PMID:Antiarrhythmic and nonantiarrhythmic drugs for sudden cardiac death prevention. 2050 77

The metabolic syndrome is a constellation of metabolic disorders including obesity, hypertension, and insulin resistance, components which are risk factors for the development of diabetes, hypertension, cardiovascular, and renal disease. Pathophysiological abnormalities that contribute to the development of the metabolic syndrome include impaired mitochondrial oxidative phosphorylation and mitochondrial biogenesis, dampened insulin metabolic signaling, endothelial dysfunction, and associated myocardial functional abnormalities. Recent evidence suggests that impaired myocardial mitochondrial biogenesis, fatty acid metabolism, and antioxidant defense mechanisms lead to diminished cardiac substrate flexibility, decreased cardiac energetic efficiency, and diastolic dysfunction. In addition, enhanced activation of the renin-angiotensin-aldosterone system and associated increases in oxidative stress can lead to mitochondrial apoptosis and degradation, altered bioenergetics, and accumulation of lipids in the heart. In addition to impairments in metabolic signaling and oxidative stress, genetic and environmental factors, aging, and hyperglycemia all contribute to reduced mitochondrial biogenesis and mitochondrial dysfunction. These mitochondrial abnormalities can predispose a metabolic cardiomyopathy characterized by diastolic dysfunction. Mitochondrial dysfunction and resulting lipid accumulation in skeletal muscle, liver, and pancreas also impede insulin metabolic signaling and glucose metabolism, ultimately leading to a further increase in mitochondrial dysfunction. Interventions to improve mitochondrial function have been shown to correct insulin metabolic signaling and other metabolic and cardiovascular abnormalities. This review explores mechanisms of mitochondrial dysfunction with a focus on impaired oxidative phosphorylation and mitochondrial biogenesis in the pathophysiology of metabolic heart disease.
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PMID:Mitochondrial biogenesis in the metabolic syndrome and cardiovascular disease. 2072 11

In this article, we review the evidence supporting the use of eplerenone for improving cardiovascular prognosis. Activation of the renin-angiotensin-aldosterone system plays a major role in the pathogenesis of heart disease, and blockage of this system has been shown to improve prognosis in several cardiovascular conditions. The 2 marketed aldosterone antagonists, spironolactone and eplerenone, improve prognosis in patients with left ventricular (LV) dysfunction and are effective antihypertensive medications. In addition, a potential role for aldosterone antagonists in the treatment of patients with heart failure and preserved LV function has been suggested and is currently being evaluated in clinical trials. In patients with myocardial infarction having LV dysfunction and evidence of heart failure, eplerenone improves cardiovascular outcomes and attenuates myocardial remodeling. In addition, eplerenone is effective for the treatment of hypertension, where it regresses both LV hypertrophy and proteinuria (2 powerful markers of increased cardiovascular risk). In contrast to spironolactone, eplerenone essentially lacks the sexual side effects that sometimes limit the use of spironolactone. Hyperkalemia is the main potential side effect of eplerenone, especially when used in combination with other medications that can cause hyperkalemia. Adequate patient selection and monitoring are therefore of utmost importance when using this medication. In conclusion, eplerenone is a medication that offers the cardiovascular therapeutic and prognostic benefits of aldosterone antagonism but with fewer side effects compared to spironolactone.
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PMID:Review article: eplerenone: an underused medication? 2087 42


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