Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased oxidative stress and endothelial dysfunction are commonly observed in patients with chronic heart failure (HF). The relation between myeloperoxidase (MPO), an inflammatory marker with mechanistic links to plaque vulnerability and abnormal ventricular remodeling, and degrees of severity in chronic HF has not been reported. Plasma MPO levels were measured in 105 normal controls (no history of HF or left ventricular dysfunction) and 102 patients with chronic systolic HF (left ventricular ejection fraction <50%), and the relations among plasma MPO levels, plasma B-type natriuretic peptide levels, and the left ventricular ejection fraction were examined. Plasma MPO levels in patients with chronic systolic HF were significantly elevated compared with those of healthy controls (1,158 +/- 2,965 vs 204 +/- 139 pM, p <0.0001). Plasma MPO levels increased in parallel with increasing New York Heart Association class (p <0.0001) and were correlated with plasma B-type natriuretic peptide levels (Spearman's r = 0.39, p <0.0001). Levels of MPO were strongly associated with the prevalence of HF (unadjusted odds ratio 30.3, 95% confidence interval 11.1 to 94.5) and remained significant when adjusted for age and B-type natriuretic peptide (odds ratio 27.7, 95% confidence interval 3.6 to 371.1). In conclusion, in a cohort of patients with chronic HF, plasma MPO levels were elevated compared with those of normal controls and were associated with worsening functional class.
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PMID:Plasma myeloperoxidase levels in patients with chronic heart failure. 1695 Jan 88

Owing to the common coincidence of osteoporosis and vascular disease, pathophysiological links between both disorders have long been sought. The osteoprotegerin (OPG)/receptor activator of NF-kappaB (RANK)/receptor activator of NF-kappaB ligand (RANKL) cytokine network, a key regulatory system in bone homeostasis, has been implicated recently in vascular calcification, changes in matrix composition and diabetic macroangiopathy, aortic aneurysm development, heart failure and, most importantly, advanced atherosclerosis, plaque destabilization and manifestation of cardiovascular diseases. The concept of an active role of RANKL and OPG in vascular pathophysiology is intriguing and is gaining increasing support from both epidemiological and basic research. OPG serum level is considered to be a stable and reliable indicator of the overall activity of the OPG/RANK/RANKL axis and may find application as a biomarker of vascular risk and prognosis. RANKL in turn may be a suitable target for novel therapies. Pharmacological strategies for specific interference with the OPG/RANK/RANKL axis are currently being developed and evaluated in osteoporosis therapy.
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PMID:The osteoprotegerin/RANK/RANKL system: a bone key to vascular disease. 1717 97

Transforming growth factor beta (TGF-beta) is a cytokine engaged in a wide range of diverse and often contradictory functions. Its effect on the cardiovascular system is also ambiguous; on the one hand, there is a strong evidence for so-called 'protective cytokine hypothesis'considering TGF-beta to be an anti-atherogenic and plaque-stabilizing factor, but on the other hand, TGF-beta has been proven to exert some proinflammatory effects. Moreover, besides the positive aspect of a profibrotic and reparative action of TGF-beta, there are also some disadvantages: TGF-beta plays a significant role in postangioplasty restenosis, post-infarction myocardial remodeling (resulting in the development of heart failure) and in numerous other circulatory disorders where fibrosis and vascular remodeling takes part in pathology. The aim of the paper was to review and discuss the unwanted effects of TGF-beta in the circulatory system, and to outline the possible pharmacological strategies to interfere with TGF-beta-dependent pathways and prevent these disturbances.
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PMID:Transforming growth factor beta and cardiovascular diseases: the other facet of the 'protective cytokine'. 1722 May 37

Obesity is an important risk factor for heart disease. Whether weight loss affects the severity of heart failure induced by viral myocarditis is a matter of debate. We hypothesized that weight loss could improve cardiac dysfunction by inducing cardiac expression of a cardioprotective cytokine, adiponectin. We examined the relationship between weight loss by food restriction and heart failure due to viral myocarditis in obese KKAy mice. We intraperitoneally injected encephalomyocarditis virus (500 plaque-forming units/mouse) into KKAy mice fed ad libitum as a control (CF) or 60% restriction of that eaten by ad libitum (RF). The 14-day survival rate was 0% in FF, whereas it was 23% in RF (P<0.01). Heart weight/body weight ratio in RF was lower than that in FF on day 5 after viral inoculation (P<0.05). Histological scores for myocardial necrosis and inflammation on day 5 were significantly lower in RF than in FF (P<0.05). Circulating adiponectin level on day 0 was significantly elevated in RF compared with that in FF (32+9 vs. 22+2 microg/mL, P<0.05). Comparative expression of cardiac adiponectin mRNA in RF was significantly higher than that in FF (5.1+0.3 vs. 1+0.2, P<0.05). Cardiac tumor necrosis factor-alpha (TNF-alpha) mRNA in RF was significantly decreased compared with that in FF on day 5 (P<0.05). Cardiac expression of nuclear factor kappa B was reduced and that of peroxisome proliferator-activated receptor gamma mRNA was increased in RF in comparison with FF on day 0. Cardiac adiponectin mRNA was negatively correlated with cardiac TNF-alpha mRNA (r=-0.555; P=0.0097). Weight loss improved the survival and myocardial damage in obese mice with viral myocarditis, with cardiac induction of adiponectin. The induction of adiponectin might provide benefit through a cardioprotective effect against acute heart failure due to viral myocarditis in obese subjects.
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PMID:Reduced-energy diet improves survival of obese KKAy mice with viral myocarditis: induction of cardiac adiponectin expression. 1727 7

ST-elevation myocardial infarction is due to the occlusion of a coronary artery, mainly due to a rupture of an atherosclerotic plaque with superimposed thrombosis. The main therapeutic goal is to restore the blood flow within the culprit artery as quickly as possible. In this review we discussed the several approaches which have been employed to reach this target. Primary percutaneous coronary intervention (PCI) is considered the best treatment option, as it is associated to lower in-hospital mortality, reduced risk of reinfarction and stroke, lower rate of intracranial bleeding and ventricular rupture from myocardial hemorrhage compared with fibrinolytic therapy. Also, it is superior to facilitated PCI, i.e. immediate planned PCI after i.v. thrombolytic therapy administration, because of lower mortality, reinfarction rate, strokes and bleedings. Rescue PCI after failed thrombolysis was associated with a reduction of early severe heart failure and improved survival at 1 year, in patients with moderate to large infarctions, compared to conservative medical therapy, in a pooled analysis of 9 randomized trials, carried out in the balloon era. Also in the stent era, a meta-analysis of 5 randomized trials found a significant 36% reduction in the risk of 30-day mortality, a trend to lower risk of heart failure, although a marginally increased risk of thromboembolic stroke, in the rescue PCI arm. However, rescue PCI is not associated with a better long-term clinical outcome. Laser thrombectomy before PCI could be a useful additional strategy which might be compared to standard stenting in future randomized studies.
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PMID:Acute myocardial infarction interventional procedures: primary percutaneous coronary intervention versus facilitated percutaneous coronary intervention, rescue angioplasty, rescue excimer laser. 1728 82

Myocardial imaging with radionuclide biochemical tracers has provided advanced diagnostic approaches for patients with coronary artery disease and heart failure. Since the biochemical information includes cellular events such as metabolism, inflammation, and sympathetic drive, it can be regarded as one of 'Molecular Imaging'. In this chapter, I introduce topics on clinical evaluation of cellular pathophysiology in cardiovascular diseases with radionuclide biochemical imaging: detection of coronary vulnerable plaque to predict the occurrence of acute coronary syndrome and estimation of altered myocardial metabolism and sympathetic drive to estimate the severity of myocardial failure.
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PMID:[Clinical evaluation of cellular pathophysiology in cardiovascular diseases with radionuclide biochemical imaging]. 1730 74

Cardiovascular mortality is remarkably high in patients who are on hemodialysis. Soluble CD154 (sCD154), a protein that belongs to the TNF receptor superfamily, has been implicated in the pathogenesis of atheromatous plaque destabilization and thrombotic events. The predictive value of sCD154 as a marker for clinical outcome in patients with ESRD was investigated. A total of 232 patients were prospectively followed for 52 mo. At study entry, clinical characteristics were documented and plasma concentrations of sCD154 and those of conventional risk predictors were analyzed. The time and cause of any hospitalization and death were documented during the entire follow-up. Survival rates were compared by Kaplan-Meier and Cox regression analyses. A total of 122 patients died, 64 of cardiovascular disease, including 20 cases of fatal atherothrombotic diseases (myocardial infarction, stroke, mesenteric ischemia). All 20 cases of fatal atherothrombotic events had high sCD154 plasma levels (cutoff >6.42 ng/ml) at study entry. The total number of fatal and nonfatal atherothrombotic events was 66. Only five atherothrombotic nonfatal events occurred in patients with sCD154 <6.42 ng/ml, whereas 61 fatal and nonfatal events were seen in patients with sCD154 > or =6.42 ng/ml (P < 0.005). This was confirmed by Kaplan-Meier curves for fatal atherothrombotic events (P = 0.0214) and the combined end point fatal and nonfatal atherothrombotic events (P = 0.0039). Cox regression analysis revealed that high sCD154 is an independent predictor (relative risk 6.80; 95% confidence interval 1.64 to 28.26; P = 0.008) for the combined end point death or hospitalization as a result of atherothrombotic events. Death or hospitalizations as a result of any other reason (arrhythmia, heart failure, infectious diseases, and cancer) were not linked to sCD154 plasma concentrations. In conclusion, sCD154 predicts nonfatal and fatal atherothrombotic events (myocardial infarction, stroke, mesenteric ischemia) but not death and hospitalization as a result of any other reason in stable patients who have ESRD and are on hemodialysis.
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PMID:Soluble CD154 is a unique predictor of nonfatal and fatal atherothrombotic events in patients who have end-stage renal disease and are on hemodialysis. 1731 26

Biologic agents are an important new class of drugs, offering targeted treatment for chronic skin diseases such as psoriasis. The biologic therapy efalizumab is an anti-CD11a monoclonal antibody, which was approved by the European regulatory agency in 2004 for the treatment of moderate-to-severe plaque psoriasis. Here we describe our 2-year experience in treating over 100 patients with moderate-to-severe psoriasis with efalizumab at two dermatology centres in Italy. Overall, we found efalizumab is efficacious for a large subset of patients, regardless of previous therapies received, and has an easily manageable safety profile. We believe one important quality of efalizumab is the stability and maintenance of clinical response over time. We found that most patients who respond to treatment experience a long-term clearing of psoriasis with only mild recurrence events. Our experience with individual cases provides specific insights into efalizumab re-treatment, the use of efalizumab in patients with a history of heart failure, and the management of patients who become pregnant or conceive while receiving efalizumab therapy. In summary, our off-trial experience in over 100 patients confirms the efficacy and safety of efalizumab in the treatment of moderate-to-severe plaque psoriasis.
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PMID:Long-term treatment of plaque psoriasis with efalizumab: an Italian experience. 1737 19

In bone and teeth formation, coordinated calcification is a highly desirable biological process. However, heterotopic calcification at unwanted tissue sites leads to dysfunction, disease and, potentially, to death and therefore requires prevention and treatment. With the recent discovery of calcification inhibitors we now know that biological calcification is not passive but a complex, active and highly regulated process. Calcification at vascular sites is the most threatening localization and manifests as part of atherosclerosis or arteriosclerosis. Atherosclerosis is often accompanied by intimal plaque calcification, whereas arteriosclerosis is characterized by calcification of the media. The severity of calcification of cerebral or coronary atherosclerotic plaques is associated with an increased incidence of events such as stroke or myocardial infarction. Medial calcification is the major cause of arterial stiffness, which contributes to left ventricular dysfunction and heart failure. Patients with chronic kidney disease are at especially increased risk for both intimal and medial calcification. In this context, it is currently thought that calcium-regulatory factors including fetuin-A, matrix Gla protein, osteoprotegerin, and pyrophosphates act in a local or systemic manner to prevent calcifications of the vasculature, and that dys-regulations of such calcification inhibitors may contribute to progressive calcifications. Nephrolithiasis represents another process of unwanted calcification responsible for significant morbidity. More than 80% of renal stones contain calcium. Urinary factors inhibiting calcification are citrate, glycosaminoglycans, Tamm-Horsfall protein, and osteopontin. This review summarizes current experimental and clinical data underlining the biological importance of these calcification inhibitors.
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PMID:Inhibitors of calcification in blood and urine. 1737 84

The Heinz Nixdorf Recall Study, which was inaugurated in 2000, is an ongoing population-based study to evaluate the prediction of cardiovascular events by integrating new imaging and nonimaging modalities in risk assessment. A focus is the additional prognostic value of coronary artery calcification (CAC). Currently used risk stratification algorithms often describe the individuals' risk based on few established risk factors only inaccurately. Using noninvasive quantification of CAC progression, the natural history of atherosclerosis with its repetitive, frequently subclinical plaque ruptures, may detect an unstable course of the disease long before the disease irreversibly manifests in sudden death or myocardial infarction. While the independent additional prognostic value of CAC quantification has been shown in asymptomatic patients at intermediate risk, only few studies provided evidence for an independent prognostic value of serial CAC measurements. In the Heinz Nixdorf Recall Study, the impact of established and new risk factors, e.g., the metabolic syndrome, psychosocial and environmental risk factors, or genetic variables, can be assessed. Further, the association of CAC progression with the incidence of other cardiovascular diseases such as heart failure or aortic or aortic valve calcification can be described. Since April 2006, the participants of the study return to the study center 5 years after baseline recruitment to assess health status and to determine the risk factor profile. Based on recently published data, serial CAC measurements have been granted allowing for (1) characterization of the natural history of CAC progression, and (2) identification of its determinants. The rationale of serial CAC quantification is discussed in this article.The Heinz Nixdorf Recall Study will contribute to the appraisal of new imaging modalities in risk stratification.
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PMID:[Assessment of the natural history of coronary artery calcification and identification of its determinants. Rationale of the 2nd part of the Heinz Nixdorf Recall Study]. 1740 53


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