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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerosis, a chronic systemic disease of the vasculature with an inflammatory component, is the primary cause of cardiovascular morbidity and mortality in industrialized countries. Impairment of vascular endothelial cell function in atherosclerosis and in conditions associated with increased cardiovascular risk are important determinants of disease progression. Reduced endothelium-dependent relaxation in the coronary and systemic circulation due to decreased bioavailability of nitric oxide (NO) and increased release of oxygen-derived free radicals promotes the adhesion of leukocytes, thrombosis, inflammation, cell proliferation, and increases in vascular tone. In addition to decreases in bioactive NO, enhanced production of the 21-amino acid peptide endothelin-1 contributes to the progression of atherosclerosis. This paper discusses mechanisms and therapeutic approaches to improving endothelial pathways in atherosclerosis. Restoration of endothelium-derived NO bioactivity through inhibition of the renin-angiotensin system, the endothelin system, or statin therapy improves vascular function in experimental hypercholesterolemia, hypertension and heart failure. These treatments may also have therapeutic benefit for patients at risk or with overt atherosclerosis, and are likely to reduce vascular and myocardial complications of this disease.
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PMID:Endothelium and atherogenesis: endothelial therapy revisited. 1181 71

Hypertrophic cardiomyopathy is a relatively common genetic disorder with heterogeneity in mutations, forms of presentation, prognosis and treatment strategies. Hypertrophic cardiomyopathy is recognized as the most common cause of sudden cardiac death that occurs in young people, including athletes. The clinical diagnosis is complemented with the ecocardiographic study, in which an abnormal myocardial hypertrophy of the septum can be observed in the absence of a cardiac or systemic disease (arterial systemic hypertension, aortic stenosis). The annual sudden mortality rate is 1% and, in selected populations, it ranges between 3 and 6%. The therapeutic strategies depend on the different subsets of patients according to the morbidity and mortality, sudden cardiac death, obstructive symptoms, heart failure or atrial fibrillation and stroke. High risk patients for sudden death may effectively be treated with the automatic implantable cardioverter-defibrillator.
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PMID:[Hypertrophic cardiomyopathy. Arrhythmia in hypertrophic cardiomyopathy]. 1296 40

Atherosclerosis is a chronic systemic disease of the vasculature with an inflammatory component. It accounts for the majority of cardiovascular morbidity and mortality in industrialized countries and its incidence is increasing in developing countries. The impairment of vascular endothelial cell function in atherosclerosis and in conditions associated with increased cardiovascular risk is an important determinant of disease progression. The reduction of endothelium-dependent relaxation in the coronary and systemic circulation in atherosclerosis is in part due to decreased bioavailability of nitric oxide and increased release of oxygen-derived free radicals. Atherosclerosis also increases the formation of vasoconstrictors and growth factors, adhesion of leukocytes, thrombosis, inflammation, cell proliferation, as well as increases in vascular tone. Here we review mechanisms and therapeutic approaches to improve endothelial pathways in atherosclerosis. Restoration of NO bioactivity through pharmacological inhibition of the renin-angiotensin system, statin therapy, or endothelin receptor blockade, ameliorates vascular function in experimental hypercholesterolemia, hypertension and heart failure. These treatments also have therapeutic benefit for patients at risk or with overt atherosclerosis, to reduce vascular and myocardial complications of this disease.
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PMID:Endothelial therapy of atherosclerosis and its risk factors. 1532 Aug 38

COPD is a major cause of death and disability worldwide. Treatment of COPD improves lung function but is unlikely to slow the steady downhill course of the disease or reduce mortality. In COPD, numerous abnormalities can be found outside the lung. These include systemic inflammation, cachexia, and skeletal muscle dysfunction. Thus, COPD has been called a systemic disease. Convincing data demonstrate that COPD causes neurohumoral activation. By precedents derived from chronic heart failure and other diseases characterized by neurohumoral activation, we propose that the negative consequences of neurohumoral activation, namely inflammation, cachexia, effects on ventilation, and skeletal muscle dysfunction, give rise to a self-perpetuating cycle that contributes to the pathogenesis of COPD, and which may involve respiratory muscle dysfunction as well as systemic inflammation. This concept may further help explain the increased cardiovascular morbidity and mortality in COPD patients. Currently, little is known about the effect of treatments directed at neurohumoral activation and COPD. As this aspect of COPD becomes better understood, new insights may direct novel therapeutic approaches.
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PMID:Neurohumoral activation as a link to systemic manifestations of chronic lung disease. 1630 21

Systemic sclerosis (scleroderma) is a chronic, progressive connective tissue disease characterized by typical skin changes and internal organ involvement. Arterial pulmonary hypertension is found in approximately 10-15% of patients with systemic sclerosis, and is considered as one of the most fatal complications of the disease. When pulmonary hypertension secondary to scleroderma related interstitial lung disease, left-sided cardiac insufficiency and thrombo-embolic disease is also taken into account, the frequency of pulmonary hypertension in systemic sclerosis may be as high as.50%. Recent investigations brought new information considering the pathogenesis of pulmoanry hypertension and allowed new therapeutic approches to be introduced. Early diagnosis of pulmonary hypertension is a key issue in clinical practice, but it is a challange in patients with systemic disease such as systemic sclerosis. Current review presents up to date information on the pathogenesis, early diagnosis and treatment of pulmonary hypertension related to systemic sclerosis.
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PMID:[An up date on pulmonary hypertension related to systemic sclerosis]. 1652 4

Churg-Strauss syndrome (CSS) is a rare systemic disease characterized by necrotizing vasculitis and peripheral eosinophilia. Cardiac involvement is considered common and is given a high rank among the causes of morbidity and mortality. The aim of this study was an update on the cardiac manifestations of this syndrome using a noninvasive approach. Sixteen patients with CSS were compared with a gender- and age-matched group of 20 healthy subjects. All patients but 1 were receiving treatment (steroids and/or immunosuppressive drugs). According to the Birmingham vasculitis activity score, 12 patients were in an active phase, and 4 were in drug-induced remission. All subjects underwent M-B-mode echocardiography and Doppler tissue echocardiography. Heart failure, life-threatening arrhythmias, and other prominent manifestations of heart disease were not observed. No differences were found in left ventricular diameter, volume, mass, or ejection fraction. The 2 groups did not differ in right ventricular diameter and pulmonary pressure. Few and nonspecific changes were detected by 2-dimensional echocardiography, including subclinical pericardial effusion and mitral regurgitation, in fewer than half the subjects. Subjects with CSS showed an impairment of ventricular relaxation. Changes were more prominent in the right ventricle. The peak velocity (PV) of early diastolic tricuspid inflow (E) was about 8% less than in controls, and the velocity of late diastolic inflow (A) was 35% greater. The E/A(PV) ratio was, on average, 33% less. In the left ventricle, E(PV) was 11% less and A(PV) 11% greater. The E/A ratio was decreased by 22%. Doppler analysis of tissue kinetics confirmed these indications. In the right ventricle, E(PV) was decreased by 10% and A(PV) was increased by 20% in the patient group. The E/A(PV) ratio was decreased by 29%. In the left ventricle, in which different sites were sampled, the average changes were -15%, +1%, and -23%, respectively. In the left ventricle, the velocity of systolic contraction was also decreased by 12%. Because of the small group size, only some of these differences were statistically significant. In conclusion, these moderate changes, devoid of clinical correlates, contrast with early reports emphasizing cardiac morbidity and poor prognosis in this syndrome.
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PMID:Cardiac involvement in the Churg-Strauss syndrome. 1667 97

Present review focused on the recent advance and clinical application of exercise test in cardiology. Exercise intolerance is considered as one of clinical essential feature in patients with heart failure. Cardiac dysfunction induces systemic disorders including motor muscle and vasculature, and then limits exercise performance through direct and indirect pathway. Parameters of exercise test consist of subjective indexes such as NYHA functional class, and objective evaluations such as cardiopulmonary exercise test(CPX). Especially, we discussed the parameters of CPX provided many indexes, for example peak VO2, VE/VCO2 slope and deltaVO2/Work rate. These various indexes have different clinical meanings among each other. Low value of peak VO2, which reflected both disturbances of central and peripheral factors, is reported to result in poor survival rate. Although VE/VCO2 slope similarly predicts the prognosis, it thought to be mediated through a different way. We concluded that exercise test is important to understand the pathophysiological feature of heart failure as a systemic disease.
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PMID:[Recent advance of exercise test in clinical cardiology concerning heart failure]. 1668 70

Vomiting and abdominal pain are common pediatric complaints encountered by emergency physicians. The differential diagnosis of abdominal pain is extensive. Herein, we report 2 cases with fatal myocarditis who initially presented with abdominal pain and vomiting. Both cases were presented with abdominal pain, vomiting, and loose stools. On arrival at our emergency department, hypotension, tachycardia, and cyanotic extremities were found. Their serum troponin-I levels were elevated. The echocardiogram demonstrated poor left ventricular performance and a decreased ejection fraction. In both cases, an arrhythmia and a coma developed within hours and were shortly followed by death. The clinical presentations of acute myocarditis are variable, ranging from an initial mild discomfort to acute progressive heart failure, and at times, even death. Abdominal pain may be a manifestation of systemic disease, an extra-abdominal lesion, or myocarditis. Although myocarditis associated with abdominal pain or vomiting remains a diagnostic challenge to physicians, it should be considered in the differential diagnosis of children with gastritis and hypotension or who are refractory to rehydration therapy.
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PMID:Myocarditis presenting as gastritis in children. 1680 47

Amyloidosis is an uncommon systemic disease characterized by deposition of insoluble fibrillar protein in different organs and the prognosis is poor if the heart is involved. Experience with management of cardiac amyloidosis is difficult because of its rare occurrence, late presentation and ineffective treatment. Since 1995, we have encountered and prospectively followed up 16 cases of cardiac amyloidosis in our cardiac centre. We believe this is the largest series of cardiac amyloidosis reported in Chinese patients. The 1-year, 3-year and 5-year survival rates were 40%, 25% and 17%, respectively. The major cause of death was cardiac-related. Those patients with overt heart failure or with untreated amyloidosis had a dismal prognosis (mean survival of 2.2 months and 3.5 months, respectively). Those who received specific treatment for the underlying amyloidosis had a better outcome with an average survival of 33.4 months.
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PMID:Cardiac amyloidosis - experience in a tertiary cardiac referral centre. 1738 27

Sleep-disordered breathing, broadly characterized by obstructive sleep apnea (OSA) and central sleep apnea (CSA), is an increasingly recognized public health burden. OSA, consisting of apneas or hypopneas associated with respiratory efforts in the face of upper airway narrowing or collapse, is a common disorder that can be effectively treated with continuous positive airway pressure (CPAP). OSA not only results in daytime sleepiness and impaired executive function, but also has been implicated as a possible cause of systemic disease, particularly of the cardiovascular system. CSA, which may coexist with OSA, has gained attention because of the association of Cheyne-Stokes respiration with an ever-increasing prevalence of heart failure in an aging population. This article reviews some of the extensive literature on pathophysiologic mechanisms as they may relate to the development of cardiac and vascular disease and examine the evidence suggesting OSA as a specific cause of certain cardiovascular conditions. Available evidence regarding the implications of CSA in the context of heart failure is discussed.
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PMID:Sleep-disordered breathing and cardiovascular risk. 1742 25


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