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

It is known that local and systemic inflammatory processes play an important role in the genesis and development of atheroclerotic lesions and in the pathophysiology of acute coronary syndromes. This hypothesis is supported by findings of elevated parameters of the "inflammatory" reaction in the affected blood vessels but also in the blood of atherosclerotic patients. Known risk factors do not explain quite satisfactorily epidemiological cardiovascular phenomena and different manifestations of coronary heart disease. It is very probable that also Chlamydia pneumoniae is a risk factor. This assumption is based on evaluation of seroepidemiological data, examination of atherosclerotic plaques not only in humans but also in animal models with chlamydial infection. Based on retrospective and prospective evaluation of case-records the authors analyzed the incidence of cardiovascular complications in 83 patients with acute myocardial infarction (AIM), incl. 51 patients (31 men and 20 women, mean age 64.4 +/- 3.4 years who had a non-specific inflammation and chlamydial infection, and 32 patients (24 men and 8 women, mean age 64.7 +/- 3.6 years) who had chlamydial infections but no non-specific inflammation (in the blood). These patients were selected from all patients hospitalized during 1998-2001. When diagnosing acute myocardial infarction we applied WHO criteria, and the presence of at least two of three criteria was necessary: a history of prolonged (more than 20 min). stenocardia, electrocardiographic changes typical for ischaemia and/or necrosis and elevation of myocardial enzymes in serum, Non-specific inflammatory activity was present in patients (i.e. positive) if the following laboratory parameters were recorded: C-reactive protein > 5 mg/l assessed by the radial immunodiffusion method; fibrinogen > 4 mg/l assessed by the coagulation method according to Claus; leukocytes > 9.6 x 10(3)/microliter, leukocytes were counted automatically in a Coulter chamber; lymphocytes > 3.4 x 10(3)/microliter. Red cell sedimentation rate > 20 mm/hour. The activity was evaluated as positive when all parameters were elevated. The presence of chronic infection with Chlamydia pneumoniae was assessed qualitatively by antibody positivity (IgG) in serum using the microimmunoflurescent method (using a set from Labsystems Co.). The incidence of associated risk factors (obesity, smoking, diabetes, hyperlipidaemia and hypertension) is higher in the sub-group of patients with Chlamydia infections without inflammation, however, the difference is not statistically significant. The incidence of cardiovascular attacks was higher in the sub-group of patients with chlamydial infection and concurrent inflammation as compared with the sub-group of patients with chlamydial infection without inflammation. In case of re-infarction of the myocardium, a sudden cerebrovascular attack, death and arrhythmia the difference was statistically significant, while in case of cardiac failure and cardiogenic shock the difference was not significant. Patients with acute myocardial infarction with chlamydial infection and a concurrent non-specific inflammation had to be treated more often by combined (i.e. more intense) treatment, thrombolytic treatment, PTCA and surgery (bypass) of the coronary vessels as compared with patients with Chlamydia infections but without inflammation. The authors assume therefore that not only different risk factors but also the effect of non-specific inflammation and Chlamydia infection contribute towards the increased number of cardiovascular postinfarction complications. Therefore a therapeutic approach involving eradication of infection and suppression of the inflammatory reaction should be considered.
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PMID:[Effect of chronic Chlamydia infection with non-specific inflammation on cardiovascular complications in acute myocardial infarct]. 1272 71

The prevalence and incidence of chronic heart failure (HF) have now reached epidemic proportions. However, the issue of the prevention of HF has been raised only recently. New US guidelines have introduced a new classification system that includes 4 categories: patients at risk, patients with asymptomatic left ventricular dysfunction, patients with symptomatic HF, and those with refractory HF. Because coronary artery disease is the major cause of HF, its risk factors are also those of HF. Hypertension favors the development of HF through accelerated atherosclerosis and increased left ventricular wall stress and hypertrophy. Left ventricular hypertrophy is also a powerful risk factor for HF, independent of blood pressure. Angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, and diuretics are the antihypertensive agents that have been associated with favorable effects in patients with overt HF. Therefore, they may be preferred in the prevention of this syndrome. Diabetes is the most frequent noncardiac comorbidity of HF and is independently associated with an increased risk. Normalization of glycemic and glycosylated hemoglobin levels is a desirable goal of treatment. However, no direct evidence exists in the prevention of HF. A greater control of the other risk factors (eg, hypertension, hyperlipidemia) is, on the other hand, particularly important. Beta-blockers and ACE inhibitors have both been shown to have favorable effects across all spectrums of severity of HF. The ACE inhibitor ramipril has also been shown to prevent the development of HF in patients at risk without left ventricular dysfunction. The role of antiplatelet agents, warfarin, and statins is clear in the prevention of the coronary artery disease. However, it has not been adequately assessed in patients with HF and awaits the results of ongoing trials.
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PMID:Prevention and management of chronic heart failure in patients at risk. 1272 47

A 41 year old woman with type 2 diabetes, hypertension, and hyperlipidaemia but no known heart disease received 130 DC shocks for repeated cardiac arrests due to ventricular tachyarrhythmias over 48 hours. She was stabilised by intravenous amiodarone and had a defibrillator implanted. Serial ECGs did not change, but raised troponin I confirmed myocardial infarction as the underlying cause. Electrical storm is an uncommon and dramatic but usually treatable syndrome of recurrent ventricular arrhythmias. Frequent precipitants of electrical storm include recent worsening heart failure, hypokalaemia, hypomagnesaemia and myocardial ischaemia. Amiodarone is the antiarrhythmic agent of choice and implantable cardioverter defibrillator improves long term outcome.
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PMID:Successful resuscitation of a patient with electrical storm. 1274 67

Peripheral arterial disease, which is caused by atherosclerotic stenosis or occlusion of the leg arteries, is an important manifestation of systemic atherosclerosis. The age-adjusted prevalence of symptomatic and asymptomatic peripheral arterial disease is approximately 12% in the general population. The overall prevalence and incidence of the disease is likely to increase with the aging of the population. Peripheral arterial disease is a relatively benign condition in terms of local disease. Five years after the diagnosis, 75% of the patients remain clinically stable. On the contrary, life expectancy, even in the absence of any history of myocardial infarction or ischemic stroke, has decreased by 10 years. These patients have approximately the same relative risk of death from cardiovascular causes as do patients with history of coronary or cerebrovascular disease. Moreover, the severity of peripheral arterial disease is closely associated with the risk of myocardial infarction and death from vascular disease. The lower the ankle-brachial index, the greater the risk of cardiovascular events. Furthermore, peripheral arterial disease is a significant independent predictor for cardiovascular mortality also in coronary patients. The risk factors associated with peripheral arterial disease are essentially the same as for coronary heart disease: older age, cigarette smoking, diabetes mellitus, hypertension, and hyperlipidemia. The excess morbidity and mortality for cardiovascular disease in these patients has not been fully explained. Patients with peripheral arterial disease show a systemic endothelial dysfunction and an increase in the serum concentration of activated white blood cells, endothelin, and C-reactive protein that may trigger acute coronary syndromes. In peripheral arterial disease the functional status is often severely impaired. Peak exercise performance has decreased to about 50% of that of age-matched controls, equivalent to moderate-severe heart failure. Epidemiological studies support the concept that patients affected by peripheral arterial disease, without established coronary heart disease, have a coronary heart disease high risk equivalent. In spite of this, peripheral arterial disease remains an underdiagnosed and undertreated disease. As the role of cardiologists is expanding, the purpose of this review was to awaken the clinician to the significance of lower limb atherosclerotic occlusive diseases.
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PMID:[Why are cardiologists to be concerned about obliterating arterial disease of the lower leg?]. 1278 66

Only early detection and treatment is likely to stem the current epidemic of heart failure (HF). Several common cardiovascular and metabolic conditions increase the risk of developing symptomatic HF, but its detection by a simple and reliable screening method has proved elusive. HF screening sessions were conducted in September and November 2001. Members of the community with HF risk factors (e.g., hypertension, coronary artery disease, diabetes mellitus, hyperlipidemia) were invited--all specifically without a history of HF. The screening included a history review, health history questionnaire, measurement of blood pressure and pulse, as well as a measurement of B-type natriuretic peptide (BNP) level. A total of 233 individuals attended these two sessions: 108 men and 125 women (mean age, 63 years). Of the 233 subjects screened, the majority (92%) had >or=1 risk factor with an average of 2.8 risk factors for HF. The most common risks included hyperlipidemia (112), hypertension (112), age >65 years (105), cigarette smoking (105), coronary artery disease (60), and diabetes mellitus (54). Many subjects also had symptoms consistent with HF, with most (182, 82%) recording >or=1 symptom. Blood pressure measurements revealed a mean systolic of 139 mm Hg and mean diastolic of 79 mm Hg; on the screening days, 48% and 59% of subjects demonstrated either systolic or diastolic blood pressures above normal, respectively. BNP levels ranged from 0-479 pg/mL with an average of 40 pg/mL. A total of 24 subjects (10.3%) had a BNP level >100 pg/mL, and a total of 32 subjects (13.7%) had a level >80 pg/mL. The follow-up data showed that all 24 subjects saw their physician within 6 months after the screening. By 12 months following the initial screening program, 21 of the 24 subjects with elevated BNP levels (88%) underwent further testing and 18 of the 24 (67%) had changes in their medications. BNP screening identifies subjects at high risk for developing HF. Most subjects at risk have multiple risk factors and abnormal blood pressure. Approximately 10% of this population tested with an abnormal level of BNP, higher than the Food and Drug Administration-assigned cut-point diagnostic for HF. Increased public and physician awareness and information are needed to transform screening opportunities into a strategic approach to improve health care and HF prevention.
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PMID:High incidence of elevated B-type natriuretic peptide levels and risk factors for heart failure in an unselected at-risk population (stage A): implications for heart failure screening programs. 1282 70

Hyperlipidemia is a common problem in solid organ transplant recipients. In this study we evaluated the role of pre-transplant renal replacement therapy on early and late changes of serum lipid levels in children following renal transplantation. In 46 children with chronic renal failure (median age 10.3 years) and 12 children with heart failure (median age 5.0 years), cholesterol and triglycerides were measured before and during follow-up after transplantation. Children with renal failure had significantly higher serum lipids than controls ( n=34, median age 9.2 years) and patients with heart failure. Pre transplantation, cholesterol and triglycerides were significantly lower in the hemodialysis than in the peritoneal dialysis population, whereas conservatively treated children had intermediate levels. After transplantation, serum cholesterol converged towards a mean level of 208 mg/dl and triglyceride levels converged towards a uniform level of 195 mg/dl at 9 months post transplant. The ratio of cholesterol/high-density lipoprotein significantly decreased from 4.7 to 3.8. The pattern of "post-transplant hyperlipidemia" was similar in both renal and cardiac allograft recipients. Hence, the early post-transplant changes of serum lipid pattern are markedly dependent on the mode of pre-transplant renal replacement therapy. Later, serum lipid levels were no longer influenced by prior renal replacement therapy and showed a new pattern of "post-transplant hyperlipidemia" in all children.
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PMID:Serum lipid pattern unifies following renal transplantation in children. 1288 78

Accumulating evidence indicates that reactive oxygen species (ROS) play major roles in the initiation and progression of cardiovascular dysfunction associated with diseases such as hyperlipidemia, diabetes mellitus, hypertension, ischemic heart disease, and chronic heart failure. ROS produced by migrating inflammatory cells as well as vascular cells (endothelial cells, vascular smooth muscle cells, and adventitial fibroblasts) have distinct functional effects on each cell type. These include cell growth, apoptosis, migration, inflammatory gene expression, and matrix regulation. ROS, by regulating vascular cell function, can play a central role in normal vascular physiology, and can contribute substantially to the development of vascular disease.
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PMID:Reactive oxygen species in the vasculature: molecular and cellular mechanisms. 1458 Dec 95

In the last decade the number of patients with congestive heart failure has increased noticeably and today heart failure is one of the major problems in civilized countries. While in earlier decades arterial hypertension was the main reason for developing heart failure, today coronary artery disease has become the focus of attention. However, arterial hypertension, diabetes and hyperlipidemia are also main risk factors for developing coronary artery disease. In addition to non-pharmacological management with reduced fluid intake and periodical exercise training particularly in stable heart failure, in the last decade some special drug compounds have demonstrated a significant reduction in mortality in great double blind randomized trials. ACE-inhibitors and betablockers are essential components in treating congestive heart failure. Angiotensin-II-receptorblockers are indicated if ACE inhibitors and/or beta-blockers are not tolerated. The combined use of all three compounds was shown to result in a further reduction of mortality in the recently presented CHARM study. In progressive heart failure the use of diuretics is necessary and effective especially when fluid overload exists. Not treating heart failure is followed by high mortality, as we know, and so adequate and uncompromising treatment of hypertension is the most important approach to prevent the further development of heart failure.
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PMID:[Therapeutical strategies in hypertensive patients presenting heart failure symptoms]. 1500 83

Mitochondriopathies (MCPs) are either due to sporadic or inherited mutations in nuclear or mitochondrial DNA located genes (primary MCPs), or due to exogenous factors (secondary MCPs). MCPs usually show a chronic, slowly progressive course and present with multiorgan involvement with varying onset between birth and late adulthood. Although several proteins with signalling, assembling, transport, enzymatic function can be impaired in MCP, most frequently the activity of the respiratory chain (RC) protein complexes is primarily or secondarily affected, leading to impaired oxygen utilization and reduced energy production. MCPs represent a diagnostic challenge because of their wide variation in presentation and course. Systems frequently affected in MCP are the peripheral nervous system (myopathy, polyneuropathy, lactacidosis), brain (leucencephalopathy, calcifications, stroke-like episodes, atrophy with dementia, epilepsy, upper motor neuron signs, ataxia, extrapyramidal manifestations, fatigue), endocrinium (short stature, hyperhidrosis, diabetes, hyperlipidaemia, hypogonadism, amenorrhoea, delayed puberty), heart (impulse generation or conduction defects, cardiomyopathy, left ventricular non-compaction heart failure), eyes (cataract, glaucoma, pigmentary retinopathy, optic atrophy), ears (deafness, tinnitus, peripheral vertigo), guts (dysphagia, vomiting, diarrhoea, hepatopathy, pseudo-obstruction, pancreatitis, pancreas insufficiency), kidney (renal failure, cysts) and bone marrow (sideroblastic anaemia). Apart from well-recognized syndromes, MCP should be considered in any patient with unexplained progressive multisystem disorder. Although there is actually no specific therapy and cure for MCP, many secondary problems require specific treatment. The rapidly increasing understanding of the pathophysiological background of MCPs may further facilitate the diagnostic approach and open perspectives to future, possibly causative therapies.
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PMID:Mitochondriopathies. 1500 63

Breathing-related sleep disorders, particularly obstructive sleep apnea, have been largely undiagnosed in people with cardiovascular disease, probably due to limited health care provider awareness of the association between the two conditions. Solid evidence is emerging that the apneic events that occur during sleep lead to acute and chronic hemodynamic changes during wake time, including elevated sympathetic tone, decreased stroke volume and cardiac output, increased heart rate, and changes in circulating hormones that regulate blood pressure, fluid volume, vasoconstriction, and vasodilation. Obstructive sleep apnea is associated with known cardiovascular risk factors such as obesity and hyperlipidemia, and is considered by many sleep clinicians to be an independent risk factor for hypertension. Additionally, sleep apnea has been implicated in the pathogenesis of heart failure and stroke. Treatment with positive airway pressure during sleep eliminates the apneic events and the ensuing acute hemodynamic changes. Improvements in daytime blood pressure and left ventricular function also have been noted in persons with hypertension and heart failure. Because effective treatment is available for sleep apnea, this condition needs to be diagnosed and treated in persons with cardiovascular disease.
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PMID:Sleep-disordered breathing and the association with cardiovascular risk. 1501 52


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