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

Kasabach-Merritt syndrome is characterized by thrombocytopenia and bleeding tendency leading to disseminated intravascular coagulation with giant hemangiomas. We present a very low birth weight infant with this syndrome who underwent four operations. A male baby (1179 g, 37 cm) was born at a gestational age of 28 weeks and 6 days by caesarean section. A large hemangioma, 7 x 8 cm in size, was recognized on the left thigh. As associated consumption coagulopathy (Kasabach-Merritt syndrome) was diagnosed with platelet count 5.1 +/- 10(4) mm-3 and fibrinogen 49 mg.dl-1. Despite treatment with liniac X-ray radiation, systemic steroid and component transfusion, coagulopathy became worse with extremely low platelet count of 1.1 x 10(4) mm-3. Infusion of dopamine and dobutamine was necessary for high output cardiac failure. On day 9, PDA ligation was performed. Cerebro-ventricular drainage, ventricuro-peritoneal shunt and shunt revision were required on day 15, 49 and 88, respectively, for hydrocephalus due to intraventricular hemorrhage. Main anesthetics used were fentanyl and sevoflurane. Major problems encountered by anesthetists were: bleeding tendency, water and electrolyte management, body temperature control, and immaturity and fragility of premature infant. Coagulopathy in Kasabach-Merritt syndrome must be a risk factor for intraventricular hemorrhage, which is a characteristic complication of a very low birth weight infant.
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PMID:[Anesthetic problems in a very low birth weight infant with Kasabach-Merritt syndrome]. 881 2

The epidemiologic approach to investigation of atherosclerotic cardiovascular disease has provided many insights into the preclinical and clinical spectrum of the disease. The hazard of developing atherosclerotic cardiovascular disease is substantial with coronary heart disease (CHD), the most common and most lethal feature. The outlook in those who manage to survive the initial episode is also serious, with a 10-year mortality rate of 37% for persons with angina and a 55% rate for those sustaining a myocardial infarction. Fifteen percent of persons developing CHD present with a fatal event, and 38% of infarctions go unrecognized. The presence of atherosclerosis in one vascular territory imposes an increased risk of its appearing in another area at two to six times the general population rate. The major cardiovascular risk factors adversely affect all arterial vascular territories so that correction of risk factors targeted at one particular atherosclerotic outcome may also favorably influence the other risk factors. Coronary disease is the most prevalent lethal hazard of hypertension, dyslipidemia, glucose intolerance, and cigarette smoking. These risk factors cluster and optimal therapy must improve the whole risk profile. Women share the same risk factors for CHD as men. Although women have a lower absolute risk for most risk factors, a high total/HDL cholesterol ratio, left ventricular hypertrophy, and diabetes each tend to eliminate the female advantage. Menopause also promptly escalates risk threefold. Although women tend to have a lower incidence than men, the initial attack is just as highly lethal in women, and their subsequent outlook as survivors is at least as serious as for men. Sudden death is a pre-eminent feature of coronary disease and cardiac failure. Coronary disease increases sudden death risk 3.3-fold and cardiac failure 4.8-fold. Sudden death incidence varies in relation to the same cardiovascular risk factors as coronary heart disease, with no unique risk factors identified. However, multivariate combinations of these in a profile can identify high-risk candidates for sudden death as well as coronary attacks in general. The key to prevention of sudden death is to prevent coronary attacks and cardiac failure. Despite aggressive cardiac revascularization and treatment of hypertension, congestive heart failure (CHF) has not decreased in prevalence, and innovations in the treatments of overt failure have not substantially improved survival. Median survival is only 1.7 years for men and 3.2 years for women. The conditional probability of developing CHF can be estimated using a logistic function comprised of age, systolic pressure, vital capacity, heart rate, ECG-left ventricular hypertrophy (LVH), glucose intolerance, x-ray enlargement, and presence of CHD and heart murmurs. Eighty percent of CHF events occur in persons in the upper quintile of multivariate risk. Continued clinical, metabolic, and epidemiologic research have expanded and refined atherosclerosis risk factors. The lipid connection is now concerned with the apoprotein makeup of the lipids, subfractions of lipids, and Lp(a). The diabetic influence is now focused on insulin resistance. Ambulatory monitoring is being used to evaluate blood pressure and silent ischemia. Fibrinogen and leukocyte counts have emerged as possible indicators of unstable lesions. Prospects for primary and secondary prevention are good if public health measures, health education, and preventive medicine are implemented based on existing knowledge of correctable or avoidable risk factors. The potential for more effective prevention continues to expand, and great advances have already been made in countries where aggressive preventive measures have been implemented to correct the major established risk factors.
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PMID:Hazards, risks, and threats of heart disease from the early stages to symptomatic coronary heart disease and cardiac failure. 921 Oct 12

Many risk factors operate in both coronary heart disease and stroke, especially ischaemic stroke--age, sex, social class, blood pressure, pre-existing vascular disease (angina, myocardial infarction, cardiac failure, diabetes and peripheral vascular disease, transient ischaemic attack and stroke), atrial fibrillation and fibrinogen, smoking, alcohol and height. Total cholesterol has also recently been recruited to this list. The various mechanisms involved in stroke and its subtypes and the epidemiological problems in evaluating aetiological factors in stroke make the comparison with coronary heart disease more difficult. The recent discrepancy between much of the epidemiology and the clinical trials evaluating the role of lipids in stroke has spurred the systematic review (meta-analysis) of major prospective observational studies. These will provide a clearer assessment about the quantitative comparison of some of the more important risk factors for stroke and coronary heart disease in the near future.
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PMID:Are risk factors for stroke and coronary disease the same? 973 88

Malnutrition, inflammation and atherosclerotic cardiovascular disease occur at high prevalence, and often concomitantly, in conjunction with chronic renal failure. Several features of malnutrition (e.g., increased oxidative stress, increased plasma levels of fibrinogen, Lp(a), and inflammation) may all, alone or in concert, increase the risk of cardiovascular disease. Recent findings suggest malnutrition and hypoalbuminaemia in chronic renal failure to be largely the consequence of such factors as heart failure, chronic infection and inflammation, that simultaneously trigger the development of atherosclerotic cardiovascular disease. Central to this scenario is the involvement of proinflammatory cytokines which may cause muscle wasting, hypoalbuminaemia, anorexia, and accelerated atherosclerosis. It is unlikely that the high mortality due to atherosclerotic disease among patients with chronic renal failure can be substantially reduced unless new treatment strategies are developed which address the complex relationships that exist between malnutrition, inflammation and cardiovascular disease.
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PMID:[Strong connection between malnutrition, inflammation and arteriosclerosis. Improved treatment of renal failure if underlying factors are attacked]. 1057 60

We describe the case of a patient with a neonatal giant cutaneous hemangioma with high-output cardiac failure and Kasabach-Merritt syndrome and successfully treated with transcutaneous arterial embolization aimed at controlling severe congestive heart failure and consumption coagulopathy. A patient was admitted to the neonatal care unit on the first day of age because of a large hemangioma on his right lateral chest wall and respiratory distress, associated with cardiac failure resulting from arteriovenous shunting. On the second day of age the platelet count decreased to 5.7 x 10(4)/microliter and fibrinogen level was 85 mg/dl. The values of prothrombin time and activated partial thromboplastin time were prolonged. Intravenous predonisone therapy was started immediately, but bleeding tendency was getting worse and the evidence of congestive heart failure persisted. On the third day the patient then underwent embolization of feeding arteries with microcoils. The cardiac failure and thrombocytopenic coagulopathy had improved significantly without complications. We conclude that transcutaneous arterial embolization is an effective and safe treatment in this neonate and should be considered for the treatment of control high-output cardiac failure and coagulopathy in infants with hemangioma and Kasabach-Merritt syndrome.
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PMID:Successful transcutaneous arterial embolization of a giant hemangioma associated with high-output cardiac failure and Kasabach-Merritt syndrome in a neonate: a case report. 1064 62

Five decades of epidemiologic research have established that blood pressure elevation is a common and powerful contributor to all of the major cardiovascular diseases, including coronary disease, stroke, peripheral artery disease, renal disease, and heart failure. The common variety of hypertension designated benign essential hypertension was not shown to be either benign or essential. Although clinicians favor the diagnosis and treatment of hypertension in terms of diastolic blood pressure elevation and categoric cut points, epidemiologic data show a more important influence of systolic blood pressure, and a continuous, graded influence of blood pressure even within what is regarded as the normotensive range. An important revelation in epidemiologic hypertension research is that hypertension usually occurs in conjunction with other metabolically linked risk factors; therefore, less than 20% occurs in isolation. The other risk factors that tend to accompany hypertension include glucose intolerance, obesity, left ventricular hypertrophy, and dislipidemia (elevated total, LDL, and small dense LDL cholesterol levels, raised triglyceride, and reduced HDL cholesterol levels). Clusters of three or more of these additional risk factors occur at four times the rate expected by chance. This clustering is attributed to an insulin resistance syndrome promoted by abdominal obesity. The amount of risk factor clustering accompanying elevated blood pressure was observed to increase with weight gain. Based on Framingham Study data the prevalence of insulin resistance syndrome in the general population could be as high as 22% in men and 27% in women. Risk of coronary disease, the most common and most lethal sequel to hypertension, increased stepwise with the extent of risk factor clustering. Among persons with hypertension, about 40% of coronary events in men and 68% in women are attributable to the presence of two or more additional risk factors. Only 14% of coronary events in hypertensive men and 5% of those in hypertensive women occurred in the absence of additional risk factors. Other important features of risk stratification of hypertension are the presence of an elevated heart rate and left ventricular hypertrophy, and an elevated fibrinogen that often accompany hypertension. Recent population-based data reported suggest that elevated renin accompanying hypertension may independently enhance the risk of coronary events. Because clustering of other major risk factors with hypertension is the rule, the prudent physician should routinely screen for the presence of these other factors. Multivariate risk assessment profiles are now available for coronary disease, stroke, peripheral artery disease, and heart failure, to enable physicians to pool all the relevant risk factor information so as to arrive at a composite risk estimate. Hypertensive patients are more appropriately targeted for therapy by such risk stratification and the goal of the therapy should be to improve the multivariate risk profile.
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PMID:Risk stratification in hypertension: new insights from the Framingham Study. 1067 82

The Framingham Study was initiated in 1948 to investigate an epidemic of coronary disease in the USA, using a prospective epidemiological approach. Insights were provided into the prevalence, incidence, full clinical spectrum and predisposing factors. The major "risk factors" (a term coined by the Framingham Study) for coronary disease, stroke, peripheral artery disease and heart failure were identified and clinical misconceptions dispelled about isolated systolic hypertension, left ventricular hypertrophy, dyslipidemia, atrial fibrillation and glucose intolerance. Average values for blood lipids, blood pressure, body weight, glucose and fibrinogen were shown to be dangerously suboptimal and to have a continuous graded relationship to cardiovascular disease without critical values. Dyslipidemia, glucose intolerance and elevated fibrinogen were shown to have smaller hazard ratios in the elderly, but this was offset by a higher absolute risk. Diabetes was shown to operate more strongly in women, eliminating their advantage over men. Serum total cholesterol was shown to derive its atherogenic potential from its LDL component and also to reflect cholesterol being removed in the HDL fraction. The total/HDL-cholesterol ratio was demonstrated to be the most efficient lipid profile for predicting coronary disease. LDL was shown to be correlated with hemostatic factors, suggesting that there would be additional benefits to lowering LDL. High triglyceride associated with reduced HDL, indicating insulin resistance and small dense LDL, was shown to be associated with excess coronary disease. All the risk factors tended to cluster, and this was shown to be promoted by insulin resistance induced by weight gain. Multivariate risk profiles were produced to facilitate risk stratification of candidates for coronary disease, stroke, peripheral artery disease and heart failure. The Framingham Study is now engaged in quantifying the independent contributions of homocysteine Lp(a), insulin resistance, small dense LDL, C reactive protein, clotting factors and genetic determinants of cardiovascular disease. We are now able to estimate the lifetime risk of all the atherosclerotic cardiovascular disease outcomes.
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PMID:The Framingham Study: ITS 50-year legacy and future promise. 1087 16

Sudden death is most common and often the first manifestation of coronary heart disease although its risk is difficult to predict. It has been studied mainly in patients with severe ventricular arrhythmia or recent myocardial infarction, but little is known about the different risk factors for short- and long-term risk of sudden death in patients with stable angina. To assess risk factors for sudden death in patients with stable angina and angiographically proven coronary artery disease, 319 consecutive patients were recruited prospectively and followed-up. Patients with clinical heart failure or recent myocardial infarction were excluded. Clinical, angiographic and biological variables were recorded. The association between each variable and the risk of sudden death was assessed in univariate and logistic multivariate analysis. There were 25 sudden deaths during the follow-up period (97+/-29 months). The univariate predictors in the short-term (2 years) were: peripheral arterial disease, left ventricular hypertrophy, low density lipoprotein cholesterol and ejection fraction. The independent predictors were: peripheral arterial disease (relative risk: 6.3), ejection fraction (relative risk 1.05) and low density lipoprotein (relative risk: 1.8). In the long-term (8-10 years), body mass index, coronary score, ejection fraction and fibrinogen were univariate predictors. Only body mass index (relative risk: 1. 2), ejection fraction (relative risk: 1.06) and fibrinogen (relative risk: 2) remained independent predictors. The risk factors for sudden death in stable angina were time-dependent, peripheral arterial disease appeared as the best predictor with LDL for short time, and body mass index (obesity: index >27) and fibrinogen for long time. Ejection fraction was the only time-independent predictor.
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PMID:Short- and long-term risk factors for sudden death in patients with stable angina. 1110 69

Atherosclerosis and coronary artery disease (CAD) are now the commonest sequelae of hypertension and all clinical manifestations of CAD occur in excess in persons with elevated blood pressure. Risk increases in relation to the extent of blood pressure elevation whether this is in the systolic or diastolic component, at any age and in either sex. Even isolated systolic hypertension increases cardiovascular risk. Elevated pressures are often accompanied by lipid abnormalities, hyperglycemia, elevated fibrinogen, obesity, and ECG abnormalities, all of which augment the risk. These risk factors associated with hypertension influence the coronary risk potential more than the nature of the blood pressure elevation. Although blood pressure makes an independent contribution to CAD, the risk at any level of pressure is markedly influenced by the cardiovascular risk profile. In mild to moderate hypertension in particular, the risk of CHD is concentrated in those who have impaired glucose tolerance, increased total/HDL ratio, ECG abnormalities, and smoke cigarettes. One or more of these associated risk factors also predisposes to other cardiovascular sequelae of hypertension, including stroke, peripheral vascular disease, and cardiac failure. The presence of organ involvement indicated by proteinuria, evidence of impaired ventricular function, or left ventricular hypertrophy greatly escalates the risk and usually indicates a compromised coronary circulation. Most myocardial infarctions and sudden deaths occur prior to the appearance of such evidence. Hypertensive risk assessment requires consideration of the multivariate risk profile because of the interdependence of the risk factors. The nature and urgency of treatment is better determined from such a risk profile than from the blood pressure parameters alone. Optimal preventive management of hypertension requires more than normalization of the blood pressure if coronary sequelae are to be avoided.
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PMID:Influence of multiple risk factors on the hazard of hypertension. 1152 37

Many acquired risk factors may be identified to avoid the scholarly nature of these interminable lists, they may be reclassified with respect to their originality or their mechanism of action and those of current interest, whose data is still often hypothetical but recent, can be underlined. The following order may be proposed: risk factors which cannot be changed: age (which remains the principal factor) and gender (women being at higher risk than men); true acquired risk factors such as cancer, dysimmune conditions (more specifically, the antiphospholipid syndrome) and hormone replacement therapy (oestroprogestative contraception which has been updated by the debate about "third generation pills" and the risk related to progesterone-like substances themselves; hormone replacement therapy of the menopause which still has no clinical trials to assess "our" forms with natural hormones administered transdermally or transmucosally). Smoking has also been accused of being a risk factor for venous thrombosis in the latest clinical trials. Metabolic factors increase the risk of thrombosis: this is established for obesity, still suspected for hyperhomocystonaemia, the abnormalities being the result of complex gene-environment interactions. Other dysmetabolic conditions (diabetes, hypercholesterolaemia, hypertriglyceridaemia), responsible for arterial complications, are not clearly related to increased venous thromboembolic risk although a preventive effect of statins (yet another I) has just been reported. Similarly to these metabolic factors, the origin of which, genetic or environmental, is difficult to establish, interest has recently been shown in quantitative and functional changes in blood clotting factors. This has been established for arterial disease for fibrinogen but, in addition to this factor which slightly increases the risk of venous thrombosis, increases of factor VIII independent of inflammatory conditions, of blood group and Von Willebrand factor, which all influence the level of factor VIII, an increase by 150% of the normal increases the risk of venous thromboembolic disease by 3 or 4 times. As for factor VIII, increases in factor IX, factor XI, and resistance to activated C protein (independently of the Leiden mutation on the gene for factor V), are also associated in increased venous thromboembolic risk. Without knowing into which category to classify them, previous personal and family history of thromboembolic disease, in the absence of the already mentioned hereditary risk factors, must be noted. Finally, amongst the acquired risk factors, the authors also list conditions of blood stasis and vascular lesions with or without hypercoagulability (surgery, prolonged hospital stays, cardiac failure, paralysis, pregnancy...). Of these acquired conditions which increase the risk of thrombotic complications, particular attention has been given over the last few years to forced immobilisation in uncomfortable positions as in certain forms of transport. Although clinical reports have discordant results, it would seem that the risk is increased and the benefits of supportive elastic stockings have been confirmed. If the acquired risk is identified and quantified for a patient, it allows evaluation of global risk and the installation of appropriate therapeutic measures.
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PMID:[Venous thromboembolic pathology. New acquired risk factors or new data on acquired risk factors]. 1179 76


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