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)

Cardiovascular disease (CVD) is a leading cause of premature death in the UK and a major cause of ill health and disability. Whilst death rates from CVD have been falling since the late 1970s in the UK, levels of morbidity (such as angina) do not seem to be falling and may even be rising in some age-groups, especially as the population ages. There is broad consensus that lifestyle factors, including physical activity and diet, are fundamental determinants of heart disease risk. Current recommendations to reduce cardiovascular risk include maintaining a healthy body weight, eating five or more portions of fruit and vegetables each day, reducing intake of fat (particularly saturated fatty acids), reducing salt intake and eating one portion of oily fish per week. Although some improvements have been made in recent years (e.g. a reduction in total fat intake), national studies suggest that more effective campaigns are required to increase awareness of the benefits of these dietary changes. The present paper will discuss how the dietary messages relating to CVD are best communicated to the general public and will identify some of the main barriers to their implementation.
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PMID:Diet and cardiovascular disease in the UK: are the messages getting across? 1469 93

Syncope, defined as a transient loss of consciousness and postural tone with spontaneous recovery and no neurologic sequelae, is among one of the most common causes of consultation with a physician. The diagnostic workup is complex but can be simplified if focused on the underlying condition. Prognosis is highly dependent on the presence or absence of structural heart disease, primarily the presence of cardiomyopathy regardless of etiology, particularly if the left ventricular (LV) function is less than 35%. The diagnostic approach to the patient with recurrent syncope and no structural heart disease is targeted to rule out neurally mediated causes. This approach usually includes a tilt table test (ie, head-up tilt), carotid sinus massage in patients older than 55 years, and an adenosine challenge test in patients who remain with unexplained syncope. Unexplained syncope in patients with reduced LV function (< 35%) may be potentially life-threatening. Infrequent causes of syncope should be sought in younger patients with a family history of sudden cardiac death. Channelopathies such as the long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia are among this variety. Therapy should address the potential mechanism of syncope. In neurally mediated causes, restoration of orthostatic tolerance, primarily by increasing volume during orthostatic stress, is recommended. Physiologic countermaneuvers and increase in salt and water intake are usually the initial therapy. With syncope in patients with an LV dysfunction (< 35%), an ICD is frequently recommended after ruling out common causes of syncope. Syncope in the elderly is usually multifactorial and therapy should include reassessment of multiple medications, which can promote neurally mediated syncope as well as searching for bradycardic causes. Empiric pacing may be used in this complex group of patients.
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PMID:Current Management of Syncope: Treatment Alternatives. 1532 13

Advanced heart failure, also be defined as stage D heart failure, characterized by advanced structural heart disease and marked symptoms of heart failure at rest despite dietary modification, salt restriction and maximal medical therapy including ACE inhibitors, angiotensin II receptor blockers, digitalics, diuretics and beta blockers. These patients require frequent hospitalizations and specialized interventions such as heart transplantation, implantation of mechanical assistance devices, continuous intravenous inotropic therapy to palliate symptoms, or continued terminal care.
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PMID:[Management of advanced or refractory heart failure]. 1568 Jan 39

Individuals homozygous for the autosomal recessive disorder CF are known to have low blood pressure, thought to be caused by greatly increased sweat salt loss. We examined whether carriers of the CF gene also have low blood pressure. Our pilot studies had suggested an effect limited to females, leading to 2 further studies in white females. In the first, blood pressure was measured in 232 known CF mutation carriers and compared with 246 mutation-negative control subjects. The carriers showed a significantly lower rate of increase in systolic blood pressure with age than the controls, especially after age 50 (3.5% per decade compared with 5.4% per decade, P=0.010). In a small substudy, sweat sodium and chloride levels were highest in those CF carriers with the lowest blood pressures. In the second study, CF carrier status was investigated in 563 normotensive females and in 607 women with essential hypertension diagnosed to test whether a lower incidence of carriers in the hypertensives suggested a protective effect. Twenty-five of the normotensives (4.4%) were carriers compared with 21 (3.5%) of the hypertensive group (P=0.45). Older CF carrier females had lower systolic and diastolic pressures than matched control subjects, with a tendency for blood pressure to increase less with age. This could result in significant reduction in stroke and heart disease. The effect on blood pressure is insufficient to prevent hypertension, though it remains conceivable that the severity might be ameliorated in carriers.
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PMID:Blood pressure and the cystic fibrosis gene: evidence for lower pressure rises with age in female carriers. 1547 85

The excess risk of hypertension in black Americans continues to be a major health concern. Although there is considerable information regarding these disease trends, much of the major underpinnings of the etiology of hypertension remain unclear. The excess mortality in blacks due to heart disease, renal failure, and stroke are clearly directly related to the excess burden of hypertension. Amid the recent findings about the pathophysiology of hypertension, some clear differences in the effects of overweight, salt sensitivity, and vascular biology emerge along ethnic lines. These differences may shed some light on the development of more effective treatment strategies. Based on our current knowledge, aggressive management of hypertension in blacks is critical. This review highlights what is known about various factors affecting hypertension and its treatment in black Americans.
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PMID:Hypertension in black patients: special issues and considerations. 1548

1. If one was to design a hormone to protect the heart, it would have a number of features shown by the cardiac natriuretic peptides atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP). These hormones are made in cardiomyocytes and are released into the circulation in response to atrial and ventricular stretch, respectively. Atrial natriuretic peptide and BNP can reduce the preload and after-load in normal and failing hearts. They reduce blood volume over the short term by sequestering plasma and over the longer term by promoting renal salt and water excretion and by antagonizing the renin-angiotensin-aldosterone system at many levels. Each of these actions affords indirect benefit to a volume- or pressure-threatened heart. 2. Recent studies have identified additional modes of action of the natriuretic peptides that may also confer cardioprotective benefits, especially in heart disease. The emerging findings are: (i) that ANP and BNP antagonize the cardiac hypertrophic action of angiotensin II and continue working under conditions where endothelial nitric oxide (NO) function is compromised, such as in the presence of high glucose in diabetes; (ii) they potentiate the bradycardia caused by inhibitory ('autoprotective') cardio-cardiac reflexes; and, furthermore, (iii) BNP can suppress cardiac sympathetic nerve activity in humans, including those with heart failure. Thus, it appears that natriuretic peptides can shift sympathovagal balance in a beneficial direction (away from the sympathetic). The vagal reflex and antihypertrophic actions of the peptides are mediated by particulate guanylyl cyclase (pGC) natriuretic peptide receptors. 3. The multiple synergistic actions of the natriuretic peptides make them and their pGC receptors attractive targets for therapy in heart disease. Encouragingly, exogenous natriuretic peptides remain effective even when endogenous peptide levels are raised, as is the case in heart failure. They also remain effective in disease states where other protective mechanisms, such as the NO system, have become ineffective, offering yet further encouragement for the therapeutic use of the natriuretic peptides.
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PMID:Cardioprotective functions of atrial natriuretic peptide and B-type natriuretic peptide: a brief review. 1556 95

Injury to the myocardium disrupts geometric integrity and results in changes to intracardiac pressure, wall stress and tension, and the pattern of blood flow through the heart. Significant disruption to pump function results in heart failure which is defined in terms of symptoms: breathlessness and fatigue, signs of salt and water retention, and neurohormonal activation. This syndrome most commonly occurs in the context of injury due to ischaemic heart disease and dilated cardiomyopathy but because patients with congenital heart disease (CHD) are born with sometimes gross distortions of cardiac anatomy they too are subject to the forces that drive heart failure. This paper explores the available data relating to the clinical and neurohormonal manifestations of heart failure in patients with congenital heart disease and describes how, by additionally exploring events at a cellular level, we may be able to arrive at a definition of heart failure relevant to this population.
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PMID:Towards defining heart failure in adults with congenital heart disease. 1559 75

Epidemiology in the past was concerned essentially by the study of infectious diseases which were the cause of huge mortalities especially since urbanisation was initiated. Epidemics of pest, typhus, cholera, influenza a.o. were common. The epidemics were halted by better hygiene, vaccination and antibiotics. Since the second world war epidemiology was dominated by an "epidemic" of new chronic diseases, especially heart disease and cancer. This was due to an increase in life span and to an increase in smoking habits and in the intake of saturated fat and a too small intake of fruit and vegetables combined with a too high intake of salt (NaCl). Gradually epidemiology evolved as the study of the causes, the distribution, the risk factors and the prevention of chronic diseases, but also including accidents, suicide, depression a.o., diseases with a mass occurrence at the population level. The importance of nutrition as a determinant of health gradually became recognized, but remains undervalued by the medical profession. Mortality at the population level follows some simple mathematical laws and can be represented accurately (r2>0.99) between the ages of 35 and 84 year by either Gompertz equations (ln mortality versus age) or by a polynomial equation (ln mortality versus age, age2). This is valid for all populations and both sexes and remains valid at times of great and rapid changes in mortality. This shows that measures for prevention should be directed towards the total population. The future of epidemiology should be directed towards the slowing of the ageing process at the population level by a healthy life style consisting of: not smoking, avoiding obesity, a fair amount of physical activity and a healthy nutrition i.e little salt, little saturated fat, an adequate amount of omega-3 fatty acids and a large amount of fruit and vegetables, with an occasional glass of red wine. This contains the secret of a long and healthy life. Conceptually it will be important to determine whether a maximum human life span, genetically determined, exists. A maximal rectangularization of the mortality curve should then be the ultimate goal. At the same time the possible re-emergence of old and new infectious diseases (SARS, Ebola, BSE, AIDS) should be kept in mind.
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PMID:Epidemiology: past, present and future. 1564 67

We have used molecular dynamics simulations to investigate the effect of phosphorylation and mutation on the cytoplasmic domain of phospholamban (PLB), a 52-residue protein that regulates the calcium pump in cardiac muscle. Simulations were carried out in explicit water systems at 300 K for three peptides spanning the first 25 residues of PLB: wild-type (PLB(1-25)), PLB(1-25) phosphorylated at Ser16 and PLB(1-25) with the R9C mutation, which is known to cause human heart disease. The unphosphorylated peptide maintains a helical conformation from 3 to 15 throughout a 26-ns simulation, in agreement with spectroscopic data. Comparison with simulations of a fourth peptide truncated at Pro21 showed the importance of the region from 17 to 21 in preventing local unfolding of the helix. The results suggest that residues 11-16 are more likely to unfold when specific capping motifs are not present. It is proposed that protein kinase A exploits the intrinsic flexibility of the 11-21 region when binding PLB. In agreement with available CD and NMR data, the simulations show a decrease in the helical content upon phosphorylation. The phosphorylated peptide is characterized by helix spanning residues 3-11, followed by a turn that optimizes the salt-bridge interaction between the side chains of the phosphorylated Ser-16 and Arg-13. Replacing Arg-9 with Cys results in unfolding of the helix from C9 and an overall decrease of the helical conformation. The simulations show that initiation of unfolding is due to increased solvent accessibility of the backbone atoms near the smaller Cys. It is proposed that the loss of inhibitory potency upon Ser-16 phosphorylation or R9C mutation of PLB is due to a similar mechanism, in which the partial unfolding of the cytoplasmic helix of PLB results in a conformation that interacts with the cytoplasmic domain of the calcium pump to relieve its inhibition.
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PMID:The alpha-helical propensity of the cytoplasmic domain of phospholamban: a molecular dynamics simulation of the effect of phosphorylation and mutation. 1576 55

The excess risk for hypertension in black Americans continues to be a major health concern. Although there is considerable information regarding these disease trends, many of the major underpinnings of the etiology of hypertension remain unclear. The excess mortality in blacks due to heart disease, renal failure, and stroke is clearly directly related to the excess burden of hypertension. Amid the recent findings about the pathophysiology of hypertension, some clear differences in the effects of overweight, salt sensitivity, and vascular biology emerge along ethnic lines. These differences may shed some light on the development of more effective treatment strategies. Based on our current knowledge, aggressive management of hypertension in blacks is critical. This review highlights what is known about various factors affecting hypertension and its treatment in black Americans.
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PMID:Hypertension in black patients: special issues and considerations. 1606 Oct 41


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