Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurrence of the C3F allele was investigated in the following three groups: 69 consecutive referred patients with untreated essential hypertension, including borderline hypertension; 70 patients with established and treated essential hypertension, already attending the same outpatient clinic, and 62 age- and sex-matched normotensive healthy subjects without clinical signs of atherosclerosis or familial predisposition to hypertension. In the three groups the C3F allele was found in 38.2%, 29% and 20%, respectively. Among the treated hypertensive patients with C3F gene, 40% had coronary heart disease (CHD) compared to 6.1% among the C3F negative (P less than 0.005), and the relative risk of CHD among the treated hypertensive patients with this allele was found to be 10.2 (P less than 0.002). The C3F gene was present in 72.7% of the treated patients with CHD. In the untreated patients the occurrence of CHD was low, and no differences between C3F positive and negative patients could be demonstrated. No association of the C3F allele with familial predisposition to hypertension was found. This study provides further evidence of a positive association of the C3F allele with atherosclerosis, and it is concluded that this allele in a hypertensive patient might accelerate the atherosclerotic process, with subsequent premature development of vascular complications.
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PMID:Association between coronary heart disease and the C3F-gene in essential hypertension. 68 71

Borderline hypertension is widespread. Though the increased blood pressure appears to be innocent, and upon rest frequently returns to the normal range, signs of complex and profound alteration of the physiologic control of the circulation can already be found. The pathophysiology of borderline hypertension is of particular interest since it may reveal clues about the processes which initiate the hypertension rather than the consequences of the primary blood pressure elevation. Patients with borderline hypertension are at a higher risk of developing future sustained hypertension and its consequences. The risk, however, is not sufficient to justify treatment in all cases. Patients must be followed to observe blood pressure trends and treatment attempted in the selected minority which has the highest risk. The determination of risk is based on repeated measurements of blood pressure and on the assessment of risk factors for atherosclerosis and for future hypertension.
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PMID:Borderline hypertension. An overview. 85 4

As hypertension advances, secondary pathophysiologic changes are induced in multiple organs. Consequently, we investigated the pathophysiology of the earliest forms of hypertension--e.g., borderline hypertension. Borderline hypertension is associated with abnormal autonomic control of the circulation; sympathetic drive to the heart, blood vessels, and kidney is increased, cardiac parasympathetic inhibition is decreased, and plasma norepinephrine is increased. The hemodynamic picture is one of increased cardiac output not met by adequate vasodilation. The condition of "hyperkinetic" borderline hypertension is a precursor of more severe hypertension. In due course, a transition from high cardiac output to high vascular resistance occurs, while the enhanced sympathetic tone recedes toward normal values. The mechanism of hemodynamic transition is easily understood: cardiac output decreases due to structural changes and receptor downregulation, whereas ensuing vascular hypertrophy increases vascular resistance. The apparent regression of plasma norepinephrine values is explained in the framework of our hypothesis of the "blood pressure-seeking properties of the central nervous system." Large body mass and overweight are a consistent feature of borderline hypertension. A recent study in Tecumseh, Michigan shows that weight, plasma norepinephrine, a hyperkinetic state, and plasma insulin values are correlated in the general population. The explanation of this interrelationship will greatly advance our understanding of hypertension. From the pathophysiological viewpoint, the paradoxical outcome of clinical trials involving older antihypertensive medication is not surprising. The complexity of pathophysiologic interrelationships and the fact that risk factors for atherosclerosis are increased in hypertension suggest that reduction of blood pressure cannot be expected to ameliorate all consequences of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic and neurohumoral evidence of multifaceted pathophysiology in human hypertension. 169 32

Mental arithmetic and mirror tracing were compared in 40 untreated patients with borderline hypertension, tested in random sequence in standardized protocols. Both tasks significantly increased systolic and diastolic blood pressure, heart rate, cardiac index, plasma renin, and decreased peripheral resistance. Mental arithmetic also increased cholesterol, triglycerides and HDL; plasma catecholamines were not changed significantly. Lipid changes were correlated with blood pressure changes. These methods will be useful in exploring the relationships between hemodynamic reactivity to stress, and the presence and progression of atherosclerosis, as well as testing the effects of antihypertensive drugs on stress-induced changes that may influence atherosclerotic complications of hypertension.
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PMID:Hemodynamic and endocrine effects of mental stress in untreated borderline hypertension. 226 Nov 52

The Tecumseh project investigates the evolution of hypertension in a healthy population. Of 946 subjects aged 18 through 38 years, 124 had clinic blood pressure readings higher than 140/90 mm Hg (the mean for borderline hypertensive subjects was 130/94 mm Hg). Compared with normotensive subjects, borderline hypertensive subjects had higher home blood pressures (mean, 12/7 mm Hg higher). Their childhood and postpubertal blood pressures were elevated (6/4 mm Hg higher than normal at age 6 years and 12/7 mm Hg higher than normal at age 21 years), and hypertensive target organ changes were detected. Borderline hypertensive subjects also had elevated minimal forearm resistance (0.22 U higher than normal), decreased stroke index (1.8 mL/m2 lower than normal), and impaired ventricular diastolic relaxation (mitral Doppler peak early diastolic blood flow [E] to peak late diastolic blood flow [A] ratio 0.13 lower than normal). Borderline hypertensive subjects had significant abnormalities in other coronary risk factors (cholesterol levels were 0.39 mmol/L higher, triglyceride levels were 0.45 mmol/L higher, high-density lipoprotein levels were 0.08 mmol/L lower, insulin levels were 38 pmol/L higher, and 16.5% more of them were overweight). Borderline hypertension is neither transient nor innocuous. Its association with other predictors of atherosclerosis calls for clinical attention.
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PMID:The association of borderline hypertension with target organ changes and higher coronary risk. Tecumseh Blood Pressure study. 236 31

A clinical definition of borderline hypertension is offered that includes increased risk of complications but no proof that interventions will be effective in reducing those complications. Defining an average blood pressure level permits improved prediction of individual risk. Simple clinical assessment permits definition of overall risk for hypertension and atherosclerosis. The vigor of intervention should be matched to the level of overall absolute risk. Pharmacologic treatment is appropriate for patients with borderline pressure elevation who have hypertensive target organ changes or a history of hypertensive complications. Patients with borderline hypertension deemed to be at intermediate to high risk but without target organ injury should receive nonpharmacologic (NP) instruction to reduce overall cardiovascular risk. The average blood pressure level, other atherosclerosis risk factors, and the effects of NP measures on these variables should be reevaluated at 6-12-month intervals in this group. Those at low risk should be cautioned about excessive weight gain and should have annual blood pressure measurements.
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PMID:Management of the patient with borderline hypertension. 242 65

The pathophysiology of various stages of hypertension is different. In early hyperkinetic borderline hypertension, the sympathetic drive to the heart and blood vessels is increased while the parasympathetic cardiac inhibition is decreased. The elevated cardiac output, vascular resistance, and blood pressure at that stage can be fully normalized by autonomic blockade. As hypertension advances, a hyperkinetic circulation is less evident, since beta-adrenergic responsiveness and cardiac compliance tend to decrease. Simultaneously hypertrophy of the resistance vessels increases the baseline vascular resistance and the vessels' responsiveness to constrictive stimuli. Eventually a picture of a normal cardiac output/high vascular resistance typical for established essential hypertension emerges. As the blood vessels become hyperreactive, the same degree of vasoconstriction/blood pressure elevation can be achieved with less sympathetic tone. In that phase the sympathetic overactivity is less evident, as the brain resets itself to maintain the same blood pressure elevation with a small amount of sympathetic discharge. While sympathetic overactivity may be less evident in established hypertension, it remains an important pathophysiologic factor, not only for the maintenance of blood pressure, but also for a number of other abnormalities in hypertension. Hypertension is intimately associated with higher levels of pressure-unrelated risk for development of atherosclerosis: dyslipidemia, overweight, and hyperinsulinemia. Furthermore, a number of factors in hypertension favor a poorer outcome from coronary heart disease. These pressure-independent factors increase the risk of coronary thrombosis, arrhythmic deaths, and coronary spasms. Sympathetic overreactivity appears to be crucially implicated in the evolution of this added coronary risk in hypertension. Understanding the pathophysiology of coronary risk and its relationship to sympathetic overreactivity in hypertension is helpful in seeking further improvements in clinical practice. At present antihypertensive treatment is less efficacious in reducing coronary events in hypertension than would be expected. Judicious use of appropriate drugs promises to further improve the efficacy of antihypertensive treatment in those patients who, in addition to high blood pressure, also have other associated risk factors.
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PMID:Abnormalities of autonomic nervous control in human hypertension. 806 76

Heat-shock proteins protect cells from damage but are also often the target of immune responses in inflammation and may therefore both induce and perpetuate the chronic inflammation characterizing atherosclerosis. Hypertension is a well-established risk factor for atherosclerosis, and recently, borderline hypertension also has been related to atherosclerosis. The present study investigated the possible role of heat-shock proteins in borderline hypertension and their relation to atherosclerosis by investigating antibody titers against the 65-kD heat-shock protein (HSP65). Sixty-six men with borderline hypertension and 67 age-matched normotensive men (diastolic pressure, 85 to 94 and < 80 mm Hg, respectively) were recruited from a population screening program. Titers of antibodies to HSP65 were determined by enzyme-linked immunosorbent assay. The presence of carotid atherosclerosis was determined by B-mode ultrasonography. Twenty-seven individuals had atherosclerotic plaques: 48 were smokers (more than one to two cigarettes per day). Borderline hypertensive men had higher anti-HSP65 reactivity than normotensive control subjects (P = .034). Smokers with atherosclerosis had low levels of antibodies to HSP65 compared with nonsmokers with atherosclerosis (P = .002). Furthermore, when high-risk individuals (borderline hypertension plus plaque, n = 15) were compared with matched low-risk individuals (normotensive with no plaque, n = 15), the high-risk men had significantly enhanced antibody titers to HSP65 (P = .041). In conclusion, we demonstrate that serum antibody titers to HSP65 are enhanced in individuals with borderline hypertension, which may indicate an ongoing immune reaction in the artery wall.
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PMID:Association of serum antibodies to heat-shock protein 65 with borderline hypertension. 903 77

This article describes the objectives and protocol of the HAROLD study, a trial designed to assess whether home blood pressure (BP), 24-hour ambulatory BP, left ventricular structure and function, and albumin excretion rate are more accurate predictors of outcome than traditional sphygmomanometric BP in elderly subjects with borderline hypertension. Development of sustained hypertension (BP > or = 160/95 mmHg) and incidence of morbid events over a 5-year follow-up are considered soft and hard endpoints, respectively. Patients with blood pressure values between 140/90 and 159/94 mmHg after three months of observation and who have never been treated, are eligible for the study; these subjects must be 60 to 79 years old, and free from other important risk factors for atherosclerosis. Baseline exams, which include plasma renin and insulin, 24-hour urine collection for detection of microalbuminuria, and echo-doppler cardiac examination are repeated after three and five years follow-up, or when subjects develop sustained hypertension. To recruit a large enough number of subjects to allow a sufficient number of endpoints (over 1000 subjects), the study is conducted as a multicenter trial. Ninety Italian Hospital Centers have agreed to participate in the study.
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PMID:Optimizing the assessment of the elderly patient with borderline hypertension: the Hypertension and Ambulatory Recording in the OLD (HAROLD) study. 945 97

-Elevated antibody levels to oxidized low-density lipoprotein (aOxLDL) have been shown to correlate with the degree of atherosclerosis in some studies. On the other hand, immunization of experimental animals with OxLDL, leading to enhanced aOxLDL levels, inhibits the development of the disease. The role of antibodies to OxLDL during different stages of disease development is thus not clear. The objective of this study was to determine the level of aOxLDL in early cardiovascular disease, such as borderline hypertension (BHT). Seventy-three men with BHT were matched with 75 age-matched normotensive (NT) men (diastolic blood pressures, 85 to 94 and <80 mm Hg, respectively). Antibody levels to epitopes of OxLDL were determined by use of conventional and chemiluminescence ELISA techniques. Presence of carotid atherosclerosis was determined by B-mode ultrasonography; atherosclerotic plaques were detected in 29 individuals. BHT men had significantly lower aOxLDL levels of IgG class (P=0.001) and IgM class (P=0.001) than NT controls, as determined using chemiluminescence ELISA. Similar results were obtained using conventional ELISA, with which aOxLDL of IgG (P=0. 0002) and IgM (P=0.026) classes and antibody levels to malondialdehyde-LDL were significantly lower in BHT individuals. There was no difference in antibody levels between individuals with or without carotid atherosclerosis. It is not clear whether the decreased aOxLDL levels in BHT are due to a decreased immune reaction to OxLDL or to an increased consumption of aOxLDL due to binding to early atherosclerotic lesions. The possible implications of these findings are discussed.
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PMID:Autoantibodies to OxLDL are decreased in individuals with borderline hypertension. 993 Oct 81


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