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

The pharmacological class of calcium channel antagonists (CCA) is, with beta-adrenergic antagonists, diuretics, converting enzyme inhibitors and alpha-adrenergic antagonists, one of the first line monotherapies of essential hypertension, according to the recommendations of the "Fifth Joint National Committee on Detection, Evaluation and Treatment of Hypertension". CCA have several advantages for the treatment of hypertension: the blood pressure lowering effect is due to a reduction of total peripheral vascular resistance, which are primarily abnormally increased in hypertension; the antihypertensive efficacy of CCA is comparable to that of other commonly used antihypertensive drugs; CCA induce a significant regression of left ventricular hypertrophy, a factor of morbidity and mortality which is considered to be independent of the level of mean arterial pressure; CCA have vasodilating properties on the coronary circulation; CCA are generally well tolerated, from both clinical and biological points of view. The challenge for CCA concerns three domains related to the morbidity/mortality of hypertension (coronary and cerebrovascular events) a better antihypertensive efficacy for the whole period of 24 hours, a better prevention of cerebrovascular events and an effect on the development of atherosclerosis.
 ...
PMID:[Calcium antagonists and arterial hypertension]. 809 51

Coronary calcific deposits are always associated with coronary atherosclerosis. Sensitive radiographic technology can detect coronary calcium before atherosclerosis becomes symptomatic. A total of 1461 asymptomatic high-risk adult subjects were studied with digital subtraction fluoroscopy to detect coronary calcium. Risk factor data were recorded including age, sex, family history, smoking history, diabetes history, body mass index, systolic blood pressure, left ventricular hypertrophy on ECG, total serum cholesterol level, high-density lipoprotein (HDL) cholesterol, and total cholesterol/HDL ratio. Digital subtraction fluoroscopy in the left anterior oblique projection was performed in all subjects. The prevalence of calcific deposits in at least one major coronary artery was high (58.3%). Eleven percent had coronary calcium in all three major arteries. Multivariate logistic regression analysis showed significant correlations (p < 0.05) between the prevalence of coronary calcium and age, smoking history (relative risk = 1.30), diabetes history (relative risk = 1.24), and family history (relative risk = 1.26). In older subjects (at least 65 years of age), smoking and serum lipoproteins assumed greater importance as contributors to coronary calcium, whereas in younger subjects a history of diabetes was more significant. Coronary calcific deposits are prevalent in high-risk asymptomatic subjects. Their occurrence is closely related to most known risk factors.
 ...
PMID:Prevalence of fluoroscopic coronary calcific deposits in high-risk asymptomatic persons. 819 79

The clinical coincidence of hypertension, obesity and non insulin diabetes mellitus (NIDDM) has long been recognized. Increasing interest has also been recently focused on the possible role of insulin and insulin resistance in mediating this association. There is also evidence that hyperglycemia per se may have a role in the pathogenesis of hypertension and atherosclerosis in NIDDM patients. Glucose is a determinant to cellular ion homeostasis, promoting an increase of intracellular calcium and suppressing intracellular free magnesium and pH. Moreover, hyperglycemia promotes glycosilation of proteins and the consequent accumulation of advanced glycosilation end products in tissues. It has recently been suggested that iter is a cellular ionic basis for the clinical and epidemiological linkage of hypertension, left ventricular hypertrophy (LVH), obesity and non insulin dependent diabetes mellitus (NIDDM). These clinical conditions may be different expressions of a common underlying defect in ion handling, displayed by elevated cytosolic free calcium and suppressed free magnesium levels. Therapeutically, reversal of this excess free calcium accumulation and/or free magnesium deficit with ion specific agents, such as calcium channel blocker drugs, may thus ameliorate not only the elevated blood pressure of hypertension but also the concurrent cardiac, vascular and metabolic aspects of the hypertensive states.
 ...
PMID:Diabetes, hypertension and atherosclerosis: pathophysiological role of intracellular ions. 820 15

Hypertension has two main effects on the heart; it increases afterload, causing left ventricular hypertrophy, and precipitates the risk factor for coronary atherosclerosis. Left ventricular hypertrophy is an independent risk factor, but hypertension is a clustering of cardiovascular risks with many metabolic abnormalities, one of which is the recently described endocrinological Syndrome X (hyperinsulinaemia, resistance to insulin-stimulated glucose uptake, glucose intolerance, high triglyceride levels, low HDL and hypertension, which is apparently unrelated to the cardiological Syndrome X (angina with normal coronary arteries). However, the link between both Syndromes X may be the derangement of microvasculture, particularly endothelial dysfunction of nitric oxide (NO) production.
 ...
PMID:Global and regional ischaemia in left ventricular hypertrophy reactive to hypertension. 828 58

Antihypertensive treatment in the diabetic patient is a critical issue because hypertension has an impact on all of the vascular complications of diabetes, including nephropathy, retinopathy, atherosclerosis, and left ventricular hypertrophy. These complications are a consequence of altered endothelial-vascular smooth muscle interrelations that ultimately enhance vasoconstriction and alter the remodeling processes in the vascular wall. Several observations suggest that the renin-angiotensin system (RAS) may be an important contributor to these processes in diabetes mellitus. In both animal and human studies, angiotensin-converting enzyme (ACE) inhibitors have been demonstrated to slow the progression of glomerulosclerosis, prevent abnormal remodeling processes in the heart following injury, and slow the progression of atherosclerosis. In particular, ACE inhibitors appear to protect the kidney more than would be expected from simply the lowering of blood pressure and decreasing of intraglomerular pressure, possibly because angiotensin II has both hemodynamic and direct effects on the glomerulus. Paradoxically, however, the activity of the circulating RAS is low in diabetic patients. Part of these seemingly inconsistent observations may be due to (1) potential activity of tissue RASs, (2) increased sensitivity to angiotensin II in diabetes, or (3) an effect of ACE inhibition on other systems in addition to the RAS. Investigation of these mechanisms will be important in determining the therapeutic role of inhibition of the RAS in diabetes mellitus.
 ...
PMID:Systemic hypertension and the renin-angiotensin system in diabetic vascular complications. 828 77

Thirty essential hypertensive subjects had their BP measured by 24h ambulatory monitoring before (first placebo period) and after exposure to antihypertensive therapy with either enalapril (four weeks) or nitrendipine (six weeks). Similar measures of BP were obtained during a second placebo period intercalated between the two active drugs. The 24h averages of systolic and diastolic pressures were higher during placebo (148 +/- 3/91 +/- 1 mmHg, respectively) than during treatment periods. Four weeks of treatment with enalapril reduced arterial pressure to a 24h average of 137 +/- 1/86 +/- 1 mmHg while nitrendipine given for six weeks lowered BP to an average of 135 +/- 1/84 +/- 1 mmHg. The antihypertensive effect of the drugs was of a comparable magnitude (P > 0.05). In addition both drugs produced analogous reductions in BP during the day (07.00 to 23.00 h). In contrast, the nocturnal fall in BP was significantly greater during treatment with nitrendipine. Average systolic and diastolic pressures between 23.00 h and 07.00 h were 133 +/- 1 mmHg and 82 +/- 2 mmHg with enalapril compared with 129 +/- 3 mmHg (P < 0.01) and 77 +/- 3 mmHg (P < 0.01) with nitrendipine, respectively. These data suggest that antihypertensive agents show important differences in terms of their action on the mechanisms that regulate BP during sleep. Medications that amplify the otherwise physiological fall in BP during sleep may add risk to patients with impaired coronary vasodilator reserve owing to ventricular hypertrophy, coronary atherosclerosis, or both.
 ...
PMID:Nocturnal hypotension and ACE inhibitors. 834 98

The effects of age, atherosclerosis, hypertension, and hypercholesterolemia on vascular function of the coronary circulation were studied by subselective intracoronary infusions of acetylcholine, which releases endothelium-derived relaxing factor, and papaverine, which directly relaxes vascular smooth muscle, in normal patients (n = 18; no risk factors for coronary artery disease), in patients with evidence of early atherosclerosis but normal cholesterol levels and normal blood pressure (n = 12), in patients with hypertension without left ventricular hypertrophy (n = 12), and in patients with hypercholesterolemia (n = 20). Papaverine-induced maximal increases in coronary blood flow were significantly greater in normals, but no differences were noted between the groups of patients with early atherosclerosis, with hypertension, and with hypercholesterolemia. The capacity of the coronary system to increase blood flow in response to acetylcholine was similar in normal and normocholesterolemic patients with epicardial atherosclerosis and/or hypertension but was significantly impaired in patients with hypercholesterolemia, irrespective of evidence of epicardial atherosclerotic lesions. Age (r = -0.62, P < 0.0001) and total serum cholesterol levels (r = -0.70; P < 0.0001) were the only significant independent predictors of a blunted coronary blood flow response to acetylcholine. Thus, hypercholesterolemia and advanced age selectively impair endothelium-mediated relaxation of the coronary microvasculature in response to acetylcholine, whereas endothelial dysfunction is restricted to epicardial arteries in age-matched normocholesterolemic patients with evidence of coronary atherosclerosis and/or hypertension.
 ...
PMID:Endothelium-mediated coronary blood flow modulation in humans. Effects of age, atherosclerosis, hypercholesterolemia, and hypertension. 834 4

To study the clinical picture of coronary heart disease with concomitant arterial hypertension of various genesis, 172 patients were examined, out of them the cause of arterial hypertension was hypertensive disease in 54, chronic pyelonephritis in 40, chronic glomerulonephritis in 37, and stenotic atherosclerosis of renal arteries in 29, endocrine disease in 12 patients. The patients were divided into 2 groups: (1) 148 with stenotic atherosclerosis of coronary arteries and (2) 24 patients with intact coronary arteries. Comparison of these patient groups revealed no clear-cut correlation between the age and the detection of exercise-induced angina, as well as the duration of arterial hypertension. There was no correlation between the detection of the anginal syndrome and ECG changes. The incidence of the anginal syndrome was 62.2% in Group 1 and 47.7% in Group 2. It was established that the detection of the anginal syndrome correlated well with the severity of left ventricular hypertrophy and values of blood pressure, despite nosological entities.
 ...
PMID:[The clinical characteristics of ischemic heart disease in patients with arterial hypertension of different origins]. 837 62

While the circulating renin-angiotensin system (RAS) plays an important role in short-term maintenance of cardiovascular homeostasis, recent studies point to a role in long-term cardiovascular regulation for endogenous RAS in target tissues. This article focuses on the multiple effects of tissue angiotensin enzyme (ACE) and angiotensin II (Ang II), its active peptide product. Ang II has been shown to be a potent growth factor in vascular smooth muscle cells. Depending on the local conditions, the vascular response may be either hypertrophy or hyperplasia. The molecular mechanisms involved in the interactions of Ang II with endothelium- and smooth muscle-derived cell products may play important roles in the modulation of vascular structure in hypertension and vascular injury. Evidence also points to a role for Ang II in the development of left ventricular hypertrophy in hypertension. In addition, cardiac RAS may contribute to the pathophysiology of heart failure. Experimental and clinical studies with ACE inhibitors point to a role for tissue ACE activity in the development of atherosclerosis, as well as cardiac hypertrophy and remodeling.
 ...
PMID:Local expression and pathophysiological role of renin-angiotensin in the blood vessels and heart. 839 69

Conventional risk factors (especially high arterial pressure, elevated cholesterol and glucose levels, and cigarette smoking) are useful predictors of morbid atherosclerotic and hypertensive events, and their control variably reduces the incidence of events. However, both the ability to predict risk and the ability to reduce it by modification of established risk factors are limited. These limitations occur in part because the progression from risk factor exposure to morbid events depends on the variable likelihood that individuals exposed to the same risk factors will progress through two stages: the development of asymptomatic or "preclinical" anatomic and functional cardiovascular disease in response to standard risk factors and other variables, and the precipitation of morbid events by progression of preclinical disease or by the action of additional "triggering" mechanisms in the presence of preclinical disease. Advances in diagnostic methodology now make possible accurate noninvasive detection in many asymptomatic individuals of preclinical disease such as left ventricular hypertrophy, carotid atherosclerosis, and renal dysfunction. Progress in elucidating stimuli to left ventricular hypertrophy and systemic atherosclerosis suggests that focusing research separately on these two stages of disease evolution is a fruitful strategy. The closer relation of measures of preclinical disease than risk factors with the subsequent risk of complications indicates that their detection improves clinical risk stratification. However, critical testing of whether clinical outcome is improved or treatment cost is lowered by basing antihypertensive or antihyperlipidemic treatment decisions in part on the presence of preclinical cardiovascular disease is needed before this strategy is adopted on a widespread scale.
 ...
PMID:Role of preclinical cardiovascular disease in the evolution from risk factor exposure to development of morbid events. 840 91


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>