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)

Although indapamide has been used for many years as a first-line treatment of hypertension, it is only recently that some of its activities on the changes of the cardiovascular system, brought on by age and high blood pressure, have been studied. Indapamide appears to reduce blood pressure by a combined diuretic and direct vascular activity reducing vascular reactivity and total peripheral resistance. In addition, it has discrete effects on a number of interrelated systems that may protect the cardiovascular system. Indapamide reduces intracellular calcium levels, maintains magnesium ions, but reduces phosphate ions that may be involved in arterial rigidity. Circulating catecholamines remain unchanged but there is a reduction in normetanephrine, suggesting a reduction in sympathetic tone. It stimulates prostacyclin synthesis, increases levels of circulating prostacyclin, reduces platelet aggregation and stimulates the vasodilation elicited by endothelium-derived relaxing factor in the presence of bradykinin. In addition, it inhibits the formation of the vasoconstrictor prostanoid, thromboxane A2. The free radical scavenging activity of indapamide could also protect the vascular smooth muscle from the reperfusion injury of cerebral and myocardial ischemia. Indapamide induces a reduction in cerebral ischemia after carotid ligation. Unlike some other antihypertensives, it does not upset the high-density/low-density lipoprotein-cholesterol balance, reducing the possible risk of atherosclerosis. Moreover, the combination of binding to elastin and reduction in uptake of calcium and phosphate into the smooth muscle could be a mechanism for reducing arterial rigidity seen in the elderly and hypertensive patient. In hypertensive patients, these properties induce an improvement in arterial compliance, and in the long term a reduction in left ventricular hypertrophy. These pharmacologic and clinical results, together with a good antihypertensive efficacy and acceptability, suggest that indapamide may be a preferential agent in the long-term cardiovascular protection of the hypertensive patient.
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PMID:Cardiovascular protective properties of indapamide. 218 50

Patients with aortic stenosis develop widely variable patterns of left ventricular hypertrophy and dysfunction. We postulated that coronary atherosclerosis (CAD) may be associated with impaired left ventricular function and chamber dilatation in patients with aortic stenosis. Left ventricular mass and volumes were quantified from two-dimensional echocardiography and correlated with coronary angiography in 78 patients with severe aortic stenosis and no previous myocardial infarction or regional wall motion abnormalities. Eighteen patients (group 1) had smooth coronary arteries, 25 patients had irregular coronary arteries with 50% or less stenosis (group 2), and 35 patients had obstructive CAD (group 3). Even though the calculated valve area was similar in all three study groups, group 1 patients had higher values for ejection fraction (65 +/- 9%, 51 +/- 17%, and 48 +/- 13%; p = 0.0002), systolic mass-to-volume ratio (9.2 +/- 3.9, 5.6 +/- 2.8, and 5.2 +/- 2.2; p = 0.0001), and cardiac index (2.9 +/- 0.7, 2.5 +/- 0.7, and 2.3 +/- 0.6 l/min.min2; p = 0.015) than patients in groups 2 and 3, respectively (mean +/- SD). Mean circumferential wall stress was inversely related to severity of CAD. Multivariate analysis showed that CAD is an independent predictor of ejection fraction and mass-to-volume ratio in this group of patients. Thus, in an elderly population with severe aortic stenosis, patients with both obstructive and nonobstructive CAD have an increased incidence of left ventricular enlargement and systolic dysfunction.
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PMID:Coronary atherosclerosis is associated with left ventricular dysfunction and dilatation in aortic stenosis. 224 30

The relationship between diuretic therapy and possible increased risk of coronary heart disease (CHD), especially sudden death, is controversial. The initial report from the Multiple Risk Factor Intervention Trial (MRFIT) raised the possibility that the increased CHD mortality observed in a subset of special intervention men with hypertension and certain electrocardiographic abnormalities on their baseline examination might be an unexpected adverse effect of diuretic therapy. Subsequent reports from the MRFIT have revealed a stronger association of CHD mortality to hydrochlorothiazide than to chlorthalidone. There was no consistent relationship of CHD mortality to the dose of either drug, to the most recent serum potassium level, or to the presence of ventricular premature beats. Unfavorable trends of the same magnitude were also seen among similar white men in the Hypertension Detection and Follow-up Program and in the Oslo hypertension trial, although the sample sizes in these two studies were too small to yield clearcut conclusions. Clinical studies have shown an increased risk of CHD death among hypertensive men with left ventricular hypertrophy. Such men are also noted to have a higher frequency of ventricular premature beats, even in the absence of diuretic therapy. Other studies have shown that diuretic-induced hypokalemia is accentuated in the presence of epinephrine and that low potassium levels decrease the threshold for ventricular fibrillation. Thus, although the evidence is still incomplete, it is possible that the excess CHD mortality among MRFIT special intervention men with electrocardiographic abnormalities may have been caused by a combination of increased left ventricular mass in the presence of coronary atherosclerosis, and hypokalemia caused by good compliance with diuretic therapy and accentuated by stress-induced increases in circulating catecholamines. Given the very large population of patients receiving diuretic therapy, further evaluation of this possibility is important.
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PMID:Unexpected effects of treating hypertension in men with electrocardiographic abnormalities: a critical analysis. 241 86

Hypertension increases cardiovascular morbidity and mortality two- to fourfold. The chief hazards are now atherosclerosis and coronary disease. Risk is proportional to the degree of systolic or diastolic blood pressure elevation at any age, in either sex. More than the character of blood pressure elevation, commonly associated risk factors markedly influence the hazard. The risk of coronary heart disease is concentrated in hypertensive patients with a high total/high-density lipoprotein (HDL)-cholesterol ratio, impaired glucose tolerance, high fibrinogen, electrocardiographic (ECG) abnormalities, and who are cigarette smokers. Evidence of organ involvement such as left ventricular function are hallmarks of impending cardiovascular sequelae. Electrocardiogram-left ventricular hypertrophy (ECG-LVH) behaves like myocardial infarction in its clinical course, predisposing at the same rate to sudden death, infarction, cardiac failure, and stroke. Consideration of cardiovascular risk factors is required to evaluate properly the need for treatment, select the best treatment, set goals, and determine the efficacy of treatment. Awaiting evidence of organ involvement is dangerous since the first such evidence is often a sudden death, stroke, or myocardial infarction. Optimal treatment must improve the composite risk profile as well as lower the blood pressure.
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PMID:Risk factors in hypertension. 246 76

The manifestations of cardiac involvement in hypertension include: (1) the development of hypertensive heart disease characterized by left ventricular hypertrophy (LVH), and (2) the consequences of coronary atherosclerosis, as angina pectoris, myocardial infarction, and sudden cardiac death. Whereas the former is directly related to increased blood pressure, the latter are sequelae of atherosclerosis per se, and hypertension acts only as a risk factor in this regard. This can partially explain why antihypertensive treatment is effective in diminishing the incidence of congestive heart failure, which is the final consequence of LVH, but is not very effective in preventing coronary complications. It is generally accepted about LVH that increased arterial pressure is the major stimulus to cardiac hypertrophy in hypertension; however, there are a lot of both quantitative and qualitative events suggesting that other factors beside blood pressure levels can modulate the development of LVH, in particular neurohumoral influences. From a morphological point of view, hypertrophy of the cardiac muscle is defined as an increase in the size of existing myocardial fibers. In most experimental models, myocardial hypertrophy is associated with myosin isoenzymatic changes, consisting in a shift from the faster migrating isoenzyme V1 to V3, a form that migrates more slowly. However these changes do not occur in all animal species and particularly in humans. In the hypertrophied human ventricle, a decreased ATPase activity of myofibrils was observed, probably related to changes in myosin light chains. Presently the changes in ATPase activity and in ventricular contractility do not still have a clear molecular basis in humans.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heart and hypertension. 252 4

The main goal in treating hypertensive patients is to reduce the incidence of complications, especially on the heart. The lowering of blood pressure do not seem enough. Some properties, not shared by all antihypertensive drugs, are likely to allow some protection against heart and coronary diseases. These properties are: the absence of deleterious effects on glucids, lipids and kaliemia; the ability to induce left ventricular hypertrophy regression, antiarrhythmics effects, anti-ischemic effects and the ability to improve arterial compliance. Calcium inhibitors share all these properties and also have some more original and beneficial effects on arterial spasm and may be on progression of atherosclerosis. For all these reasons, a great interest arise for this new therapeutic class in hypertension. However we are still waiting for the demonstration of a true cardiac protection in hypertension with controlled long term trials.
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PMID:[Calcium inhibitors and cardioprotection]. 252 38

Hypertension increases cardiovascular morbidity and mortality two to four-fold. The chief hazards are now atherosclerosis and coronary disease. The risk is proportional to the degree of systolic or diastolic blood pressure elevation at any age, in either sex. More than the character of the blood pressure elevation, commonly associated risk factors markedly influence the hazard. The risk of coronary heart disease is concentrated in hypertensives with a high total/high density lipoprotein (HDL) cholesterol ratio, impaired glucose tolerance, high fibrinogen, those with ECG abnormalities and cigarette smokers. Evidence of organ involvement such as left ventricular hypertrophy, proteinuria or impaired left ventricular function are hallmarks of impending cardiovascular sequelae. The presence of ECG-LVH behaves like myocardial infarction in its clinical course, predisposing at the same rate to sudden death, myocardial infarction, cardiac failure and stroke. Consideration of all cardiovascular risk factors is required to evaluate properly the need for treatment, select the best treatment, and set goals and determine the efficacy of treatment. Waiting until there is evidence of organ involvement is dangerous since the first such evidence is often sudden death, a stroke or a myocardial infarction. Optimal treatment must improve the composite risk profile as well as lower the blood pressure. This can be achieved by hygienic (dietary) measures or pharmacological therapy in those who do not respond to diet alteration, weight control and exercise.
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PMID:An integrated view of hypertension. 260 26

Drug treatment of hypertension reduces morbidity and mortality most effectively in moderate to severe cases. However, most patients have only mild hypertension, for which traditional drug treatment is not consistently successful. Angiotensin converting enzyme (ACE) inhibitors provide superior control of mild hypertension. They have a haemodynamically favourable mechanism of action, are well tolerated and can produce a predictable response within a narrow and convenient dose range. Further, ACE inhibitors are lipidneutral, and they positively affect some of the mechanisms conducive to the development of atherosclerosis. Further research in this area is warranted. The ACE inhibitors may also help prevent end-organ damage in hypertensive patients who also have diabetes, kidney disease, left ventricular hypertrophy or a combination of these disorders. The case for renoprotection in diabetic hypertensives is strong enough to recommend preferential use of ACE inhibitors for these patients. The positive effects shown in left ventricular hypertrophy may also be produced by other modern antihypertensive agents, while the advantages of ACE inhibitors in essential hypertension with renal damage remain largely conjectural. There have been encouraging clinical results, but ongoing larger trials may provide a more definitive answer.
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PMID:Angiotensin converting enzyme inhibitors and the progress of antihypertensive therapy. 268 2

The calcium antagonists, although initially restricted to the treatment of angina pectoris, are now finding widespread application as safe and effective therapy for hypertension. These drugs reduce systemic vascular resistance and thus address the usual primary physiologic defect in high blood pressure. Reduction of blood pressure with these agents appears to lead to the concomitant reduction of hypertension-induced ventricular hypertrophy and improvement of ventricular function. Unlike other vasodilators, calcium antagonists do not secondarily lead to sodium retention or stimulation of the renin-angiotensin-aldosterone and sympathoadrenal systems. They are effective in the treatment of angina pectoris and may inhibit the onset or progression of atherosclerosis. As calcium antagonists primarily block voltage-operated, as opposed to receptor-operated, sarcolemmal calcium channels, they may be rationally and effectively combined with agents such as converting enzyme inhibitors and adrenergic antagonists. Calcium antagonists have important interactions with drugs relevant to the treatment of cardiac disease. The combination of verapamil and beta blockers or disopyramide and diltiazem with amiodarone should be avoided; caution is advised in the concomitant use of calcium antagonists and digoxin or the major antiarrhythmic agents.
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PMID:The actions and role of calcium entry blockers in hypertension: cardiac considerations. 268 25

The prevalence of microscopic atheroma in the proximal left anterior descending coronary artery was studied in thirty young males aged 20 to 29 years, living in Mexico City, who died in urban accidents. All of them were either unemployed or labor workers with a socioeconomical status considered to be representative of the majority of young males living in Mexico City. It was found that coronary atheroma was present in 11 of them (33%) with variable degrees of luminal obstruction. In two of them the luminal obstruction was greater than 75%. The prevalence found in this group was significantly different to that found in younger and older males who also died in accidents. Since the prevalence of coronary atheroma was not related to ventricular hypertrophy, valvular or congenital heart disease our findings indicate that in Mexico City as in other geographical regions, coronary atherosclerosis is not an unusual finding in males in the third decade of life, with a low socioeconomical status.
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PMID:[Prevalence of microscopic coronary atheroma in young adults from Mexico City]. 293 72


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