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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of hypertension on the heart include the development of left ventricular hypertrophy, impairment of left ventricular function leading to heart failure and accelerated coronary atherosclerosis leading to ischemic heart disease. The precise role of hypertension in precipitating these cardiac events is poorly understood, and the effect of antihypertensive drugs in preventing or reversing these abnormalities is surprisingly unclear. Current understanding of the pathophysiology and therapeutic responses of these cardiac manifestations of hypertension will be examined.
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PMID:Role of drugs for systemic hypertension and their effect on the heart. 296 Feb 28

Cardiac transplantation is frequently associated with accelerated coronary atherosclerosis and immune-mediated microvascular injury. To determine if orthotopic cardiac transplantation impairs the capacity of the coronary vasculature to vasodilate and conduct hyperemic blood flow, maximal coronary vasodilator reserve was measured in 25 cardiac allograft recipients with no evidence of rejection 6-57 months after transplantation and in 20 normal subjects. Left ventricular wall thickness was assessed echocardiographically, and epicardial coronary anatomy was evaluated by quantitative coronary angiography. Coronary vasodilator reserve (CVDR) was measured in all patients with a coronary Doppler catheter and a maximally vasodilating dose of intracoronary papaverine. CVDR measured in the transplant recipients with normal coronary arteries, left ventricular function, and wall thickness (5.0 +/- 0.3 [mean +/- SEM] peak/resting velocity; range, 3.8-7.3; n = 16) was not different from that of normal subjects (4.8 +/- 0.2; range, 3.7-8.3). CVDR in the five cardiac allograft recipients with diffuse coronary atherosclerosis producing 30 +/- 5% narrowing (range, 25-38%) of epicardial vessel diameter also was normal (5.1 +/- 0.3; range, 4.3-6.2; n = 5). The CVDR was reduced, however, in two of the four cardiac allograft recipients with left ventricular hypertrophy. In the only transplant recipient in whom a regional wall motion abnormality was present, CVDR was abnormal in the vascular distribution of the hypokinetic wall segment (1.8) but was normal in the artery that supplied normally functioning myocardium (4.0). These findings demonstrate that in the absence of allograft rejection, acquired left ventricular hypertrophy, and regional wall motion abnormalities, coronary vasodilator reserve is normal after orthotopic human cardiac transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary vasodilator reserve after human orthotopic cardiac transplantation. 297 19

New methods of investigation (ECG, echocardiography, angiography, histology) allow a better understanding of the pathophysiology of valvular aortic stenosis (VAS) associated with coronary atherosclerosis. The progressive decrease in valvular aortic area modifies the coronary blood flow and leads to myocardial ventricular hypertrophy. These two mechanisms worsen left ventricular function. A significant atherosclerotic stenosis on a large coronary artery creates a considerable reduction of the available coronary blood flow. This reduction is permanent: present at rest, it is obviously increased during exercise. The study of the relationship between the severity of the VAS and the myocardial hypertrophy (MH) is of great interest. It seems that in VAS with coronary artery disease, different situations exist: (i) when the hypertrophy is severe (left ventricular mass greater than 180 g m-2), the angina pectoris is more attributable to the VAS than to the coronary lesions. Thus the removal of the aortic outflow obstruction is the most essential therapy; (ii) when the hypertrophy is less severe (left ventricular mass less than 180 g m-2), surgical treatment of the valvular lesion and myocardial revascularization are justified.
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PMID:Valvular aortic stenosis and coronary atherosclerosis: pathophysiology and clinical consequences. 304 6

More than half of the United States population over 65 years of age has essential hypertension. In 1984, there were 10 million elderly hypertensive persons and this number will reach 25 million in the near future. These patients are at high risk for congestive heart failure, stroke, heart attack, and dissecting aneurysm. Successful reduction of blood pressure can lower these risks considerably, but rational treatment depends on understanding the complex pathophysiology of hypertension in older patients. In fact, treatment that does not take into account the combined effects of aging and hypertension on the cardiovascular system and the kidneys may do more harm than the hypertension itself. Among the prominent age-related cardiovascular changes are stiffening of the arterial tree, with or without a contribution from atherosclerosis. This reduces arterial compliance and increases afterload, resulting in the left-ventricular hypertrophy seen in old age and leading to a progressive rise in systolic pressure. There is considerable shrinkage of the kidneys, due primarily to loss of glomerular and tubular tissue in the cortex, along with sclerosis of the glomeruli and formation of tubular diverticula. Arteriolar changes lead to reduced renal blood flow, the shunting of blood around the glomeruli, and thus a reduction in glomerular filtration rate. Renal water and electrolyte excretion are changed, making homeostasis more difficult to maintain, and the renin-angiotensin system is altered, helping to blunt the kidneys' response to pressure changes. Essential hypertension superimposed on all the foregoing effects exacerbates them. Peripheral resistance is usually markedly elevated in older hypertensive persons, which increases afterload directly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology of hypertension in older patients. 304 95

Current theory suggests that life began in a prebiologic era, progressed to a ribonucleic-deoxyribonucleic cellular era, and finally entered an era characterized by multicellular organisms. If this progression is correct, it is not surprising that, as medicine studies living organisms with increasing sophistication, factors that are initially discovered to have systemic effects are, in many instances, later determined to have paracrine, autocrine or even intracellular ("intracrine") effects. This schema is potentially of value in analyzing the pathogenesis of cardiovascular disease and, in particular, the development of the sequelae of hypertension. A case is made for the idea that the actions of common peptide and nonpeptide factors at local tissue levels can play an important role in the development of atherosclerosis and left ventricular hypertrophy. In making this case, the potential roles of insulin, angiotensin II and other vasoactive factors are considered. In addition, it is argued that some peptide and nonpeptide factors with cardiovascular impact may operate in the intracellular environment, thus broadening prospects for study and intervention. Finally, genomic alterations either spontaneously occurring or resulting from chronic stimulation or viral infection are considered and their potential role is discussed.
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PMID:Emerging issues in the cellular biology of the cardiovascular system. 305 99

Arterial hypertension (AH) is an excessive elevation of the arterial blood pressure (ABP) in the systemic circulation. It is, however, arbitrary to define a limit between normal and pathological ABP, since the ABP varies in a continuous fashion with the population. Occasional measurement of the blood pressure by sphygmomanometer is rather inaccurate but still remains the method of reference. A more precise determination of the ABP is possible by using the stress blood pressure profile and ambulatory measurement which are prognostically far superior to occasional measurement. AH is not a disease but a risk factor--quantitative and independent of the cardio-vascular system because it contributes to atherosclerosis and regional ischemic processes. The genesis of the so called essential AH still remains unclear, but it is getting better known: from a genetic factor of predisposition, the respective roles of the salt and the kidney as a filter are determining, along with the more or less appropriate action of hormonal factors of the sodium excretion. This is combined with the complex and synergistic action of potent vasopressor mechanisms such as the sympathetic nervous system and the renin-angiotensin systems--circulating as well as in the tissues. AH presents haemodynamic abnormalities, which vary according to age, and among which the elevation of systemic vascular resistances is most characteristic. This is combined with a lack of compliance of the large arterial vessels, and secondarily, a hypertrophy, partially adaptive, of the entire cardiovascular system. This includes left ventricular hypertrophy which has harmful effects on intracardiac and coronary haemodynamics, resulting in an increased mortality. It is therefore necessary that the treatment, not only decrease the blood pressure, but also take into account the regional vascular outputs while respecting and improving the renal, cerebral and coronary circulations with general improvement of the vascular compliance. The treatment must also result in an early and lasting decrease of the myocardial hypertrophy. This is why the new anti-hypertensive treatments (conversion enzyme inhibitors and calcium inhibitors) represent a desirable therapeutic alternative to the classical treatment. Their prescription follows a few general rules, but must, however, remain very personalized with evaluation of the results at two levels: individual control of the ABP and mass benefit in terms of decreased cardiovascular morbidity and mortality.
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PMID:[Essential arterial hypertension. From notion to treatment]. 306 94

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

The effect of hypertension, hyperlipidemia, and the combination of both on acute and chronic myocardial ischemia were evaluated in a total of 30 male rabbits. After preliminary hypertension and/or hyperlipidemic load by loading of the abdominal aorta and/or cholesterol feeding, acute ischemia was produced by clipping of the left coronary artery. The banding produced elevation of carotid arterial pressure and left ventricular hypertrophy. Cholesterol feeding resulted in severe atheromatous changes in all sizes of coronary arteries. The intimal thickening was due to foam cell accumulation in all arteries examined. Animals pretreated with the combination of hypertension and hyperlipidemia displayed the most severe cardiolmegaly with advanced coronary atherosclerosis and chronic ischemic lesions of the myocardium, i.e., perivascular patchy fibrosis in the subendocardial area. Furthermore, electron microscopic detection of ultrastructural myocardial damage, involving glycogen depletion, sarcoplasmic edema, mitochondrial swelling, and contractile abnormalities, was also most frequent in this group. These changes were quantitated using the ischemic score. These results confirm the hypothesis that fatal ischemic injuries may occur clinically in human hearts with coronary insufficiency due to coexistence of hypertensive cardiomegaly and severe coronary atherosclerosis. They offer a model for further study of these combined effects.
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PMID:An ultrastructural study on ischemic lesions in rabbits' hearts with pressure overload and hyperlipidemia. 315 60

Copper deficiency has been shown to result in severe cardiovascular lesions in several species of animals. The principal carbohydrate in the copper-deficient diet most often used with rats is sucrose, which is known to have adverse effects on carbohydrate and lipid metabolism and thus may contribute to cardiovascular disorders. These observations prompted experiments in which starch and fructose were substituted for sucrose in a copper-deficient diet, to see if the effects of the copper deficiency might be modified. In the hearts from rats fed copper-deficient diets with fructose or sucrose, there was marked, mostly ventricular hypertrophy, and mild to severe myocardial inflammation, degeneration, and fibrosis. Aneurysm of the left ventricle and pericarditis also were common. Hearts from the starch, copper-deficient groups were much less hypertrophic, and very few were affected by myocardial inflammation, degeneration, or fibrosis. Defects of elastin or other structures were not observed in the aortas or pulmonary or coronary arteries of any specimens.
Atherosclerosis 1988 Dec
PMID:Dietary fructose exacerbates the cardiac abnormalities of copper deficiency in rats. 324 Mar 32

Ambulatory blood pressure monitoring allows one to evaluate the blood pressure profile over a 24-hr period. It has been demonstrated that an average of daily pressure readings is more predictive of cardiovascular complications of hypertension than casual monitoring of blood pressure. On the other hand, there is no conclusive evidence that the higher degree of blood pressure variability found in hypertensive patients is related to increased hypertensive morbidity. The absence of a physiological decrease in arterial pressure during sleep is associated with complications of hypertension such as atherosclerosis and left ventricular hypertrophy as well as with impairments of the autonomic nervous system.
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PMID:Diagnostic information provided by ambulatory blood pressure monitoring. 330 98


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