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

The Joint National Committee Reports IV (1988) and V (1992) have emphasized individualization of drug therapy for patients with hypertension-a departure from the "stepped" care approach of initiating therapy with diuretics as advocated by the JNC I-III in the 1970's and 1980's. This review highlights individualization or "patient profiling" using calcium channel blockers as first-line treatment strategy for patients with primary hypertension--especially in the patient who has attendant risk factors and sequelae. The calcium channel antagonists, especially effective in elderly and Black patients, have proven efficacy in reducing left ventricular hypertrophy and improving diastolic function in patients with hypertensive heart disease. The heart rate limiting calcium antagonist, verapamil, has been found effective in outcome trials of reducing death and reinfarction rates post myocardial infarction and is an alternative therapy for the beta blocker intolerant hypertensive post myocardial infarction. More vascular specific dihydropyridines (felodipine, isradipine, and amlodipine) may be preferable to rate limiting agents in hypertensives with sinus node or AV conduction disorders and in those with impaired left ventricular systolic function. Verapamil and diltiazem have been effective in preliminary trials in reducing proteinuria and preserving renal function in both diabetic and non diabetic hypertensives. Calcium channel antagonists appear to prevent the progress of atherosclerosis independent of their antihypertensive properties. Further, they have theoretic value in improving endothelial mediated vasodilation.
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PMID:Individualization of therapy for hypertension in the 1990's: the role of calcium antagonists. 785 64

Oxidative modification of low-density lipoprotein (LDL) cholesterol may contribute to atherosclerosis by several mechanisms demonstrated in vitro. Antioxidants have been shown to inhibit this process in vitro, and there is evidence from animal studies that they protect against atherosclerosis in vivo. The results of human studies examining the association between antioxidants and cardiovascular disease (coronary heart disease, hypertensive heart disease, and stroke) have been equivocal, although evidence is accumulating that suggests a beneficial effect. Recently, monounsaturated fatty acids incorporated into LDL have been shown to be resistant to oxidation in vitro, compared to polyunsaturated fatty acids. Results from short-term clinical studies are consistent with this finding, as are some epidemiologic data, which suggest that diets containing monounsaturated fatty acids are associated with decreased mortality from cardiovascular disease. The overall roles of antioxidants and particular fatty acids in preventing atherosclerosis require further elucidation.
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PMID:Antioxidant status, fatty acids, and cardiovascular disease. 802 72

In this report, some of the underlying pathophysiological alterations associated with the independent risk from hypertensive heart disease and left ventricular hypertrophy are discussed. Emphasized are the classically described coronary hemodynamic alterations of decreased coronary blood flow and flow reserve with increased coronary vascular resistance and minimal coronary resistance; more recent concepts of endothelial dysfunction are emphasized. Additionally, increased collagen deposition within the ventricular walls and perivascularly participates importantly. These changes are exacerbated by the aging process and perhaps by increased dietary salt intake. Consequences of these functional and structural changes include further endothelial dysfunction, impairment of coronary hemodynamics, and ventricular contractile function (diastolic as well as systolic). The clinical consequences of these alterations are angina pectoris (with or without atherosclerosis), myocardial infarction, cardiac failure, lethal dysrhythmias, and sudden cardiac death. Thus, not all that is clinically recognized as "left ventricular hypertrophy" is true myocytic hypertrophy with structural remodeling; other important comorbid changes occur that directly affect risk, including ventricular fibrosis, impaired coronary hemodynamics, and endothelial dysfunction.
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PMID:State of the Art lecture. Risk mechanisms in hypertensive heart disease. 1052 61

Acute myocardial ischemia, which results from a significant imbalance between myocardial oxygen demands and myocardial oxygen supply, occurs in as many as six million persons with atherosclerotic coronary artery disease in the United States. Accordingly, a clear understanding of the physiologic and pathophysiologic factors that influence coronary artery blood flow is important to the clinician and provides the basis for the judicious use of medications for the treatment of patients with atherosclerotic coronary artery disease. This review discusses the endothelial, metabolic, myogenic, and neurohumoral mechanisms of coronary blood flow regulation and the interaction of the different mechanisms in the regulation of coronary blood flow. The importance of nitric oxide in coronary blood flow regulation is emphasized. We also discuss the common clinical problems of hyperlipidemia and coronary atherosclerosis, coronary artery spasm, and systemic arterial hypertension that result in coronary artery endothelial dysfunction, the impaired production and increased inactivation of nitric oxide, and impairment in coronary blood flow regulation. This information is important to clinicians because more than forty million people in the United States have atherosclerotic or hypertensive heart disease and therefore are at risk for significant myocardial complications due to impairment of coronary blood flow regulation.
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PMID:Coronary artery blood flow: physiologic and pathophysiologic regulation. 1062 79

Mechanisms underlying risk associated with hypertensive heart disease (HHD) and left ventricular hypertrophy (LVH) are discussed in this report and provide a rationale for understanding this very common and important cause of death from hypertension and its complications. Emphasized are impaired coronary hemodynamics, endothelial dysfunction, and ventricular fibrosis from increased collagen deposition intramurally and perivascularly. Each is exacerbated by aging and, perhaps, also by increased dietary salt intake. These functional and structural changes promote further endothelial dysfunction, altered coronary hemodynamics, and diastolic as well as systolic ventricular contractile function in HHD. The clinical endpoints of HHD include angina pectoris (with or without atherosclerosis of the epicardial coronary arteries), myocardial infarction, cardiac failure, lethal dysrhythmias, and sudden death. The major concept to be derived from these alterations is that not all that is clinically recognized as LVH is true myocytic hypertrophy and structural remodeling. Other major co-morbid changes occur that serve to increase cardiovascular risk including impaired coronary hemodynamics, endothelial dysfunction, and ventricular fibrosis.
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PMID:Ischemia and fibrosis: the risk mechanisms of hypertensive heart disease. 1082 97

The increased cardiovascular morbidity and mortality in hypertension are related to the target organs (ie, heart, brain, kidneys) involvement from vascular disease. Left ventricular hypertrophy (LVH), the major expression of cardiac involvement, is both a structural and functional adaptation to the afterload imposed by the vascular disease. Without this adaptation, cardiac failure would result much earlier in the natural history of hypertensive heart disease (HHD). However, LVH imposes an independent risk that is even greater than the risk associated with the height of systolic or diastolic pressure. The mechanisms that explain this risk have not been defined precisely; several have been postulated. Among these are the following: 1) coronary hemodynamic alterations associated with HHD (ie, increased coronary vascular and minimal vascular resistance, reduced coronary blood flow and flow reserve, and increased blood viscosity); 2) enhanced predisposition for lethal cardiac arrhythmias, cardiac failure, and accelerated atherosclerosis of the coronary arteries (with exacerbation of the ischemia); and 3) collagen deposition and ventricular fibrosis. From the earliest controlled therapeutic trials, deaths from stroke and coronary heart disease were significantly reduced. However, more recent data have indicated that the prevalence of cardiac failure (CHF) continues to rise progressively. The nature of the CHF is no longer primarily from systolic dysfunction, but is now chiefly from diastolic dysfunction. Diastolic dysfunction occurs primarily in the elderly hypertensive patient or in the patient with ischemic heart disease, both of which are associated with increased collagen deposition. Indeed, these effects continue to be suggested by the data from the Framingham Heart Study as well as NHANES-III that indicate CHF is the most common diagnosis occurring in hospitalized patients over 65 years of age. In this report, both experimental and clinical evidence demonstrating that increased ventricular fibrosis occurs in the spontaneously hypertensive rats and in hypertensive patients are provided, and that treatment with the newer antihypertensive agents reduce ventricular hydroxyproline (ie, collagen) content while, at the same time, improve coronary hemodynamics.
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PMID:Fibrosis and ischemia: the real risks in hypertensive heart disease. 1141 56

African Americans experience higher morbidity and mortality than Whites do as a result of hypertension and associated cardiovascular disease. Chronic psychosocial stress has been considered an important contributing factor to these high rates. The authors describe the rationale and design for a planned randomized controlled trial comparing Transcendental Meditation, a stress-reduction technique, with lifestyle education in the treatment of hypertension and hypertensive heart disease in urban African Americans. They pretested 170 men and women aged 20 to 70 years over a 3-session baseline period, with posttests at 6 months. Outcomes included clinic and ambulatory blood pressure, quality of life, left ventricular mass measured by M-mode echocardiography, left ventricular diastolic function measured by Doppler, and carotid atherosclerosis measured by beta-mode ultrasound. This trial was designed to evaluate the hypothesis that a selected stress reduction technique is effective in reducing hypertension and hypertensive heart disease in African Americans.
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PMID:Behavioral treatment of hypertensive heart disease in African Americans: rationale and design of a randomized controlled trial. 1176 29

Variations in the validity of hospital discharge diagnoses can complicate the assessment of trends in incidence of acute myocardial infarction (AMI). To clarify trends in the validity of discharge codes, the authors compared event classification based on published Atherosclerosis Risk in Communities (ARIC) Study criteria with the presence or absence of an International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) hospital discharge code for AMI (code 410). Between 1987 and 2000, 154,836 coronary heart disease events involving hospitalization in the four ARIC communities had ICD-9-CM codes screened for AMI. The sensitivity of ICD-9-CM code 410 for classifying AMI in men (sensitivity = 0.65, 95% confidence interval (CI): 0.63, 0.66) was statistically significantly greater than that found for women (sensitivity = 0.60, 95% CI: 0.58, 0.62) and was greater in Whites (sensitivity = 0.67, 95% CI: 0.65, 0.68) than in Blacks (sensitivity = 0.50, 95% CI: 0.47, 0.53). The ethnic difference was related to a greater frequency of hypertensive heart disease and congestive heart failure codes encompassing AMI among Blacks as compared with Whites. The authors found that although the validity of ICD-9-CM code 410 to identify AMI was generally stable from 1987 through 2000, differences between Blacks and Whites and across geographic locations support investment in validation efforts in ongoing surveillance studies.
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PMID:Trends in the sensitivity, positive predictive value, false-positive rate, and comparability ratio of hospital discharge diagnosis codes for acute myocardial infarction in four US communities, 1987-2000. 1558 65

Hypertension represents a complex, multifactorial disease and contributes to the major causes of morbidity and mortality in industrialized countries: ischemic and hypertensive heart disease, stroke, peripheral atherosclerosis and renal failure. Current pharmacological therapy of essential hypertension focuses on the regulation of vascular resistance by inhibition of hormones such as catecholamines and angiotensin II, blocking them from receptor activation. Interaction of G-protein coupled receptor kinases (GRKs) and regulator of G-protein signaling (RGS) proteins with activated G-protein coupled receptors (GPCRs) effect the phosphorylation state of the receptor leading to desensitization and can profoundly impair signaling. Defects in GPCR regulation via these modulators have severe consequences affecting GPCR-stimulated biological responses in pathological situations such as hypertension, since they fine-tune and balance the major transmitters of vessel constriction versus dilatation, thus representing valuable new targets for anti-hypertensive therapeutic strategies. Elevated levels of GRKs are associated with human hypertensive disease and are relevant modulators of blood pressure in animal models of hypertension. This implies therapeutic perspective in a disease that has a prevalence of 65million in the United States while being directly correlated with occurrence of major adverse cardiac and vascular events. Therefore, therapeutic approaches using the inhibition of GRKs to regulate GPCRs are intriguing novel targets for treatment of hypertension and heart failure.
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PMID:Regulation of GPCR signaling in hypertension. 2006 Aug 96

The early part of the new millennium witnessed reports of a growing burden of cardiovascular disease in Sub-Saharan Africa (SSA). However the contribution of ischemic heart disease and stroke to this increasing burden relative to that caused by hypertensive heart disease, cardiomyopathy and rheumatic heart disease was not clear. Over the last decade, data from the continent has begun to clarify this issue and suggests three main points. The burden of ischemic heart disease relative to other causes of heart disease remains low particularly in the black Africans majority. Stroke caused predominantly by hypertension is now a major cause of disability and premature death. Third, the burden of risk factors for atherosclerosis is increasing rapidly in most urban and some rural regions. A concerted effort to understand the primary drivers of this increase in cardiac risk factors is required to prevent a future epidemic of atherosclerosis and its sequelae.
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PMID:Recent advances in the epidemiology, outcome, and prevention of myocardial infarction and stroke in sub-Saharan Africa. 2368 Aug 88


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