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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Once the rules for understanding of complex congenital heart disease were reviewed in part I, the purpose in this second part is show how the clinical diagnosis is made. The first requirement is to separate patients into two groups: neonates and infants. A critical route based on five clue data: patient's age, presence or absence of cyanosis, presence or absence of myocardial failure, pulmonary blood flow estimated on x chest film, and presence of either right or left ventricular hypertrophy or both in ECG, is matched. This approach is helpful to reduce possibilities to diagnosis in congenital heart disease.
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PMID:[Understanding and diagnosis of complex congenital cardiopathies. II]. 141 55

Over the past decade we have seen a shift in the strategy for the treatment of hypertension, from stepped therapy--involving a highly structured, unvarying series of steps--to recommendations for more individualized treatment. How shall we accomplish that goal? Severe hypertension provides a clear indication to bypass earlier recommendations. Demographic data such as age, gender, and race, often cited, have proved less helpful. Concomitant medical problems, which are found in greater than 50% of hypertensive patients, are most often the crucial determinants in the selection of antihypertensive therapy. Concurrent coronary artery disease, diabetes mellitus, heart failure, azotemia, asthma, chronic obstructive pulmonary disease, borderline cognitive dysfunction, anxiety, and depression are all common. Each has implications for antihypertensive therapy. Moreover, blood pressure reduction is a surrogate for our real goal, which is reduction of cardiovascular risk. Thus, consideration of concomitant medical problems has extended to left ventricular hypertrophy, obesity, hyperlipidemia, and insulin resistance as additional risk factors in hypertension. Consideration of all of these factors makes it possible to individualize antihypertensive therapy in most patients.
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PMID:Evolution of the treatment of hypertension: what really matters in the 1990s? 151 35

Cardiac adaptation to hemodynamic stress involves both quantitative (hypertrophy) and qualitative (pattern of gene expression) changes. Our previous studies have shown that advancing age in the rat is associated with diminished capacity to develop left ventricular hypertrophy in response to either ascending aortic constriction (AoC). In this study, we examined whether the expression of protooncogenes and contractile protein genes in response to AoC differs between adult (9-mo-old) and old (18-mo-old) rats. RNA was isolated from the left ventricles of AoC animals of both age groups subjected to a similar hemodynamic stress. Immediately after AoC, the levels of the ventricular expression of c-fos and c-jun protooncogenes were markedly lower in the old rats than in the adult animals. 5 d after the operation, the ratio of beta- to alpha-myosin heavy chain mRNAs increased significantly after AoC in both age groups. In contrast, AoC was associated with a marked reduction in the levels of mRNAs encoding sarcoplasmic reticulum Ca(2+)-ATPase (by 69%) and cardiac calsequestrin (by 49%) in the old rats but not in the adults. The mRNAs encoding atrial natriuretic factor and skeletal alpha-actin increased in response to AoC only in the adult rats. There were no significant differences in expression of the cardiac alpha-actin mRNA among the experimental groups. These data suggest that (a) the expression of protooncogenes in response to acute pressure overload is significantly reduced in the aged rats and (b) the pattern of expression of the contractile protein gene in response to AoC in the old rats differs qualitatively as well as quantitatively from that in younger animals. These age-related differences may play a role in the higher frequency of heart failure in the aged during hemodynamic stress.
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PMID:Age-related differences in the expression of proto-oncogene and contractile protein genes in response to pressure overload in the rat myocardium. 153 37

We investigated biochemical and structural changes in collagen in ventricles in right ventricular hypertrophy (RVH) induced by monocrotaline injection in Sprague-Dawley rats. Rats injected with monocrotaline showed significant RVH after 2 weeks compared with the vehicle-treated rats (controls). After 4 weeks, the monocrotaline-treated rats showed severe RVH with heart failure. After 2 weeks, the proportion of type III collagen in the right ventricles (RV) of the monocrotaline-treated rats increased significantly compared with controls, with a concomitant decrease in type I collagen. After 4 weeks, there was a significant increase in the proportion of type III and type V collagens in the RV. In the left ventricles (LV), the proportion of collagen types was similar in the monocrotaline-treated and control rats at 2 and 4 weeks. There was no significant difference in collagen concentration (% collagen in dry defatted tissue) between the monocrotaline-treated rats and controls at either 2 or 4 weeks in the LV and RV. Scanning electron microscopy revealed that the collagen fibrillar sheaths around the myocytes in the endomysium of the RV had thickened and formed a dense network in the monocrotaline-treated rats. In the perimysium, tendon-like collagen fibers increased and became thicker than those in the RV of controls. Giant coiled perimysial fibers were also observed in the monocrotaline-treated RV. These structural changes were more pronounced after 4 weeks of monocrotaline-treatment: Loss of myocytes was evident and was accompanied by replacement fibrosis, where dense collagen fibers aggregated parallel to the long axes of the myocytes. Our results show that biochemical and structural remodeling of collagen occurred in the RV but not in the LV during the development of RVH and heart failure, providing important clues to the pathogenesis and pathophysiology of RVH and cardiac failure in response to pressure overload.
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PMID:Biochemical and structural remodeling of collagen in the right ventricular hypertrophy induced by monocrotaline. 153 90

Left ventricular hypertrophy (LVH) constitutes a powerful independent risk factor in hypertensive heart disease. Although initially the wall stress, i.e., left ventricular afterload, remains normal, the coronary reserve is diminished due to disturbances in the microcirculation. This is also shown in the commonly present silent ischemia episodes in Holter monitoring. LVH also causes ventricular dilation and heart failure. Apart from systolic wall stress LVH is modulated by the trophic effects of the sympathetic nervous system and angiotensin II and genetic factors. Long-term antihypertensive treatment must therefore focus on regression of both LVH and the microvascular abnormalities. A step approach for the treatment of the LVH has been recommended on the basis of the experience of this working group with calcium antagonists and ACE inhibitors, whereas the place of beta-blockers is as yet unclear. Preliminary data indicate that coronary flow rescue can also be improved after chronic antihypertensive treatment.
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PMID:Therapeutic effect on left ventricular hypertrophy by different antihypertensive drugs. 153 67

Whether cardiac hypertrophy is a compensatory response or a cause of decompensation has been an interesting and important controversy in cardiology. The purpose of this study is to assess qualitative and quantitative changes in biological factors involved in the evolution and the development of right ventricular hypertrophy (RVH) and right ventricular failure in response to pressure overload in rats with pulmonary hypertension induced by monocrotaline injection, and to clarify the process from compensation to deterioration in cardiac hypertrophy biochemically and morphologically. Significant RVH was produced in rats at 2 weeks after single subcutaneous injection of monocrotaline, and signs of right ventricular failure became obvious at 4 weeks as RVH became more severe. In the right ventricle of these rats, we found that: 1) myosin isoenzymes shifted from V1 to V3 both at 2 and 4 weeks; 2) total collagen content increased, and type III and type V collagens increased with a relative decrease in type I collagen at both 2 and 4 weeks; 3) intracellular Ca2+ transient recorded from isolated myocytes showed a lower peak and slower descent slope compared to those of control rats; 4) ultrastructural changes observed by scanning electron microscopy at 1 and 2 weeks disappeared gradually as heart failure developed, and degeneration or destruction of mitochondria or sarcoplasmic reticulum became remarkable at 3 and 4 weeks. These findings suggest that cardiac hypertrophy might be an ominous sign of cardiac failure rather than a benign adaptive process, at least in this model.
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PMID:Changes in contractile and non-contractile proteins, intracellular Ca2+ and ultrastructures during the development of right ventricular hypertrophy and failure in rats. 153 55

We examined the effect of age on capacity for myocardial hypertrophy, pressure-generating ability and coronary circulation after imposition of pressure-overload. Marked right ventricular and cellular hypertrophy was observed 1 week after pulmonary artery constriction in the developmental phase of rats (2 months of age) and after 3 weeks in the young-adult rats (7 months). In old rats (18 months) similar increases in peak right ventricular pressure did not produce significant hypertrophy even after 3 weeks. The right ventricular hypertrophy at the organ and cell levels in response to pressure-overload decreased with age. In vivo pressure-generating ability, which was determined by maximum isovolumic pressure during pulmonary artery occlusion, correlated with the degree of myocardial hypertrophy in each age group. During the ascending aortic constriction experiment the age-associated diminution in hypertrophic response was also observed in the left ventricle. Coronary dilator capacity, which was determined after brief ischemia in an isolated, blood-perfused, beating but nonworking heart model, was decreased in the presence of myocardial hypertrophy in young-adult rats (7 months) and in the absence of significant myocardial hypertrophy in old rats (18 months). The age-associated diminution in capacity for myocardial hypertrophy, pressure-generating ability and maladaptation in the coronary circulation may explain the higher incidence of heart failure or increased vulnerability of the myocardium to ischemic episodes during hemodynamic stress in aged patients.
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PMID:Aging effects on myocardial hypertrophic response and coronary circulation in pressure-overload. 153 57

The risk for cardiovascular complications is already substantially increased in persons with borderline elevation of arterial pressure (141-159/90-94 mmHg and transiently below). It increases progressively with higher grades of hypertension. The main aim of treatment is thus a significant improvement in survival for the patient. Persons with raised blood pressure (BP) have often additional cardiovascular risk factors such as deranged carbohydrate metabolism, dyslipidemia, left ventricular hypertrophy, smoking and others. Treatment of hypertensive patients should thus not only normalize BP but should at the same time reduce associated risk factors or at least not increase them. Conventional antihypertensive treatment based on thiazides in high doses or beta-blocking agents led to marked reduction of strokes and heart failure, but did not satisfactorily reduce coronary heart disease or sudden cardiac death. It has been suspected that other cardiac risk factors are insufficiently influenced or eventually even deteriorated by conventional therapy, thus counteracting partly a beneficial effect of lowered BP. Beta-blockers however have at least a secondary preventive effect after myocardial infarction. Newer antihypertensive drugs such as ACE-inhibitors, calcium antagonists and alpha 1-blockers reduce left ventricular hypertrophy and are at least neutral with regard to metabolism of lipids and carbohydrates. The non-thiazide diuretic indapamide and the serotonin (S2-) blocker ketanserin likewise are neutral with regard to glucose and lipid metabolism. The efficacy of these new drugs regarding long term survival is as yet undetermined. Persisting borderline or established hypertension should as a rule always be approached with basic non-pharmacologic measures: loss of overweight, reduction of alcohol intake, exercise, avoidance of high salt foods, abstention from smoking and withdrawal of BP-raising drugs. If antihypertensive medication is indicated, potential first line drugs are ACE-inhibitors, calcium antagonists, beta-blockers, thiazides at low dose, indapamide, ketanserin, the alpha 1-blocker prazosin and others; initially as monotherapy, if needed in combinations of 2 or 3. Older patients or those will with additional disturbances such as diabetes, hypercholesterolemia, nephropathy, heart failure, ischemic heart disease, arrhythmias, claudication, asthma and others need problem-adjusted modifications of treatment.
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PMID:[Antihypertensive therapy in the nineties]. 153 54

Despite multiple, interdisciplinary group recommendations, we are still on uncertain ground when it comes to treatment of most aspects of hypertension. Seven major areas of controversy include mild hypertension, the relevance of hypertension and lipids, hypertensive agents and electrolyte imbalance, treatment and regression of left ventricular hypertrophy, isolated systolic hypertension, ambulatory blood pressure monitoring and overtreatment of hypertension--the "j shaped curve." Although our knowledge of these aspects has advanced tremendously, significant doubts exist as to our present approach. Key publications are reviewed to evaluate our present knowledge and recommendations are made. The 1988 recommendations of the Joint National Committee on Detection, Evaluation and Treatment of Hypertension both answered and raised some questions regarding treatment of high blood pressure. We lack information on the treatment outcomes and many of us remain unconvinced that our present approach is the best we can do. Many other questions abound. Should the treatment of mild hypertension be as aggressive as it is at present or should systolic hypertension in the elderly be treated at all? There are striking variations and recommendations of other groups outside the United States which reaffirm our lack of evidence. Ideally, we ought to be able to reduce or abolish the recognized poor outcomes of treated hypertension: heart attack, heart failure, stroke, renal failure and retinopathy. Adequate control of blood pressure has gone a long way towards preventing stroke, accelerated hypertension and hypertensive encephalopathy. Congestive heart failure has also been reduced. There is a singular lack of evidence of the influence on either total mortality or morbidity from coronary events.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New controversies in hypertension: questions answered, answers questioned. 154 98

Fifty-four patients hospitalized in Niger for complications from hypertension between September 1988 and October 1989 were studied. The following complications were observed: left ventricular hypertrophy (56%), coronary vascular defect (35%), left heart deficiency (26%), cardiac failure (32%), retinopathy (56%), renal insufficiency (35%), and stroke (24%). The most frequent risk factor was Type A personality (76%), followed by stress (48%), excess weight (37%), tobacco use (35%), hyperuricemia (35%), hypercholesteremia (17%), and diabetes (15%). Complications from hypertension may well become a major problem for African countries as they develop.
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PMID:Hospitalizations in Niger (West Africa) for complications from arterial hypertension. 158 Oct 14


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