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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The impact of treatment on prognosis of patients with chronic congestive heart failure depends not only on pharmacological therapy but also on nonpharmacological aspects of patient management. Patient compliance, life style changes, salt and fluid restriction, detailed patient information and measures of self control greatly affect therapeutic efficacy. Reasons for hospitalizations and emergency room visits: In an analysis of 82 admissions of patients for decompensated chronic congestive heart failure we found poor compliance with drug treatments or dietary instructions as causally related factors in 30 patients, uncontrolled hypertension in 22 patients, acute infection in 18 and acute myocardial ischemia in 18 patients. More than half of the patients had weight gain before decompensation, that had not been adequately answered by changes in medication. Inadequate patient information: Inadequate knowledge about necessary life style changes at the time of hospital discharge is often found in patients with chronic heart failure. Less than 50% of these patients remembered correctly the instructions on key issues of necessary life style changes and diet. Drug treatment of heart failure: Recent controlled drug trials have not gained enough weight in therapeutic decisions of physicians treating heart failure patients. While ACE-inhibitors have been shown to improve longevity in congestive heart failure only 6% of patients with heart failure are treated with these drugs, while 5% are treated with calcium antagonists which have not been proven to be of symptomatic or prognostic benefit and may be harmful as well in this disease. Inadequate dosage in patients with chronic renal failure or in elderly patients as well as inadequate choice of drugs lead to side effects in a considerable percentage of patients.
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PMID:[Effects of patient information, compliance and medical control on prognosis in chronic heart failure]. 182 Feb 95

The clinical syndrome of congestive heart failure can result from inadequate myocardial contraction (systolic myocardial failure), from pseudo-heart failure due to circulatory overload, or from failure of the ventricles to fill at low pressure (diastolic myocardial failure). The presence of systolic or diastolic heart failure is most precisely defined by an examination of left ventricular pressure-volume relations. Diastolic failure commonly coexists with systolic dysfunction. However, in many patients, diastolic dysfunction may exist alone or as the predominant physiologic disturbance. This is especially true in such common disease states as systemic hypertension and ischemic heart disease. Like systolic heart failure, diastolic failure results in significant morbidity and mortality. Diastolic heart failure may correlate better with prognosis for symptoms and survival than traditional indices of systolic function. The presence of predominantly diastolic dysfunction in large numbers of patients with the diagnosis of congestive heart failure has important therapeutic implications.
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PMID:Prognosis in heart failure: is systolic or diastolic dysfunction more important? 182 Mar

Diastolic dysfunction is an important cause of the clinical syndrome of congestive heart failure. Traditionally, the syndrome of pulmonary congestion due to the elevation of left heart filling pressure has been attributed to the depressed ability of the heart to eject blood during systole, with a secondary increase in left ventricular volume. However, heart failure can also occur when the left ventricle fails to receive blood during diastole at low filling pressures. With a mild degree of resistance of the left ventricle to diastolic filling, the initial hemodynamic manifestation may just be the elevation of left ventricular diastolic pressure and pulmonary venous pressure. More severe resistance to left ventricular filling may cause an inadequate extent of diastolic filling and insufficient myofiber stretch, which results in the depression of stroke volume. In this review, the factors contributing to diastolic dysfunction are discussed, with a particular focus on the role of diastolic heart failure in patients with ischemic heart disease or hypertrophy.
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PMID:Significance of diastolic dysfunction of the heart. 182 70

Eleven patients with congestive heart failure class II-IV (NYHA) caused by ischemic heart disease were studied before and three months after adding enalapril to their treatment with furosemide. After an infarction the heart dilates gradually, mainly as a result of slippage of myocardial fiber bundles. It is known that the addition of an ACE-inhibitor to the medical treatment unloads the heart and gradually, within a period of 3 months, reduces heart size. Objectives of this study were to demonstrate remodelling by recording diastolic pressure-volume relations before and after treatment. The study addresses the question of whether regression of dilation, induced by the ACE-inhibitor treatment, improves the oxygen supply-demand ratio and, as a result, the contractility of the heart muscle. Treatment resulted in a reduction of vascular resistance (1479 to 1182 dyn.s.cm-5, p less than 0.05) and of the left ventricular end-diastolic (130 to 108 ml per m2 body surface area, p less than 0.05) and end-systolic (102 to 81 ml per m2 body surface area, p less than 0.01) volume index. The slope of the end-systolic pressure-volume relation, measured using vena cava occlusion and beat-to-beat recording of pressure and volume loops, remained unchanged. Indices of oxygen-supply demand ratio such as a drop of ejection fraction during exercise and parameters of active diastolic relaxation also did not change. Addition of an ACE-inhibitor induces regression of ventricular dilation, but no indications were found that it improves the condition of the cardiac muscle.
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PMID:Cardiac remodelling and myocardial contractility in patients with congestive heart failure treated with furosemide and enalapril. 182 82

The transmitral flow velocity pattern of 28 Type 1 diabetic patients and 39 age-matched healthy control subjects was studied for determination of left ventricular diastolic function. No patient had systemic hypertension, congestive heart failure, or ischaemic heart disease by clinical or electrocardiographic criteria. Echocardiographic measures of systolic ventricular function were within normal range in all subjects. The ratio of early to late transmitral peak flow velocity (ve/va) was significantly decreased in the diabetic patients (1.3 +/- 0.1 (+/- SE) vs 1.6 +/- 0.1, p less than 0.05), while other Doppler derived variables did not show any significant difference. No correlation of ve/va with duration of diabetes was found (r = -0.27), but it correlated with age in both groups (both r = -0.40, p less than 0.05). Furthermore, a significant correlation was found between ve/va and heart rate (r = -0.55 for diabetic patients, p less than 0.01; r = -0.58 for control subjects, p less than 0.01). After matching for heart rate (24 diabetic patients and 24 control subjects) no significant decrease of ve/va was observed in the diabetic group.
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PMID:Diastolic ventricular function in type 1 diabetic patients: a study using Doppler echocardiography. 182 33

Among dialysis patients, only 23% have a normal echocardiogram, about 10% have recurrent or chronic congestive heart failure, and 17% have asymptomatic ischemic heart disease. The predisposing factors for congestive heart failure are dilated cardiomyopathy, hypertrophic hyperkinetic disease, and ischemic heart disease. Dilated cardiomyopathy, a disorder of systolic function, includes among its risk factors age, hyperparathyroidism, and smoking. Hypertrophic disease results in diastolic dysfunction, and its predictors include age, hypertension, aluminum accumulation, anemia, and, perhaps, hyperparathyroidism. Ischemic heart disease is due to the presence of coronary artery disease and also to nonatherosclerotic disease caused by the reduction in coronary vasodilator reserve and altered myocardial oxygen delivery and use. The clinical outcome of congestive heart failure is comparable to that of nonrenal patients with medically refractory heart failure. Left ventricular hypertrophy is an important independent determinant of survival. A subset have hyperkinetic disease with severe hypertrophy and have a bad survival, as low as 43% have a 2-yr survival after the first admission to hospital with cardiac failure. The prognosis for those with dilated cardiomyopathy is less severe but is worse than those with normal echocardiogram. The survival of patients with symptomatic ischemic heart disease was little different from that of patients without symptoms, suggesting that the underlying cardiomyopathies had an adverse impact on survival independent of ischemic disease. Much research needs to be undertaken on the risk factors, natural history, and therapy of the various types of cardiac disease prevalent in dialysis patients.
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PMID:The natural history of myocardial disease in dialysis patients. 183 84

Left ventricular hypertrophy (LVH) has been identified as a significant risk factor for future cardiovascular morbidity and mortality. LVH and its sequelae such as myocardial ischemia, impaired filling and contractility, ventricular arrhythmias, and congestive heart failure can be reduced by specific antihypertensive agents. Future clinical trials will determine whether a reduction of LVH will ultimately improve its inherent ominous prognosis.
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PMID:Hypertension: left ventricular hypertrophy, ventricular ectopy, and sudden death. 183 4

Left ventricular hypertrophy is the most important cardiovascular consequence of chronic systemic hypertension. While ventricular hypertrophy is an adaptive response to increased work load that preserves cardiac output, it nonetheless has adverse consequences. These include gradual systolic and diastolic dysfunction leading to congestive heart failure, an increased incidence of ventricular arrhythmias, accelerated atherosclerosis of the coronary arteries, and alterations (anatomic and physiologic) in the coronary microvasculature. Additionally, the presence of hypertension and hypertrophy increases the likelihood of poor outcome when ischemic heart disease occurs. Chronic systemic hypertension is prevalent among African Americans, who are therefore at risk for the development of left ventricular hypertrophy and the increase in mortality that accompanies the hypertrophic response.
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PMID:Left ventricular hypertrophy resulting from systemic hypertension: adaptive advantage and adverse consequences. 183 25

Heart period and arterial pressure short term variabilities contain rhythmic oscillations which might provide information on neural mechanisms regulating cardiovascular function. Continuous electrocardiographic and/or arterial pressure signals, after appropriate analogue to digital conversion, furnish the time series which constitute the basis for spectral analysis of their variabilities. Under stationary conditions, this methodology can be utilized to assess both total variability and the power and center frequency of each rhythmic component. Human physiological and animal studies support the hypothesis that the low frequency (LF) component, around 0.1 Hz, is a marker of sympathetic modulation of both R-R and arterial pressure variabilities, while the high frequency (HF) component, around 0.25 Hz, is a marker of vagal modulation of R-R variability. LF/HF ratio of R-R variability is a marker of sympatho-vagal balance. Spectral components when assessed for a 24-hour period evidence marked circadian rhythmicity with sympathetic predominance during the day and vagal predominance at night. Various pathophysiological conditions including arterial hypertension, ischemic heart disease, cardiac transplantation, congestive heart failure, Chagas' disease and diabetic neuropathy have been explored with this methodology, and a new quantitative evaluation of the alterations in sympatho-vagal balance which seem to characterize these abnormal states has been obtained. The study of cardiovascular rhythmicity, i.e. an analysis performed in the frequency domain, although based on indirect spectral markers, seems to offer a new clinical tool for the exploration of cardiovascular neural control in health and disease.
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PMID:Neurovegetative regulation and cardiovascular diseases. 184 Aug 13

Ionic biology involving Ca2+, Na+, K+ and Mg2+ across the cell membrane and in the development of the action potential is reviewed with reference to cardiac arrhythmia. K+ and Mg2+ deficiency which frequently occur together lead to abnormal ionic transfer of Na+, K+ and Ca2+ with development of automaticity, triggered impulses and reentrant tachycardia. Tachycardia occurring in acute myocardial ischemia, congestive heart failure, hypertensives on diuretics and digitalis toxicity is examined according to the concept of ionic imbalance. A protocol for prevention and treatment of cardiac tachyarrhythmia is proposed with this concept in mind.
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PMID:Magnesium-potassium interactions in cardiac arrhythmia. Examples of ionic medicine. 184 52


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