Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of atrial natriuretic peptide (ANP) were determined in 34 male patients undergoing diagnostic right heart catheterization. Patients with effort angina exhibited significant higher ANP levels at rest (259 +/- 42 pg/ml; n = 7) than patients without signs of coronary heart disease (78 +/- 30 pg/ml; n = 8). Patients with effort angina also had higher ANP levels at rest than patients exhibiting impaired cardiac function on exertion without signs of ischemia (105 +/- 15 pg/ml; n = 4), patients with only minimal functional alterations due to infarction residues (95 +/- 27 pg/ml; n = 7), or patients with only borderline changes of ST-segments during exertion (61 +/- 19 pg/ml; n = 8). In contrast, mean pulmonary capillary or right atrial pressures were not significantly different between the various groups of patients. The patients with effort angina also exhibited the highest ANP levels during bicycle exercise (846 +/- 238 pg/ml). There was only a weak to moderate linear correlation between ANP levels and pulmonary or right atrial pressures in the whole group of patients (r = 0.1-0.6). The plasma levels of epinephrine and norepinephrine and of ANP were not significantly correlated, with the exception of norepinephrine levels during exercise (r = 0.54). Our observations suggest that in patients with effort angina there may exist additional stretch-independent factors stimulating the release of ANP, possibly associated with repetitive myocardial ischemia.
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PMID:[Increased plasma level of atrial natriuretic peptide in patients with stress-induced coronary insufficiency: stretch-independent release of atrial natriuretic peptide?]. 214 Dec 8

The data obtained in a prospective study made it possible, using Markov's analysis, to assess different forms of coronary heart disease (CHD) of long duration and to elaborate an unsophisticated scale for estimating individual risk of death from that disease. The Markov's analysis demonstrated a high enough probability (over 20%) of transformation to a remission for patients with all forms of CHD, with the probability being the least for persons with painless ischemia. The most unfavorable prognosis was assumed for patients who suffered myocardial infarction of had associated angina pectoris of effort and ischemic alterations as shown by the ECG. The highest death rate is predicted for the latter group (about 54% during 20 years). In the group of persons with painless ischemia, the death rate approaches that among patients with a history of myocardial infarction (32 and 39%, respectively). Isolated angina pectoris of effort has the most favorable prognosis.
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PMID:[The long-term prognosis of the course of different forms of ischemic heart disease and a scale for assessing its risk of death]. 214 40

Many clinical studies have shown an increased insulin response to oral glucose in patients with ischemia of the heart, lower limbs, or brain. Hyperinsulinemia also occurs in patients with angiographically proved atherosclerosis without ischemia and thus appears to be related to arterial disease and not to be a nonspecific response to tissue injury. Fasting insulin levels and insulin responses to intravenous stimuli, including glucose, tolbutamide, and arginine, are normal, suggesting a gastrointestinal factor may be involved in the increased insulin response to oral glucose. In patients with atherosclerosis, insulin sensitivity appears to be normal or enhanced with respect to both glucose and lipid metabolism. Five population studies have shown that insulin responses to glucose are higher in populations at greater risk of cardiovascular disease. Many of the hyperinsulinemic populations also had upper-body obesity, hypertriglyceridemia, lower high-density lipoprotein (HDL) levels, and hypertension. These prospective studies support an independent association between hyperinsulinemia and ischemic heart disease, although their results differ in detail. Hyperinsulinemia is associated with raised triglyceride and decreased HDL cholesterol levels. Total and low-density lipoprotein (LDL) cholesterol is less closely related to hyperinsulinemia. Upper-body adiposity is associated (in separate studies) with coronary heart disease, diabetes, hyperinsulinemia, and hypertriglyceridemia. Insulin and blood pressure are closely related in both normotensive and hypertensive people. Although obesity and diabetes are often found in hypertensive people, hyperinsulinemia also occurs in nonobese nondiabetic hypertensive people. Thus, hyperinsulinemia is closely associated with a cluster of cardiovascular risk factors, i.e., hypertriglyceridemia, low HDL levels, hypertension, hyperglycemia, and upper-body obesity. There is a possibility that insulin has a role in the sex differences in ischemic heart disease incidence and their absence in diabetes, but additional work is required for its clarification. Long-term treatment with insulin results in lipid-containing lesions and thickening of the arterial wall in experimental animals. Insulin also inhibits regression of diet-induced experimental atherosclerosis, and insulin deficiency inhibits the development of arterial lesions. Insulin stimulates lipid synthesis in arterial tissue; the effect of insulin is influenced by hemodynamic factors and may be localized to certain parts of the artery. In physiological concentrations, insulin stimulates proliferation and migration of cultured arterial smooth muscle cells but has no effort on endothelial cells cultured from large vessels. Insulin also stimulates cholesterol synthesis and LDL binding in both arterial smooth muscle cells and monocyte macrophages.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Insulin and atheroma. 20-yr perspective. 199 42

Cardiac failure, which used to be rare in coronary heart disease, is now its most common complication. Coronary heart disease can cause or appear as cardiac failure through one or more of 12 mechanisms: acute myocardial infarction, acute reversible ischemia, right ventricular dysfunction, cardiogenic shock, acute mitral regurgitation, ventricular septal perforation, cardiac free wall rupture, ischemic cardiomyopathy, ventricular aneurysm, coexisting diseases, iatrogenesis, and pseudoheart failure. An understanding of the responsible mechanism or mechanisms is essential not only for appropriate treatment but also for prognostication. Various therapeutic modalities, both medical and surgical, should be able to improve not only symptoms but also survival. Current efforts in the management of patients with cardiac failure as a result of coronary heart disease should be aimed at prevention, both primary and secondary.
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PMID:Cardiac failure in coronary heart disease. 220 Feb 54

With this study including 9 patients with angiographically proven coronary heart disease it could be shown that a monotherapy with nifedipine in the galenic preparation as Adalat SL (Bayer AG, Leverkusen, FRG) is efficient in reducing myocardiac ischemia and concomitantly raising working capacity during bicycle ergometry as well after first time application of this drug as after continuous therapy with 1 tablet twice daily during 4 weeks. This findings are true both at normal environmental conditions (1000 ft above sea level) and at conditions of altitude induced hypoxia (9000 ft above sea level), simulated in a hypobaric chamber. There was no development of drug tolerance during continuous therapy with 1 tablet of Adalat SL twice a day. Out of these findings the conclusion can be drawn that in patients with coronary heart disease receiving protective therapy with Adalat SL there is no remarkably higher risk of episodes of angina pectoris or even myocardiac infarction at altitudes up to 9000 ft above sea level than is to be expected during daily life.
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PMID:[Modification of physical fitness of patients with coronary heart disease with nifedipine during a stay at altitude]. 223 49

In the Whitehall study, 18,388 subjects aged 40-64 years completed a questionnaire on intermittent claudication. Of these subjects, 0.8% (147) and 1% (175) were deemed to have probable intermittent claudication and possible intermittent claudication, respectively. Within the 17-year follow-up period, 38% and 40% of the probable and possible cases, respectively, died. Compared with subjects without claudication, the probable cases suffered increased mortality rates due to coronary heart disease and cerebrovascular disease, but the mortality rate due to noncardiovascular causes was not increased. Possible cases demonstrated increased mortality rates due to cardiovascular and noncardiovascular causes. This difference in mortality pattern may be due to chance. Possible and probable cases still showed increased cardiovascular and all-cause mortality rates after adjusting for coronary risk factors (cardiac ischemia at baseline, systolic blood pressure, plasma cholesterol concentration, smoking behavior, employment grade, and degree of glucose intolerance). Intermittent claudication is independently related to increased mortality rates. It is not a rare condition, and simple questionnaires exist for its detection. The latter can be usefully incorporated in cardiovascular risk assessment and screening programs.
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PMID:Intermittent claudication, heart disease risk factors, and mortality. The Whitehall Study. 224 47

To clarify the central effects of physical training on patients with coronary heart disease, 81 subjects were selected for the present study. Evaluations of the oxygen transport system function were performed according to the definition proposed by Bruce and others in terms of FAI (functional aerobic impairment), LVI (left ventricular impairment) or MRI (myocardial reserve impairment), CRI (chronotropic reserve impairment) and PCI (peripheral circulatory impairment). Remarkable improvement in left ventricular impairment was found in those patients with single vessel disease or those who experienced disappearance of chest pain after the completion of the program. In another series of study on myocardial perfusion performed on 11 patients with coronary heart disease, improvement in ischemia was also demonstrated in 7 of 8 patients who revealed redistribution pattern in 201TL exercise stress images specifying myocardial ischemia. In conclusion, exercise training could induce improvements not only the left ventricular functions characterized by increased maximal pressure rate product and maximal heart rate, but also in myocardial ischemia. Further studies are needed to specify its effects, since natural progression or regression of the disease process itself may influence the results.
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PMID:Physical training of the patients with coronary heart disease: noninvasive strategies for the evaluation of its effects on the oxygentransport system and myocardial ischemia. 228 45

The determinants of the altered whole blood filterability observed during coronary ischemia are still under discussion. Since no studies have been carried out to date on what exactly causes these alterations during the early stages of controlled ischemia in coronary heart disease, a model was set up using a bicycle ergometer test (with a 25 W increase every 2 minutes). Blood samples were taken from 48 stable angina pectoris patients and from a group of 28 matched controls before and immediately after exercise and 8 minutes later. Plasma viscosity, the filterability (through 5 microns diameter pore filters) of whole blood, erythrocytes, and polymorphonuclear and mononuclear leukocytes (separated by density gradient) were monitored. Alterations in whole blood filterability could be linked only to an impairment in polymorphonuclear cell filterability in those stable angina pectoris patients who reported chest pain and/or whose ST segment depression was greater than or equal to 2 mm.
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PMID:Stable angina pectoris and controlled ischemia: what causes the abnormalities in whole blood filterability? 229 74

The effect of a controlled-release formulation of isosorbide-5-mononitrate (IS-5-MN) was studied in patients with coronary heart disease (CHD), with the aim of comparing the acute effect with that after chronic administration on parameters of ischemia. To determine whether any tolerance developed, several aspects of ischemia were observed: ECG signs, clinical parameters, and left ventricular function. Fifteen patients with angiographically proven CHD were examined with 12-lead exercise ECG before, 2 h and 4 h after the first dose and after 10 days of therapy with 60 mg IS-5-MN (Coleb-Duriles) once daily. After 7 days, three radionuclide ventriculographies were performed: control, 2 h after nitrate and 2 h after 75 mg gallopamil. Plasma concentrations of IS-5-MN were measured before every exercise test. The results showed a reduction of total ST-segment depression from 0.59 mV to 0.29 mV after 2 h (NS) and 4 h (P less than 0.05) on the 1st day and from 0.48 mV to 0.32 mV (P less than 0.05) and 0.31 mV (NS) after 10 days. The severity of angina pectoris was diminished by about 50%. The effect on exercise duration and time to ST-segment depression by more than 0.1 mV remained unchanged after 10 days, whereas the effect on blood pressure, heart rate and time to onset of angina was attenuated. The mean decrease in ejection fraction (EF) from rest to exercise was reduced from--5.9% to -1.9% (P less than 0.05) after nitrate, while an increase of +1.4% was seen after gallopamil (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of tolerance after chronic administration of controlled-release isosorbide-5-mononitrate. Interaction of nitrate and gallopamil. 235 12

Based on the therory of promoting flow of qi and dispersing blood stasis, the KUO GUAN QU YU LING coronary--dilating and stagnation--dispersing) powder in capsules were prepared for the treatment of 60 cases of coronary heart disease. After a 30 day course of treatment, cardiac ischemia was improved in 64.7% and the symptom of angina pectoris was relieved in 61.7% of the patients. This drug also acted to reduce blood lipids and to improve left cardiac function. Pharmacological study indicated that this preparation improved the tolerance of cardiac muscle against anoxia and prevented ventricular fibrillation and cardiac damage from ischemia.
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PMID:Observations on the treatment of coronary heart disease by kuo guan qu yu ling. 236 65


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