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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the implications of transient myocardial ischaemia following acute myocardial infarction we compared ambulatory ST segment monitoring with exercise treadmill testing in 170 patients (mean age 58 years) at 4-8 weeks after admission. Ambulatory monitoring detected transient ischaemia (265 episodes; 249 (94%) silent) in 53/170 patients (31%) which was less frequent than ischaemia during exercise testing (90 patients; 53%) (P less than 0.0001). However, patients displaying transient ambulatory ischaemia (i) achieved less total exercise (248.7 +/- 17.2 vs 318.7 +/- 14.1 s; means +/- SEM) (P less than 0.006), (ii) developed exercise ST deviation earlier (172.4 +/- 14.3 vs 244.8 +/- 16.2 s) (P less than 0.0004) and (iii) had more widespread exercise ischaemia (3.8 +/- 0.3 vs 2.5 +/- 0.2 ECG leads) (P less than 0.005). Positive ambulatory ST segment monitoring was infrequently found (12/80 patients; 15%) in the presence of a negative exercise test but did identify the majority of patients (9/11 patients; 82%) with easily provoked exercise ischaemia and hence strongly positive exercise tests. These data suggest a limited role for routine 24 h ambulatory monitoring after myocardial infarction for the diagnosis of ongoing ischaemia but raise the possibility of an important place for this test in prognosis and risk stratification.
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PMID:Transient ischaemia after acute myocardial infarction: relationship to exercise ischaemia. 204 Mar 22

Plasma levels of catecholamines, beta-thromboglobulin (BTG) and arginine vasopressin (AVP), and degree of pain were examined in 22 patients with suspected uncomplicated myocardial infarction within 24 h following onset of chest pain. Sixteen patients developed infarction with peak creatine phosphokinase at 1280 Ul-1 (range 293-3770 Ul-1). Fifteen healthy men served as controls (C). Arterial adrenaline levels were significantly higher in patients with pain (1.15 +/- 0.23 nmol l-1, n = 8, mean value +/- SEM) than in those without pain (0.60 +/- 0.10 nmol l-1, n = 14, P less than 0.05). Plasma catecholamines were moderately but significantly elevated in myocardial infarction; the concentration of arterial adrenaline was 0.83 +/- 0.14 nmol l-1 and that of arterial noradrenaline was 2.70 +/- 0.28 nmol l-1 compared with 0.44 +/- 0.04 nmol l-1 (P less than 0.025) and 1.47 +/- 0.05 nmol l-1 (P less than 0.0005), respectively, in C. One week later, plasma catecholamines had returned to baseline levels. Plasma BTG showed borderline elevation (1.0 +/- 0.1 pmol l-1) compared with C (0.6 +/- 0.1 pmol l-1, P = 0.04), and remained unchanged 1 week later. Plasma AVP was at baseline level. Uncomplicated myocardial infarction, regardless of size, was associated with only moderately increased sympathetic tone. Plasma adrenaline was related more to the degree of pain than to the presence of acute myocardial infarction. Arterial adrenaline may be a sensitive marker of sympatho-adrenal activity related to pain.
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PMID:Increased arterial adrenaline is related to pain in uncomplicated myocardial infarction. 214 43

1. To examine the metabolic effects of increases in circulating endogenous plasma catecholamines, we measured plasma glucose, potassium and magnesium in 14 patients undergoing elective coronary artery bypass grafting. The patients were randomized into two groups and received either sodium nitroprusside (a direct-acting vasodilator) or trimetaphan camsylate (a ganglion-blocking agent) for routine control of blood pressure during the operation. 2. There were significant differences between the two groups in the levels of all three metabolic variables studied. Plasma glucose levels rose in both groups, but were significantly higher in the sodium nitroprusside group [peak levels 9.14 (SEM 0.72)mmol/l compared with 6.71 (0.88) mmol/l, P less than 0.001, analysis of variance]. The cardioplegia solution caused a large increase in plasma magnesium in both groups but in the sodium nitroprusside group the level rose higher [to 1.59 (0.12)mmol/l compared with 1.34 (0.06)mmol/l] and fell faster (P less than 0.05, analysis of variance). In the group receiving sodium nitroprusside, plasma potassium fell, by a mean of 0.34mmol/l, as plasma catecholamine levels rose; no such fall was seen in the group receiving trimetaphan camsylate (P less than 0.05, analysis of variance). 3. It is concluded that the sympathoadrenal system is important in causing metabolic changes during cardiopulmonary bypass and may be relevant in other conditions such as acute myocardial infarction.
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PMID:Effects of circulating endogenous catecholamines on plasma glucose, potassium and magnesium. 215 47

Coronary artery reperfusion established by thrombolytic agents early in the evolution of an acute myocardial infarction is known to result in the salvage of otherwise jeopardized heart muscle. Recently, experimental evidence has suggested that reactive products of oxygen are formed as a result of reperfusion and can increase the amount of myocardial tissue that becomes irreversibly damaged. The purpose of the present study was to determine if the thrombolytic agent, streptokinase, could serve to scavenge reactive species of oxygen, thereby protecting the myocardium by a mechanism independent of its ability to lyse an occlusive thrombus. Rabbit isolated hearts were perfused at a constant rate with Krebs-Henseleit buffer (25 ml/min, 31 degrees C, pH 7.4) using a modified Langendorff method. Changes in the permeability of the coronary vascular bed were determined with 125I-labeled albumin added to the perfusion buffer. An intraventricular fluid-filled latex balloon connected to a pressure transducer maintained the left ventricle in an isovolumic state and was used to detect changes in myocardial contractility throughout the study protocol. Electrolysis of the oxygenated Krebs-Henseleit perfusion buffer with a 20 mA direct current for 2 min, delivered with a stainless-steel anode (proximal) and a platinum cathode (distal), resulted in the generation of reactive products of oxygen. Perfusion of the isolated heart with buffer containing the products of electrolysis resulted in an increase in mean coronary artery perfusion pressure, from 48 +/- 3 to 121 +/- 6 mm Hg [mean +/- SEM (n = 17)], and an increase in the left ventricular end-diastolic pressure, from 10 +/- 1 to 54 +/- 6 mm Hg. The addition of streptokinase (150 U/ml) or heparin (20 U/ml) to the perfusion medium attenuated the observed increase in coronary artery perfusion pressure from 42 +/- 3 to 73 +/- 9 mm Hg (n = 9) or from 43 +/- 2 to 98 +/- 9 mm Hg (n = 9), respectively. In addition, streptokinase prevented the increase in the left ventricular end-diastolic pressure (11 +/- 1 to 36 +/- 5 mm Hg, n = 9) and preserved left ventricular function as determined by the pressure-volume relationship. Myocardial accumulation of 125I-labeled albumin after exposure of the heart to the reactive products of oxygen was attenuated by the addition of streptokinase or heparin to the buffer solution. The data suggest that streptokinase and, to a lesser extent, heparin may preserve myocardial and coronary vascular function by scavenging reactive oxygen species.
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PMID:Protection of myocardial function and coronary vasculature by streptokinase. 245 50

Previous work has shown that in experimental animal models a lower incidence of arrhythmias and sudden death was observed if the animals were fed cod liver oil or fish oil. After a 48-h control period starting, on average, 8 days after the onset of symptoms, 18 men who were recovering from acute myocardial infarction were given 20 ml d-1 cod liver oil for 6 weeks, either immediately after the control period, weeks 0-6 (n = 10), or during weeks 6-12 (n = 8). Forty-eight-hour Holter monitoring was carried out before cod liver oil administration and at the end of weeks 6 and 12. The eicosapentaenoic acid content of plasma phospholipids was increased by 230% during cod liver oil administration. However, no significant change was observed in the 24-h prevalence of ventricular extrasystoles or other arrhythmias during the study period. The mean ln number of ventricular extrasystoles was 2.95 +/- 0.51 (+/- SEM) during cod liver oil ingestion and 2.63 +/- 0.30 when not taking cod liver oil.
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PMID:Cod liver oil does not reduce ventricular extrasystoles after myocardial infarction. 247 49

Reocclusion of the coronary artery occurs after thrombolytic therapy of acute myocardial infarction despite routine use of the anticoagulant heparin. However, heparin is inhibited by platelet activation, which is greatly enhanced in this setting. Consequently, it is unclear whether thrombin induces acute reocclusion. To address this possibility, we examined the effect of argatroban [MCI9038, (2R,4R)-4-methyl-1-[N alpha-(3-methyl-1,2,3,4-tetrahydro-8- quinolinesulfonyl)-L-arginyl]-2-piperidinecarboxylic acid], a specific thrombin inhibitor, on the response to tissue-type plasminogen activator in a closed-chest canine model of coronary thrombosis. MCI9038 prolonged the thrombin time and shortened the time to reperfusion (28 +/- 2 min vs. 59 +/- 7 min in controls; mean +/- SEM, n = 5, P less than 0.01). At the highest dose, 2.5 mg/kg per hr, complete reocclusion was prevented in four of the five experimental animals, whereas reocclusion occurred in all five controls. However, reperfusion was complicated by cycles of decrease flow, which were abolished by the thromboxane A2 antagonist, GR32191. GR32191 at 1 mg/kg combined with MCI9038 at 0.5 mg/kg per hr prevented reocclusion, whereas, at these doses, either drug alone was without effect. In addition, thromboxane A2 biosynthesis, determined as excretion of its metabolite 2,3-dinor-thromboxane B2, was increased after reperfusion at all doses of MCI9038. These data demonstrate that thrombin impairs thrombolysis induced by tissue-type plasminogen activator in vivo and induces acute reocclusion. Furthermore, the response to thrombin inhibition may be impaired by continued formation of thromboxane A2.
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PMID:Role of thrombin and thromboxane A2 in reocclusion following coronary thrombolysis with tissue-type plasminogen activator. 250 92

Plasma concentrations of immunoreactive atrial natriuretic peptide (mean (SEM] were measured in 135 patients admitted to two coronary care units with myocardial infarction, ischaemic chest pain, or non-ischaemic chest pain. Concentrations were significantly higher in patients with acute myocardial infarction not treated with systemic thrombolysis (60.4 (14.3) pg/ml) than in patients with non-ischaemic chest pain (21.1 (4.3) pg/ml). Patients with ischaemic chest pain had intermediate values (39.3 (7.1) pg/ml). Patients with acute myocardial infarction treated with intravenous streptokinase had normal concentrations of plasma atrial natriuretic peptide (20.2 (3.6) pg/mg), which were significantly lower than those in patients with myocardial infarction not given streptokinase. These changes could not be explained by factors such as age, pre-existing hypertension, renal dysfunction, or cardiac failure, nor treatment other than streptokinase. Raised plasma concentrations of atrial natriuretic peptide in acute myocardial infarction may be a homoeostatic response acting to reduce atrial pressures by natriuresis, diuresis, and venodilatation. The lower concentrations of atrial natriuretic peptide in patients with acute myocardial infarction treated with streptokinase may reflect a short term beneficial haemodynamic effect of streptokinase.
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PMID:Plasma atrial natriuretic peptide in patients with acute myocardial infarction: effects of streptokinase. 252 82

Neutrophils contribute to the healing of and scar formation in myocardium after ischemic injury. Many recent studies indicate that neutrophils may be involved in the genesis and propagation of myocardial ischemia. To characterize neutrophil function in ischemic heart disease, neutrophil chemotaxis, leukotriene B4 (LTB4) generation, and elastase release in plasma were measured in 20 patients with stable angina, 17 patients with unstable angina or acute myocardial infarction (AMI), and 20 age-matched control subjects. Neutrophils from patients with stable angina exhibited markedly increased chemotactic activity and LTB4 generation as compared with the age-matched control subjects (p less than 0.01). Neutrophils of nine of 17 patients with unstable angina or AMI clumped spontaneously ex vivo and exhibited marked pseudopod formation and granule extrusion on electron microscopy. Subsequent chemotactic activity and LTB4 generation by neutrophils from these patients was less than in patients with stable angina, suggesting previous in vivo activation. Plasma levels of peptide B beta, a product of fibrin degradation by human neutrophil elastase, were approximately 15-fold higher (p less than 0.001) in patients with unstable angina or AMI (588 +/- 171 pmol/l, mean +/- SEM) compared with those in patients with stable angina (37 +/- 25 pmol/l) or control subjects (40 +/- 22 pmol/l), confirming intense in vivo neutrophil activation. Our study shows enhanced neutrophil function in patients with ischemic heart disease. The increased neutrophil chemotactic activity and LTB4 generation may be markers of stable angina pectoris. Intense neutrophil activation in unstable angina or AMI, as manifested by morphologic changes in neutrophils and elastase release, may relate to ongoing in vivo cellular activation.
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PMID:Neutrophil function in ischemic heart disease. 253 59

Immediately after balloon dilation of a fresh thrombotic coronary lesion, 5 patients had angina, ST segment elevation, and a striking reduction of blood flow in the dilated artery. A mean (SEM) pressure gradient across the dilated lesion of only 3(1) mm Hg and an average minimum lesion diameter of 1.7 mm indicated that the decline in resting blood flow was not due to obstruction at the site of the original lesion. Neither distal vascular emboli nor side branch occlusions were visible on the angiogram. An increase in distal coronary artery pressure during a subsequent balloon inflation suggested that the site of vasoconstriction was distal to the origin of collateral vessels. The syndrome lasted 48-80 min and was not reversed with nitroglycerin or thrombolytic drugs. Papaverine lessened the syndrome transiently on one occasion. Such microvascular constriction, caused by release of potent vasoconstrictors from the clot, may partly explain the failure of emergency angioplasty to reduce infarct size in acute myocardial infarction.
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PMID:Intense microvascular constriction after angioplasty of acute thrombotic coronary arterial lesions. 256 3

An increase in R wave amplitude and a diminution of S wave amplitude, together with ST segment elevation, have been described as very early electrocardiographic changes during clinical and experimental acute myocardial infarction. The genesis of these QRS changes remains unclear. We assessed the quantitative relationship between the local conduction delay and the formation of the giant R wave, using multiple epicardial, intramural unipolar, and bipolar electrodes in 30 open-chest pigs with acute transmural myocardial ischemia. Blood pressure, heart rate, serum electrolytes, hematocrit, and left ventricular size remained constant, or varied insignificantly throughout the experiments. In nonischemic pigs, transmural left ventricular activation occurred nearly simultaneously, and the activation time was not correlated with the net QRS potential. During acute ischemia, a giant R wave developed at all of the electrodes located within the ischemia region; R wave amplitude began to increase 1 min after coronary artery ligation (p less than 0.05), compared to control amplitude and peaked at 8 min (p less than 0.0001). The degree of conduction delay at a given site was correlated linearly with the local R wave amplitude (average of correlation coefficients +/- SEM at 1 min, r = 0.64 +/- 0.08, and at 8 min, r = 0.81 +/- 0.06). The magnitude of the R wave potential and the conduction delay were greater in regions deep inside the ischemic zone than in the border and normal areas (p less than 0.0001), and were greater in subepicardial than in subendocardial areas (p less than 0.05). In summary, during transmural ischemia, conduction is markedly slowed, and an orderly and discrete wavefront advances toward the center of the ischemic zone from lateral and subendocardial areas. When depolarization is complete in the rest of the heart, this slow activation front becomes temporally isolated and its progression gives rise to a giant R wave, which appears in recordings from overlying electrodes.
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PMID:Origin of the giant R wave in acute transmural myocardial infarction in the pig. 263 38


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