Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten patients with severe congestive heart failure after acute myocardial infarction were treated with 40 mg isosorbiddinitrate-retard every 4 hours and additional sublingual nitroglycerine. There was a prompt improvement of hemodynamic parameters which was maintained for 24 hours: pulmonary capillary wedge pressure (PCW) decreased within 10 min from 26 +/- 5 (X +/- SEM) to 17 +/- 2 mm Hg (p less than 0.01) and mean arterial pressure from 109 +/- 7 to 98 +/- 6 mm Hg. The heart rate remained constant, and the cardiac index improved from 2.3 +/- 0.2 to 2.5 +/- 0.21/min/m2. The fall in blood pressure was dependent on the pretreatment pressure: it was significantly greater in patients with elevated blood pressure and only slight in those with a low pretreatment blood pressure. In the presented series of patients neither adverse effects or symptoms nor a critical reduction of blood pressure were observed. Combined oral treatment with isosorbiddinitrate and nitroglycerine can therefore be carried out without invasive blood pressure monitoring.
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PMID:[Peroral nitrate therapy in severe cardiac insufficiency following acute myocardial infarct]. 10 29

Pulmonary artery wedge and plasma colloid osmotic pressures and their relationship to pulmonary edema were investigated in 26 patients with acute myocardial infarction of whom 14 developed pulmonary edema. In the absence of pulmonary edema, both the pulmonary artery wedge pressure and plasma colloid osmotic pressure were in normal range; after onset pulmonary edema, a moderate increase in pulmonary wedge pressure and reduction in plasma colloid osmotic pressure were observed. When the gradient between the plasma colloid osmotic pressure and the pulmonary artery wedge pressure was calculated, highly significant differences were demonstrated (P less than 0.002). In the absence of pulmonary edema, this gradient averaged 9.7 (plus or minus 1.7 SEM) torr; following appearance of pulmonary edema, it was reduced to 1.2 (plus or minus 1.3) torr. During therapy with digoxin and furosemide, reversal of pulmonary edema was closely related to a concomitant change in the colloid osmotic-hydrostatic pressure gradient. These observations indicate that both increases in pulmonary capillary pressure and decreases in colloid osmotic pressure may follow the onset of pulmonary edema. Such decline in colloid osmotic pressure and especially the reduction in colloid osmotic-hydrostatic capillary pressure gradient may favor transudation of fluid into the lungs.
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PMID:Pulmonary edema related to changes in colloid osmotic and pulmonary artery wedge pressure in patients after acute myocardial infarction. 23 2

A radioimmunoassay was developed to measure serum levels of the B isoenzyme of creatine kinase(ATP: creatine N-phosphotransferase, EC 2.7.3.2) (CPK) in order to evaluate the time course and frequency of MB isoenzyme elevation in patients with acute myocardial infarction. The method can identify as little as 0.2 ng of the B portion of the CPK-MB isoenzyme, does not significantly crossreact with CPK-MM isoenzyme, and is not affected by storage of serum at --20 degrees CPK isoenzyme containing B subunits was detected in 48 out of 51 sera from normal adults; serum levels in these individuals ranged between 1.2 and 12.5 ng/ml [mean +/- SEM was 2.7 +/- 0.30 ng/ml]. The mean serum level of CPK-B isoenzyme in a pool of sera obtained from 100 normal subjects was 2.9 +/- 0.35 ng/ml; two patients with rhabdomyolysis that were studied had serum CPK-B isoenzyme levels of 2.5 and 3.5 ng/ml, respectively. In contrast, serum levels of the CPK-B isoenzyme were markedly elevated in sera from 18 patients with acute myocardial infarcts when obtained within 12 hr after hospital admission; the mean +/- SEM concentration was 56 +/- 7.8 ng/ml. We performed serial determinations on 14 patients with acute myocardial infarcts and demonstrated that maximal serum CPK-B levels occurred within the first 12 hr after admission and were lower thereafter. The serum concentration of B-containing CPK isoenzyme in 19 additional patients admitted with chest pain but without acute myocardial infarction was 3.4 +/- 0.50 ng/ml. Thus, radioimmunoassay measurement of CPK-B isoenzyme appears to be a useful and sensitive test for the detection of acute myocardial infarcts in patients.
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PMID:Radioimmunoassay of creatine kinase-B isoenzyme in human sera: results in patients with acute myocardial infarction. 26 11

Platelets may contribute to the pathogenesis of atherosclerosis and to the complications of coronary atherosclerosis, acute myocardial infarction, unstable angina, and sudden cardiac death. In addition, platelets may contribute to saphenous vein aortocoronary graft occlusion. Of 104 men with coronary artery disease, platelet survival (SURV) (chromium51 labeling) was shortened in 68% (3.1+/-0.03 days [average+/-SEM]; normal, 3.7+/-0.03 days; P greater than .001). Three platelet-suppressant drugs, sulfinpyrazone, clofibrate, and dipyridamole increased SURV. Saphenous vein graft occlusion was associated with shortened SURV. Of 36 men with occlusion of at least one graft, SURV was shortened in 35 (2.5+/-0.08 days), whereas in 19 with all grafts open, SURV was shortened in six (3.5+/-0.10 days; P less than .01). These drugs increased SURV (2.3 +/- 0.08 to 2.7 +/- 0.11 days; P less than 0.1) and were associated with improved graft patency (four of 32 grafts after initial bypass vs 30 of 34 grafts open after second operation).
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PMID:Platelet-suppressant therapy in patients with coronary artery disease. 30 69

Serum creatine kinase (CK) isoenzyme MB and total CK activity concentrations in 11 patients with acute myocardial infarction (AMI) were compared with the corresponding enzyme activities in 25 patients after coronary bypass surgery, not complicated clinically by AMI. Peak CK-MB occurred 2 +/- 0 (mean +/- SEM) hours after the end of surgery (mean duration of operation 6 hours), but 17 +/- 1 hours from the onset of symptoms in AMI. The plasma half"life for CK-MB was 11 +/- 1 hours under both conditions. Peak total CK was found after about 20 hours in both series of patients. Total CK half-life was 17 +/- 2 hours in AMI, but 30 +/- 3 hours following surgery. CK kinetics were thus different in these two situations, indicating different mechanisms for the elevations of serum CK-MB activity. In conclusion, the time course for the transient CK-MB elevation following bypass surgery should be considered in the diagnosis of peri operative infarction.
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PMID:Serum CK-MB kinetics in acute myocardial infarction and after coronary bypass operations. 31 44

Left ventricular end-diastolic pressure (P) and volume (V) were measured in 12 patients with acute myocardial infarction. It was assumed that the diastolic P-V relationship was exponential and corresponded to the formula P=be KV. In 7 patients submitted to volume loading, several data points of this relationship were obtained and at zero volume, the mean intercept with the ordinates was 0.037+/-0.015 kPa (SEM) (0.28+/-0.12 mmHg). In the other 5 patients, the P-V curve was plotted through this intercept and the pressure and volume co-ordinates obtained by control. The K coefficient (passive elastic modulus) was greater, and the normalised left ventricular compliance index (dV/VdP) was smaller in the infarct group than in the control group. This suggests decreased left ventricular compliance during the acute phase of myocardial infarction. By comparing left ventricular function curves plotted using either end-diastolic pressure or end-diastolic volume as the stretch index it is possible to evaluate the relative participation of decreased compliance and depressed contractility in global left ventricular function.
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PMID:Left ventricular compliance in acute myocardial infarction in man. 87 Jan 96

The effect of hyaluronidase on myocardial ischemic injury was examined in 13 patients with acute myocardial infarction, and the results were compared with 11 patients who did not receive hyaluronidase. A 35-electrode precordial mapping method was used to assess the rate of resolution of ST segment elevations. In the 11 control patients, the sum of ST segment elevations (sigmaST) fell after 2 hours to an average of 93.5% plus or minus 17.3% (SEM) and after 24 hours to 89.6% plus or minus 7.6% of the initial values, while the number of electrodes exhibiting ST segment elevations exceeding 0.1 mV (NST) fell to 98.0% plus or minus 12.3% and 94.3% plus or minus 10.4% of the initial values respectively. In the hyaluronidase-treated group, at the same time sigmaST fell significantly more (P less than 0.05), to 54.1% plus or minus 5.0% and 51.3% plus or minus 11.8% and NST was also more markedly reduced (P less than 0.05) to 50.7% plus or minus 7.8% and 50.1% plus or minus 12.4%, thus indicating that hyaluronidase can accelerate the reduction of myocardial ischemic injury in patients with acute myocardial infarction.
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PMID:Effects of hyaluronidase administration on myocardial ischemic injury in acute infarction. A preliminary study in 24 patients. 111 65

Precordial electrocardiographic mapping has been proposed as a method for evaluating the extent of myocardial injury in patients with acute myocardial infarction. To assess the relationship between direct measures of myocardial cell damage and findings obtained by precordial mapping, the left anterior descending coronary artery (LAD) was occluded in dogs instrumented for simultaneous recording of epicardial and precordial electrocardiograms. The sum in millivolts of ST-segment elevation recorded from 30 electrodes placed in a Silastic grid sutured to the epicardium (EPIsigmaST) was compared to that recorded from 30 precordial electrodes (PresigmaST). While ischemic injury was: 1) maintained constant with a fixed occlusion; 2) reduced by partial reperfusion; 3) increased by addition of a second occlusion; or 4) increased repeatedly by intermittent infusions of isoproterenol, EPIsigmaST and PresigmaST were always closely correlated in each of the 16 dogs studied: r equal 0.92 plus or minus 0.01 (SEM). In seven control dogs, 30 minutes after coronary occlusion, PresigmaST had fallen to 77.4 plus or minus 6.6% of its value 15 minutes postocclusion. In seven experimental dogs, two branches of the LAD were occluded. Fifteen minutes after double occlusion, one occlusion was released; 30 min after the initial occlusion PresigmaST had fallen significantly more than control, to 43.1 plus or minus 13.1% of its value 15 minutes postocclusion. Simultaneously, epicardial sites in the reperfused area also showed normalization of ST segments and 24 hours later exhibited normal myocardial creatine phosphokinase activity and normal histologic appearance. During the same experiment, the mean precordial R wave voltage of sites with ST-segment elevations exceeding 0.15 mV 15 minutes following occlusion fell significantly (P less than 0.05) more in the control group (from 1.14 plus or minus 0.15 to 0.75 plus or minus 0.06 mV) than in the reperfused group (from 1.06 plus or minus 0.09 to 0.96 plus or minus 0.17 mV) during the ensuing 45 minutes. Thus, more rapid normalization of PresigmaST or preservation of precordial R wave voltage reflected the actual prevention of myocardial necrosis by reperfusion. These findings demonstrate the usefulness of precordial electrocardiographic mapping for evaluation changes in myocardial ischemic injury. Sites at which appearance of epicardial ST segment is not a reliable index of ischemic injury were associated with the development of intraventricular conduction blocks with Q to intrinsic deflection intervals exceeding 40 mesc or QRS durations exceeding 65 msec; these changes were associated with precordial RSR' configurations. Such sites, whether recorded from precordial or epicardial leads, should be excluded from ST-segment measurements used in the assessment of myocardial ischemia.
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PMID:Evaluation of precordial electrocardiographic mapping as a means of assessing changes in myocardial ischemic injury. 113 19

To examine whether atrial natriuretic factor (ANF) is secreted adequately in the early phase of myocardial infarction, plasma ANF concentration and clinical parameters, including hemodynamic variables, were studied in 118 patients with acute myocardial infarction (AMI). The patients were divided into 2 subgroups according to the absence (group A, n = 41) or presence (group B, n = 77) of a history of valvular heart disease, previous myocardial infarction, hypertension, or renal failure. Although no significant difference in atrial pressure after the infarction was found between the 2 groups, the plasma ANF level was significantly lower in group A than in group B (76 +/- 6 vs. 185 +/- 26 pg/ml; mean +/- SEM, p < 0.01). Plasma ANF was correlated with pulmonary capillary wedge pressure in group B (r = 0.54, p < 0.001), whereas no relationship with hemodynamic parameters was observed in group A. In 56 of the 118 patients (group A, n = 18; group B, n = 38), the pulmonary arterial plasma level was significantly higher in group A (p < 0.05), whereas the difference was not significant in group B. Seven of the 8 expired cases among these 56 patients had peripheral plasma ANF levels of more than 150 pg/ml, which were higher than those in pulmonary arterial plasma. These observations suggest firstly that the plasma level of ANF is lower in patients with a new onset of myocardial infarction compared to those with a history of cardiac or renal diseases, and secondly that stimulated ANF release originates not only from the right side of the heart, but also from additional site(s), particularly in patients with chronic ventricle overload and a poor prognosis.
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PMID:Plasma atrial natriuretic factor in patients with acute myocardial infarction. 128 94

It has been reported that intraaortic balloon pumping can prevent reocclusion after coronary angioplasty for acute myocardial infarction. The speculated mechanism has been the production of markedly enhanced diastolic coronary perfusion pressure; however, most studies have reported that intraaortic balloon pumping has little effect on coronary blood flow. To assess the effectiveness of this procedure, we studied 12 patients with acute anterior myocardial infarction who were undergoing coronary angioplasty and intraaortic balloon pumping. After successful angioplasty, coronary blood flow velocity was measured with a coronary Doppler catheter before and during intraaortic balloon pumping. Although mean coronary blood flow velocity was unchanged, intraaortic balloon pumping increased peak coronary blood flow velocity from 34.6 +/- 5.0 cm/sec (mean +/- SEM) to 46.7 +/- 5.8 cm/sec (p < 0.005). Such an increase in peak coronary blood flow velocity seemed to be a mechanism by which intraaortic balloon pumping could prevent reocclusion after coronary angioplasty for acute myocardial infarction.
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PMID:Effects of intraaortic balloon pumping on coronary hemodynamics after coronary angioplasty in patients with acute myocardial infarction. 144 77


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