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)

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

To compare angiographically-determined coronary artery disease in diabetic patients with controls, 1,653 patients coming to cardiac catheterization were reviewed retrospectively to find 37 diabetic and 79 control patients matched for sex, age (+/- 3 years), and risk factors (hypertension, hyperlipidemia, and smoking). The severity of coronary artery disease was assessed using an angiographic grading system. The following results were obtained: 16 of 37 diabetic patients (43%) had three-vessel disease compared to 20 of 79 controls (25%). Seventy-six of 111 (68%) diabetic vessels were diseased compared to 110 of 237 control vessels (46%) (P less than 0.005). The total coronary score reflecting total extent of disease for diabetic patients was 371 (mean 10.0 +/- (SEM) compared to 594 for controls (mean 7.5 +/- 0.7, (P less than 0.01). Diabetic patients had a statistically similar number of diffusely diseased vessels as controls (28% vs 22%). There were only three of 76 diabetic vessels (4%) considered inoperable compared to seven of 110 (6%) control vessels. We conclude that diabetic patients with chest pain have more coronary artery disease than nondiabetics, but no more diffuse or inoperable disease.
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PMID:Diffuse coronary artery disease in diabetic patients: fact or fiction? 61 80

Twenty patients with fixed coronary artery obstruction were studied during rapid atrial pacing and methoxamine infusion. During pacing to heart rates of 142 +/- 4 (mean +/- SEM) beats per minute coronary sinus flow increased from 108 +/- 8 to 187 +/- 15 cc/min and myocardial oxygen consumption increased by + 80 +/- 11%. During methoxamine infusion that raised arterial systolic pressure to 196 +/- 5 mm Hg, similar increases in coronary sinus flow (to 179 +/- 13 cc/min) and myocardial oxygen consumption (+ 77 +/- 12%) occurred. Chest pain and ischemic ST segment changes developed in 17 and 14 patients respectively during atrial pacing, an incidence significantly greater (P less than 0.05) than during infusion of methoxamine (6 and 3 patients). Myocardial lactate extraction which averaged 26 +/- 4% during control was decreased to 10 +/- 8% during pacing and to 24 +/- 7% during methoxamine; the difference between decreases was not significant. The data show that at similar increases in myocardial oxygen consumption stress of increased heart rate results in more myocardial ischemia than stress of increased afterload.
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PMID:Effects of pharmacologically-induced hypertension on myocardial ischemia and coronary hemodynamics in patients with fixed coronary obstruction. 61 96

First heart sound (S1) energy spectra in isovolumic systole, hemodynamics, and angiographic left ventricular wall motion (LVWM) at rest and with atrial pacing were compared in 27 patients who underwent diagnostic cardiac catheterization and angiography because of chest pain. Eighteen patients were found to have coronary artery disease (CAD) and nine patients, normal coronary arteries. Eleven of the 18 CAD patients (61%) had a mean reduction in the spectral energy of S1 of 6.5 +/- 1.4 (SEM) dB below control (-52%), during interruption of ischemic stress of rapid atrial pacing, compared to only one of nine patients without CAD (P less than 0.05). Only five CAD patients (28%) had an abnormal rise (greater than or equal to 5 mm) in left ventricular end-diastolic pressure (LVEDP) either during or upon interruption of pacing, and six (33%) had ischemic ST-segment depression greater than or equal to mv in the ECG. Similarly two patients free of CAD (22%) had an abnormal increase in LVEDP, and none had ECG evidence of ischemia. Seventeen CAD patients (94%) had segmental LVWM abnormalities at rest or with interruption of pacing, while three patients with normal coronary arteries (33%) had abnormal angiographic LVWM (P less than 0.01). Thus, reduction is S1 spectral energy is a common accompaniment of myocardial ischemia. In the present study, it was more frequently observed than abnormalities in either the ECG or LVEDP, but was not was consistently seen as segmental left ventricular wall motion abnormalities.
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PMID:Spectral energy of the first heart sound in acute myocardial ischemia. A correlation with electrocardiographic, hemodynamic, and wall motion abnormalities. 62 70

The etiology of chest pain in patients with the anginal syndrome and normal coronary arteriograms has not been established. There has been no explanation for the association of electrocardiographic, hemodynamic, and myocardial metabolic abnormalities consistent with myocardial ischemia observed in some patients with this disorder. Historical, clinical, laboratory, and hemodynamic data of 45 patients (24 females, 21 males), mean age 47.5 years, with chest pain and normal coronary arteriograms are reviewed. Left ventriculograms were analyzed utilizing the single-plane cineangiographic measurement of left ventricular volume. Systolic ejection fractions for the 45 patients ranged from 0.66 to 0.91 (mean 0.80 +/- 0.01 SEM). Ventricular volumes determined angiographically revealed mean end-diastolic and end-systolic volumes of 83 +/- 5 ml and 18 +/- 2 ml, respectively. The mean changes in longitudinal and transverse segmental axis shortening that occurred during ventricular systole were 28.8% and 50.7%, respectively. These elevated values for ejection fraction, and reduced measurements of ventricular volumes, indicate that some patients with chest pain and normal coronary arteriograms may have small hearts with hyperdynamic ventricular contraction. These findings suggest that hyperdynamic ventricular contraction may play a causative role in the development of transient, angina-like chest pain in these patients. The etiology of the proposed hyperdynamic ventricle is unknown, but it may be attributable to increased beta-sympathetic stimulation of the myocardium.
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PMID:Elevated ejection fractions in patients with the anginal syndrome and normal coronary arteriograms. 73 29

The effects of intravenous propranolol on left ventricular wall motion and hemodynamics were studied in 16 patients, 12 with significant coronary artery disease and four with chest pain but no coronary disease. Eight patients received 0.10 mg/kg and eight received 0.15 mg/kg of propranolol intravenously. All underwent atrial pacing at a constant rate. Left ventricular angiograms were performed before and 20 minutes after propranolol. At both doses, propranolol caused no significant change in left ventricular systolic or diastolic pressures, either before or immediately following ventriculography. Cardiac index fell significantly (3.4 plus or minus 0.2 [SEM] to 2.6 plus or minus 0.1 L/min/m-2) with the higher dose only. Of the ten patients with coronary artery disease and adequate ventriculograms, one patient had a normal left ventricle, two had regional hypokinesis, only three had areas of hypokinesis and akinesis, two had dyskinetic and akinetic areas, and two had areas of hypokinesis, akinesis and dyskinesis. No changes in regional contractility occurred with propranolol except for a minimal increase in hypokinesis in one patient at each dosage and equivocal development of a new area of slight hypokinesis in one patient and minimal apex of dyskinesis in another at the higher dosage. Of the four patients without coronary artery disease, two were affected by propranolol, one with initial regional akinesis and dyskinesis had slight worsening with propranolol and one with regional hypokinesis developed a definite new area of hypokinesis. Therefore, propranolol, even in large intravenous doses, resulted in no significant change in left ventricular wall motion in patients with coronary artery disease.
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PMID:Left ventricular wall motion response to intravenous propranolol. 113 15

In order to evaluate the effects of intracoronary acetylcholine on coronary resistance vessels, oxygen saturation in coronary sinus blood was continuously measured to compare its dynamic changes during intracoronary injection of acetylcholine in both patients with variant angina and control subjects. Group 1 consisted of 6 patients without coronary artery disease. Group 2 consisted of 10 patients with variant angina and spasm in the left anterior descending coronary artery. A fiberoptic reflection oximetry system was used for the continuous measurement of coronary sinus venous oxygen saturation. Acetylcholine (20 micrograms) was injected directly into the left coronary artery over 30 s. In the group 1 patients, coronary sinus venous oxygen saturation was increased from 39 +/- 2% (mean +/- SEM) to 54 +/- 3% at 30 s, continuously climbed to 70 +/- 3% at 60 s and then gradually decreased to 53 +/- 5% at 120 s after the initiation of intracoronary injection of acetylcholine. In contrast, in the group 2 patients, coronary sinus venous oxygen saturation was transiently increased from 39 +/- 2% to 56 +/- 4% at 30 s, reversed, decreased to 52 +/- 4% at 60 s and then rapidly decreased to 36 +/- 3% at 120 s with the onset of chest pain associated with electrocardiographic ischemic changes. Coronary arteriography during attacks demonstrated a total or subtotal occlusion of the left anterior descending coronary artery due to severe spasm in all of the 10 patients. The extent of increases in coronary sinus venous oxygen saturation at 30 s after acetylcholine injection was not significantly different between the two groups (group 1: 15 +/- 4%, group 2: 17 +/- 3%). Heart rate, blood pressure and rate-pressure product were essentially unchanged at 30 s after intracoronary injection of acetylcholine in both groups. These data suggest that in control adult humans, coronary blood flow was increased through dilatation of resistance vessels by acetylcholine, while in patients with variant angina, coronary blood flow was transiently increased by dilatation of resistance vessels, after which it was suddenly decreased by spasm of an epicardial artery induced by this agent. Relaxant responses to acetylcholine of coronary resistance vessels appear to be preserved well in patients with variant angina.
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PMID:Biphasic changes (initial increase and late decrease) in coronary sinus venous oxygen saturation during anginal attacks induced by intracoronary acetylcholine in patients with variant angina. 130 Dec 47

The purpose of this study was to evaluate the significance of increased Tl-201 uptake by the lungs after oral dipyridamole testing. In conjunction with myocardial perfusion scintigraphy, intravenous dipyridamole has been recently approved as an alternative to exercise for the evaluation of coronary artery disease in patients who cannot adequately exercise, and it will largely replace oral dipyridamole testing. This study contributes to the understanding of the significance of increased lung thallium uptake during pharmacologic stress testing. Oral dipyridamole, 400 mg, was administered to 192 patients undergoing Tl-201 imaging for clinical indications. Mild adverse effects occurred in 31% of patients (chest pain, nausea, headache, or flushing). Dipyridamole had minimal hemodynamic effects. The lung/heart thallium activity ratio was determined in 152 patients. These were subdivided into four groups according to the presence or absence of ischemia, transient myocardial perfusion defect, or scar as indicated by a fixed myocardial perfusion defect. In 61 patients without transient myocardial perfusion defect or fixed myocardial perfusion defect (group 1), the lung/heart thallium activity ratio was 0.39 +/- 0.01 (mean +/- SEM). In 31 patients without transient myocardial perfusion defect but with fixed myocardial perfusion defect (group 2), the lung/heart thallium activity ratio was higher, 0.44 +/- 0.02 (P less than 0.05). In 27 patients with transient myocardial perfusion defect but no fixed myocardial perfusion defect (group 3) and in 33 patients with both transient myocardial perfusion defect and fixed myocardial perfusion defect (group 4), the lung/heart thallium activity ratio was 0.51 +/- 0.03 and 0.52 +/- 0.03, respectively, both significantly higher than either group 1 or group 2 (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of increased Tl-201 uptake by the lungs in patients undergoing oral dipyridamole-thallium myocardial imaging. 161 45

Experimental coronary occlusion is accompanied by an acute impairment of the baroreceptor-heart rate reflex. This study was planned to determine whether this impairment also occurs in humans. In 30 patients admitted to a coronary care unit for an anterior (n = 14) or inferior (n = 16) transmural myocardial infarction (MI), we measured 1) the increase in RR interval induced by stimulating carotid baroreceptors through progressive reductions in neck chamber pressure, 2) the increase in RR interval induced by stimulating arterial baroreceptors through intravenous boluses of phenylephrine, and 3) the reduction in RR interval induced by deactivating arterial baroreceptors through intravenous boluses of nitroglycerin. Measurements were performed 49.5 +/- 2.4 hours (mean +/- SEM) after the MI. The results were compared with those of five age-matched patients admitted to the coronary care unit for chest pain and found free from ischemic heart disease. The sensitivity of the carotid baroreceptor-heart rate reflex (slope of the linear regression of RR interval over neck pressure changes) was markedly less in MI than in control patients (3.8 +/- 0.5 vs. 5.9 +/- 0.6 msec/mm Hg, p less than 0.05), the reduction being similar in patients with anterior and inferior MI. This was the case also for the baroreflex sensitivity measured by the phenylephrine and the nitroglycerin methods (slope of the linear regression of RR interval over systolic blood pressure changes). However, 10.2 +/- 0.3 days later, the baroreflex sensitivity measured by all three methods increased significantly (p less than 0.05 or 0.01) and became similar to that of control subjects, which showed no significant change from the early to the late period after admission into the coronary care unit. Thus, MI is accompanied by an acute marked impairment of the baroreceptor control of the heart in humans, and this is the case both for an anterior and an inferior MI. The impairment is largely transient in nature, however, and a clear-cut recovery of the baroreflex can be seen a few days later.
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PMID:Early alterations of the baroreceptor control of heart rate in patients with acute myocardial infarction. 210 4

Treadmill testing (TMT) was performed on 76 frail but ambulatory subjects, between 64 and 84 years of age, who had common health problems contributing to physical limitations but had no clinically apparent heart disease. The subjects achieved a mean symptom-limited maximal heart rate of 140.1 +/- 2.07 (SEM) beats per minute which was 80.2 +/- 2.1% of the predicted maximum for age. By standard criteria, ischemic responses were noted in only 5 subjects (6.6%). Three responses were categorized as inconclusive (multifocal ventricular ectopy, chest pain without electrocardiographic change, and prompt ST depression upon standing). TMT was well tolerated, with no significant difficulties encountered. Even for those frail elderly with diseases and physical impairments, symptom-limited TMT may be used with low risk to quantify functional capacity and for exercise prescription. Attempts to screen more intensively for cardiac disease may be irrelevant to their immediate need for maintaining function.
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PMID:Treadmill exercise electrocardiography in the elderly with physical impairments. 214 24


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