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)

Oxyhemoglobin dissociation (OHD) curves were performed on whole blood (WB) from 20 patients with anginal pain, normal hemodynamics, and normal coronary arteries, as demonstrated by selective coronary cinearteriography. OHD curves in 19 of 20 patients, from zero to full saturation, were nearly identical to those in normal control subjects with values for P(50) (Po(2) at 50% saturation and pH 7.4) of 26.7+/-1.5 (mean+/-SD of the mean) torr (mm Hg) and red blood cell (RBC) levels of 2,3-diphosphoglyceric acid (2, 3-DPG) of 0.72+/-0.10 (mean+/-SD of the mean) M/M hemoglobin (Hb). Normal values for nonsmoking adults were: P(50), 26.6+/-1.4 (mean+/-SD of the mean) torr: and RBC 2,3-DPG, 0.81+/-0.09 (mean+/-SD of the mean) M/M Hb. Mean levels of carbon monoxide were normal at 0.14+/-0.01 (mean+/-SEM) ml/100 ml WB in 10 patients who were nonsmokers and 0.45+/-0.15 (mean+/-SEM) ml/100 ml WB in 10 smokers. In one patient, a heavy smoker with markedly elevated blood carbon monoxide levels, an abnormal leftward shift of the OHD curve was observed. This was corrected after discontinuation of smoking. In utilizing these methods, we could not detect consistent abnormalities of Hb affinity for oxygen at rest in the patients studied, which suggests that a defect in oxygen transport at rest is an unlikely explanation for the symptoms of chest pain in patients with the anginal syndrome and normal coronary arteriograms.
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PMID:Hemoglobin affinity for oxygen in the anginal syndrome with normal coronary arteriograms. 484 50

Responses of heart rate and blood pressure to transient myocardial ischemia were analyzed in patients with variant angina. Heart rate changes during ST segment elevation were examined by means of a Holter ECG monitoring system. All 27 ST segment elevations from 10 patients with anterior ischemia were accompanied by an increase in heart rate by 12 +/- 2 bpm (mean +/- SEM, p less than 0.001) at peak ST segment elevation. With inferior ischemia in nine patients, heart rate decreased significantly by 4 +/- 1 bpm (n = 28, p less than 0.001). However, 9 of these 28 ST segment elevations showed a biphasic response of heart rate, that is, an initial increase and subsequent decrease. Such heart rate changes were not different between ST segment elevations with and without chest pain. With chest pain systolic blood pressure rose in anterior ischemia by 42 +/- 5 mm Hg (n = 10, p less than 0.001) but fell in inferior ischemia by 22 +/- 8 mm Hg (n = 7, p less than 0.05). We conclude that a different cardiovascular reflex occurs in response to inferior versus anterior ischemia and it is independent of chest pain.
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PMID:Reflex heart rate and blood pressure changes during ST segment elevation in patients with variant angina. 649 87

Previous reports have suggested that creatine kinase isoenzymes are elevated in patients with chronic renal failure and thus are less useful in the evaluation of chest pain in such patients. Our data in 88 patients with chronic renal failure receiving maintenance dialysis confirm this observation for total plasma creatine kinase. However, elevations in MB and BB creatine kinase, although statistically significant, were biologically unimpressive (5.9 +/- 0.05 [SEM] IU/L compared with 4.8 +/- 0.04 IU/L for MB creatine kinase [p less than 0.02], and 5.5 +/- 0.08 ng/ml compared with 3.2 +/- 0.05 ng/ml for BB creatine kinase [p less than 0.0002] ), and were unlikely to cause diagnostic confusion. In 92% of patients with chronic renal failure, plasma MB creatine kinase activity was within the normal range (less than 13 IU/L). Eight percent of patients manifested abnormal MB creatine kinase values; the highest was 20 IU/L. The glass bead method for measuring MB creatine kinase was used to avoid the potential confusion induced by non-creatine kinase-mediated fluorescence, which occurs in the region of MB and BB creatine kinase on electrophoresis. The infrequent and modest increases in plasma MB creatine kinase observed in patients with chronic renal failure should be appreciated, but it should not cause diagnostic confusion, because acute myocardial infarction usually results in more substantial elevations of MB creatine kinase.
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PMID:Unmasking artifactual increases in creatine kinase isoenzymes in patients with renal failure. 674 38

Although coronary artery disease and gastroesophageal reflux disease are common conditions which, therefore, may coexist, it is unknown whether or not the presence of one affects the other. We performed esophageal acid perfusion tests, with concurrent blood pressure, heart rate, and 12-lead electrocardiographic monitoring, in 37 patients, 25 with angiographically documented coronary disease and 12 with normal coronary arteries. Rate-pressure product, an index of myocardial work load, was calculated. In patients with coronary disease who developed chest pain during acid perfusion, rate-pressure product increased from 10.0 +/- 1.0 x 10(3) (mean +/- SEM) basally to 15.2 +/- 1.5 x 10(3) (p less than 0.001), and 3 of 9 patients showed concomitant electrocardiogram evidence of myocardial ischemia. In addition, in coronary disease, 64% of patients with infrequent or absent reflux symptoms by history had positive acid perfusion tests, and 56% of patients with coronary disease who developed pain during esophageal acid perfusion could not distinguish that pain from their usual angina. We conclude that in coronary disease, acid perfusion (and, presumably, gastroesophageal reflux) resulting in chest pain causes rate-pressure product elevation and can induce myocardial ischemia. The presence of esophageal acid sensitivity is not accurately predicted by clinical history in coronary disease, and pain of esophageal origin is often confused with angina.
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PMID:Esophageal acid perfusion in coronary artery disease. Induction of myocardial ischemia. 686 55

In this double-blind randomized study, 19 patients with acute transmural myocardial infarction were treated with methylprednisolone administered 4.4 +/- 0.7 hours (+/- SEM) after the onset of chest pain, and were compared with 21 patients who received placebo 4.5 +/- 0.4 hours after the start of clinical symptoms. The two groups were comparable in reference to sex, prevalence of risk factors, clinical status on admission, location of myocardial infarction and magnitude of ischemic injury as assessed by standard ECGs and precordial ST-segment and QRS maps. The treated patients, however, were older than the patients who received placebo. Methylprednisolone in an i.v. dose of 2.0 g was administered on admission and a similar dose was infused 3 hours later. Placebo administration followed an identical schedule. Mortality, cardiac rupture, incidence of ventricular arrhythmias, blocks, extension of myocardial infarction, pericarditis, postinfarction chest pain, persistent ST-segment elevation at discharge, and change in Killip class during hospitalization were the same in both groups. Peak enzyme values, and changes in ECG variables pertaining to resolution of ST-segment elevation or development of QRS evolutionary alterations were similar in both groups. Follow-up for 6 months did not reveal any differences in the clinical course of the two groups. Methylprednisolone infused in a total dose of 4.0 g within 12 hours after the onset of chest pain in patients with acute transmural myocardial infarction does not result in any demonstrable beneficial or harmful effects.
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PMID:Effects of methylprednisolone on the ischemic damage in patients with acute myocardial infarction. 704 10

The candidacy for streptokinase (SK) infusion was studied in 95 patients displaying ECG evidence of acute or impending infarction who were catheterized within 5 hours of the onset of chest pain. Intracoronary SK was administered to 84 patients in whom occlusions of the infarct-related vessel were identified, with early recanalization having been achieved in 74 (88%). Because of completeness of studies, a data base of 72 patients was employed for further analysis. Recanalization was sustained at follow-up in 45 of 55 patients (82%). Spontaneous thrombolysis was demonstrated at follow-up in five patients (8%) initially resistant to SK, and rethrombosis occurred in 10 patients (18%). Preservation of R waves relative to Q wave depth was limited to patients with less than 90% residual stenosis. Eight of nine patients with continuing thrombolysis and patients with recanalized occlusions of the left anterior descending coronary artery displayed more impressive increases in mean (+/- SEM) ejection fraction (47% +/- 4% to 53% +/- 5% [p less than 0.05], and 47% +/- 3% to 52% +/- 5, respectively). The ejection fraction also increased significantly in 15 patients with pre-SK values of less than 50% (41% +/- 2% to 48% +/- 3%; p less than 0.05). Ventricular function deteriorated in SK failures. Reperfusion arrhythmias occurred in 28 of 62 recanalized patients (45%). Minor bleeding tendencies were displayed in 18 of 72 patients (25%). Major hemorrhages, one of which may have been fatal, occurred in four patients (5.6%). Of 84 patients, four (4.7%) died, two of whom were in cardiogenic shock when first seen. In contrast, there were 11 deaths (11.8%) in a consecutive simultaneously enrolled series of 93 control patients with similar entry criteria (p less than 0.05). Two additional SK-treated patients died, 16 and 30 days after treatment, both more than a week after surgical revascularization. It is concluded that SK recanalization is a promising new therapy that may decrease mortality and preserve myocardial function in certain circumstances. Its efficacy in a setting closer to the mainstream of cardiologic practice extends the favorable experience issuing from earlier clinical investigations.
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PMID:Intracoronary streptokinase in clinical practice. 712 13

The feasibility of imaging the inflammatory response to acute transmural myocardial infarction in man using biologically active indium-111 (111In)-labeled autologous leukocytes was assessed in 36 patients. Indium-111 leukocytes (approximately 500 microCi) were injected i.v. 18-112 hours after the onset of chest pain. Cardiac imaging was performed 24 hours later with a mobile gamma camera. Twenty-one patients had positive images and 15 had negative images. The percent of positive images increased as the interval between infarction and 111In-leukocyte injection shortened; all patients injected within 24 hours of infarction had positive images. Patients with positive images were injected with 111In leukocytes earlier after infarction (mean +/- SEM, 43 +/- 4 vs 63 +/- 7 hours; p less than 0.05) and were younger (53 +/- 2 vs 65 +/- 3 years; p less than 0.05) than those with negative images. Several other parameters that could possibly have affected the imaging results were examined and were not significantly different in patients with positive and negative images. These included peak serum creatine kinase, location of infarction, incidence of pericarditis, use of antiinflammatory drugs (aspirin and indomethacin) or membrane-active antiarrhythmic drugs (lidocaine and procainamide), peripheral leukocyte count and cell labeling efficiency. The function of the labeled cell was similar in patients with positive and negative images. Six patients with acute infarction serving as controls and given free 111In oxine and six patients with stable coronary artery disease given 111In leukocytes all had negative cardiac images.
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PMID:Imaging the inflammatory response to acute myocardial infarction in man using indium-111-labeled autologous platelets. 747 38

Time delays to fibrinolytic treatment and outcome were assessed in 100 consecutive patients, with suggestive symptoms and electrocardiographic changes of acute myocardial infarction, admitted to the coronary care unit of this hospital. All patients admitted from out-of-hospital had access to a mobile coronary care unit. Initially, 40 patients called a general practitioner, 30 called the '999' operator, 12 called the mobile coronary care unit, 10 reported directly to the Accident and Emergency Department, seven were in-hospital and one spoke to the general practitioner's receptionist. Subsequently, 59 patients were attended by the mobile coronary care unit, 34 were admitted via the Accident and Emergency Department and seven had symptoms in-hospital. Thrombolytic therapy was initiated in 45/59 (76%) patients by the mobile coronary care unit staff and in 29/34 (85%) patients in the Accident and Emergency Department by cardiac staff. The remaining 26 patients received thrombolytic treatment in the hospital coronary care unit or cardiac department. The mean (+/- SEM) time from symptom onset to the initiation of thrombolytic therapy was 127 (+/- 11 min) for those patients treated by the mobile coronary care unit staff and for those treated in the Accident and Emergency Department was 187 (+/- 13 min) (P = 0.005). Multiple regression analysis showed significant reductions in total time delay if patients received thrombolytic therapy by the mobile coronary care unit staff out-of-hospital, when chest pain began in-hospital, or if patients had a previous myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Time delays to lytic therapy and outcome in 100 consecutive patients with a history suggestive of acute myocardial infarction in an area with access to a mobile coronary care unit. 805 97

The sympathetic nervous system is activated in acute myocardial infarction (MI). Scarce data exist, however, regarding the release of the sympathetic cotransmitter neuropeptide Y (NPY) during the acute and early convalescent phases after acute MI. Plasma NPY determination was obtained on days 1 and 3 after admission from 47 patients with acute MI and from eight control patients with acute chest pain without MI. Samples were also obtained on day 30 from the 39 survivors from the original MI cohort. Plasma NPY peaked on day 3 in the MI group (day 1: mean = 46.0 pmol/L, SEM = 6.4 pmol/L; day 3: mean = 60.8 pmol/L, SEM = 5.7 pmol/L; day 30: mean = 27.2 pmol/L, SEM = 4.1 pmol/L; days 1 to 3: p = 0.002; days 3 to 30: p < 0.001), whereas in the control group a nonsignificant decrease from day 1 (mean = 42.6 pmol/L, SEM = 12.3 pmol/L) to day 3 (mean = 34.0 pmol/L, SEM = 5.6 pmol/L) was observed. Plasma NPY levels were significantly increased in patients with MI on day 3 (p = 0.044), but not at baseline compared with the control group. No significant association between plasma NPY and plasma catecholamines, clinical heart failure, or 1-month survival was evident. These results suggest that increased plasma levels of the vasoconstrictory and cardiodepressant sympathetic neurotransmitter NPY are present in the recovery phase of MI, but with a plasma profile distinct from that of catecholamines.
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PMID:Plasma neuropeptide Y levels in the acute and early convalescent phase after myocardial infarction. 815 14

We measured serum hepatocyte growth factor (HGF) in patients with acute myocardial infarction, angina pectoris, and other heart diseases. In patients with acute myocardial infarction, blood was collected at the time of admission. Serum HGF was elevated within 3 hours in 8 of 10 patients (80%) with acute myocardial infarction after onset of chest pain (9.4 +/- 3.2 ng/mL, mean +/- SEM, values in normal subjects <0.39 ng/mL). Mean value of serum HGF was 11.0 +/-2.6 ng.mL (n=11) in patients who admitted to the hospital between 6 and 9 hours and 13.1 +/- 5.7 ng.mL between 12 and 24 hours after onset. Elevated HGF levels were significantly more frequent than those of creatine kinase within 3 hours, and elevated levels correlated well with those of serum creatine kinase at 6-9 hours after onset of acute myocardial infarction. No increase in serum HGF value was found in patients with angina pectoris or other heart diseases. Thus, measurement of HGF is a sensitive method for early diagnosis of acute myocardial infarction.
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PMID:Increased circulating hepatocyte growth factor in the early stage of acute myocardial infarction. 861 66


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