Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-two patients presenting with acute transmural inferior wall myocardial infarction underwent cardiac catheterization and angiography within 12 hours of onset of symptoms. Twelve lead electrocardiograms performed within 11/2 hours of catheterization revealed the following: Seventeen patients exhibited ST-segment depression in the anterior precordial leads in addition to inferior wall changes (group A). Fifteen patients did not manifest any ST-segment changes in the anterior precordial leads (group B). Clinical, arteriographic, and ventriculographic variables were compared between the two groups. No significant differences were observed with regard to age, sex, risk factors for coronary disease, duration of symptoms prior to angiography, Killip class, number of inferior leads with ST-segment elevation, or initial creatine kinase. The extent of coronary artery disease as well as the prevalence of severe disease in the left anterior descending artery were similar for both groups. Biplane left ventriculography revealed no significant differences between the two groups with regard to global or local left ventricular function.
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PMID:[Significance of precordial ST segment depressions in acute inferior infarct--correlation with coronary angiography and ventriculography findings in the acute infarct phase]. 399 56

The early electrocardiographic results in 100 patients surviving their first myocardial infarction who thereafter underwent serial radionuclide ventriculography were reviewed. Site of infarction was anterior in 46 and inferior in 54, with lateral extension in two patients. Those with "reciprocal" S-T segment depression of more than 1 mm in the acute phase (n = 53) sustained larger infarcts on the basis of enzyme criteria (mean peak serum creatine kinase, +/- SD, 2,203 +/- 1,271 versus 1,544 +/- 1,197 IU/liter, p less than 0.02), with a higher incidence of ventricular akinesis and dyskinesis. Reciprocal change was more common during inferior infarction (n = 33) than anterior infarction (n = 20). Despite equivalent peak enzyme levels following anterior and inferior infarction with reciprocal S-T depression (mean peak creatine kinase 2,330 versus 2,128, NS), there was marked sparing of left ventricular function in the latter group (mean left ventricular ejection fraction 0.31 +/- 0.14 versus 0.42 +/- 0.09, p less than 0.01). Of 17 patients who died within two years of infarction, 14 had reciprocal changes. Patients who died after anterior infarction with reciprocal changes (n = 5) had poor left ventricular function compared with those who died after inferior infarction (n = 9; left ventricular ejection fraction, +/- SD, 0.21 +/- 0.05 versus 0.38 +/- 0.11, p less than 0.01). One third of those recovering from inferior infarction with reciprocal changes subsequently had positive results on exercise testing, and of the nine patients who died, five had good left ventricular function (left ventricular ejection fraction 0.44 to 0.50). Infarct size and ventricular wall motion abnormality proved to be of major importance in the production of inferior reciprocal S-T change during anterior infarction, and subsequent mortality was related to poor left ventricular function. The proximity of the precordial leads to left ventricular myocardium may increase the detection of concomitant anterior ischemia during inferior infarction, and those who exhibit reciprocal change are presumably at risk from left main stem or anterior descending lesions but with reasonably good ventricular function represent a more attractive population for invasive investigation.
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PMID:Clinical significance of "reciprocal" S-T segment depression in acute myocardial infarction. Relative contributions of infarct size and ischemia at a distance. 399 58

To elucidate the functional and prognostic significance of right ventricular dysfunction after acute inferior wall myocardial infarction, 74 consecutive patients with inferior infarction were prospectively evaluated with gated equilibrium blood pool imaging at rest, submaximal exercise thallium-201 scintigraphy and coronary angiography before hospital discharge. In addition, symptom-limited stress thallium-201 scintigraphy was performed in 61 patients at 3 months, and all patients were followed up clinically for 23 +/- 15 months. Utilizing predetermined radionuclide angiographic criteria, 47 patients (Group I) had normal right ventricular function, 12 patients (Group II) had mild to moderate dysfunction and 15 patients (Group III) had severe right ventricular dysfunction. There were no significant differences among the groups with regard to age, history of prior myocardial infarction, peak creatine kinase values, maximal Killip functional class, number or type of in-hospital complications, left ventricular ejection fraction, prevalence of multivessel disease or the distribution and severity of disease affecting the infarct-related vessel. Exercise tolerance as assessed by treadmill time, blood pressure-heart rate product and peak work load in METS was comparable among the three groups, both before hospital discharge and at 3 month follow-up. No differences in indicators of exercise-induced ischemia were noted among the groups, including the prevalence of redistribution thallium-201 defects, ST segment depression or symptoms of chest pain. Finally, cardiac mortality, reinfarction rate and the incidence of medically refractory angina pectoris were similar in the three groups. Thus, right ventricular dysfunction after acute inferior wall myocardial infarction does not appear to limit exercise tolerance or identify a subgroup of patients at higher risk for recurrent cardiac events.
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PMID:A prospective clinical, scintigraphic, angiographic and functional evaluation of patients after inferior myocardial infarction with and without right ventricular dysfunction. 404 48

The characteristics of 93 patients in whom electrocardiographic recordings were obtained within 12 hours of the onset of non-Q-wave myocardial infarction were studied. Patients were divided into the three groups according to what electrocardiographic changes were seen. Forty nine patients had ST segment depression, 35 had ST segment elevation, and nine had T wave changes. Patients with ST segment depression had a higher rate of pump failure and multivessel disease than the other two groups. There were no significant differences in peak serum creatine kinase activity among the three groups. Twelve of 13 patients who died of non-Q-wave myocardial infarction in hospital had ST segment depression. Furthermore nine of them had attacks of non-Q-wave myocardial infarction with severe ST segment depression in many leads. At necropsy five of six patients who had shown severe ST segment depressions in many leads at the onset of non-Q-wave myocardial infarction were found to have circumferential subendocardial lesions with triple vessel disease. This study suggests there are electrocardiographic subtypes of non-Q-wave myocardial infarction that are associated with specific patient characteristics.
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PMID:Classification of non-Q-wave myocardial infarction according to electrocardiographic changes. 405 88

The influence of the administration of pharmacologic doses of hydrocortisone on the extent and severity of acute myocardial ischemic injury and on subsequent necrosis after acute coronary occlusion was investigated in 28 dogs. In order to study acute myocardial injury, repeated epicardial electrocardiograms were recorded from 10 to 15 sites on the anterior surface of the left ventricle. Average ST segment elevation (ST) and the number of sites in which ST segment elevation exceeded 2 mV (NST), indices of the magnitude and extent of myocardial injury, respectively, were analyzed at 30 and 60 min after coronary occlusion. In the control group ST and NST did not change significantly in this time interval while in the treated group, which received 50 mg/kg hydrocortisone just after the 30 min recording, ST fell from 3.5+/-0.8 to 1.1+/-0.4 mV (P<0.01) and NST was reduced from 6.7+/-1.1 to 1.4+/-0.8 (P<0.01). In order to study the influence of hydrocortisone on necrosis, epicardial ST segment elevation 15 min after coronary occlusion was compared to myocardial creatine phosphokinase activity (CPK) and histologic appearance 24 h later in each site. In a control group (14 dogs) a relationship was established between ST segment elevation at 15 min (in millivolts) and CPK activity (in international units per milligram of protein) 24 h later: log CPK = -0.0611ST + 1.26 (N = 102 specimens, r = -0.79). In the treated groups, hydrocortisone (50 mg/kg i.v.) was given either at 30 min after occlusion (seven dogs) or at 6 h after occlusion (six dogs). Both groups received supplementary doses of hydrocortisone (25 mg/kg) 12 h after occlusion. The two treated groups exhibited less CPK depression than that expected from ST segment elevation at each site, with slopes of the regression lines which were significantly less steep: log CPK = -0.0288ST + 1.26 (N = 48, r = -0.71) and log CPK = -0.0321ST + 1.31 (N = 48, r = -0.76) in the (1/2) h and 6 h groups, respectively. Histologically, sites with ST segment elevations of less than 2 mV at 15 min after occlusion exhibited normal appearance 24 h later. Sites with ST segment elevations (> 2 mV) in the control group showed histologic changes compatible with early myocardial infarction in 96% of specimens, while this occurred only in 61% and 63% of specimens, respectively, in the treated groups, showing that over one third of the sites were protected from undergoing necrosis due to the intervening hydrocortisone treatment. Thus pharmacological doses of hydrocortisone prevent myocardial cells from progressing to ischemic necrosis even when administration is initiated 6 h after coronary occlusion.
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PMID:Reduction of experimental myocardial infarct size by corticosteroid administration. 468 84

The effects of coronary artery reperfusion 3 hr after coronary occlusion on contractile function and the development of myocardial damage at 24 hr was studied experimentally. In 14 control and 6 reperfused dogs, relationships between epicardial ST segment elevation 15 min after coronary occlusion and myocardial creatine phosphokinase activity (CPK) and histologic appearance 24 hr later were examined. The electrocardiograms were recorded from 10 to 15 sites on the left ventricular epicardium and transmural samples for CPK and histology were obtained from the same sites where epicardial electrocardiograms had been recorded. An inverse relation existed between ST segment elevation (mv) 15 min after occlusion and log CPK activity (IU/ mg of protein) 24 hr later, log CPK = - 0.06ST + 1.26. In dogs subjected to coronary artery reperfusion, there was significantly less CPK depression (log CPK = - 0.01ST + 1.31, [P < 0.01]) than that expected from the control group. In the control group 97% of specimens showing ST segment elevations over 2 mv at 15 min showed abnormal histology 24 hr later. In contrast, in the reperfused group 43% of sites exhibiting elevated ST segment at 15 min showed abnormal histology 24 hr later. In six additional dogs it was shown that the paradoxical movement of the left ventricular wall could be reversed within 1 hr of perfusion. Therefore, by enzymatic and histologic criteria, as well as by functional assessment, coronary artery reperfusion 3 hr after occlusion resulted in salvage of myocardial tissue.
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PMID:Coronary artery reperfusion. I. Early effects on local myocardial function and the extent of myocardial necrosis. 505 63

Although patients with acute inferior myocardial infarction often manifest S-T segment depression in precordial electrocardiographic leads, the pathophysiologic abnormalities associated with this finding are poorly understood. To examine this problem, electrocardiographic findings on admission were compared with results of radionuclide cineangiography performed within 38 hours of the onset of symptoms in 25 patients with inferior infarction. Summation of S-T depression in leads V1 through V4 permitted the separation of patients into two groups: Group A (11 patients with 0.20 mV or less of S-T depression) and Group B (14 patients with 0.45 vM or more of S-T depression). The radionuclide cineangiogram revealed inferior wall dysfunction in all patients. Additional posterolateral dysfunction was seen in 13 patients, all in Group B. Patients in Group B had a relatively larger infarction (peak creatine kinase Units - 756 +2- 358 in Group A versus 1,566 +/- 983 units in Group B, p less than 0.01) and greater functional impairment (ejection fraction - 45 +/- 12 in Group A versus 33 +/- 12 in Group B, p less than 0.01). The relation between precordial S-T segment depression and posterolateral dysfunction appears to be largely independent of electrocardiographic evidence of "true posterior infarction." Thus moderate or severe anterior precordial S-T depression in patients with acute inferior infarction is a sensitive and specific indicator of relatively extensive myocardial damage, primarily involving the posterolateral region.
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PMID:Anterior S-T segment depression in acute inferior myocardial infarction: indicator of posterolateral infarction. 611 61

Strict electrocardiographic, enzymatic, scintigraphic, and hemodynamic criteria for perioperative myocardial infarction (MI) were defined and related to serial assessments of left ventricular performance during rest and exercise in patients seen early and late after coronary artery bypass graft operation. Global left ventricular performance was determined by radionuclide ventriculography from which changes in the pattern of serial postoperative ejection fractions (EF) were obtained. Patients were divided into two groups based on the presence or absence of perioperative MI, and were matched in pairs on the basis of preoperative EF and extent as well as location of coronary artery obstructions. The results indicate that neither short- nor long-term depression in resting EF occurred subsequent to perioperative MI. However, an exercise-related increase in EF eight months postoperatively was depressed in patients who had perioperative MI compared with those who did not. Patients with new Q waves and abnormal postoperative elevation in serum levels of the myocardial isoenzyme of creatine kinase (CK-MB) had a greater early decrease in EF compared with patients without evidence of perioperative MI. However, seven days after operation, the EF in both groups returned to preoperative levels. Patients with abnormal technetium 99m-pyrophosphate scintigrams had changes in perioperative EF similar to those in patients without MI. The presence of low cardiac output syndrome immediately after operation was associated with immediate and short-term decreases in EF, which were not seen in any of the other patient subgroups.
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PMID:Changes in left ventricular performance related to perioperative myocardial infarction in coronary artery bypass graft surgery. 630 34

The development of and recovery from a severe yet nonlethal myocardial injury following hyperkalemic cardioplegia and prolonged hypothermic global ischemia was examined over 14 days in a rat model of heterotopic intraabdominal cardiac isograft transplantation. Mitochondrial enzymatic markers of myocardial ischemic injury and light microscopic signs of damage were examined. Eighteen hearts were arrested in situ using hyperkalemic cardioplegia and subjected to a mean of 38 min of ischemia at 20 degrees C as transplantation was achieved. No changes in mitochondrial creatine kinase (CKm) activity, mitochondrial malate dehydrogenase (MDHm) activity, their ratio, or morphologic evidence of injury were found during 8 days of reperfusion. In a second group of 66 hearts, the duration of hypothermic cardioplegic ischemia was extended by 120 min before transplantation. Neither unreperfused hearts nor hearts reperfused for only 1 hr demonstrated significant depression of enzyme activities or microscopic evidence of injury. However, after 1 day of reperfusion, CKm and MDHm activities were depressed to 36 and 44% of control levels (P less than 0.05). These activities had returned to control levels by 2 days of reperfusion and remained stable for 12 days thereafter. Light microscopic analysis revealed cellular injury to be maximal at 1 to 2 days of reperfusion with gradual improvement noted over the following 12 days. These observations suggest the existence of a mitochondrial injury following prolonged cardioplegic arrest and hypothermic global ischemia that is maximal after 24 hr of reperfusion but shows evidence of improvement thereafter. These findings justify aggressive support of the poorly functioning heart for the first few days after prolonged global ischemia.
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PMID:Progression and resolution of myocardial reflow injury. 637 96

Comparative hemodynamic measurements recorded in 19 cases of septic shock associated with Neisseria meningitidis bacteremia and in 20 shock cases associated with bacteremia due to other Gram-negative bacilli showed a significantly higher incidence of early myocardial depression in the cases with meningococcal infection. Echocardiographic, ECG, and serum enzyme (CK-MB isoenzyme) studies closely correlated with impaired myocardial contractility and development of cardiogenic shock in patients with meningococcal bacteremia. Autopsy of the heart from three patients who succumbed to shock confirmed the presence of myocarditis with intracellular Gram-negative diplococci. Our observations suggest that the onset of cardiac dysfunction precedes clinical manifestations of shock.
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PMID:Myocardial depression in septic shock caused by meningococcal infection. 643 70


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