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P Lechleitner

Publications and source records attributed to P Lechleitner.

At least 37 records · Page 2Linked to original sources
PubMed1994

Concentration time courses of troponin and myosin subunits after acute myocardial infarction.

BACKGROUND: As a result of the limited sensitivity and specificity of creatine kinase and lactate dehydrogenase (LDH) as well as their isoenzymes, there is increasing interest in the use of cardiac contractile proteins for the diagnosis of acute myocardial infarction (AMI) and myocardial damage. METHODS: This study compared the release of creatine kinase, creatine kinase MB, myoglobin, cardiac troponin I (cTnI), cardiac troponin T (cTnT), cardiac myosin light chain-1 (cMLC-1), and beta-type myosin heavy chains (bMHC) in serial blood samples from 13 patients (10 men, three women; median age 54 years, range 40-74 years) with first-time AMI (11 Q-wave, two non-Q-wave AMI; three anterior and 10 inferior wall AMI). All but one patient received intravenous thrombolytic treatment. RESULTS: Myoglobin was the first marker to increase in blood after AMI and showed the earliest peak levels, whereas bMHC increased latest, showing the latest peak levels. cTnI and cTnT increased significantly earlier than cMLC-1 and bMHC. cTnI and cTnT increased and reached peak levels parallel to each other, but the latter tended to stay increased longer. cTnT time courses were biphasic in the majority of AMI patients, unlike cTnI time courses. cMLC-1 release was mostly biphasic. cMLC-1 allows diagnosis during the acute phase as well as several days after the onset of AMI. The time courses of bMHC were usually monophasic. Its delayed appearance makes it useful for the diagnosis of remote infarction. In contrast to cTnI and cTnT, cMLC-1 and bMHC time courses were not significantly influenced by early reperfusion. CONCLUSION: Our results demonstrate the impact of the intracellular compartmentation of an intramyocardial protein (cytosolic, structurally bound, or structurally bound with soluble pool) on its concentration time course after AMI, particularly on the rapidity of its release.

Adult↗
PubMed1993

Cardiac troponin T release in acute myocardial infarction is associated with scintigraphic estimates of myocardial scar.

BACKGROUND: This study compared clinical-chemical estimates of infarct size with scintigraphic estimates of myocardial scar in patients with first-time acute myocardial infarction (AMI). METHODS: Levels of the cardiac isoform of the contractile protein troponin T (TnT), of creatine kinase (CK), and of the isoenzyme MB of CK (CK MB) were tested in serially drawn blood samples from 21 patients (two females and 19 males; median age, 55 years). Of these 21 patients, five had anterior- and 16 had inferior-wall AMI; all patients received intravenous thrombolytic therapy. Single-photon emission computed tomography (SPECT) with technetium-99m-isonitrile (Tc-sestamibi) was performed at rest after the onset of AMI (median time, 5 weeks). Scintigraphic defects were calculated using "bull's-eye" polar coordinate maps. All patients had an uncomplicated course between discharge and myocardial scintigraphy. RESULTS: Scintigraphic defect sizes ranged from 3.2% to 47.8% of the left ventricle (median, 27.3%). Cardiac TnT and CK MB release correlated closely with each other and with scintigraphic estimates of myocardial scar. Significant correlates were found between cardiac TnT and CK MB peak values (r = 0.87, P = 0.0001), CK MB peaks and Tc-sestamibi defect sizes (r = 0.73, P = 0.0014), and TnT peaks and scintigraphic defect sizes (r = 0.73, P = 0.0011). CONCLUSIONS: Because animal studies have already shown a very close correlation between histologic infarct size and SPECT Tc-sestamibi defect size, our results indicate that cardiac TnT is a useful marker to assess infarct size noninvasively in man.

Adult↗
PubMed1993

Goodpasture's syndrome. Unusual presentation after exposure to hard metal dust.

An unusual case of Goodpasture's syndrome in a 26-year-old man with occupational exposure to hard metal dust is described. The patient developed a life-threatening interstitial lung disease that was followed by a rapidly progressive glomerulonephritis two months later. To our knowledge, association of Goodpasture's syndrome and hard metal exposure has not been reported previously.

Adult↗
PubMed1993

Granulocyte elastase in acute myocardial infarction.

Plasma concentrations of polymorphonuclear granulocytes elastase (PMN elastase) in complex with alpha-1 proteinase inhibitor are a marker of neutrophil activation. The latter complex, creatine kinase and cardiac troponin T, were measured in peripheral venous blood samples serially drawn in 39 patients with acute myocardial infarction. Of the total, 29 received intravenous thrombolytic therapy either with streptokinase (n = 15), urokinase (n = 7) or recombinant tissue type plasminogen activator (n = 7). Creatine kinase activities and cardiac troponin T concentrations were used as markers of myocardial tissue injury. In all patients with acute myocardial infarction, PMN elastase was elevated (median 80 micrograms/l, interquartile range 71 to 100 micrograms/l). Peak and cumulative (area under curve) concentrations of PMN elastase did not correlate closely with determinants of myocardial injury (r < 0.2, n.s.). PMN elastase increased during the first 6 h after starting thrombolytic therapy, whereas it decreased in conventionally treated patients and 12 h later increased. Maximum concentrations of PMN elastase, however, were not significantly higher in patients with thrombolytic therapy than in those without. In acute myocardial infarction patients with complications such as cardiac arrest with subsequent resuscitation (n = 5), cardiac rupture (n = 1) or cardiogenic shock (n = 2), PMN elastase plasma concentrations were significantly higher (p = 0.04) than in uncomplicated infarctions. In the complicated patients, changes in elastase concentrations paralleled or even preceded changes in the clinical presentation. Therefore, thrombolytic treatment seems not to significantly influence the amount of systemic neutrophil activation, but plasma PMN elastase could be a useful marker to monitor and identify complications in acute myocardial infarction.

Adult↗
PubMed1993

Plasma immunoreactive endothelin in the acute and subacute phases of myocardial infarction in patients undergoing fibrinolysis.

Endothelin is a potent vasoconstrictor of coronary arteries. We measured plasma concentrations of immunoreactive endothelin (irET) in 46 patients with confirmed acute myocardial infarction (AMI). When compared with irET concentrations in healthy individuals who served as controls, irET concentrations in patients were already significantly elevated at the time of admission (P = 0.002) and remained significantly elevated for at least 2 days after AMI (P < 0.01). IrET concentrations peaked 1 h (mean) after admission (8.5 +/- 3.9 ng/L, P = 0.02 compared with values at time of admission). Reperfusion of the infarct-related artery markedly influenced irET release. Before the start of thrombolytic therapy, irET concentration in patients with early reperfusion did not differ significantly from that of those without early reperfusion. However, irET time courses were significantly (P = 0.03 by analysis of variance) different in patients who did and did not have early reperfusion. In the latter, peak irET concentrations correlated closely with the angiographic left ventricular ejection fraction (r = -0.71, P = 0.03), maximum creatine kinase MB mass concentrations (r = 0.69, P = 0.01), and creatine kinase activities (r = 0.59, P = 0.03). Reflow and reversion of myocardial ischemia are associated with a reduced irET release in patients with AMI.

Adult↗
PubMed1992

Endothelin-1 in patients with complicated and uncomplicated myocardial infarction.

Endothelin-1 concentrations were measured in peripheral venous blood samples from 42 patients with acute myocardial infarction. In patients with ischemic or hemodynamic complications (n = 11), endothelin-1 concentrations were significantly higher already on admission (P = 0.008) and remained significantly higher until day 6 after admission compared to patients with uncomplicated infarctions (n = 31; P = 0.035). There were no close correlations between peak concentrations of endothelin-1 and creatine kinase or creatine kinase isoenzyme MB mass in either group. Only in complicated patients did left ventricular ejection fraction correlate closely and inversely with peak endothelin-1 concentrations (r = -0.71; P = 0.03). Therefore, plasma endothelin-1 concentrations in patients with acute myocardial infarction patients may reflect states of markedly depressed cardiac performance and recurrent myocardial ischemia.

Adult↗
PubMed1992

Calcitonin gene-related peptide in patients with and without early reperfusion after acute myocardial infarction.

Plasma concentrations of calcitonin gene-related peptide (CGRP), a potent regulator of vascular tone, creatine kinase, myoglobin, and cardiac troponin T were assessed in 31 patients with acute myocardial infarction. In patients who had sustained acute myocardial infarctions, maximum CGRP concentrations (median, 3.2 pmol/L; interquartile range, 1.5 to 4.8 pmol/L) were markedly elevated as compared with healthy control subjects (n = 23; median, 1.02 pmol/L; p = 0.02). However, no marked differences in CGRP levels were observed between patients with early reperfusion (n = 19; median, 3.5 pmol/L) and patients without early reperfusion (n = 12; median, 2.6 pmol/L; p = 0.96), as well as between those with congestive heart failure (n = 8; median, 3.9 pmol/L) and those without congestive heart failure (n = 23; median, 3.2 pmol/L; p = 0.62). CGRP did not correlate closely with myocardial protein release or hemodynamic parameters (heart rate and blood pressure) or the occurrence of arrhythmias. Therefore we conclude that elevated peripheral venous CGRP concentrations in patients who have sustained an acute myocardial infarction are independent of successful reperfusion and hemodynamic state. Although the cause of CGRP increase is not yet identified, CGRP may play a role in the regulation of coronary vascular tone in patients after acute myocardial infarction.

Adolescent↗
PubMed1992

Early diagnosis of acute myocardial infarction by a newly developed rapid immunoturbidimetric assay for myoglobin.

OBJECTIVE: To evaluate a rapid immunoturbidimetric assay for myoglobin and to investigate its clinical usefulness in the early detection of acute myocardial infarction. DESIGN: Prospective study. Immunoturbidimetrically determined myoglobin concentrations were compared with radioimmunoassay results obtained with the same blood samples. The diagnostic performance of myoglobin determination was compared with creatine kinase and creatine kinase MB activity (current standard of routine diagnosis). SETTINGS: Part 1: coronary care unit. Part 2: emergency room in a university hospital. PATIENTS: Part 1:30 patients with acute myocardial infarction admitted not later than four hours (median two hours) after the onset of symptoms. Part 2: 126 patients admitted to the emergency room with chest pain not caused by trauma (51 cases of acute myocardial infarction, 51 cases of angina pectoris, and 24 cases of chest pain not related to coronary artery disease). INTERVENTIONS: Part 1: routine treatment including intravenous thrombolytic treatment (28 patients). Part 2: routine emergency treatment without thrombolytic treatment. MAIN OUTCOME MEASURES: The analytical quality of the immunoturbidimetric myoglobin assay and a comparison between the myoglobin assay and creatine kinase and creatine kinase MB for diagnostic sensitivity and performance. RESULTS: The immunoturbidimetric myoglobin assay was fast and convenient and gave myoglobin determinations of high analytical quality. The concentration of myoglobin increased, peaked, and returned to the reference range significantly earlier than creatine kinase (p < or = 0.0001) and creatine kinase MB (p < or = 0.0002). Before thrombolytic therapy was started the diagnostic sensitivity of myoglobin was significantly higher than that of creatine kinase MB activity 0-6 h after the onset of chest pain and significantly higher (0.82 v 0.29) than creatine kinase 2-4 h after the onset of chest pain. In almost all patients (92%) plasma myoglobin concentrations were increased 4-6 h after the onset of chest pain. CONCLUSION: Myoglobin was more sensitive in detecting early myocardial infarction than creatine kinase and creatine kinase MB activity. Immunoturbidimetric myoglobin measurements could be useful in the early evaluation of patients with suspected myocardial infarction because this assay takes less than two minutes.

Clinical Enzyme Tests↗
PubMed1991

Early detection of acute myocardial infarction by measurement of mass concentration of creatine kinase-MB.

The diagnostic sensitivity and performance of immunoenzymometric measurements of creatine kinase (CK)-MB mass concentrations in the early diagnosis of acute myocardial infarction (AMI) were examined and compared with the sensitivities and performances of CK and CK-MB activity, in the context of simultaneous measurements of CK, CK-MB activity, and CK-MB mass concentrations in serially drawn blood samples obtained immediately from 36 patients with AMI and 126 patients with chest pain on admission to the emergency room of the department of internal medicine. In the 36 patients with AMI, who were all admitted no later than 4 hours after the onset of chest pain, pathologic increase occurred significantly earlier in CK-MB mass than in both CK and CK-MB activity, with a median difference of 1 hour each. In patients coming to the emergency room (51 with AMI, 51 with angina pectoris and 24 with chest pain not related to coronary artery disease), CK-MB mass was the best diagnostic measurement for AMI of all markers tested (significantly higher efficiency, Youden index and likelihood ratio than both CK and CK-MB activity). Before initiating thrombolytic therapy, the sensitivity of CK-MB mass is significantly higher than CK-MB activity during the 0- to 6-hour period and significantly higher than CK activity during the 2- to 4-hour period after the onset of chest pain. Consequently, it is often possible to diagnose an AMI on the basis of increased CK-MB mass concentrations even at a time when CK and CK-MB activities are still within the reference interval.

Adult↗