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Biomedical subjects

E Fleck

Publications and source records attributed to E Fleck.

At least 253 records · Page 14Linked to original sources
PubMed1985

[Quantitative coronary angiography before and after PTCA. Rate of restenosis, analysis of modifying factors].

In 95 consecutive patients in whom 101 coronary artery stenoses were successfully dilated, angiography was performed before, immediately after and at an average of 6.6 months after the procedures with computer-derived stenosis measurements (based on three-dimensional vessel reconstruction). The results were referenced to an analysis of factors possibly exerting an influence on post-PTCA outcome. In 56 of the 101 dilated stenoses (minimal area prior to PTCA 0.83 +/- 0.57 mm2, after PTCA 4.09 +/- 1.7 mm2), the findings remained essentially unchanged throughout the six-month follow-up. 17 of the 56 dilated stenoses showed a further increase in minimal area as compared with the findings seen immediately after PTCA. A reduction of the minimal area of more than 1 mm2 from that achieved immediately after PTCA, associated with narrowing of the vascular lumen greater than 70% was found in 33 of the 101 stenoses (minimal area before PTCA 0.82 +/- 0.59 mm2, immediately after PTCA 3.92 +/- 1.55 mm2, six months post-PTCA 1.39 +/- 1.27 mm2). In twelve of the 101 stenoses, restenosis amounting to more than 1 mm2 was also observed but without critical compromise of the vascular lumen (minimal area before PTCA 0.81 +/- 0.39 mm2, immediately after PTCA 5.54 +/- 1.28, six months post-PTCA 3.22 +/- 1.43 mm2, corresponding to a mean luminal narrowing of 45 +/- 24%).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1983

Effect of postextrasystolic potentiation on amplitude and timing of regional left ventricular wall motion in ischaemic heart disease.

In order to investigate the effects of postextrasystolic potentiation on left ventricular wall motion, the left ventriculograms of 30 patients were digitised frame by frame and regional movement demonstrated by contour displays. Postextrasystolic potentiation caused significant increases in end-diastolic volume, ejection fraction, and peak ejection and filling rates. The amplitude of normally moving segments increased by 5.7 +/- 2.3 mm, regardless of initial amplitude. Hypokinetic segments moved normally if the initial amplitude was greater than 5 mm, and there was a reduced or absent response if 4 mm or less. Four specific abnormalities of timing of motion were studied during isovolumic contraction, early ejection, and isovolumic relaxation. Their timing and extent were all unaffected in postextrasystolic beats. These results thus give no evidence for the entity "reversible asynergy". Rather, they suggest that the response of local wall motion to postextrasystolic potentiation depends only on basal amplitude and increased volume change in postextrasystolic beats.

Cardiac Complexes, Premature↗
PubMed1980

[The technetium-99-m-pyrophosphate scintigram in the assessment of the size of acute myocardial infarction: comparison with CK-(MB) curves mortality (author's transl)].

While the technetium-99m-pyrophosphate scintigram enables diagnostic proof of acute myocardial infarction, its use in the evaluation of the extent of infarction has not been clearly established. This study, in 30 patients with acute myocardial infarction was, thus, undertaken to assess the relationship between the findings of the technetium-99m-pyrophosphate scintigram, with respect to infarct area and uptake pattern, the infarct size, as determined from the total CK an CK-MB curves, and the mortality. The scintigraphically determined infarct areas ranged between 1.7 and 29.3 cm2; the 20.2 plus or minus 6.0 cm2 average for anterior wall infarction (n=18, range 7.4 to 29.3 cm2) was significantly greater (p smaller than 0.005) than the 8.3 plus or minus 5.3 cm2 average for inferior infarction (n=12, range 1.7 to 15.8 cm2). Correlation coefficients between the scintigraphically and enzymatically determined infarct sizes for the entire patient population ranged from 0.71 to 0.80. Anterior infarctions correlated more closely (0.66 to 0.84) than inferior infarctions (0.46 to 0.66). The technetium-99m-pyrophosphate uptake pattern was focal in 20 patients and ring-shaped (doughnut) in ten. Infarcts with focal uptake patterns were significantly smaller than those displaying a doughnut pattern (12.2 plus or minus 6.4 vs. 24 plus or minus 4.0 cm2, p smaller than 0.005). The infarct weight calculated from the CK-MC curve with application of individually determined disappearance rate for those infarcts displaying a focal uptake pattern was 34 plus or minus 29 grams while that associated with a doughnut uptake pattern was significantly greater at 86 plus or minus 25 grams (p smaller than 0.005). During the 18 -month observation period there were six deaths; the average scintigraphic infarct area of 22.8 plus or minus 3.6 cm2 in those who died was significantly greater (p smaller than 0.005) than that of the 13.8 plus or minus 8.2 cm2 of the survivors. Of the non-survivors, five had a doughnut uptake pattern and one displayed focal uptake. In the 24 survivors, a focal uptake pattern was found in 19 and a doughnut pattern in five. Conversely, 19 of the 20 patients with a focal uptake pattern survived while only five of the ten patients with a doughnut pattern were alive after 18 months. Thus, comparison with the enzymatically determined infarct weight as well as the mortality indicate that the technetium-99m-pyrophosphate scintigram yields clinically relevant data with regard to infarct size. Since no patient with an infarct area of less than 17 cm2 died within the 18-month observation period, designation of scintigraphically determined infarct size as small (smaller than 17 cm2) and large (larger than 17 cm2) was enabled. The corresponding cut-off point between large and small infarctions as determined enzymatically has been designated at 65 grams. Accordingly, agreement was found in 70% (14 of 20 patients) with scintigraphically small infarcts and in 80% (8 of 10 patients) with scintigraphically large infarcts...

Acute Disease↗
PubMed1976

[Influence of nitrates on regional myocardial blood flow and left ventricular wall motion].

Regional myocardial blood flow was measured by means of a computerized gamma-camera system in 30 patients with coronary artery disease (CAD) and in 14 healthy control subjects. Ventricular wall motion was quantitatively analyzed in 65 CAD-patients. Global and semiregional blood flow measurements yielded only limited information. In contrast, measurements of regional blood flow permitted detection of hypoperfused myocardium and the effects of pharmacologic intervention. The administration of 15 mg isosorbide dinitrate (ISDN) resulted in an increase in blood flow in post-stenotic hypoperfused myocardial regions of 20p.c. and a decrease in flow through normal myocardium of 14 p.c. These observations represent the adaption of flow to a newly-established level of metabolic demand. This increase in blood flow coupled with a reduction in afterload leads to improved ventricular wall motion in 65-75 p.c. of areas of hypokinetic myocardium and, to a markedly lesser degree, in only 20-25 p.c. of akinetic regions. Dyskinetic regions show no improvement. As compared with the 13ml/loog/min increase in blood flow seen after intracoronary administration of 0.45 mg ISDN in normal coronary vessels, the compromised dilatory capacity of diseased coronary vessels results in a relatively small increase in flow of 6 ml/100 g/min. The reduction of the extravascular component of coronary resistance, thus, appears to be the mechanism primarily responsible for the therapeutic effect of nitrates.

Coronary Circulation↗