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Biomedical subjects

U Tebbe

Publications and source records attributed to U Tebbe.

185 records · Page 11Linked to original sources
PubMed1979

[Ventricular and myocardial function in mitral regurgitation (author's transl)].

Left ventricular and myocardial performance were analyzed in 9 patients with chronic volume overload by mitral regurgitation from biplane cineventriculograms, simultaneous pressure recordings and cardiac output (thermodilution method) determinations. In spite of a considerable regurgitant fraction (49 +/- 17% of total stroke volume) cardiac index on the average is normal (CI = 3.3 +/- 0.7 l . min-1). The main compensatory mechanism to maintain cardiac ouput in hypertorphy (WED = 1.1 +/- 0.2 cm; LVMI = 216 +/- 62 g . m-2; LVMI/EDVI = 1.3 +/- 0.3 g . ml-1) and dilatation (EDVI = 163 +/- 37 ml . m-2). An increase of preload is of minor importance (PLVED = 15 +/- 7 mmHg; sigma ED = (40 +/- 19) x 10(3) dyn . cm-2). Left ventricular enlargement and wall mass are related to the degree of clinical heart failure (NYHA). Enddiastolic volume on the average is more increased than total stroke volume (89 +/- 31 ml . m-2). Ejection fraction (EF = 54 +/- 7%) was depressed despite a normal afterload (sigma tej = (171 +/- 37 x 10(3) dyn. cm-2; sigma max = (247 +/- 48 x 10(3) dyn . cm-2). The reduced ejection fraction and diminished myocardial power are related to an impairment of myocardial function (VMW . sigma tej = (83 +/- 39) x 10(3) dyn . cm-2 . s-1; VMW . sigma tej/ln sigma ED = 7.9 +/- 3.6 x 10(3) dyn . cm-2 . s-1). In comparable degrees of heart failure myocardial function is more compromised in patients with mitral than with aortic regurgitation.

Adult↗
PubMed1979

[Removal of an acute occluding coronary thrombosis by means of a Sones-catheter (author's transl)].

In a 60-year-old male patient thrombotic occlusion of a dominant right coronary artery was recanalized by means of a Sones-Catheter (8F) two hours after the clinical onset of myocardial infarction. Before recanalization the inferior wall of the left ventricle was akinetic. After recanalization this akinesia and the clinical symptoms of myocardial infarction was almost completely relieved. As evidenced by ECG and enzymes there was only a minor necrosis of the inferior wall. After one week ventricular function angiographically was completely normal. In the right coronary artery there was a 50 percent proximal stenosis, thrombi were completely abolished. Possible implications of this case are discussed.

Acute Disease↗
PubMed1979

[Left ventricular diastolic pressure-volume relations during exercise (author's transl)].

UNLABELLED: Left ventricular diastolic pressure-volume relations (PVR) were analysed from biplane ventriculograms and simultaneous pressure measurements in 33 patients at rest (R) and during ergometer exercise (E) (8 normals [N], 8 patients with coronary artery disease [CAD], 8 patients with congestive cardiomyopathy [COCM], 5 patients with aortic insufficiency [AI] and 5 patients with pressure overload (4 with aortic stenosis [A-St.] and 1 coarctation of the aorta). In N and AI diastolic PVR was essentially unchanged with E, the time constant of isovolumic relaxation (T) decreased significantly (N: delta T = -24.4 +/- 11.6%, p less than 0.001; AI: delta T = -27.3 +/- 6.8%, p less than 0.005). In CAD diastolic PVR was shifted upwards in all cases with angina pectoris during E (7/8), minimal rate of left ventricular pressure change (dp/dtmin) and T did not change significantly. In COCM diastolic PVR was shifted upwards in 4 cases, while dp/dtmin increased significantly (R = -1107 +/- 327, E = -1508 +/- 626 mm Hg-s-1, p less than 0.05), T on the average was unchanged (R = 53 +/- 10.5, E = 51 +/- 14.2 msec). In A-St. in 3 of 4 cases diastolic PVR was significantly shifted upwards with E, dp/dtmin increased (R = -1633 +/- 93, E = -2093 +/- 170 mm Hg-s-1, p less than 0.001), T in contrast to N and AI was prolonged (R = 33.8 +/- 4, E = 39.9 +/- 1.9 msec). CONCLUSION: In N and AI diastolic ventricular function is not altered with exercise. In COCM and especially in A-St., however, there are similar alterations like in CAD with angina pectoris. Changes in T indicate that shifts of the PVR with exercise in non-ischemic heart disease are related to a disturbed ventricular relaxation.

Adolescent↗