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Biomedical subjects

K D Schick

Publications and source records attributed to K D Schick.

9 recordsLinked to original sources
PubMed1994

African Homo erectus: old radiometric ages and young Oldowan assemblages in the Middle Awash Valley, Ethiopia.

Fossils and artifacts recovered from the middle Awash Valley of Ethiopia's Afar depression sample the Middle Pleistocene transition from Homo erectus to Homo sapiens. Ar/Ar ages, biostratigraphy, and tephrachronology from this area indicate that the Pleistocene Bodo hominid cranium and newer specimens are approximately 0.6 million years old. Only Oldowan chopper and flake assemblages are present in the lower stratigraphic units, but Acheulean bifacial artifacts are consistently prevalent and widespread in directly overlying deposits. This technological transition is related to a shift in sedimentary regime, supporting the hypothesis that Middle Pleistocene Oldowan assemblages represent a behavioral facies of the Acheulean industrial complex.

Animals↗
PubMed1989

Myocardial bridges at multiple sites over the left coronary artery in a patient with hypertrophic cardiomyopathy.

In a 47-year-old male with hypertrophic cardiomyopathy, coronary angiography revealed three myocardial bridges associated with significant systolic narrowing of the left coronary artery. Measurements during pacing and exercise demonstrated no sign of myocardial ischemia. Ten-year follow-up was uneventful. Thus, the prognosis of myocardial bridges, even when located at multiple sites across the left coronary artery, seems benign.

Angiography↗
PubMed1985

[Unusual rhythm disorders with a DDD pacemaker].

A tachycardia caused by an inadvertent change of the lead connections in a patient with a DDD pacemaker is reported. This was demonstrated by operating in different modes (i.e. AOO, VOO) by displaying the marker channel graphically and by X-ray examination revealing unchanged lead positions.

Electrocardiography↗
PubMed1984

[Spontaneous regression of residential stenosis of the infarct vessel following successful percutaneous transluminal coronary recanalization].

In 64 out of 90 patients with thrombolysis by intracoronary streptokinase (PTCR) in the acute stage of myocardial infarction coronary angiography was performed in the chronic stage after 28 +/- 20 days. 52 of 56 successfully treated patients had a patent infarct vessel in the chronic stage. 36 of these patients showed a spontaneous regression from the subacute to the chronic stage. In 49 of the 56 patients (age: 53.4 +/- 10.4 years) a residual stenosis of more than 75% after PTCR was found; in the chronic stage only 31 patients had a stenosis of more than 75%. Of 10 patients with a spontaneous regression of 25% or more (age: 48.0 +/- 14.9 years) 8 had a one-vessel disease. The infarct vessel was in 6 patients the left anterior descending, in 4 patients the right coronary artery and in no case the left circumflex branch. The results suggest that the indication for invasive interventions, such as acute coronary angioplasty or bypass surgery, does not only depend on the degree of the residual stenosis directly after reperfusion. If possible, the decision for further invasive treatment should depend on the clinical follow-up.

Adult↗
PubMed1983

[Sinus node suppression by ventricular stimulation in retrograde block].

In a patient with a sick-sinus syndrome atrial pacing revealed an abnormal prolongation of the sinus node recovery time. During ventricular pacing no retrograde ventriculoatrial conduction could be detected. In spite of this, complete atrial standstill occurred reproducibly during fixed-rate ventricular pacing. After ventricular pacing was stopped a pause of some seconds ("overdrive recovery") was observed before the reoccurrence of normal sinus rhythm. We have no explanation for this unique finding, unless concealed ventriculosinoidal conduction is postulated.

Electrocardiography↗
PubMed1982

[Nifedipine in hypertrophic obstructive cardiomyopathy].

The effects of nifedipine on left-ventricular dynamics were assessed in 6 patients with hypertrophic obstructive cardiomyopathy (HOCM). After intravenous infusion of 3 mg nifedipine the mean aortic pressure decreased from 100 +/- 14 to 85 +/- 8 mm Hg (P less than 0.001). Heart rate increased from 70 +/- 5 to 93 +/- 5 beats per minute (P less than 0.001). This led to an increase of cardiac index from 3.0 +/- 0.5 to 3.8 +/- 0.9 l/min . m2 (P less than 0.01), whereas the stroke volume index decreased from an average of 49 +/- 11 to 42 +/- 12 ml/m2 (P less than 0.05). A marked diminution of outflow obstruction was demonstrable in 3 patients with intraventricular pressure gradients. The left-ventricular enddiastolic pressure rose from 14 +/- 3 to 18 +/- 6 mm Hg (P less than 0.02) in all patients. This effect was accompanied by a clear-cut coronary dilatation, evidenced by an increase of oxygen saturation in the coronary sinus from 29 +/- 4 to 54 +/- 9% (P less than 0.001). Thus nifedipine leads to diminished outflow obstruction and concomitant increase of cardiac output in hypertrophic cardiomyopathy. Inhibition of contraction does not seem to be compensated by peripheral effects. Coronary dilatation demonstrable in HOCM patients permits protection against coronary spasms and thus an additional antianginous effects.

Adolescent↗
PubMed1980

[Variable acute effects of prazosin on left ventricular failure (author's transl)].

The effect of 2.5 mg prazosin orally was monitored for one hour by cardiac catheterisation in 11 patients with cardiac insufficiency as a result of primary cardiomyopathy. Mean pressures of the pulmonary capillary bed and pulmonary artery decreased on average by 9 mm Hg, of the right atrium by 2.5 mm Hg and systemically by 8 mm Hg. Judging by the increase of cardiac index patients were divided into a group of 7 "responders", all showing congestive cardiomyopathy, and a group of 4 "nonresponders" with various cardiomyopathies. During prazosin treatment cardiac index increased by 23% and pulmonary arteriole resistance decreased by 4% and pulmonary arteriole resistance increased by 41%. It is concluded that not all forms of left ventricular failure respond favourably to prazosin. Divergent effects of prazosin may possibly be caused by unequal effects on pre- and after-load of both ventricles and on variable behaviour of lung arteriole resistance.

Adult↗