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G R Fricke

Publications and source records attributed to G R Fricke.

9 recordsLinked to original sources

[Pulsed Doppler echocardiography in aortic valve disease].

The diagnostic value of pulsed Doppler echocardiography (PDE) had not been sufficiently assessed up until now. Invasive catheter velocitometric measurements in the central vessels give quantitative information on the blood movement across the aortic and pulmonary valves. It is particularly useful in the quantification of aortic regurgitation. We successfully investigated 52 patients by means of PDE (ATL 500 A); 20 were suffering pure aortic incompetence, 11 pure stenosis and 21 had combined stenosis and regurgitation. Fifteen patients without aortic valvular disease served as controls. Our findings were compared with the results of cardiac catheterization and angiography in each case. In addition, 14 patients with aortic regurgitation were studied invasively by catheter velocitometry. The obtained regurgitation values were compared to the PDE method. In the PDE the underlying criteria for the assessment of the recordings were as follows: formal analysis of the analog signal and of the turbulence content during systole and diastole; in the flow velocity tracings aortic incompetence showed a steep increase with high peak to peak aortic velocities and scant turbulence formation; the reverse flow during regurgitation was accompanied by a high grade turbulent velocity pattern. The area under the diastolic (regurgitant) flow velocity curve (the time-amplitude integral) corresponded significantly with the angiographic severity of aortic insufficiency (r = 0.87). In aortic stenosis, turbulence formation leads to an approximately flat velocity profile across the ascending aorta, if the region in the vicinity of the valve is omitted. The flow velocity analog signals are considerably disturbed. However, the turbulence content which can be qualitatively estimated from the recordings, correlates well with the calculated valve area. In combined aortic valve stenosis and incompetence, the prevailing turbulent pattern does not always permit one to assess sufficiently the severity of the stenotic component, whereas the grade of incompetence can be, in general, evaluated. PDE complements the existing non-invasive techniques and probably essentially enriches non-invasive diagnostics.

Aortic Valve Insufficiency↗

Klinefelter's syndrome and mitral valve prolapse. an echocardiographic study in twenty-two patients.

It is well known that the incidence of mitral valve prolapse is increased in various hereditary and humoral disorders, particularly in diseases with abnormal collagene structure and metabolism. We consecutively investigated, both clinically and echocardiographically, 22 patients with Klinefelter's syndrome (Mean age: 35 +/- 15.8 years). On clinical examination one third (7 patients) showed clinical signs of connective tissue weakness, 9 patients were obese. In 3 patients without a history of rheumatic fever mitral regurgitation was present. A mid-systolic click was heard in 12 patients, in 8 of them a click-murmur syndrome. Mitral regurgitation has been found in 3 patients. Echocardiographic ally, 12 of 22 patients (55%) revealed mitral valve prolapse which was not correlated with the degree of the chromosomal aberration. The incidence of mitral valve prolapse in an otherwise healthy male population is reported to be approximately 6%. Thus, in Klinefelter's syndrome, the frequency of mitral valve prolapse is found to be markedly increased. Regarding the nosological implications of mitral valve prolapse, it is recommended to thoroughly examine patients cardiologically. Furthermore, since mitral valve prolapse bears a higher risk of malignant cardiac arrhythmias, chest pain and endocarditis, an antiarrhythmic treatment and--if indicated--antibiotic prophylaxis has to be instituted. Those patients also should be advised to adjust their life style appropriately.

Adolescent↗

Optimization of the regular frequency of the heart in atrial fibrillation in relation to the cardiac output.

In atrial fibrillation an optimal frequency value has been derived to give the maximum cardiac output. A multiple, non-linear regression analysis of phasic aortic flow velocity in 12 patients with atrial fibrillation yields the parameters: (i) upper limiting frequency, fc; and (ii) 'optimal' frequency of the heart fo = fc/2. fo is defined at maximum cardiac output in resting conditions. An estimate of fc may be obtained from the carotid pulse tracing in a non-invasive way for the individual patient. The maximum cardiac output at fo ranges between 100% and 125% of the cardiac output was measured in the atrial fibrillatory state with irregular excitation of the ventricles. The greater the degree of irregularity of atrial fibrillation, the more expressed was the potential rise in cardiac output at the optimal regularization frequency. In chronic atrial fibrillation a regular excitation of the ventricles could be achieved by pharmacological agents, such as Verapamil or by ventricular pacing, without restitution of normal sinus rhythm. In critically ill patients with atrial fibrillation and the low cardiac output syndrome the heart rate should be adjusted to the individual cardiac output-related optimal frequency.

Aorta↗