We evaluated dynamic effects of the carotid sinus baroreflex on ventriculoarterial coupling. In seven anesthetized, vagotomized dogs, we bilaterally isolated carotid sinuses and randomly changed carotid sinus pressure while measuring aortic pressure, aortic flow, and left ventricular pressure. Estimating left ventricular end-systolic elastance (E.) and effective arterial elastance (Ea) on a beat-to-beat basis, we determined transfer functions from the carotid sinus pressure to Ees (HE,,) Figure 1 illustrates the basic framework of the ventriculoarterial coupling in the pressure-volume plane. End-systolic elastance (Ees), which represents contractility of the left ventricle, is the slope of the end-systolic pressure-volume relation (line A in Figure 1). Effective arterial elastance (Ea), which in the steady state approximates arterial resistance divided by the cardiac cycle length, is the slope of the end-systolic pressure-stroke volume relation (line B in Figure 1). Increases in Ea reflect increases in arterial resistance or heart rate. The end-systolic equilibrium point that re-
SUMMARYTwo siblings presented with symptoms of left ventricular dysfunction and ventricular arrhythmias. Echocardiography and left ventriculography revealed dilatation, diffuse hypokinesis and apical aneurysm of the left ventricle in both cases. Myocardial infarction was unlikely by history and examinations. We diagnosed them as cases of familial dilated cardiomyopathy complicated by left ventricular aneurysm.
Additional Indexing Words: Dilated cardiomyopathyLeft ventricular aneurysm ILATED cardiomyopathy with left ventricular aneurysm has been rarely reported,1),2) and there are no reports of familial occurrence of this association. We report herein two siblings with dilated cardiomyopathy complicated by left ventricular aneurysm.
CASE REPORT Case 1:A 56-year-old man was admitted to our clinic because of the gradual onset of chest discomfort and dyspnea lasting for a few hours. He had been suffering from the symptoms for 14 years, but had no history of chest pain suggestive of ischemic heart disease or myocarditis.On admission, an electrocardiogram (ECG) showed sustained ventricular tachycardia. After electrical cardioversion, ECG showed Q waves in leads III, aVF, and V1-V3, diffuse ST-T abnormalities, complete left bundle branch block, and first-degree atrioventricular block (Fig. 1). Frequent,
We evaluated the advantages of the autoregressive (AR) model over the conventional Fourier transform in estimating aortic input impedance. In 10 anesthetized open-chest dogs, we digitized aortic pressure and flow at 200 Hz for 51.20 s under random ventricular pacing and subdivided them into five segments. We obtained aortic input impedance over the frequency range of 0.1-20 Hz both by AR model and by Fourier transform for various lengths of data, i.e., from one to four consecutive segments. For any given data length, the impedance spectrum estimated by the AR model was smoother than that obtained by the Fourier transform. To evaluate the accuracy of the estimated impedance, we predicted instantaneous aortic pressure of the fifth segment by convolving corresponding aortic flow with the impulse response of aortic input impedance. The prediction error was less with the AR model than that resulting from Fourier transform as long as the number of the segments was less than four. We conclude that the AR model provides a more accurate estimate of aortic input impedance than does the Fourier transform when data length is limited.
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