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  • Title: [Studies on the genesis of the aortic thudding sound in patients with aortic insufficiency, with special reference to the aortic flow pattern (author's transl)].
    Author: Fukuda N, Oki T, Asai M, Ohshima C, Takemura H, Murao A, Niki T, Mori H.
    Journal: J Cardiogr; 1981 Sep; 11(3):747-63. PubMed ID: 7320553.
    Abstract:
    To clarify the genesis of the aortic thudding sound (AK), phono-, mechano- and pulsed Doppler echocardiography were performed in 16 patients with pure aortic insufficiency (AI), 3 with AI associated with mild aortic stenosis (AIs) and 5 with AI associated with mitral insufficiency (AI + MI). The results obtained were as follows: 1) AK was composed of two components, that is, one (AK1) occurred in early systole and the other (AK2) near the end point of an ejection systolic murmur. Patients studied were divided into 4 groups following the appearance of AK1 and/or AK2: group with only AK1 (4 cases), group with only AK2 (7 cases), group with both AK1 and AK2 (5 cases) and group without AK (8 cases). 2) AK1 was a low frequency sound and was well recorded from the cardiac base to the right supraclavicular region. AK1 was not observed in cases with mild to moderate AI and with AI associated with mild AS. In atrial fibrillation, when the preceding R-R intervals were long, AK1 was loud and appeared in early systole, and when short, small and in mid-systole. Marked augmentation of AK1 was observed in the first beat after premature ventricular contraction with a compensatory pause. 3) AK2 was also low in frequency and was most intensively recorded near the apex. Although the intensity of AK2 tended to increase in the severe cases of AI, AK2 could be observed in mild to moderate cases. Intensity of AK2 also showed the post-extrasystolic potentiation similar to that of AK1. 4) The carotid pulse showed pulsus bisferiens in all cases with AK2 (group with only AK2 and group with both AK1 and AK2). On the other hand, in cases without AK2 (group without AK and group with only AK1), carotid pulse showed a monophasic systolic wave except 3 cases. These results suggested that there was a close relationship between AK2 and pulsus bisferiens in the carotid pulse. (5) In the apex cardiogram (ACG), systolic notches coincident with AK1 and/or AK2 were observed in 10 of 12 cases with AK2 and in 4 of 9 cases with AK1. In cases without AK, however, no notch was seen in ACG. Therefore, these notches might be resulted from the shock of the anterior chest wall produced simultaneously with the occurrence of AK. 6) Flow patterns at the left ventricular outflow tract (aortic flow patterns) were recorded in 13 cases, including 3 with only AK1, 2 with only AK2, 3 with both AK1 and AK2 and 5 without AK. In 5 of 13 cases the flow patterns were recorded simultaneously with phonocardiograms. Systolic aortic flow showed biphasic patterns in all cases with AK2, and monophasic patterns in cases without AK2. AK1 occurred coincidentally with the first peak of the biphasic flow patterns, and AK2 with the second peak. These results suggested that AK1 might be produced by rapid ejection of massive amount of blood containing a regurgitant flow into the aorta with the ordinarily distensiblwe aortic wall, and AK2 by the clash between the second ejected flow and the reflected flow returning from the peripheral artery against the first ejected flow.
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