Bouramoue C, Vacheron A, Audoin J, Gilles R, di Matteo J
Sem Hop. 1975 Mar 14;51(13):855-70.
The authors studied systolic murmurs in 89 cases, 50 of aortic stenosis, 14 cases of obstructive cardiomyopathy and 20 cases of mitral incompetence. This systolic murmur is characterised by its exceptional intensity, its raspy character at the base, becoming softer at the apex and in the axilla, the presence of a thrill and irradiation into the neck in 50 to 75% of cases. The etiological diagnosis was ensured precisely by 1) pharmaco-dynamic tests: amyl nitrite accentuates the systolic ejection murmurs and attenuates murmurs due to mitral regurgitation. 2) careful analysis of diastole: a systolic murmur extending into early diastole, a third sound or an opening snap and a low-pitched diastolic murmur, suggest mitral incompetence. A high-pitched diastolic murmur is in favour of aortic stenosis. 3) the carotid arteriogram and catheterisation show the characteristic abnormalities of the carotid arteriogram found in aortic valve disease and the existence of a trans-aortic or intra-ventricular pressure gradient, when there is an obstruction to left ventricular jection. The F wave of the apex cardiogram or left atrial reflux of the contrast medium during cineangiocardiography, confirm mitral incompetence. The main phono-hemodynamic and phono-anatomical correlations have been emphasized: 1. The intensity of the systolic murmur is directly proportional to the degree of obstructive cardiomyopathy or mitral incompetence, but does not parallel the degree of the sub-valvular apparatus. 3. The maximum intensity of the murmur occurs all the later when the stenosis is tight, whilst it is earlier in severe obstructive cardio-myopathy. 4. The lozange shape of the murmur of mitral incompetence on phono-cardiography is, above all, due to those cases with lesions of the sub-valvular apparatus. Finally, a study of the sound recorded by the Allard-Laurens micromanometer permitted us to determine the mechanism of this irradiating systolic murmur.
作者研究了89例患者的收缩期杂音,其中50例为主动脉瓣狭窄,14例为梗阻性心肌病,20例为二尖瓣关闭不全。这种收缩期杂音的特点是强度异常,在心底部粗糙,在心尖部和腋窝处变柔和,50%至75%的病例存在震颤并向颈部传导。病因诊断通过以下方法准确确定:1)药效动力学试验:亚硝酸异戊酯可增强收缩期喷射性杂音并减弱二尖瓣反流引起的杂音。2)仔细分析舒张期:收缩期杂音延伸至舒张早期、第三心音或开瓣音以及低调舒张期杂音提示二尖瓣关闭不全。高调舒张期杂音提示主动脉瓣狭窄。3)颈动脉造影和心导管检查显示主动脉瓣疾病中颈动脉造影的特征性异常以及左心室射血受阻时跨主动脉或心室内压力梯度的存在。心尖心电图的F波或心血管造影时造影剂的左心房反流证实二尖瓣关闭不全。主要的心音动力学和心音解剖学相关性已得到强调:1. 收缩期杂音的强度与梗阻性心肌病或二尖瓣关闭不全的程度成正比,但与瓣膜下装置的程度不平行。3. 狭窄越严重,杂音的最大强度出现得越晚,而在严重梗阻性心肌病中则出现得较早。4. 二尖瓣关闭不全在心音图上的菱形杂音形状,首先是由于瓣膜下装置病变的病例。最后,对阿拉德 - 劳伦斯微测压计记录的声音进行研究,使我们能够确定这种传导性收缩期杂音的机制。