Absent septal q wave: a marker of the effects of abnormal activation pattern on left ventricular diastolic function.

H B Xiao, D G Gibson

Cardiac Department, Royal Brompton National Heart and Lung Hospital, London.

OBJECTIVE--To investigate the possible mechanical associations of the presence or absence of the septal q wave. STUDY DESIGN--Retrospective and prospective study of 63 patients with various left ventricular diseases and 10 controls by electrocardiography, echocardiography, and pulsed Doppler recordings. SETTING--Tertiary cardiac referral centre. PATIENTS--73 subjects were studied. 26 had absent septal q waves and a QRS duration < 120 ms, 25 had classic left bundle branch block, and the rest had a normal electrocardiogram. Pathologically, 34 had left ventricular disease and 29 had a structurally normal heart. 10 subjects with structurally normal hearts and normal septal q waves were taken as controls. RESULTS--The timing of left ventricular minor axis motion was consistently normal in patients with abnormal activation, but long axis motion was considerably altered, with delayed "post-ejection shortening" of a mean amplitude of 4 mm. The post-ejection shortening began 10 (15) ms and reached its peak 90(20) ms after aortic closure (A2). Peak lengthening rate did not differ from normal (6.2 (3.5) v 8.5 (3.5) cm/s, NS) though it occurred significantly later. Post-ejection shortening was unrelated to age, amplitude of left ventricular wall motion, or QRS axis on the surface electrocardiogram. Post-ejection shortening was commoner when QRS duration was > 115 ms, but an absent septal q wave predicted its presence with a specificity of 90% and sensitivity of 86%. In patients with a post-ejection shortening, the onset of left ventricular systolic long axis shortening was delayed and the extent of its lengthening during the pre-ejection period increased, indicating delayed and incoordinate onset of tension development. During diastole, post-ejection shortening was associated with a prolonged isovolumic relaxation period and the time from A2 to the onset of transmitral flow. Peak mitral E wave flow velocity was reduced due to a fall in acceleration time although acceleration rate itself was unchanged. CONCLUSION--Loss of the normal septal q wave is associated with considerable mechanical consequences throughout the cardiac cycle, from the pre-ejection period to atrial systole, and apparently causes asynchronous subendocardial function.

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