OBJECTIVE: To study the early effects of coronary angioplasty on resting left ventricular long axis function, reflecting that of the subendocardium. DESIGN: Prospective echocardiographic and Doppler examination of patients with coronary artery disease, before and after single vessel coronary angioplasty. SETTING: A tertiary referral centre for cardiac diseases with facilities for invasive and non-invasive investigation. PATIENTS: 23 patients with significant left coronary disease being considered for coronary angioplasty. RESULTS: Before angioplasty the mean (SD) isovolumic relaxation time was longer than normal (75(19) ms v 55 (10), p < 0.001) with a significant increase in transverse dimension change before mitral valve opening, and peak rate of early diastolic thinning (8(3) v 10.4 (2.6) cm/s (p < 0.001)) was reduced. Long axis motion was frequently abnormal. The interval from the onset of the Q wave to the onset of shortening was prolonged (118 (30) ms v 90 (19) at the left site and 115 (26) ms v 81 (9) at the septal site, p < 0.001) and the onset of early diastolic rapid lengthening delayed with respect to the aortic valve closure sound (A2) by 85 (34) ms v 58 (11) at the left site and 88 (33) ms v 60 (9) at the septal site (p < 0.001). Although overall amplitude was reduced at the septal site only (1.23 (0.3) cm v 1.5 (0.4), p < 0.05), the extent (0.8 (0.2) cm v 1.04 (0.3) at the left site and 0.66 (0.2) cm v 0.9 (0.3) at the septal site, p < 0.001) and peak rate (6.2 (2) cm/s v 10 (2.5) at the left site and 5.4 (2.3) cm/s v 8.5 (2) at the septal site, p < 001) of early diastolic lengthening were both much lower than normal. The E/A ratio on transmitral Doppler was modestly reduced (1.0 (0.7) v 1.4 (0.4), p < 0.05). After angioplasty: isovolumic relaxation time shortened to 64 (18) ms (p < 0.001) and left ventricular incoordination regressed. Long axis shortening with respect to Q (98 (32) ms v 118 (30) at the left site and 94 (23) ms v 115 (26) at the septal site, p < 0.01) and that of lengthening with respect to A2 both normalised. Early diastolic peak lengthening rate increased (7.5 (2.1) cm/s v 6.2 (2) at the left site, and 6.3 (2.4) cm/s v 5.4 (2.3) at the septal site, p < 0.001). The early diastolic peak thinning rate of the posterior wall significantly increased (10 (3.5) cm/s v 8 (3), p < 0.005) as did mitral E/A ratio 1.2 (0.7) v 1.0 (0.7), p < 0.05). CONCLUSION: Long axis motion, representing the function of longitudinally arranged subendocardial fibres, is consistently abnormal in the resting state in coronary artery disease. These systolic and diastolic abnormalities return towards normal after successful angioplasty, suggesting that they are the direct effect of coronary artery stenosis.
OBJECTIVE: To study the early effects of coronary angioplasty on resting left ventricular long axis function, reflecting that of the subendocardium. DESIGN: Prospective echocardiographic and Doppler examination of patients with coronary artery disease, before and after single vessel coronary angioplasty. SETTING: A tertiary referral centre for cardiac diseases with facilities for invasive and non-invasive investigation. PATIENTS: 23 patients with significant left coronary disease being considered for coronary angioplasty. RESULTS: Before angioplasty the mean (SD) isovolumic relaxation time was longer than normal (75(19) ms v 55 (10), p < 0.001) with a significant increase in transverse dimension change before mitral valve opening, and peak rate of early diastolic thinning (8(3) v 10.4 (2.6) cm/s (p < 0.001)) was reduced. Long axis motion was frequently abnormal. The interval from the onset of the Q wave to the onset of shortening was prolonged (118 (30) ms v 90 (19) at the left site and 115 (26) ms v 81 (9) at the septal site, p < 0.001) and the onset of early diastolic rapid lengthening delayed with respect to the aortic valve closure sound (A2) by 85 (34) ms v 58 (11) at the left site and 88 (33) ms v 60 (9) at the septal site (p < 0.001). Although overall amplitude was reduced at the septal site only (1.23 (0.3) cm v 1.5 (0.4), p < 0.05), the extent (0.8 (0.2) cm v 1.04 (0.3) at the left site and 0.66 (0.2) cm v 0.9 (0.3) at the septal site, p < 0.001) and peak rate (6.2 (2) cm/s v 10 (2.5) at the left site and 5.4 (2.3) cm/s v 8.5 (2) at the septal site, p < 001) of early diastolic lengthening were both much lower than normal. The E/A ratio on transmitral Doppler was modestly reduced (1.0 (0.7) v 1.4 (0.4), p < 0.05). After angioplasty: isovolumic relaxation time shortened to 64 (18) ms (p < 0.001) and left ventricular incoordination regressed. Long axis shortening with respect to Q (98 (32) ms v 118 (30) at the left site and 94 (23) ms v 115 (26) at the septal site, p < 0.01) and that of lengthening with respect to A2 both normalised. Early diastolic peak lengthening rate increased (7.5 (2.1) cm/s v 6.2 (2) at the left site, and 6.3 (2.4) cm/s v 5.4 (2.3) at the septal site, p < 0.001). The early diastolic peak thinning rate of the posterior wall significantly increased (10 (3.5) cm/s v 8 (3), p < 0.005) as did mitral E/A ratio 1.2 (0.7) v 1.0 (0.7), p < 0.05). CONCLUSION: Long axis motion, representing the function of longitudinally arranged subendocardial fibres, is consistently abnormal in the resting state in coronary artery disease. These systolic and diastolic abnormalities return towards normal after successful angioplasty, suggesting that they are the direct effect of coronary artery stenosis.