Incidence and characteristics of segmental postsystolic longitudinal shortening in normal, acutely ischemic, and scarred myocardium.

OBJECTIVE: Myocardial longitudinal shortening after aortic valve closure (postsystolic shortening [PSS]) is considered a marker of pathology with diagnostic potential. However, PSS can also occur in healthy subjects. We, therefore, investigated the occurrence and characteristics of PSS in control subjects and patients, and how to distinguish normality from disease. METHODS: In 20 young control subjects, 10 older control subjects, 30 patients with acute myocardial infarction (acute ischemia), and 10 patients with postischemic myocardial scar, longitudinal myocardial deformation was measured with Doppler tissue strain rate (SR) imaging. Segmental SR and strain were visually and quantitatively analyzed and compared. RESULTS: In young control subjects, PSS was found in 98 of 313 segments (31%) and showed gaussian distribution (median 1.3%). During ejection time, median peak SR was -1.4 s(-1) and median strain -16.6%. In older control subjects, parameters differed only slightly. In acutely ischemic and scarred myocardium, both systolic strain and SR were significantly reduced or inverted. In disease, PSS occurred significantly more often (78% and 79%, respectively), was significantly higher in magnitude, and its peak occurred later than in young and older control subjects. CONCLUSION: PSS is a normal finding in healthy subjects occurring in approximately one-third of myocardial segments and, thus, is not always a marker of disease. Our data indicate that pathologic PSS can be detected by coexisting reduction in systolic strain and, second, by exceeding a postsystolic strain magnitude cutoff.

Strain rate imaging for the assessment of preload-dependent changes in regional left ventricular diastolic longitudinal function.

BACKGROUND: Strain rate imaging is a new and intriguing way of displaying myocardial deformation properties by means of echocardiography. With high frame rate strain rate imaging we observed a spatial inhomogeneity in diastolic longitudinal strain rates in healthy persons. A base-to-apex time delay in diastolic lengthening could be seen both in early diastole and at atrial contraction. METHODS AND RESULTS: We investigated this consistent finding and its dependence on loading conditions in 20 healthy volunteers. Propagation velocities of lengthening of 91 +/- 31 cm/s (E-wave) and 203 +/- 11 cm/s (A-wave) at rest (equal to time delays of 104 +/- 29 ms and 56 +/- 24 ms, respectively) increased significantly to 101 +/- 27 cm/s (E) and 283 +/- 17 cm/s (A) with lifting the volunteers' legs. Applying nitroglycerin sublingually and sitting upright significantly decreased propagation velocities (E-wave 76 +/- 20 cm/s, A-wave 172 +/- 93 cm/s and E-wave 66 +/- 17 cm/s, A-wave 150 +/- 64 cm/s, respectively). Free lateral walls showed a lower propagation velocity than septal walls. CONCLUSION: We conclude that the propagation velocities of left ventricular lengthening waves are dependent on preload changes and increase with increasing preload.