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Apex-to-Base Dispersion in Regional Timing of Left Ventricular Shortening and Lengthening

Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota

View larger version (25K): [in a new window]   Figure 1 Arrangement of 14 sonomicrometry crystals in the left ventricular (LV) free wall. The black and gray circles indicate the location of subepicardial and subendocardial crystals and the black lines indicate the pair of crystals used for measuring longitudinal and circumferential deformations. LMCA = left main coronary artery; RV = right ventricle.

View larger version (21K): [in a new window]   Figure 2 Bipolar electrograms obtained from apical and basal segments of the left ventricular free wall. Vertical dotted lines mark the time points of steepest portion of initial bipolar QRS waveforms and end of T-wave. Note the apex-to-base direction of depolarization. The direction is reversed (base to apex) during repolarization in both subendocardium (arrow 1) and subepicardium (arrow 2). ECG = electrocardiogram.

View larger version (26K): [in a new window]   Figure 3 Distribution of bipolar electrical activation (A and B) and repolarization (C and D) intervals measured from eight pigs. Data are shown as mean ± SD. Endo and Epi = subendocardium and subepicardium, respectively. *Apex versus base; Endocardium versus epicardium (p = 0.01 and 0.04, respectively, for apex-endo vs. apex-epi and base-endo vs. base-epi electric activation intervals; p = 0.003 for apex-endo vs. apex-epi repolarization intervals).

View larger version (34K): [in a new window]   Figure 4 Distribution of time intervals for reaching 10%, 20%, 40%, and 80% of peak longitudinal and circumferential shortening in left ventricular subendocardium (A and B) and subepicardium (C and D). Data are shown as mean ± SD. A = apex; B = base; M = mid. *Apex versus base (p = 0.004, 0.01, 0.02, and 0.06, respectively for 10% to 80% shortening time intervals in panel A; and 0.002, 0.0001, 0.001, and 0.005, respectively, for 10% to 80% shortening time intervals in panel C); mid versus base (p = 0.008, 0.02, 0.01, and 0.005, respectively, for 10% to 80% shortening time intervals in panel A; and 0.006, 0.0004, and 0.0004, respectively, for 10% to 40% shortening time intervals in panel C); apex versus mid (p < 0.0001 for 80% shortening time interval in panel C).

View larger version (30K): [in a new window]   Figure 5 Distribution of time intervals for the onset and 20% longitudinal and circumferential lengthening of left ventricular subendocardium (A and B) and subepicardium (C and D). Data are shown as mean ± SD. A = apex; B = base; M = mid. *Apex versus base (p = 0.002 and <0.0001, respectively, for onsets and 20% lengthening time intervals in panel A and 0.0004 and 0.008, respectively, for onsets and 20% lengthening time intervals in panel D); mid versus base (p = 0.0005 and 0.01, respectively, for the onsets and 20% lengthening time intervals in panel A); apex versus mid (p = 0.006 and 0.001, respectively, for onset and 20% lengthening time intervals in panel D).

View larger version (33K): [in a new window]   Figure 6 Example of the apex-to-base longitudinal deformation sequence of the subendocardial region of the left ventricular (LV) free wall. Onset of lengthening (arrows) occurs earlier in the apical segment and is delayed in the basal segments into the phase of isovolumic relaxation. Phase 1 = isovolumic contraction; 2 = ejection; 3 = isovolumic relaxation; 4 = early diastole; 5 = late diastole. Ao = aorta; ECG = electrocardiogram. LA = left atrium.

View larger version (39K): [in a new window]   Figure 7 Example of the apex-to-base circumferential deformation sequence of the subepicardial region of the left ventricular (LV) free wall. Onset of lengthening (arrows) occurs earlier in the basal segment and is delayed in the apical segments beyond the phase of isovolumic relaxation into the early diastolic period. Phases 1 to 5 are described in Figure 6.

View larger version (24K): [in a new window]   Figure 8 Comparison of circumferential post-systolic shortening (PSS) in the apical subepicardium with hemodynamic pressure tracings. The repolarization wave in epicardial bipolar tracing (arrow) extends well beyond the aortic valve closure and beyond the T-wave on the surface electrocardiogram. The right panel shows linear regression analysis and correlation between the period of diastole occupied by post-systolic subepicardial contraction (Tpeak, X-axis) in the eight pigs and the diastole time period required for reaching minimum left ventricular (LV) diastolic pressures (TLVmin, Y-axis). Values on both axes are expressed as percentage of the entire diastolic relaxation period. Ao = aortic; AVO = aortic valve opening; EMG = electromyogram; LA = left atrial; MVO = mitral valve opening; Tpeak = time to peak strain; TVLVmin = time-to-minimum LV pressure.

View larger version (22K): [in a new window]   Figure 9 Linear regression analysis and correlation of the apex-to-base difference in the onset of circumferential lengthening (X-axis) with the isovolumic relaxation (IVR) duration (Y-axis, A) and the time interval required for reaching minimum left ventricular (TLVmin) diastolic pressures (Y-axis, B).

View larger version (28K): [in a new window]   Figure 10 Integrated overview of the left ventricular mechanical sequence during a cardiac cycle. Electric and mechanical activation are initiated in the apical subendocardial region. The subendocardial myofibers (right-handed helix) shorten, producing a brief twist along the right-handed helix direction during the isovolumic contraction period (phase 1) (33). During ejection (phase 2), the subendocardial and subepicardial layers shorten sequentially from the apex toward the base. The direction of apical twist is along the left-handed helix direction owing to dominating intrinsic twist imparting features of subepicardial myocytes (21), while the basal region torques briefly along the right-handed helical direction. Shortening of the subepicardium near the apex and the subendocardium near the base continues beyond aortic valve closure during the isovolumic relaxation (phase 3). This is accompanied with untwisting of the relaxed subendocardial layer with lengthening and enlargement of the left ventricular (LV) cavity at the apex. Shortening of the subepicardium near the apex continues briefly beyond the isovolumic relaxation period and is accompanied with further opening of the left ventricular cavity during early diastole (phase 4). The subsequent period of diastole is characterized by relaxation in both layers. The relaxation is further facilitated in the later phase of diastole by atrial contraction (phase 5). Phases 1 to 5 are described in Figure 6.