Apex-to-base dispersion in regional timing of left ventricular shortening and lengthening

Partho P. Sengupta, Bijoy K. Khandheria, Josef Korinek, Jianwen Wang, Arshad Jahangir, James B. Seward, Marek Belohlavek

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Abstract

OBJECTIVES: We investigated whether the onset and progression of regional left ventricular (LV) shortening and lengthening parallel the apex-to-base differences in depolarization and repolarization. BACKGROUND: Limited information exists regarding apex-to-base differences in longitudinal and circumferential deformation sequence of the LV. METHODS: The apex-to-base differences in electric activation and the progression of longitudinal and circumferential shortening and lengthening sequences were determined in 8 porcine beating hearts in situ by implanting bipolar electrodes and an array of 14 sonomicrometry crystals in the LV free wall. RESULTS: Electric activation started at the apical subendocardium and showed significant delay in reaching the LV base. The onsets of mechanical activation and subsequent 20%, 40%, and 80% peak longitudinal shortenings required longer time to occur at base compared to the apex. The repolarization sequence propagated in reverse, with the base repolarizing before the apex. Subendocardial longitudinal shortening at base and subepicardial circumferential shortening at apex continued beyond the period of LV ejection, resulting in an apex-to-base gradient in the onset of lengthening. This gradient correlated with the duration of isovolumic relaxation (r = 0.85, p = 0.004) and the time required for reaching the lowest LV diastolic pressure (r = 0.70, p = 0.04). CONCLUSIONS: Apex-to-base delay in mechanical shortening of LV parallels the apex-to-base direction of the electric activation sequence. Basal subendocardial and apical subepicardial regions deform through a characteristic phase of postsystolic shortening. Short-lived apex-to-base and subendocardial-to-subepicardial relaxation gradients at the onset of diastole may have a physiologic significance in facilitating active restoration of the LV cavity in diastole.

Original languageEnglish (US)
Pages (from-to)163-172
Number of pages10
JournalJournal of the American College of Cardiology
Volume47
Issue number1
DOIs
StatePublished - Jan 3 2006

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Diastole
Ventricular Pressure
Electrodes
Swine
Blood Pressure
Direction compound

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Apex-to-base dispersion in regional timing of left ventricular shortening and lengthening. / Sengupta, Partho P.; Khandheria, Bijoy K.; Korinek, Josef; Wang, Jianwen; Jahangir, Arshad; Seward, James B.; Belohlavek, Marek.

In: Journal of the American College of Cardiology, Vol. 47, No. 1, 03.01.2006, p. 163-172.

Research output: Contribution to journalArticle

Sengupta, Partho P. ; Khandheria, Bijoy K. ; Korinek, Josef ; Wang, Jianwen ; Jahangir, Arshad ; Seward, James B. ; Belohlavek, Marek. / Apex-to-base dispersion in regional timing of left ventricular shortening and lengthening. In: Journal of the American College of Cardiology. 2006 ; Vol. 47, No. 1. pp. 163-172.
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abstract = "OBJECTIVES: We investigated whether the onset and progression of regional left ventricular (LV) shortening and lengthening parallel the apex-to-base differences in depolarization and repolarization. BACKGROUND: Limited information exists regarding apex-to-base differences in longitudinal and circumferential deformation sequence of the LV. METHODS: The apex-to-base differences in electric activation and the progression of longitudinal and circumferential shortening and lengthening sequences were determined in 8 porcine beating hearts in situ by implanting bipolar electrodes and an array of 14 sonomicrometry crystals in the LV free wall. RESULTS: Electric activation started at the apical subendocardium and showed significant delay in reaching the LV base. The onsets of mechanical activation and subsequent 20{\%}, 40{\%}, and 80{\%} peak longitudinal shortenings required longer time to occur at base compared to the apex. The repolarization sequence propagated in reverse, with the base repolarizing before the apex. Subendocardial longitudinal shortening at base and subepicardial circumferential shortening at apex continued beyond the period of LV ejection, resulting in an apex-to-base gradient in the onset of lengthening. This gradient correlated with the duration of isovolumic relaxation (r = 0.85, p = 0.004) and the time required for reaching the lowest LV diastolic pressure (r = 0.70, p = 0.04). CONCLUSIONS: Apex-to-base delay in mechanical shortening of LV parallels the apex-to-base direction of the electric activation sequence. Basal subendocardial and apical subepicardial regions deform through a characteristic phase of postsystolic shortening. Short-lived apex-to-base and subendocardial-to-subepicardial relaxation gradients at the onset of diastole may have a physiologic significance in facilitating active restoration of the LV cavity in diastole.",
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T1 - Apex-to-base dispersion in regional timing of left ventricular shortening and lengthening

AU - Sengupta, Partho P.

AU - Khandheria, Bijoy K.

AU - Korinek, Josef

AU - Wang, Jianwen

AU - Jahangir, Arshad

AU - Seward, James B.

AU - Belohlavek, Marek

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N2 - OBJECTIVES: We investigated whether the onset and progression of regional left ventricular (LV) shortening and lengthening parallel the apex-to-base differences in depolarization and repolarization. BACKGROUND: Limited information exists regarding apex-to-base differences in longitudinal and circumferential deformation sequence of the LV. METHODS: The apex-to-base differences in electric activation and the progression of longitudinal and circumferential shortening and lengthening sequences were determined in 8 porcine beating hearts in situ by implanting bipolar electrodes and an array of 14 sonomicrometry crystals in the LV free wall. RESULTS: Electric activation started at the apical subendocardium and showed significant delay in reaching the LV base. The onsets of mechanical activation and subsequent 20%, 40%, and 80% peak longitudinal shortenings required longer time to occur at base compared to the apex. The repolarization sequence propagated in reverse, with the base repolarizing before the apex. Subendocardial longitudinal shortening at base and subepicardial circumferential shortening at apex continued beyond the period of LV ejection, resulting in an apex-to-base gradient in the onset of lengthening. This gradient correlated with the duration of isovolumic relaxation (r = 0.85, p = 0.004) and the time required for reaching the lowest LV diastolic pressure (r = 0.70, p = 0.04). CONCLUSIONS: Apex-to-base delay in mechanical shortening of LV parallels the apex-to-base direction of the electric activation sequence. Basal subendocardial and apical subepicardial regions deform through a characteristic phase of postsystolic shortening. Short-lived apex-to-base and subendocardial-to-subepicardial relaxation gradients at the onset of diastole may have a physiologic significance in facilitating active restoration of the LV cavity in diastole.

AB - OBJECTIVES: We investigated whether the onset and progression of regional left ventricular (LV) shortening and lengthening parallel the apex-to-base differences in depolarization and repolarization. BACKGROUND: Limited information exists regarding apex-to-base differences in longitudinal and circumferential deformation sequence of the LV. METHODS: The apex-to-base differences in electric activation and the progression of longitudinal and circumferential shortening and lengthening sequences were determined in 8 porcine beating hearts in situ by implanting bipolar electrodes and an array of 14 sonomicrometry crystals in the LV free wall. RESULTS: Electric activation started at the apical subendocardium and showed significant delay in reaching the LV base. The onsets of mechanical activation and subsequent 20%, 40%, and 80% peak longitudinal shortenings required longer time to occur at base compared to the apex. The repolarization sequence propagated in reverse, with the base repolarizing before the apex. Subendocardial longitudinal shortening at base and subepicardial circumferential shortening at apex continued beyond the period of LV ejection, resulting in an apex-to-base gradient in the onset of lengthening. This gradient correlated with the duration of isovolumic relaxation (r = 0.85, p = 0.004) and the time required for reaching the lowest LV diastolic pressure (r = 0.70, p = 0.04). CONCLUSIONS: Apex-to-base delay in mechanical shortening of LV parallels the apex-to-base direction of the electric activation sequence. Basal subendocardial and apical subepicardial regions deform through a characteristic phase of postsystolic shortening. Short-lived apex-to-base and subendocardial-to-subepicardial relaxation gradients at the onset of diastole may have a physiologic significance in facilitating active restoration of the LV cavity in diastole.

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