Details

Autor(en) / Beteiligte

• Inoue, Katsuji
• Asanuma, Toshihiko
• Masuda, Kasumi
• Sakurai, Daisuke
• Higaki, Jitsuo
• Nakatani, Satoshi

Titel

Compensatory increase of left atrial external work to left ventricular dysfunction caused by afterload increase

Ist Teil von

• American journal of physiology. Heart and circulatory physiology, 2015-04, Vol.308 (8), p.H904-H912

Ort / Verlag

United States: American Physiological Society

Erscheinungsjahr

2015

Quelle

MEDLINE

Beschreibungen/Notizen

• Afterload mismatch can cause acute decompensation leading to an occurrence of acute heart failure. We investigated how the left atrium (LA) and left ventricle (LV) react to acute increases in afterload using speckle tracking echocardiography (STE). LA strain and volume were obtained by STE in 10 dogs during banding of descending aorta (AoB). Simultaneously, LA pressure was measured by a micromanometer-tipped catheter. LA peak negative strain during LA contraction, strain change during LA relaxation (early reservoir strain), and that during LA dilatation (late reservoir strain) were obtained from LA longitudinal strain-volume curves. From pressure-strain curves, the areas of A-loop and V-loops were computed as the work during active contraction and relaxation (A-work) and that during passive filling and emptying (V-work). AoB increased LV systolic pressure (105 ± 15 vs. 163 ± 12 mmHg, P < 0.01) and mean LA pressure (3.8 ± 1.2 vs. 7.1 ± 2.0 mmHg, P < 0.01). LV global circumferential strain decreased (-18.8 ± 3.5 vs. -13.2 ± 3.5%, P < 0.01), but LV stroke volume was maintained (8.4 ± 2.3 vs. 9.6 ± 3.6 ml). LA peak negative strain (-2.9 ± 2.3 vs. -9.8 ± 4.0%, P < 0.01) and early reservoir strain (4.5 ± 2.1 vs. 7.7 ± 2.4%, P < 0.05) increased by AoB, but late reservoir strain did not change (8.9 ± 3.4 vs. 6.1 ± 3.4%). A-work significantly increased (3.2 ± 2.0 vs. 19.2 ± 15.1 mmHg %, P < 0.01), whereas V-work did not change (13.3 ± 7.1 vs. 13.1 ± 7.7 mmHg %). In conclusion, LA external work during active contraction and relaxation increased as compensation for LV dysfunction during aortic banding. Atrial dysfunction may lead failure of this mechanism and hemodynamic decompensation.