TY - JOUR
T1 - Giant flow reversal in pulmonary venous flow as a possible mechanism for asynchronous pacing-induced heart failure
AU - Tabata, Tomotsugu
AU - Grimm, Richard A.
AU - Bauer, Fabrice J.
AU - Fukamachi, Kiyotaka
AU - Takagaki, Masami
AU - Ochiai, Yoshie
AU - Mazgalev, Todor N.
AU - Wilkoff, Bruce L.
AU - McCarthy, Patrick M.
AU - Thomas, James D.
N1 - Funding Information:
Supported in part by Grant NCC 9-60, National Aeronautics and Space Administration, Houston, Texas (J.D.T.), and a grant from the Myocor Inc, Maple Grove, Minnesota.
PY - 2005/7
Y1 - 2005/7
N2 - Background: Mechanistic roles of the immediate increase in left atrial (LA) pressure in pacing-induced congestive heart failure have not been clearly understood. We evaluated the impact of asynchronous rapid ventricular pacing on LA hemodynamics in this model. Methods: Transthoracic and transesophageal echocardiography and hemodynamic assessment were performed in 23 healthy mongrel dogs. Data were acquired before and 5 minutes after initiation of rapid right ventricular pacing (200/min). Results: At 5 minutes after initiation of the pacing, giant pulmonary venous (PV) flow reversal (-76 cm/s) was observed in association with 1:1 ventriculoatrial conduction or complete atrioventricular dissociation. This giant PV flow reversal corresponded to an inappropriately timed atrial contraction, especially during systole. Cardiac output (3.21 vs 2.00 L/min, P < .001) was decreased corresponding to the decrease in the forward blood volumes as described by decrease in the Doppler left ventricular (LV) outflow (8.99 vs 4.73 cm, P < .0001), mitral inflow (6.89 vs 3.19 cm, P < .0001), and PV flow (14.15 vs 7.22 cm, P < .0001) velocity integrals. As a result, there was a marked elevation of the mean pulmonary capillary wedge (9.1 vs 17.1 mm Hg, P < .001) and LV end-diastolic (8.2 vs 17.4 mm Hg, P < .01) pressures leading to congestive heart failure. Conclusions: The giant PV flow reversal seen during asynchronous rapid right ventricular pacing corresponds to an inappropriate atrial contraction, immediately elevates LA pressure, and may initially promote congestive heart failure. The increase in LV end-diastolic pressure associated with decreased LV ejection fraction caused decrease in the LV filling volume leading to further increase in the LA pressure. This sustained marked elevation in the LA pressure and LV end-diastolic pressure could contribute to the heart failure process.
AB - Background: Mechanistic roles of the immediate increase in left atrial (LA) pressure in pacing-induced congestive heart failure have not been clearly understood. We evaluated the impact of asynchronous rapid ventricular pacing on LA hemodynamics in this model. Methods: Transthoracic and transesophageal echocardiography and hemodynamic assessment were performed in 23 healthy mongrel dogs. Data were acquired before and 5 minutes after initiation of rapid right ventricular pacing (200/min). Results: At 5 minutes after initiation of the pacing, giant pulmonary venous (PV) flow reversal (-76 cm/s) was observed in association with 1:1 ventriculoatrial conduction or complete atrioventricular dissociation. This giant PV flow reversal corresponded to an inappropriately timed atrial contraction, especially during systole. Cardiac output (3.21 vs 2.00 L/min, P < .001) was decreased corresponding to the decrease in the forward blood volumes as described by decrease in the Doppler left ventricular (LV) outflow (8.99 vs 4.73 cm, P < .0001), mitral inflow (6.89 vs 3.19 cm, P < .0001), and PV flow (14.15 vs 7.22 cm, P < .0001) velocity integrals. As a result, there was a marked elevation of the mean pulmonary capillary wedge (9.1 vs 17.1 mm Hg, P < .001) and LV end-diastolic (8.2 vs 17.4 mm Hg, P < .01) pressures leading to congestive heart failure. Conclusions: The giant PV flow reversal seen during asynchronous rapid right ventricular pacing corresponds to an inappropriate atrial contraction, immediately elevates LA pressure, and may initially promote congestive heart failure. The increase in LV end-diastolic pressure associated with decreased LV ejection fraction caused decrease in the LV filling volume leading to further increase in the LA pressure. This sustained marked elevation in the LA pressure and LV end-diastolic pressure could contribute to the heart failure process.
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U2 - 10.1016/j.echo.2004.12.013
DO - 10.1016/j.echo.2004.12.013
M3 - Article
C2 - 16003269
AN - SCOPUS:21344440281
SN - 0894-7317
VL - 18
SP - 722
EP - 728
JO - Journal of the American Society of Echocardiography
JF - Journal of the American Society of Echocardiography
IS - 7
ER -