Giant flow reversal in pulmonary venous flow as a possible mechanism for asynchronous pacing-induced heart failure.
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.
Section of Cardiovascular Imaging, Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA. tommy@clin.med.tolushima-u.ac.jp
Tomotsugu
T
Tabata
Richard A
RA
Grimm
Fabrice J
FJ
Bauer
Kiyotaka
K
Fukamachi
Masami
M
Takagaki
Yoshie
Y
Ochiai
Todor N
TN
Mazgalev
Bruce L
BL
Wilkoff
Patrick M
PM
McCarthy
James D
JD
Thomas
D000818:Animals; D001783:Blood Flow Velocity; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects*; D004285:Dogs; D004452:Echocardiography / Q000379:methods; D006325:Heart Atria / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D006333:Heart Failure / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology*; D011667:Pulmonary Veins / Q000000981:diagnostic imaging* / Q000503:physiopathology*