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1.
Circulation ; 110(16): 2395-400, 2004 Oct 19.
Article in English | MEDLINE | ID: mdl-15477415

ABSTRACT

BACKGROUND: Left ventricular (LV) pacing improves hemodynamics in patients with heart failure. We hypothesized that at least part of this benefit occurs by minimization of external constraint to LV filling from ventricular interaction. METHODS AND RESULTS: We present median values (interquartile ranges) for 13 heart failure patients with LV pacing systems implanted for New York Heart Association class III/IV limitation. We used the conductance catheter method to measure LV pressure and volume simultaneously. External constraint was measured from the end-diastolic pressure-volume relation recorded during inferior vena caval occlusion, during LV pacing, and while pacing was suspended. External constraint to LV filling was reduced by 3.0 (4.6 to 0.6) mm Hg from 4.8 (0.6 to 7.5) mm Hg (P<0.01) in response to LV pacing; effective filling pressure (LV end-diastolic pressure minus external constraint) increased by 4.0 (2.2 to 5.8) mm Hg from 17.7 (13.3 to 22.6; P<0.01). LV end-diastolic volume increased by 10 (3 to 11) mL from 238 (169 to 295) mL (P=0.01), whereas LV end-systolic volume did not change significantly (-1 [-2 to 3] mL from 180 [124 to 236] mL, P=0.97), which resulted in an increase in stroke volume of 11 (5 to 13) mL from 49 (38 to 59) mL (P<0.01). LV stroke work increased by 720 (550 to 1180) mL . mm Hg from 3400 (2110 to 4480) mL . mm Hg (P=0.01), and maximum dP/dt increased by 120 (2 to 161) mm Hg/s from 635 (521 to 767) mm Hg/s (P=0.03). CONCLUSIONS: This study suggests a potentially important mechanism by which LV pacing may produce hemodynamic benefit. LV pacing minimizes external constraint to LV filling, resulting in an increase in effective filling pressure; the consequent increase in LV end-diastolic volume increases stroke volume via the Starling mechanism.


Subject(s)
Cardiac Pacing, Artificial , Heart Failure/therapy , Heart Ventricles/physiopathology , Hemodynamics , Aged , Cardiac Catheterization , Cohort Studies , Diastole , Female , Heart Failure/physiopathology , Humans , Male , Middle Aged , Models, Cardiovascular , Pressure , Systole
2.
Heart ; 90(5): 502-5, 2004 May.
Article in English | MEDLINE | ID: mdl-15084543

ABSTRACT

OBJECTIVES: To assess whether patients with congestive heart failure (CHF) and a normal QRS duration can benefit from left ventricular (VDD-LV) pacing. DESIGN: Cardiac resynchronisation is reserved for patients with a broad QRS duration on the premise that systolic resynchronisation is the mechanism of benefit, yet improvement from pacing correlates poorly with QRS duration. In CHF patients with a broad QRS duration, those with a high resting pulmonary capillary wedge pressure (PCWP) > 15 mm Hg benefit. In this acute haemodynamic VDD-LV pacing study, patients with CHF with a normal QRS duration were divided into two groups--patients with a resting PCWP > 15 mm Hg and patients with a resting PCWP < 15 mm Hg--to determine whether benefit is predicted by a high resting PCWP. PATIENTS: 20 patients with CHF, New York Heart Association functional class IIb-IV, all with a normal QRS duration (< or = 120 ms). INTERVENTIONS: Temporary pacing wires were positioned to enable VDD-LV pacing and a pulmonary artery catheter was inserted for measurement of PCWP, right atrial pressure, and cardiac output. RESULTS: In patients with a PCWP > 15 mm Hg (n = 10), cardiac output increased from 3.9 (1.5) to 4.5 (1.65) l/min (p < 0.01), despite a fall in PCWP from 24.7 (7.1) to 21.0 (6.2) mm Hg (p < 0.001). In patients with a PCWP < 15 mm Hg there was no change in PCWP or cardiac output. Combined data showed that PCWP decreased from 17.0 (9.1) to 15.3 (7.7) mm Hg during VDD-LV pacing (p < 0.014) and cardiac output increased non-significantly from 4.7 (1.5) to 4.9 (1.5) (p = 0.125). CONCLUSIONS: Patients with CHF with a normal QRS duration and PCWP > 15 mm Hg derive acute haemodynamic benefit from VDD-LV pacing.


Subject(s)
Cardiac Pacing, Artificial/methods , Heart Failure/therapy , Hemodynamics/physiology , Cardiac Output/physiology , Female , Heart Failure/physiopathology , Humans , Male , Pulmonary Wedge Pressure/physiology , Ventricular Dysfunction, Left/physiopathology , Ventricular Dysfunction, Left/therapy
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