Why the study?
Does acute ischemia during coronary angioplasty alter pulmonary impedance and right ventricular-vascular coupling in patients with single-vessel LAD disease?
Does acute ischemia during coronary angioplasty alter pulmonary impedance and right ventricular-vascular coupling in patients with single-vessel LAD disease?
Acute ischemia during coronary angioplasty alters pulsatile pulmonary artery properties and increases right ventricular power output requirements, which may contribute to right ventricular hypertrophy or failure in coronary artery disease.
Acute ischemia may raise RV power needs during angioplasty; leaves open contribution to RV failure in CAD.
Right ventricular ejection may be modified by alterations in pulmonary vascular properties during acute pulmonary hypertension. Pulmonary artery impedance and reflection properties were analyzed during coronary angioplasty in nine patients with single-vessel disease involving the left anterior descending artery by use of high-fidelity catheter recordings of pulmonary pressure and flow made before angioplasty balloon inflation and at peak ischemia. Acute pulmonary hypertension in this resting model resulted in a significant decrease in pulmonary vascular resistance (142 +/- 54 to 92 +/- 64 dyn.s.cm-5, P < 0.05), increase in low-frequency impedance (67 +/- 36 to 101 +/- 43 dyn.s.cm-5, P < 0.05), and no change in high-frequency (characteristic) impedance (38 +/- 14 to 41 +/- 13 dyn.s.cm-5). Pulmonary wave reflection amplitudes were increased, and the amount of hydraulic power expended per unit of net forward flow significantly increased (3.1 +/- 0.7 to 4.3 +/- 0.7 mW.ml-1.s-1, P < 0.001). These findings indicate that, during acute pulmonary hypertension in humans, 1) recruitment of additional resistance vessels can occur, 2) pulsatile pulmonary artery properties are significantly altered, and 3) right ventricular power output requirements are increased. Because episodic pulmonary hypertension occurs frequently in coronary artery disease, these changes may help explain eventual right ventricular hypertrophy or failure.
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Kussmaul et al. (1993) studied this question.
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