A crossover study was performed to compare the hemodynamic effects of the iso-osmolar contrast agent iodixanol (Visipaque) 320 mg I/ml to those of the low-osmolar iohexol (Omnipaque) 350 mg I/ml. The main hypothesis was that iodixanol and iohexol would affect left ventricular end-diastolic pressure (LVEDP) to different degrees. In 48 patients with reduced cardiac function (mean ejection fraction 33. 4%), one ventricular injection was performed with each contrast medium. Ventricular, aortic and right atrial pressures and heart rate were measured continuously. Cardiac output (using Fick's principle) and systemic vascular resistance were calculated. LVEDP increased with both agents, but significantly less after iodixanol than after iohexol (P < 0.01), also in subgroups of patients in whom baseline LVEDP was severely increased and in whom 3-vessel disease was present. Immediate changes in variables reflecting vasodilatation were similar with both agents. In conclusion, both contrast agents influenced hemodynamics during ventriculography, but iodixanol had significantly less influence on LVEDP than did iohexol.

The effective flow rates with human blood through an autoperfusion catheter cannot be monitored in vivo and have not been experimentally determined in vitro. The manufacturers (Advanced Cardiovascular Systems [ACS], Temecula, CA) have suggested that "the flow rate" through the Stack over the wire and the RX-60 monorail catheter is 60 ml/min with a pressure gradient of 80 mmHg. We measured human blood flow rates in vitro through these catheters under different continuous pressure regimens (between 40 and 120 mmHg), with varying hematocrit levels (between 25% and 62%). Measured blood flows at a gradient of 80 mmHg were found to vary from 32 to 65 cc/min, with hematocrit levels of 62-25%. Minor variations in the circuitry, besides the viscosity of the medium, cause significant changes in observed flow rates (such as kinking of the catheter and blood sedimentation). In vitro determinations of blood flows cannot automatically be transferred to the in vivo condition, primarily because in vitro determinations do not account for the systolic intramural pressure increase (which may overcome the aortic pressure). If such a phenomenon is also considered, then the in vitro flow rates reported here should be multiplied by a factor of 0.40-0.60 to determine effective in vivo flow rates. Such information is relevant for the clinical operator of angioplasty, especially in the treatment of patients at high risk for undergoing percutaneous transluminal coronary angioplasty.