Oren Rotman

High accuracy differential pressure measurements using fluid-filled catheters – A feasibility study in compliant tubes

High accuracy differential pressure measurements are required in various biomedical and medical applications, such as in fluid-dynamic test systems, or in the cath-lab. Differential pressure measurements using fluid-filled catheters are relatively inexpensive, yet may be subjected to common mode pressure errors (CMP), which can significantly reduce the measurement accuracy. Recently, a novel correction method for high accuracy differential pressure measurements was presented, and was shown to effectively remove CMP distortions from measurements acquired in rigid tubes. The purpose of the present study was to test the feasibility of this correction method inside compliant tubes, which effectively simulate arteries. Two tubes with varying compliance were tested under dynamic flow and pressure conditions to cover the physiological range of radial distensibility in coronary arteries. A third, compliant model, with a 70% stenosis severity was additionally tested. Differential pressure measurements were acquired over a 3 cm tube length using a fluid-filled double-lumen catheter, and were corrected using the proposed CMP correction method. Validation of the corrected differential pressure signals was performed by comparison to differential pressure recordings taken via a direct connection to the compliant tubes, and by comparison to predicted differential pressure readings of matching fluid-structure interaction (FSI) computational simulations. The results show excellent agreement between the experimentally acquired and computationally determined differential pressure signals. This validates the application of the CMP correction method in compliant tubes of the physiological range for up to intermediate size stenosis severity of 70%.

Effect of Arterial Distensibility and Stenoses on Pressure Drop in Pulsatile Flow

The most accepted standard tool of cardiologists for assessing stenoses severity in the coronary tree is coronary angiography. Information from coronary angiography is limited to geometrical data on the coronary lumen, and provides limited functional data on the severity of stenoses. In addition, histopathological studies have demonstrated that angiographic evidence of stenosis is usually detected when the cross-sectional area of a plaque approaches 40% to 50% of the total cross-sectional area of the vessel [1]. Hence, managing the intermediate coronary lesions (40% to 70% diameter stenosis) are a true challenge for cardiologists. These geometrical limitations have led to the development of several hemodynamic parameters, which functionally assess stenoses severity and the cardiovascular tree, among which the most pronounced is Fractional Flow Reserve (FFR), which is defined as the ratio of hyperemic flow in the stenosis artery to the flow in the same artery in the theoretic absence of the stenosis [2]. FFR is lesion specific and provides functional assessment of the stenosis severity by means of pressure measurement as a surrogate for flow. Under hyperemic flow conditions, FFR can be calculated as the ratio of pressures distal and proximal to a lesion. FFR values of 0.75–0.80 have been established as threshold values that distinguish normal from abnormal levels for a given measurement. Stenoses with an FFR 0.80 are considered to be ischemic ‘safe’ [2]. One of the limitations of FFR is its absolute dependency in pharmacologically-induced maximal hyperemia. The current clinical standard for coronary hyperemia is the intracoronary administration of ademosine, however in 10% to 15% of patients, intracoronary adenosine induces submaximal hyperemia only, and therefore FFR may be overestimated by up to 0.10 [3, 4].Copyright

Vulnerable Plaque Detection Using Intracoronary Thermography and Cold Saline Injection

Intracoronary Thermography (ICT) is a method which is primarily used for the detection of warmer arterial regions by a dedicated catheter with miniature temperature sensors at the catheter tip. A major goal for the ICT is to detect vulnerable plaques, which are the main cause of myocardial infraction, and hence a major life risk factor. The underlining hypothesis is that atherosclerotic lesions, which are considered as an inflammatory desease [1], will present on their intimal surface higher temperature than a normal, healthy arterial wall.Copyright

Numerical Analysis of a Novel Method for Temperature Gradient Measurement in the Vicinity of Warm Inflamed Atherosclerotic Plaques

Thermography is a method used mainly for the detection of warmer arterial wall regions, as an indication for the presence of inflamed atherosclerotic plaques. A new method, utilizing injection of cold saline to the bloodstream and measuring temperature gradients within the flow instead of the wall is numerically investigated. Results show an almost 12-fold increase in expected temperature gradients, emphasizing the usefulness of such method for novel catheter design.

Bio-Mechanical Aspects of Short Peripheral Catheter Thrombophlebitis

Venflons, or Short Peripheral Catheters (SPC), are the most common intravenous devices being used in medical practice, particularly in hospitals and intensive care units. SPC is usually inserted into veins of the upper extremities to administer fluids, medications, blood products or for prophylactic use before procedures. It has been reported that 40–80% of hospitalized patients were treated with SPCs [1, 2]. Short Peripheral Catheter Thrombophlebitis (SPCT) is the most frequent complication of treatment with, characterized by pain, tenderness, warmth, erythema, swelling and palpable thrombosis of the cannulated vein. SPCT causes patients discomfort and generally leads to catheter removal and insertion of a new catheter at a different site [3]. SPCT is a sterile inflammation [2, 3], and its pathogenesis is not well understood. Several mechanisms have been suggested for SPCT pathogenesis, such as chemical irritation of the endothelium due to infusate or catheter material, or that vein wall injury combined with stasis cause an inflammation response and thrombosis [4, 5].Copyright