Paper B Analysis of the Controlled Auxotonic

In the intact heart, there are simultaneous changes in stress and length throughout the cardiac cycle. In a recently developed digital control system for experiments on isolated papillary muscles from rabbit right ventricle, we included a controlled auxotonic twitch. This twitch allowed proportional changes in stress and length, as if the muscle was acting against an ideal spring. The auxotonic twitches had no discontinuities in length, velocity, stress, or derivative of stress and represented a smooth transition from isotonic to isometric loading. We wanted to use such twitches to analyze the dependence on auxotonic load and initial length of contraction and relaxation. Timing of contraction was independent of load when initial length was l max . Timing of relaxation was highly correlated with peak stress. Twitch prolongation at increased initial length was more pronounced at lower loads. Similar results were obtained when post extra-systolic potentiation was included as an inotropic intervention. The relations between the load dependence of auxotonic contraction and relaxation, presented in this paper, may have implications for the in vivo left ventricular function analysis

Transstenotic coronary pressure gradient measurement in humans:in vitro and in vivo evaluation of a new pressure monitoring angioplasty guide wire

\u3cp\u3eObjectives. The present study was designed to investigate 1) the feasibility and accuracy of coronary pressure measurements with a novel 0.015-in. (0.038 cm) fluid-filled guide wire, and 2) the effect of the guide wire itself on stenosis hemodynamics. Background. To assess the functional results of coronary angioplasty, measurements of the transstenotic pressure gradient have been advocated. However, this is no longer routinely measured because it is not reliable when determined with the angioplasty catheter. Methods. A fluid-filled 0.015-in. guide wire to be connected to a conventional pressure transducer was developed. Five wires were tested for their frequency response characteristics and for their accuracy in measuring hydrostatic pressure. In an in vitro model of stenosis (reference diameter 4 mm), the pressure gradient was determined at incremental flow levels for varying stenosis severity with and without a 0.015-in. guide wire through the narrowing. In 37 patients, the transstenotic pressure gradient was measured before and after angioplasty and compared with obstruction area and percent area stenosis as determined by quantitative coronary angiography. Results. The correlation between the actual pressure and the pressure recorded by the guide wire was excellent (r = 0.98) despite a slight underestimation (-3 ± 5%). Phasic pressure recordings were precluded by a long time constant of 16 ± 4 s. The presence of the guide wire produced a significant overestimation (>20%) of the pressure decrease only in cases of tight stenosis (>90% area reduction). Furthermore, a theoretic model based on the fluid dynamic equation predicted that this overestimation was inversely proportional to the reference diameter of the vessel, yet was only slightly influenced by the flow. The lesion was crossed in all but one (97%) and pressure gradient was recorded throughout the study in 34 (94%) of 36 patients. The mean pressure gradient decreased from 30 ± 19 before to 3 ± 5 mm Hg after angioplasty (p < 0.01). A curvilinear relation was found between the pressure gradient and both percent area stenosis (r\u3csup\u3e2\u3c/sup\u3e = 0.67) and obstruction area (r\u3csup\u3e2\u3c/sup\u3e = 0.72). A sharp increase in pressure gradient was noted once the stenosis exceeded 75% area reduction. Conclusions. Mean transstenotic pressure gradients can be easily and reliably recorded with a 0.015-in. fluid-filled guide wire. This ability should facilitate the functional assessment of coronary stenoses of intermediate severity and of immediate postangioplasty results.\u3c/p\u3

Coronary flow reserve calculated from pressure measurements in humans : Validation with positron emission tomography

Background Experimental studies have shown that fractional flow reserve (defined as the ratio of maximal achievable flow in a stenotic area to normal maximal achievable flow) can be calculated from coronary pressure measurements only. The objectives of this study were to validate fractional flow reserve calculation in humans and to compare this information with that derived from quantitative coronary angiography. Methods and Results Twenty-two patients with an isolated, discrete proximal or mid left anterior descending coronary artery stenosis and normal left ventricular function were studied. Relative myocardial flow reserve, defined as the ratio of absolute myocardial perfusion during maximal vasodilation in the stenotic area to the absolute myocardial perfusion during maximal vasodilation (adenosine 140 mu g.kg(-1).min(-1) intravenously during 4 minutes) in the contralateral normally perfused area, was assessed by O-15-labeled water and positron emission tomography (PET). Myocardial and coronary fractional flow reserve were calculated from mean aortic, distal coronary, and right atrial pressures recorded during maximal vasodilation. Distal coronary pressures were measured by an ultrathin, pressure-monitoring guide wire with minimal influence on the transstenotic pressure gradient. Minimal obstruction area, percent area stenosis, and calculated stenosis flow reserve were assessed by quantitative coronary angiography. There was no difference in heart rate, mean aortic pressure, or rate-pressure product during maximal vasodilation during PET and during catheterization. Percent area stenosis ranged from 40% to 94% (mean, 77+/-13%), myocardial fractional flow reserve from 0.36 to 0.98 (mean, 0.61+/-0.17), and relative flow reserve from 0.27 to 1.23 (mean, 0.60+/-0.26). A close correlation was found between relative flow reserve obtained by PET and both myocardial fractional flow reserve (r=.87) and coronary fractional flow reserve obtained by pressure recordings (r=.86). The correlations between relative flow reserve obtained by PET and stenosis measurements derived from quantitative coronary angiography were markedly weaker (minimal obstruction area, r=.66; percent area stenosis, r=-.70; and stenosis flow reserve, r=.68). Conclusions Fractional flow reserve derived from pressure measurements correlates more closely to relative flow reserve derived from PET than angiographic parameters. This validates in humans the use of fractional flow reserve as an index of the physiological consequences of a given coronary artery stenosis