Analysis of methodology for measurement of intramyocardial pressure

Nematzadeh, David; Rose, John C.; Schryver, Th.; Huang, H. K.; Kot, Peter A.

doi:10.1007/bf01935811

Cited by 20 publications

(13 citation statements)

References 25 publications

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“…In general, great care has to be taken to avoid direct contact of the sensor with the muscle and a covered or recessed transducer is used; this was recently discussed by Rabbany et al (58). It was also shown that transducer orientation may be important (54). This method was used first by Armour and Randall (6) and later by others (30,31,54,65,66).…”

Section: Microtransducer Methodsmentioning

confidence: 95%

“…This method is often called the "closed method" (54,58). An artificial cavity is created in the myocardium and pressure is measured in it.…”

Section: Isovolumic Methodsmentioning

confidence: 99%

“…Both approaches can be divided into two separate methods. This classification of methods into a total of four groups was suggested by Nematzadeh et al (54) and will be uscd here.…”

Section: Measurement Of Intramyocardial Pressurementioning

confidence: 98%

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Physiological hypotheses-Intramyocardial pressure. A new concept, suggestions for measurement

Westerhof

1990

Basic Res Cardiol

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Intramyocardial pressure is supposed to play a major role in systolic coronary flow impediment. Via its assumed relation with radial wall stress it is supposed to be similar to ventricular pressure at the endocardium and decreases linearly to negligible values epicardially. Many attempts to measure intramyocardial pressure have been reported in the literature with rather different results. For instance, with most of the various methods, intramyocardial pressures both higher and lower than left ventricular pressure have been obtained and intramyocardial pressures of more than 125 mm Hg have been found in low-loaded isobaric beats (negligible pressure development in systole). In this "physiological hypotheses paper" I suggest left ventricular pressure and intramyocardial pressure both to result from the varying stiffness of cardiac muscle over the heart cycle. For any intramuscular cavity a time varying pressure-volume (P-V) relation results from the changes in muscle stiffness, the so-called time varying elastance defined as E(t) = P(t)/V(t), and with maximal or systolic elastance called Emax. For a constant contractile state the time varying elastance (E(t)) is suggested to be almost independent of preload and afterload. This concept has been well established for the ventricular cavities, but is here proposed to hold for the interstitial space as well. If a cavity is subject to isovolumic conditions the pressure will be high, but when volume in systole decreases (ventricular ejection or squeezing out of interstitial fluid) pressures will be lower. Thus for constant load on the interstitial cavities, but different loads on the ventricle, left ventricular pressure will vary while intramyocardial pressure remains the same. For low-loaded isobaric beats where left ventricular pressure is minimal intramyocardial pressure will remain the same as during normal ventricular loads and isovolumic beats. Augmented contractility will increase Emax and this will increase left ventricular and intramyocardial pressure only by the same amount if loading conditions of both cavities remain the same. Both ventricular pressure and intramyocardial pressure arise from varying stiffness of cardiac muscle and intramyocardial pressure does not result from left ventricular pressure. A proportionality of left ventricular and intramyocardial pressure is therefore not to be expected. The results on intramyocardial pressure obtained by the different methods used in the literature should be re-interpreted taking this concept into account.

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Section: Microtransducer Methodsmentioning

confidence: 95%

“…This method is often called the "closed method" (54,58). An artificial cavity is created in the myocardium and pressure is measured in it.…”

Section: Isovolumic Methodsmentioning

confidence: 99%

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Physiological hypotheses-Intramyocardial pressure. A new concept, suggestions for measurement

Westerhof

1990

Basic Res Cardiol

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“…The size and location of infarction after coronary occlusion will generally depend upon regional oxygen demands, regional oxygen and other substrate supplies, and the size and location of the tissue bed perfused by the vessel at jeopardy. In ventricular free walls, intramural systolic tension is greater in inner than in outer wall segments (14,21); indeed, subendocardial wall tension may exceed intracavitary pressure (14,21). This pressure gradient translates into a greater oxygen demand in subendocardial than in subepicardial tissues.…”

Section: Artery a F T E R Verifying T H E S E Variables An A T T E mentioning

confidence: 97%

Myocardial infarction following acute occlusion and reperfusion of the septal coronary artery

et al. 1985

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It has been demonstrated that temporary occlusion of major epicardial arteries of the dogs produces a nontransmural myocardial infarction (MI) whose size is reduced by early reperfusion. This study was undertaken to determine the location and extent of MI following acute occlusion and reperfusion of the septal artery (SA). The SA was occluded for four hours in group I (7 dogs). Occlusion time for group II (6 dogs) was 2 hours and for group III (6 dogs) was 1 hour, followed by 2 and 3 hours of reperfusion, respectively. The hearts were then removed and cut into transverse slices from base to apex. The triphenyl tetrazolium chloride technique identified the areas of infarction, which were quantitated with a microcomputer-based graphics system. To determine the extent of necrosis across the interventricular septum (IVS), the IVS was divided into 5 transverse segments of equal depth and the amount of MI was determined for each. In group I, MI involved 3.42 +/- 0.9% (mean +/- SEM) of the left ventricle (LV) and 13.49 +/- 3.4% of the IVS. In group II, 6.11 +/- 1.3% of the LV and 25.00 +/- 5.5% of the IVS were infarcted. In group III, 5.63 +/- 1.3% of the LV and 31.9 +/- 14.3% of the septum were infarcted. MI was larger on the left side of the IVS than on the right in all groups, and the extent of MI did not differ significantly between the three groups. This study showed that early reperfusion of the SA did not reduce MI as reported for other coronary beds.

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“…This pressure was named "tissue pressure" or "intramyocardial pressure" [2]. The accuracy of its measurement depends on the size of the transducers inserted inside the left ventricular wall, large transducers providing pressure values higher than the real ones [3]. The servo-nulling method seems the solution for this problem, because it uses as sensors glass micropipettes, which are 1000 smaller than transducers used by any other method [4].…”

Section: Introductionmentioning

confidence: 99%

Measurement and calculation of the intramyocardial stress

Mihăilescu¹,

Shoucri²

2005

Modelling in Medicine and Biology VI

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By using a servo-nulling mechanism and coated glass micropipettes (20-24 µm OD), intramyocardial stress (IMS) was measured at the base of the left ventricle in isolated working and nonworking cat hearts, perfused with Krebs-Henseleit buffer. Glass micropipettes were placed at various depths inside the left ventricular wall using a micropipette holder and manipulator. Calculation of the IMS is not a simple problem because of the complex structure of the active fibres in the myocardium. However a mathematical approach has been developed that reduces the complexity of this problem. It consists in using the concept of force per unit volume of the myocardium to model the components of the stress generated by the fibers in three orthogonal directions (assuming symmetrical contraction). Important relations are derived between the stress induced by the LVP and the stress induced by the active fibres in the passive medium of the myocardium. Keywords: measurement with micropipette, intramyocardial stress, active and passive stress in the myocardium, left ventricular elastance, active force per unit volume of the myocardium, stress-strain relation in the myocardium.

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Analysis of methodology for measurement of intramyocardial pressure

Cited by 20 publications

References 25 publications

Physiological hypotheses-Intramyocardial pressure. A new concept, suggestions for measurement

Physiological hypotheses-Intramyocardial pressure. A new concept, suggestions for measurement

Myocardial infarction following acute occlusion and reperfusion of the septal coronary artery

Measurement and calculation of the intramyocardial stress

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