ASSESSMENT OF DIASTOLIC DYSFUNCTION : Invasive Modalities - 05/09/11
Résumé |
Given the access to direct invasive measurements of left ventricular (LV) chamber pressure and volume, one would presume that the analysis of diastolic function would be fairly straightforward. Certainly, many of the ambiguities associated with noninvasive echo-Doppler parameters stem from their lack of directness; however, even with such invasive data, thoughtful assessment of diastolic properties requires an understanding of the assumptions upon which the analysis is based, and the various factors that can influence the results.
There are three features of ventricular diastolic function that are most accurately and directly measured by invasive techniques. The first is the decline in ventricular chamber pressure during the period of isovolumetric relaxation (Figure 1A). Pressure can be easily and accurately determined from a high-fidelity micromanometer transducer placed within the LV cavity. Pressures after aortic valve closure but prior to mitral valve opening are analyzed to yield indexes of the rate of pressure decline. These parameters are generally referred to as time constants of relaxation. Some of the parameters are, by their definition, highly dependent upon the conditions under which the heart is contracting (i.e., net filling volume or preload, arterial impedance or afterload, pericardial and intrathoracic pressures). Some common measures can also prove problematic in diseases such as congestive heart failure, because the mathematical models upon which they rely do not consistently describe the course of pressure decay.32, 44 There are other situations, such as hypertrophic cardiomyopathy with mid-systolic cavity obliteration, where pressure decay is interrupted in mid-course, so that no single time constant can be meaningfully derived.3, 38 In the first section of this article, the author focuses on how relaxation is invasively assessed, and provides details regarding potential pitfalls of various indexing methods.
The second component is the end-diastolic pressure (EDP), that is, the pressure achieved within the ventricle at maximal filling volume, just before the onset of contraction. This is an extremely common parameter; however, its definition is often surprisingly vague. For example, EDP is frequently defined as the pressure at the time of rapid upstroke of left ventricular pressure (LVP), a rather qualitative identifier that may be difficult to precisely apply at rapid heart rates.
The third major component of diastolic function that is only directly assessable by invasive methods is passive chamber stiffness or its inverse—compliance. This is usually derived from an analysis of the simultaneous relations between LV pressures and volumes measured during the diastolic filling period.14, 26 The term diastolic chamber compliance is itself somewhat of a misnomer, in that the ΔVolume/ΔPressure ratio by which it is defined is not constant for a given heart, but itself a function of cavity volume. This is the consequence of the nonlinear properties and fiber architecture of structural proteins within myocytes such as titin6, 21, 31 and the extracellular matrix,46, 47 and is clearly represented by nonlinearity of the pressure-volume (P-V) curve (Figure 1B). As with pressure decay, diastolic P-V data are typically fit using mathematical models so as to yield stiffness measurements that are theoretically less dependent on the specific loading conditions. An important caveat in analyzing diastolic P-V relations is that they do not solely convey information about the cardiac muscle wall. Extrinsic constraining forces related to the right ventricle and pericardium can play a major role in the measured diastolic P-V curve, and can prominently influence parameters derived from such data.7, 23, 25, 45 Lastly, the relation between pressure and volume can be modified by the rate at which the heart is filled owing to viscous properties of the muscle.9, 13, 42 Nonetheless, methods have been developed that minimize these effects to obtain very reasonable assessments of diastolic stiffness.
This article focuses on the methods for measuring these two primary components of diastole. All of the data presented have been obtained in human subjects, using methods that are, if not widely available, at least well established for the diagnosis and treatment of clinical disease.
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| Address reprint requests to David A. Kass, MD, Halsted 500, Johns Hopkins Hospital, 600 N Wolfe Street, Baltimore, MD 21287, e-mail: dkass@bme.jhu.edu |
Vol 18 - N° 3
P. 571-586 - août 2000 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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