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Diastolic function in heart failure.

Kovács SJ - Clin Med Insights Cardiol (2015)

Bottom Line: One important consequence of understanding what diastolic function is, is the recognition that all that current therapies can do is basically alter the load, rather than actually "repair" the functional components (chamber stiffness, chamber relaxation).If beneficial (biological/structural/metabolic) remodeling due to therapy does manifest ultimately as improved diastolic function, it is due to resumption of normal physiology (as in alleviation of ischemia) or activation of compensatory pathways already devised by evolution.This requires advancing beyond phenomenological global indexes such as E/A, E/E', Vp, etc. and employing causality (mathematical modeling) based parameters of diastolic function easily obtained via the parametrized diastolic function (PDF) formalism.

View Article: PubMed Central - PubMed

Affiliation: Cardiovascular Biophysics Laboratory, Cardiovascular Division, Department of Internal Medicine, Washington University School of Medicine, Department of Biomedical Engineering, School of Engineering and Applied Science, Washington University in St. Louis, St. Louis, MO, USA.

ABSTRACT
Heart failure has reached epidemic proportions, and diastolic heart failure or heart failure with preserved ejection fraction (HFpEF) constitutes about 50% of all heart failure admissions. Long-term prognosis of both reduced ejection fraction heart failure and HFpEF are similarly dismal. No pharmacologic agent has been developed that actually treats or repairs the physiologic deficit(s) responsible for HFpEF. Because the physiology of diastole is both subtle and counterintuitive, its role in heart failure has received insufficient attention. In this review, the focus is on the physiology of diastole in heart failure, the dominant physiologic laws that govern the process in all hearts, how all hearts work as a suction pump, and, therefore, the elucidation and characterization of what actually is meant by "diastolic function". The intent is for the reader to understand what diastolic function actually is, what it is not, and how to measure it. Proper measurement of diastolic function requires one to go beyond the usual E/A, E/E', etc. phenomenological metrics and employ more rigorous causality (mathematical modeling) based parameters of diastolic function. The method simultaneously provides new physiologic insight into the meaning of in vivo "equilibrium volume" of the left ventricle (LV), longitudinal versus transverse volume accommodation of the chamber, diastatic "ringing" of the mitral annulus, and the mechanism of L-wave generation, as well as availability of a load-independent index of diastolic function (LIIDF). One important consequence of understanding what diastolic function is, is the recognition that all that current therapies can do is basically alter the load, rather than actually "repair" the functional components (chamber stiffness, chamber relaxation). If beneficial (biological/structural/metabolic) remodeling due to therapy does manifest ultimately as improved diastolic function, it is due to resumption of normal physiology (as in alleviation of ischemia) or activation of compensatory pathways already devised by evolution. In summary, meaningful quantitative characterization of diastolic function in any clinical setting, including heart failure, requires metrics based on physiologic mechanisms that quantify the suction pump attribute of the heart. This requires advancing beyond phenomenological global indexes such as E/A, E/E', Vp, etc. and employing causality (mathematical modeling) based parameters of diastolic function easily obtained via the parametrized diastolic function (PDF) formalism.

No MeSH data available.


Related in: MedlinePlus

(A) The current conventional triangle approximation to characterize E- and A-wave shapes. Using this approximation, Epeak, Apeak, the duration of E-wave (Edur), AT, DT, Epeak/Apeak, and EVTI/AVTI are measured. (B) The often observed curvature change (inflection point) of the E-wave contour that is not a feature of the triangle approximation to E-wave shape. See text for details.
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f1-cmc-suppl.1-2015-049: (A) The current conventional triangle approximation to characterize E- and A-wave shapes. Using this approximation, Epeak, Apeak, the duration of E-wave (Edur), AT, DT, Epeak/Apeak, and EVTI/AVTI are measured. (B) The often observed curvature change (inflection point) of the E-wave contour that is not a feature of the triangle approximation to E-wave shape. See text for details.

Mentions: Briefly, as a first approximation, E- and A-wave contours are simplified as having triangular shape, and triangle-based indexes, such as peak heights of the E- and A-waves and their ratio (Epeak, Apeak, Epeak/Apeak), the deceleration time and width of the E-wave (DT, Edur), and the velocity time integral (VTI) of the E- and A-waves (Fig. 1A), are routinely measured. The triangular approximation to E-wave shape is convenient, but current imaging technology allows the curvature of E-wave contours to be discerned (see Fig. 1B). Regrettably, the physiologically important curvature features of the E-wave are usually disregarded. However, the benefit in understanding the physical and physiologic principles that govern E-wave shape and its curvature allows additional information to be extracted as detailed below [the parametrized diastolic filling (PDF) formalism].


Diastolic function in heart failure.

Kovács SJ - Clin Med Insights Cardiol (2015)

(A) The current conventional triangle approximation to characterize E- and A-wave shapes. Using this approximation, Epeak, Apeak, the duration of E-wave (Edur), AT, DT, Epeak/Apeak, and EVTI/AVTI are measured. (B) The often observed curvature change (inflection point) of the E-wave contour that is not a feature of the triangle approximation to E-wave shape. See text for details.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4401253&req=5

f1-cmc-suppl.1-2015-049: (A) The current conventional triangle approximation to characterize E- and A-wave shapes. Using this approximation, Epeak, Apeak, the duration of E-wave (Edur), AT, DT, Epeak/Apeak, and EVTI/AVTI are measured. (B) The often observed curvature change (inflection point) of the E-wave contour that is not a feature of the triangle approximation to E-wave shape. See text for details.
Mentions: Briefly, as a first approximation, E- and A-wave contours are simplified as having triangular shape, and triangle-based indexes, such as peak heights of the E- and A-waves and their ratio (Epeak, Apeak, Epeak/Apeak), the deceleration time and width of the E-wave (DT, Edur), and the velocity time integral (VTI) of the E- and A-waves (Fig. 1A), are routinely measured. The triangular approximation to E-wave shape is convenient, but current imaging technology allows the curvature of E-wave contours to be discerned (see Fig. 1B). Regrettably, the physiologically important curvature features of the E-wave are usually disregarded. However, the benefit in understanding the physical and physiologic principles that govern E-wave shape and its curvature allows additional information to be extracted as detailed below [the parametrized diastolic filling (PDF) formalism].

Bottom Line: One important consequence of understanding what diastolic function is, is the recognition that all that current therapies can do is basically alter the load, rather than actually "repair" the functional components (chamber stiffness, chamber relaxation).If beneficial (biological/structural/metabolic) remodeling due to therapy does manifest ultimately as improved diastolic function, it is due to resumption of normal physiology (as in alleviation of ischemia) or activation of compensatory pathways already devised by evolution.This requires advancing beyond phenomenological global indexes such as E/A, E/E', Vp, etc. and employing causality (mathematical modeling) based parameters of diastolic function easily obtained via the parametrized diastolic function (PDF) formalism.

View Article: PubMed Central - PubMed

Affiliation: Cardiovascular Biophysics Laboratory, Cardiovascular Division, Department of Internal Medicine, Washington University School of Medicine, Department of Biomedical Engineering, School of Engineering and Applied Science, Washington University in St. Louis, St. Louis, MO, USA.

ABSTRACT
Heart failure has reached epidemic proportions, and diastolic heart failure or heart failure with preserved ejection fraction (HFpEF) constitutes about 50% of all heart failure admissions. Long-term prognosis of both reduced ejection fraction heart failure and HFpEF are similarly dismal. No pharmacologic agent has been developed that actually treats or repairs the physiologic deficit(s) responsible for HFpEF. Because the physiology of diastole is both subtle and counterintuitive, its role in heart failure has received insufficient attention. In this review, the focus is on the physiology of diastole in heart failure, the dominant physiologic laws that govern the process in all hearts, how all hearts work as a suction pump, and, therefore, the elucidation and characterization of what actually is meant by "diastolic function". The intent is for the reader to understand what diastolic function actually is, what it is not, and how to measure it. Proper measurement of diastolic function requires one to go beyond the usual E/A, E/E', etc. phenomenological metrics and employ more rigorous causality (mathematical modeling) based parameters of diastolic function. The method simultaneously provides new physiologic insight into the meaning of in vivo "equilibrium volume" of the left ventricle (LV), longitudinal versus transverse volume accommodation of the chamber, diastatic "ringing" of the mitral annulus, and the mechanism of L-wave generation, as well as availability of a load-independent index of diastolic function (LIIDF). One important consequence of understanding what diastolic function is, is the recognition that all that current therapies can do is basically alter the load, rather than actually "repair" the functional components (chamber stiffness, chamber relaxation). If beneficial (biological/structural/metabolic) remodeling due to therapy does manifest ultimately as improved diastolic function, it is due to resumption of normal physiology (as in alleviation of ischemia) or activation of compensatory pathways already devised by evolution. In summary, meaningful quantitative characterization of diastolic function in any clinical setting, including heart failure, requires metrics based on physiologic mechanisms that quantify the suction pump attribute of the heart. This requires advancing beyond phenomenological global indexes such as E/A, E/E', Vp, etc. and employing causality (mathematical modeling) based parameters of diastolic function easily obtained via the parametrized diastolic function (PDF) formalism.

No MeSH data available.


Related in: MedlinePlus