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A New Look at Diastole

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A New Look at Diastole
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  This article appeared in a journal published by Elsevier. The attachedcopy is furnished to the author for internal non-commercial researchand education use, including for instruction at the authors institutionand sharing with colleagues.Other uses, including reproduction and distribution, or selling orlicensing copies, or posting to personal, institutional or third partywebsites are prohibited.In most cases authors are permitted to post their version of thearticle (e.g. in Word or Tex form) to their personal website orinstitutional repository. Authors requiring further informationregarding Elsevier’s archiving and manuscript policies areencouraged to visit:http://www.elsevier.com/copyright  Author's personal copy A New Look at Diastole Julien I.E. Ho ff  man, MD a, *, Aman Mahajan, MD, PhD b ,Cecil Coghlan, MD c , Saleh Saleh, MD b , Gerald D. Buckberg, MD b a University of California at San Francisco, San Francisco, CA, USA b University of California at Los Angeles, Los Angeles, CA, USA c University of Alabama at Birmingham, Birmingham, AL, USA The word ‘‘diastole’’ comes from two Greekroots:  dia  (apart) and  stellein  (put or make); onemeaning of this combination is expansion ordilatation. Its counterpart is ‘‘systole,’’ from  sus (together) and  stellein , and the combination canbe interpreted as contraction. As early as 1628,William Harvey [1], in his publication  De MotuCordis , used these terms for these meanings.Both of these terms imply a volume change. Thesetwo periods of decreased and increased ventricu-lar volumes are separated by periods in whichvolume does not change. An isovolumic periodprecedes systolic emptying. During this periodventricular pressure rises until it exceeds aorticpressure, the aortic valve opens, and blood beginsto be ejected. This isovolumic period is termed thepresystolic period. When ventricular pressurebegins to decrease and the aortic valve closes,another isovolumic period begins, and it lastsuntil ventricular pressure decreases below atrialpressure, the atrioventricular valve opens, andblood begins to enter the ventricle. By analogyto the presystolic period, this should be termedthe ‘‘prediastolic period.’’ Care is needed in usingthese terms, because sometimes the presystolicand emptying periods are combined and called‘‘systole,’’ and the prediastolic and filling periodsare combined and called ‘‘diastole.’’ There areadvantages to keeping the four periods separatebecause di ff  erent mechanisms are associated witheach of them.Initially, studies of left ventricular functionwere confined to examining changes in pressuresand the dimensions of the long and short axes,because only these measurements could easily bemade with available tools. Left ventricularvolumes were derived from angiographic or echo-cardiographic measurements based on geometricformulas, and then much later directly by theconductance method [2]. Although torsion of theventricle (di ff  erence in rotational twisting between the base and apex of the ventricle) had beenobserved centuries ago, as initially described byBorelli in 1660 [3], it was not measured in humanbeings until the study by Ingels and colleagues in1975 [4]. Arts and colleagues [5] included torsion in their modeling of the left ventricle, and subse-quently implanted markers on the dog heart,made detailed measurements of torsion, and con-cluded that torsion was important in equalizingstresses across the ventricular wall [6]. Morerecently, torsion has been measured in the humanventricle by noninvasive measurements withtagged magnetic resonance imaging (MRI) [7,8],Doppler tissue imaging [8–12], or speckle trackingimaging [8,13–17], and described as an angularnumber that quantifies the di ff  erence betweenclockwise and counterclockwise rotation of thebase and apex of the left ventricle, respectively.These studies have confirmed the magnitude andtime course of torsion in systole and untwistingin diastole, and have shown that the rate of earlydiastolic untwisting is decreased in cardiachypertrophy because of aortic stenosis [7], dilated cardiomyopathy [16], and in myocardial ischemia * Corresponding author. University of California atSan Francisco, 925 Tiburon Boulevard, Tiburon, CA94920-1525. E-mail address:  julien.ho ff  man@ucsf.edu(J.I.E. Ho ff  man)1551-7136/08/$ - see front matter    2008 Elsevier Inc. All rights reserved.doi:10.1016/j.hfc.2008.02.013  heartfailure.theclinics.com Heart Failure Clin 4 (2008) 347–360  Author's personal copy [18]. The normal increase in untwisting with exer-ciseisdecreasedwithhypertrophiccardiomyopathy[10] or aging [13]. Ischemia, too, decreases intra- ventricular pressure gradients and apical filling[19,20].During systole there is not only a decrease inthe dimensions of the long and short axes of theventricle, but the entire ventricle, including thebase, mid, and apex undergoes rotation andreciprocal twisting leading to creation of torsion[7,15]. The torsion aids ventricular emptying inthe same way that wringing out a wet towelremoves more water than merely squeezing thetowel would [3]. At the end of systole, when theaortic valve closes, there is a rapid untwisting of the ventricle. This untwisting creates a negativepressure or a suction in the ventricular cavity,and this negative pressure helps to open the atrio-ventricular valves and draws the blood into theventricles [21–23]. As a result, most ventricularfilling (especially the rapid suction phase that ac-counts for 50% or more of left ventricular filling)occurs well before atrial contraction. Abnormaluntwisting decreases the suction, delays ventricu-lar filling, and can lead to diastolic dysfunction.The time interval between closure of the aorticvalve until opening of the mitral valve duringdeceleration of ventricular pressure is termed the‘‘isovolumic relaxation interval,’’ because ventric-ular volume does not change during this phase of developing a negative intraventricular pressure.The changes of untwisting and the creation of negative ventricular pressure have been attributedto passive elastic recoil of a ventricle below itsequilibriumvolume.Ifonestopssqueezingarubberball,the deformedballreturns toits restingvolumebecause of restoring elastic forces. If one stopstwisting a child’s swing, it untwists because of restoring forces recovering the energy of twisting.Theseanalogieshavebeenusedfortheleftventriclein early diastole. The restoring forces have beenregarded as caused by a ‘‘release of energy frompreviously distorted extra- . and intracellular . elastic structures [12].’’ The structures referred toare titin [24] and interstitial tissue [25]. There is, however, reason to believe that othermajor factors also play a part in untwisting,because recent studies (see below) have shownthat the subepicardial spiral muscle band thatforms the right half of the ventricular septum andleft ventricular outflow tract (and corresponds tothe ascending segment of the ventricular helixconfiguration) is still contracting during predias-tole (Fig. 1) [26,27]. This observation suggests that the conventional term for this phase of cardiaccycle, isovolumic relaxation (IVR), must be reex-amined to explain why such evidence of musclecontraction exists, provide a mechanical explana-tion for the muscular apparatus that may causethis normal physiologic event, examine how this Fig. 1. Sonomicrometer tracings of the descending and ascending muscle bands. From above downward are sonomi-crometer tracings of the descending and ascending muscle bands, with shortening moving down, and tracings of theleft ventricular pressure and dP/dt. Note that in prediastole (  yellow rectangle ), the ascending band is still shortening whilethe descending band is relaxing.348  HOFFMAN  et al  Author's personal copy phase may interact with events that interfere withdiastolic untwisting, and determine if better un-derstanding of its mechanisms can further ourability to use such knowledge to o ff  set adversediastolic dysfunction changes. Structural observations A brief description of the architecture of ventricular muscle is needed to make the involvedmechanisms understandable. Although obliquefibers on the left ventricular surface had beendescribed centuries ago, it was not until Streeter’sstudies that adequate details were provided[28,29]. Streeter used a T-shaped configuration,with the horizontal portion to sample the baseand the vertical portion (that he called the‘‘leg’’) to sample the muscle toward the apex. Bymaking successive sections through the left ven-tricular free wall, he showed that the fiber anglesvaried with depth (Figs. 2 and 3).At the base there were three main sets or layersof fibers. The outer (subepicardial) 20% of the leftventricular free wall has roughly parallel fibersthat run at an angle of about 20 degrees to80 degrees (mean about 50 degrees to 60 degrees)to the equatorial or short axis of the left ventricle.There is an abrupt change of direction to thefibers that occupy about 60% of the midwall andare approximately in the short axis plane at anglesof 10 degrees to   10 degrees from that plane.Another abrupt change of direction leads to the20% of deep (subendocardial) fibers that alsohave an angle of about 20 degrees to 80 degrees(mean about 60 degrees) to the equatorial plane,but in a direction opposite to the subepicardialfibers; the two oblique layers cross like an X.These findings have been confirmed by many laterstudies [30,31]. Note that because of the greaterradius of subepicardial than subendocardialfibers, there is more subepicardial than subendo-cardial muscle. At the lower left ventricular walltoward the apex Streeter found predominantlytwo layers that crossed each other at about   60degree and  þ 60 degree angles, with ‘‘zero’’ atthe mid ventricular position. This angulation isshown in the image of ‘‘leg’’ fiber angles in Fig. 3.Streeter’s studies did not include the septum,and were done on small blocks of ventriculartissue; therefore, he did not describe a spiral arrangement of fibers. His description of thebase of the free wall, however, has been corrob-orated by recent studies with di ff  usion tensorMRI, a technique that has the ability to detectanisotropy because of di ff  erences in the orienta-tion of muscle fibers [32,33]. These studies show Fig. 2. Diagrams showing method of sectioning the wall and measuring the fiber angles. ( A ) Sites of sampling. ( B  )Method of measuring angles. ( From  Streeter DD, Jr., Spotnitz HM, Patel DP, et al. Fiber orientation in the canineleft ventricle during diastole and systole. Circ Res 1969;24(3):339–47; with permission.)349 A NEW LOOK AT DIASTOLE  Author's personal copy three layers of the free wall: an outer layer witha fiber angle of about 60 degrees to the equatorialplane, a horizontal (circumferential) middle layer,and an inner layer with a fiber angle of about60 degrees in the opposite direction (see Fig. 3;Fig. 4). These transverse fibers are particularlywell shown in the imaging by Zhukov and Barr[34] (Fig. 5), together with the oblique clockwise and counterclockwise fibers of the left and righthanded helical arms of the subepicardium andsubendocardium. The circumferential muscledoes not reach the apex, which has therefore, Fig. 3. Distribution of fiber angles across the left ventricular wall at the base and the leg (near the apex). Note that thereis no circumferential layer near the apex. ( From  Streeter DD, Jr., Spotnitz HM, Patel DP, et al. Fiber orientation in thecanine left ventricle during diastole and systole. Circ Res 1969;24(3):339–47; with permission.)Fig. 4. View of left ventricular fibers in the human heart, with septum at bottom. Green: subendocardial spiral fibers.Light blue: circumferential fibers. Dark blue: fibers on right ventricular side of septum (‘‘subepicardial’’). ( Left panel  )Clockwise and counterclockwise helixes in the left ventricle, with circumferential fibers between them. ( Center panel  )Continuity of fibers from right to left ventricle. ( From  Rohmer D, Sitek A, Gullberg GT. Visualization of fiber structurein the left and right ventricle of a human heart. Lawrence Berkeley National Laboratory Report LBNL-61064, 2006;with permission.) ( Right panel  ) Apical fibers showing descending subendocardial fibers forming vortex with ascendingsubepicardial fibers. The pale blue in this figure is an artifact of the rapid change of fiber angle. ( Left panel and right panel from  Rohmer D, Sitek A, Gullberg GT. Reconstruction and visualization of fiber and laminar structure in thenormal human heart from ex vivo di ff  usion tensor magnetic resonance imaging (DTMRI) data. Invest Radiol2007;42(11):777–89; with permission.)350  HOFFMAN  et al
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