Abstract
Objective: To mechanically test the intact cardiac structure to determine the sequence of contraction within the myocardial mass to try to explain ejection and suction. Methods: In 24 pigs (30–85kg), segment shortening at the site of sonomicrometer crystals was continuously recorded. The ECG evaluated rhythm, and Millar pressure transducers measured intraventricular pressure and dP/dt. Results: Study of segment shortening defined a sequence of contraction within the myocardial mass, starting at the free wall of the right ventricle and on the endocardial side of the antero-septal wall of the left. Crystal location defined underlying contractile trajectory; transverse in right ventricle followed by basal posterior left ventricle, and from the endocardial anterior wall to the posterior apical segment and finally to the epicardial side of the anterior wall. Mean shortening fraction averaged 18±3%, with endocardial exceeding epicardial shortening by 5±1%. Epicardial segment crystal displacement followed endocardial shortening by 82±23ms in the anterior wall, and finished 92±33ms after endocardial shortening stopped, time frame that matches the interval of fast drop of ventricular pressure and the start of suction. Conclusions: Crystal shortening fraction sequence followed the rope-like myocardial band model to contradict traditional thinking, with two starting points of excitation–contraction, the right anterior free wall of the right ventricle, and the endocardial side of the anterior wall. Active suction may be due to active shortening of the epicardial fibers of the anterior wall, because relaxation was not detected when both mitral and aortic valves were closed during the interval previously termed ‘isovolumetric relaxation’.
1 Introduction
In spite of recent remarkable progress in understanding myocardial function at the genetic and molecular level, the advancement in developing a comprehensive understanding of ventricular structure has been limited to microscopic scales. These concepts are mainly based on Streeter's two-dimensional measurements of a uniformly changing angle of orientation of myocardial microscopic fibers from epicardium to endocardium [1]. Streeter's findings have helped us to recognize the intricate nature of local fiber structure and perhaps function. However, in order to understand cardiac function and its efficiency from the point of view of vectors of force generated by cardiac sarcomeres, one needs to develop a global three-dimensional model of ventricular structure adhering to the local and global dynamics of myocardial spatial architecture.
Streeter recognized the seminal conceptual framework of Krehl's Treibwerk representation of the figure of eight oblique fiber pathways, connecting inner and outer cones, and verification of this idea by the dissection techniques of Torrent-Guasp thereby vindicates the Treibwerk, showing a highly ordered compact structure [2]. The re-introduction of a helical rope-like heart muscle concept by Torrent-Guasp [3] offers a radically different view thus challenging the prevailing anatomical views of myocardial structure and function. In this concept, the ventricular structure consists of two simple loops, which start at the pulmonary artery and end in the aorta. These two components include a horizontal basal loop, comprised of right and left segments that surround the right and left ventricles, which changes direction to form an oblique dual apical loop. This change develops through a spiral fold in the ventricular band to cause a dual ventricular helix produced by now obliquely oriented fibers, forming an endocardial or descending and epicardial or ascending segment of the apical loop with an apical vortex (Fig. 1). In this view, both the outer circumferential wrap and inner helical fiber bundle, which weave through myocardial substance, provide a preferential pathway for possible sequential contractile dynamics as detailed at http://www.gharib.caltech.edu/~heart/ on a theoretical model.
The validity of any cardiac model relies upon showing that the structure can explain physiological function when activated. Torrent-Guasp's concept, if correct, may offer interesting opportunities to explain ventricular shape and mechanics based on realistic fiber shortening and dynamic rearrangement. Also, unlike the current views, it may offer a unified concept of systolic ejection and the early suction phase of ‘diastolic’ cardiac function. It provides a unifying theme because it can explain both phases of cardiac function through a sequential contractile action. This is in contrast with the conventional acceptance of elastic recoil from stored potential energy during systole to explain isovolumetric relaxation [4,5]. With Torrent-Guasp's structural model, a sequential contractile wave through the preferential helical band can induce a coil-like twisting and reciprocal twisting in the opposite direction of the left ventricle and septum to cause the physiologic events of ejection and suction.
The main objective of this paper is to mechanically test the intact cardiac structure to find the sequence of contraction within the myocardial mass. By selective placement of multiple sonomicrometer transducer-pairs we identified the principle angle of local fiber bundles at subendocardial/epicardial positions throughout the left and right heart, observed patterns of shortening, and will suggest physiologic correlation with known hemodynamic events.
2 Material and methods
All animals received humane care in compliance with the 1996 NRC Guide for the Care and Use of Laboratory Animals, available at: http://www.nap.edu/readingroom/books/labrats/contents.html
Twenty-four Yorkshire-Duroc pigs (30–85kg) were premedicated (ketamine 15mg/kg, diazepam 0.5mg/kg IM) and anesthetized with inhaled isoflurane 1.5% (MAC 1%) throughout the operation. Support with a volume-controlled ventilator (Servo 900C, Siemens-Elema, Sweden) was started after tracheostomy and endotracheal intubation. The femoral artery and vein were cannulated and arterial blood gases measured to keep oxygen and carbon dioxide tensions and pH within normal range. A balloon-tipped catheter (Model 132F5, Baxter Healthcare Corp., Irvine, CA) was advanced into the pulmonary artery through a jugular vein to measure cardiac output (thermo-dilution technique) and pulmonary artery pressure. Plasma-Lyte or Saline were added to keep LV pressure within 10–15mmHg. Cardiac outputs were measured before, during and after experimentation to ensure no hemodynamic instability. In three animals, we tested the effects of dopamine 10μg/kgmin and propranolol 50mg at the end of the experiment to evaluate variations in percentage of segment shortening (%SS).
The pericardium was incised after median sternotomy and a solid-stated pressure transducer-tipped catheter (Model MPC-500, Millar Instruments, Inc., Houston, TX) was inserted through the apex to monitor left ventricular pressure (LVP). Regional shortening within the right and left ventricle was measured with pairs of 2mm ultrasonic microtransducer crystals (Sonometrics, London, Ontario, Canada). Aortic pressure, LVP, dP/dt, and sonomicrometer crystals data were digitally processed by specific hardware and software (Sonometrics, London, Ontario, Canada). Velocity of sound through cardiac tissue was fixed to 1590m/s. Sonomicrometer measurements were recorded with a sampling rate of 195.8 samples/s, a transmitter spacing of 652μs, transmit inhibit delay of 1.81μs, and transmit pulse length of 375ns. Synchronicity between myocardial shortening was compared to left ventricular performance with 5ms precision. Sequence of contraction of different segments of the heart was then established and compared with ventricular hemodynamics. All cases were performed and analyzed by the same surgeon.
2.1 Crystal position and orientation
Four pairs of sonomicrometer crystals were positioned for each area tested (e.g. epicardial side of the anterior wall) describing an octagon with angles pointing at 0, 45, 90, 135, 180, 225, 270 and 315°. To measure the angle of the line connecting the crystals in each pair, a local coordinate was used (Fig. 2); the aortic annulus was the highest point and the apex as the lowest, in a North and South fashion. Following the North and South simile, contraction at 0° was considered when both crystals were oriented North to South, 90° East to West, 45° Southwest to Northeast and 135° Northwest to Southeast. Synchronic recordings of the four pairs of opposing crystals gave an estimate of the best angle of contraction of that area, by choosing the pair with highest %SS. In multiple occasions, two pairs recorded similar %SS (e.g. 45 and 90°). Then, a new couple of crystals was placed orientated at an angle calculated by the mean of the angles defined by the two pairs with highest contraction (following the example, at 65°) to test if this new orientation presented higher %SS. Segmental shortening was calculated as follows 
where EDL and ESL are end diastolic and end systolic length, respectively.
Epicardial and endocardial sides of the LV were separately tested as well as the free wall of the RV. In the epicardial side, crystals were placed by a 1mm cut into the epicardium. Endocardial crystals were placed by a 1mm cut in the epicardium followed by pushing the crystal into the ventricular cavity by a specific crystal introducer (1mm diameter PVC tube). When pulsatile bleeding was achieved to confirm transmural perforation, pulling from the electrical cord of the crystal brought the sensor to the endocardial wall, fixing it by a 5/0 PTFE stitch in the epicardial side. Confirmation of positioning was performed post-mortem in all hearts.
Left ventricular anterior and posterior walls were explored in all hearts. We restricted exploration of different cardiac regions to a limited number of experiments because of concern that multiple myocardium perforations might affect global heart function. We tested the RV free wall in five hearts, lateral LV wall in five hearts and apex in two. Sequence of contraction was compared to the anterior and posterior walls in each animal. %SS and angle of optimum contraction is presented as mean±SD.
3 Results
All animals remained hemodynamically stable, since mean arterial pressure was 67±16mmHg at start and 61±12mmHg at completion, mean heart rate began at 95±14 and was 102±18mmHg at experiment end, and cardiac index exceeded 2.3l/minm2 throughout the study.
3.1 LV anterior wall
Segment shortening in the endocardial wall was most powerful at angles between 80 and 90°, reaching 17–27% (Fig. 2). In contrast, %SS was reduced by placing the crystals at 0°. The onset of endocardial shortening occurred between the Q and R waves of the EKG, thus preceded the systolic rise of LVP and dP/dt (Figs. 2 and 3). Subendocardial muscle shows two distinct rates as it shortens. First, a short and steep descent followed by a longer and less steep shortening phase. A curve notch was present to divide these phases, which increased in size as crystals were placed closer to the papillary muscle (Fig. 4). The end of endocardial shortening consistently coincided with the beginning of the descent phase of the left ventricular pressure and the negative slope of dP/dt (Fig. 2).
LV anterior subepicardial shortening averaged 12±2% SS (Figs. 2 and 3) when crystal placement angle was oriented at 150±10° (approximately 60° opposite endocardial placement). Conversely, shortening extent was 6% at a 45° angulation. Compared to subendocardial shortening, the onset of subepicardial %SS displayed a consistent delay of 82±23ms time-related delay (Table 1), starting at the maximum value of dP/dt. In all studies, epicardial %SS finished 92±33ms after subendocardial contractions ended (Fig. 3).
The extent of contraction was more intense when the crystal pairs were situated near the apex in both the endocardial and epicardial sides of the left ventricle, averaging 35±5% less contraction in the basal portion.
3.2 Apical posterior wall of the left ventricle
In contrast to the anterior wall, endocardial and epicardial sides of the apical posterior wall presented near similar amount of contraction. There was a 10±5s delay in initiation of contraction (Fig. 3). However, the orientation of contraction was opposite in each side: better angle of contraction of the endocardial side was found at 0°, while at the epicardial side was 90°. This fractional shortening variance was most evident at the epicardial site, as the transverse positioning showed 19 vs. 7% for vertical placement. With endocardial placement, the vertical crystal pair showed 23 vs. 17% with transverse positioning.
Despite these differences in the direction of shortening between endo and epicardial sites in the posterior inferior LV wall, the starting point of contraction was similar, a finding different from the ∼80ms time delay in initiating shortening on the anterior wall.
3.3 Right ventricle
Two main types of shortening are found in the right ventricular free wall. In the right ventricular outflow, tract shortening pattern was more intense at an orientation of 150±10°, starting later than the lateral free wall, and simulating the pattern of LV anterior epicardial shortening. In the lateral RV free wall, close to the atrio-ventricular junction, shortening started between the Q and R waves of the EKG, synchronic with LV endocardial anterior wall. The most prominent shortening was in a transverse (%SS 23±1% at 100±5°), rather than vertical direction (10±1% at 0°), falling to 6% at 45° angulation.
3.4 Left ventricular posterior basal region
A similar maximal horizontal pattern to the RV free wall occurred in the LV posterior basal region. Angle orientation was 100±5°, but the initiation of regional shortening occurred 10±5ms after the start of RV free wall shortening.
3.5 Sequence of contraction
Shortening starts initially and simultaneously in the RV lateral free wall, and LV endocardial antero-septal wall (Fig. 2). This early shortening corresponded with the Q wave of the EKG and initial slow LVP rise, which remained below 15mmHg. After a 10±5ms delay, the event sequence continues with shortening of the LV posterior wall (Fig. 3). Shortening of right and posterior LV, and anterior endocardial wall segments began before shortening occurred in the LV subepicardial anterior wall or RV outflow tract.
Contraction at these later LV and RV segments began 82±23ms after the initial muscle contraction, corresponding to peak positive dP/dt wave, S wave of QRS, and steep LVP rise for systolic ejection. Shortening was then present in all segments during systolic ejection, so that ‘co-contraction’ of both endocardial and epicardial fibers existed during this cardiac phase. Initiation of subepicardial fiber shortening coincided with a reduction of shortening slope in subendocardial fibers (Fig. 3), but did not change the slope of segmental shortening of either the lateral LV or RV free wall.
The first regions to stop shortening were segments that started first, the LV endocardial antero-septal wall and RV free wall, then 10ms later the posterior basal LV wall. The end of contraction for these segments coincided with the onset of the negative dP/dt. In each instance, the LV epicardial component and RV outflow tract fibers continued this shortening phase for 92±33ms after the RV free wall, posterior LV, and endocardial LV segments stopped shortening. This extended time interval during epicardial segment shortening contraction corresponds to the ‘isovolumetric relaxation’ phase, and overlaps the LV rapid pressure decrease that is otherwise known as the ‘suction’ phase (Figs. 3 and 5). Consequently, a systolic shortening phase persisted throughout the entire LVP recording, so that there was no interval of isovolumetric relaxation.
The prolonged shortening of LV anterior wall epicardial fibers during the cessation of LV endocardial shortening was associated with a reversal, or upward slope of the endocardial crystal tracing (Figs. 2 and 3). Simultaneously, the basal posterior wall of the LV presented an increased distance between crystals (Fig. 3). This separation between crystals reached the point of maximum fiber stretch (i.e. separation between crystals), only surpassed by the added stretch due to ventricular filling by atrial contraction (Fig. 6).
The relationship between shortening of endo and epicardial segments was examined by use of infusions of inotropic (Dopamine) or β-blocking (Propranolol) drugs. The time delay between the start of contraction in endocardial and epicardial muscle of the anterior wall of the LV decreased to 26±7ms when 10μg/kg per min dopamine was given. Simultaneously, %SS increased from 25.7 to 29.1% in the endocardial wall, and heart rate rose from 88 to 112beats/min to confirm the inotropic stimulation. In contrast, propranolol 50mg IV prolonged this time delay to 121±20ms, reducing %SS to 19%, and slowed heart rate to 78beats/min. There was also an associated prolongation of the duration of the endocardial contraction. Thus, the interval between the end of endocardial contraction with ongoing epicardial contraction shortened, and the slope of the rapid descent of the LVP curve was less steep (Fig. 7).
4 Discussion
The intent of this study was to use sonomicrometer crystals with high temporal and spatial resolution [6] to determine contraction patterns within the myocardial mass. The crystal one-dimensional gauges provide a local view of a global concept, exploring all cardiac regions, by probing how the maximal extent of fiber shortening in preferential pathways is governed by the orientation between couples of these crystals [7]. We recognize the crystal tracings show movement of only the fibers touched by the crystals in the endocardium and epicardium. Global motion, like narrowing, shortening, lengthening and widening, that characterize visible motion shown by echocardiogram or MRI are not defined by the isolated crystals.
These local barometers do not measure thickening [6], twisting [5], torsion [4], cross fiber shearing forces [6] or inception of the calcium trigger of contraction [8]. Distinction between each of the varied factors that influence the term ‘contractility’ is not the intent of this manuscript, since no effort was made to measure deformation [7], as it influences strain of the cross fiber or transmural shearing forces [7] that may result in a motion that may not be aligned with local myofibers. However, such measurements were made by others [9], shear stress and torsion are maximal in the endocardial and approximately twice [9] that of the epicardial region, consistent findings with the maximal extent of shortening during our comparisons of displacement between couples of crystals. Additionally, our observation of the anisotropic shortening showing the heterogeneous contractile action of both endocardial and epicardial regions increasing toward the apex, compares favourably with tagging-related MRI non-invasive reports of ventricular rotational deformation in humans by Buchalter [9].
The genesis of ventricular shortening begins immediately after the Q wave on the EKG, and involves both left ventricular endocardial and right lateral free wall fibers, to be followed ∼10ms later with LV posterior shortening in the distribution of the basal loop. These three segments contract before the rapid acceleration of LV pressure for ejection. The predominant force becomes circumferential compression, thereby explaining the 13–25% narrowing of the mitral valve annulus during the isovolumetric contraction that precedes ventricular emptying [10].This narrowing occurs with a clockwise cocking of LV motion, shown by MRI and radio opaque markers. Timek et al. [11] studied ischemia, and suggested an atrial contribution to mitral annular narrowing by noting maximum widening of the annulus synchronic to atrial contraction-induced rising of EDLVP, followed by fall of the LVP and constant narrowing of mitral annular area in early systole. We studied normal hearts and support an important ventricular component to annular narrowing related to the myocardial band by showing in Fig. 6 that shortening of the basal loop, prior to the rise of LVP, produces an active narrowing by the transverse and circumferential myocardial fibers that surround the posterior and lateral basal portion of the left ventricle. The sequence from right to left segment supports the cocking motion seen by MRI and radio opaque markers.
While isovolumetric shortening involves only three segments, ejection involves the whole myocardial mass, bringing into play the later contribution of the epicardial muscle. Shortening of the epicardial segment follows ∼80ms later, and correlates with the rapid acceleration of pressure, peak positive dP/dt and end of the QRS complex. Based upon the direction of crystals, we think that the RV and posterior basal LV shortening are dominant at the initiation of contraction, and cause compression and narrowing of the chamber, together with the annulus. The oblique squeeze of the endocardial segment initiates the predominant twisting responsible for ejection with shortening of the cavity which occurs during ‘co-contraction’ with the epicardial fibers. This may initiate the torsion-like counter clockwise twisting, or wringing of a towel or with a wine press suggested by Borrelli in 1660, and now codified by non-invasive MRI recordings with tagging studies [5]. The downward movement of the ventricle during this later phase of ejection implies that the oblique endocardial segment muscle carries the dominant force during shortening for ejection.
The oblique endocardial very rapid shortening phase becomes less steep with the onset of shortening of the oppositely directed and oblique epicardial segment, that is evident during their co-contraction. This reciprocal force may become unleashed when there is cessation of endocardial segment active shortening, so the reciprocally twisting epicardial segment can then predominate and produce the apical clockwise twisting that occurs during abrupt lengthening during rapid ventricular filling.
We suspect the final phase of motion relates to the hiatus between loss of shortening in the RV, posterior LV and endocardial segment records, and ongoing shortening in the epicardial segment. This time interval is linked to the rapid descent of LV pressure (almost simulating the rapid rise for generation of pressure) and the onset of the negative phase of dP/dt recording. Consequently, an active consistent period of epicardial shortening persists during the period previously termed isovolumetric relaxation. A more precise term is late isovolumetric contraction[12]. This repetitive interval precedes a rapid filling phase that has been ascribed to reflect elastic recoil related to potential energy stored during the systolic contraction [13,14]. We believe this motion relates to muscular shortening, an oxygen requiring step that is produced by ongoing epicardial muscle shortening that overlies LV endocardial muscle, thus providing a myocyte cause for ventricular suction.
This active contractile role was also suggested by Rademaker and Shapiro [5,15] whose MRI studies showed that 50% of filling develops during this time frame, and could use inotropic infusion to accentuate of speed and rate untwisting (or reciprocal twisting in a reverse direction) for rapid filling. Brutsaert [8] further amended the infrastructure for rapid filling by a suggesting contractile phase of systole.
Clearly, discoordination of hiatus between endocardial and epicardial shortening may compromise rapid filling and derail the mechanisms for suction, so that pressure, rather than muscle motion becomes the principal filling determinant. In consequence, a contractile dysfunction may be the origin of diastolic dysfunction. Evidence for this prolongation of late systole in hearts with diastolic dysfunction is evident in studies of stunning after ischemia [16], hypertrophy during aortic stenosis [17], post-transplant dilatation, and tachycardia-induced cardiomyopathy [18].
This pattern of sequential contraction partially mirrors the architectural model of Torrent-Guasp (Fig. 1), whereby the single myofiber band divided by a basal loop (free wall of the right ventricle and posterior basal portion of the LV) and apical loop with a descending segment (endocardial) and ascending segment (that includes epicardial anterior wall fibers, right ventricle outflow track and right ventricular side septal fibers as seen in Fig. 4). Nevertheless, the contractile sequence we found defeats Torrent-Guasp's concept of progression of initiation of contraction along the visible myocardial band [3], since endocardial contraction would be expected to begin after the left posterior basal LV contraction, yet it precedes this contraction.
The sequence of contraction found better matches the known nerve-muscle anatomy. The right bundle of the His-Purkinje system, traversing the base of the anterior papillary muscle of the right ventricular free wall with no previous nervous-muscle connections, and the left bundle with multiple electric connections over a wide portion of the LV endocardium, explains how the right ventricular free wall and the endocardial side of the LV contract synchronically. The impulse from these points has to advance to the posterior wall and into the epicardial muscle. Most likely the impulse transmission spreads along spiral pathways, as suggested by Taccardi [19] to explain the spread of activation beyond the superficial Purkinje network.
We believe the excitation–contraction impulse wave is along the fibers described by Torrent-Guasp, i.e. from the right ventricle to the posterior wall along the basal loop and from the endocardium to the epicardium through the apical loop, contradicting the concept of transmission of the contraction wave from the inner to the outer wall. Recent published data correlates the axial flow spread of the impulse along the fiber bundles, with more rapid transmission along thinner than thicker fibers [12,20]. Consequently, the more slender RV and LV free wall basal loop segments shorten more quickly than the thicker papillary muscle and outer LV wall. Clearly, conduction along cell–cell via low resistance gap junctions, at a maximum velocity of 0.3mm/ms could not occur along the 80mm descending segment, and 130mm ascending segment, since 433ms would be needed in the epicardium to complete activation [21]. The beginning of excitation of most fibers that enter into contraction is only ∼105ms, and only ∼80ms in this study. Consequently conventional concepts of excitation contraction coupling may become questioned by the recorded sequence of sequential contraction in this study, and a new framework must now be considered.
Another gap in conventional thinking is our evidence of early contraction of the entire base of the heart before ejection occurs. This separation between basal contraction before papillary muscle shortening for rapid ejection starts was reported by Armour and Randall in 1970 [22], who confirmed the work of Roy and Adami in 1890 [23]. Our data supports the concept of Armour and Randall that the base of the heart forms a stiff outer shell around the bulk of myocardium (really the endocardial and epicardial or descending and ascending regions of the apical loop) responsible for ejection. Armour documented the later electrical stimulation of the base, as also shown by Sodi-Pallares [24], who confirmed a ‘mismatch’ in excitation contraction coupling.
The confirmation of oblique-oriented myocardial fibers may help explain the observations of Sallin [25], in which 50–60% ejection fraction could only be achieved with 15% shortening fibers if they were in a helical arrangement, compared to circumferential (EF 30%) or simply longitudinally oriented (EF 15%).
The helical cardiac formation is well-known anatomically, with Senec describing the internal helix, shown in Fig. 1 from his text in 1760, Pettigrew describing the apex to contain reciprocal spirals with the epicardium going from without to within, and the endocardium going from within to without. This spatial analysis also provides a functional confirmation to the observations of Richard Lower, in 1669, who described muscle fibers of the inner wall that ran opposite the fibers of the outer wall, and that contraction can be compared ‘… to the wringing of a cloth to squeeze out the water’. Our functional analysis shows that the lengthening is due to the reciprocal twist of the outer wall fibers that continue to contract after the inner wall fibers stop in the normal heart.
In conclusion, we suspect the functional sequence of excitation–contraction within the myocardial muscle that follows the anatomic model ventricular band, and that the phenomena of suction for rapid ventricular filing is caused by active contraction of the epicardial left ventricular wall fibers. These structure/function observations may produce a new term of late isovolumetric contraction, a novel concept that will replace the conventional term of isovolemic relaxation that has been used to generate elastic recoil for suction.
On the left, diagram taken from the 1760 text of Senec, showing his conception of the cardiac internal helical formation. The center image shows the apical view of the heart, from Mall's text in 1911, with the reciprocal spiral arrangement of fibers, moving from the epicardium to within the chamber from the surface, and how internal fibers emerge from the endocardium to wrap around the epicardial surface. On the right, myocardial band model of Torrent-Guasp, with the right (RS) and left segments (LS) of the basal loop in white, and the descending (DS) and ascending segments (AS) of the apical loop in black. The basal loop forms the free wall of the right ventricle and the posterior basal segments of the LV. The descending segment forms most of the thickness of the LV wall and left side of septum on its endocardial side. The ascending segment is formed by a thinner layer of myocardial fibers of the epicardial side of the anterior wall of the LV, the right side of the septum and, by the aberrant fibers that supply the RV outflow track.
Simultaneous recordings of tracings 2cm above the LV apex, showing the typical recordings obtained in the maximal fiber direction of the epicardial (ascending) and endocardial (descending) muscle, compared to the right ventricular wall. Note the (a) earlier origin and termination of contraction in the descending segment, (b) similar starting point for RV contraction, and (c) later origin and end of shortening in the ascending segment. Upper left corner circle shows the crystal angulation, as described in the text.
Simultaneous tracings of the posterior and inferior LV wall (top tracing), and anterior epicardial (middle tracing) and anterior endocardial segments (lower tracing). Note (a) earliest onset of shortening in descending endocardial segment, (b) 10ms delay in onset of shortening in posterior, inferior LV wall and (c) longer delay in onset, together with ongoing shortening in ascending (epicardial) area after descending and posterior shortening stops.
Circumferential sonomicrometer around the left ventricular mid wall, showing a notch in the endocardial tracings. A predominant notch occurs in the third tracing, where there is absent-coordinated shortening. We suspect this is due to maximum displacement by papillary muscle at mitral closure.
Chronologic sequence of contraction of both segments of the apical loop as recorded by sonomicrometer crystals. The basal loop (circumferential darkened area) is already shortening. In (A) the descending segment contracts first, to begin ejection (first solid longitudinal line), while the ascending segment is relaxed. In (B) shortly after descending segment contraction, the ascending segment starts to shorten (hatched line) to reflect both segments ‘co-contraction’ in reciprocal directions to shorten the ventricle for the rest of ejection. In (C) when the descending segment reaches its maximal contraction (second solid line), the ascending segment continues shortening to begin to lengthen the ventricle at the start of the isovolumetric contractile phase, which stops at the dotted line.
Comparison between early shortening of posterior basal loop free wall (top) and ascending (epicardial) LV free wall. Note the widening of crystals (upward trajectory) in LV free wall, while there ongoing shortening and downward trajectory continues in LV epicardial muscle, shown by distance between dotted and hatched lines. This widening event occurs during the phase of deceleration of LV pressure associated with the isovolumic period.
Sequence of contraction of different segments during a study in one subject during (a) basal conditions (top) and with dopamine (middle) or propranolol infusion (bottom). Black and hatched lines mark the start and end of shortening of endocardial and epicardial muscle, respectively. There is a delay between start of the endocardial and the epicardial myocardium of the anterior wall, which decreases with dopamine from 84±10 to 26±7ms and increases with propranolol to 121±20ms. The termination of endocardial shortening is prolonged with propranolol to (a) reduce the separation during baseline, and (b) associated with a fall in the downslope of the LV pressure tracing.
Regional direction and intensity of contraction
Presented at the C. Walton Lillehei Resident Forum Session, 84th American Association for Thoracic Surgery Meeting, Toronto, April 25-28, 2004.
