The Cardiac Suction Pump

Abstract

Introduction: Historically, the ventricular expansion process has not had the thorough analysis it deserves, the real meaning of diastolic filling being ignored in the physiological mechanism. In this regard, only systole has been given the category of being an active phase, with muscle contraction and energy consumption. How should we refer to diastolic filling? As cause or consequence of the expansion? As a result, would it be produced by venous pressure (vis a tergo) or by an active mechanism of myocardial suction?

Materials and Methods: The endo and epicardial electrical activation sequence of the left ventricle has been studied by means of three-dimensional electroanatomic mapping with a Carto navigation and mapping system that allows a three-dimensional anatomical representation, with activation maps and electrical propagation. Isochronic and activation sequence maps were generated, correlating them with the surface ECG. Endo and epicardial ventricular activation maps were also produced, obtaining detailed high-density recordings with apical, lateral and basal views.

Results: According to recordings obtained by three-dimensional mapping, the electrical impulse propagates along the helical myocardium in order to achieve two opposite forces that facilitate ventricular torsion. Transmission is longitudinal, eliciting shortening of the base-apex and radial (transverse) distance, with chamber narrowing and myocardium twisting, thus determining ventricular torsion. During the Protodiastolic Phase of Miocardial Contraction onset, the ascending band is contracting and the descending band is repolarizing. This late contraction of the ascending segment allows, in the Protodiastolic Phase, the mechanical process to achieve ventricular detorsion-lengthening and suction, generating the necessary pressure drop to draw in blood.

Conclusions: The consequence of Protodiastolic Phase of Miocardial Contraction in both ventricles is a drop in intraventricular pressure, which implies generating the mechanical conditions for subsequent diastolic filling. Thus, this phase has myocardial contraction and energy consumption. This physiological situation in both ventricles is feasible, given that by sharing the interventricular septum, the chambers are subject to a process of anatomical and functional interdependence.

Keywords: Protodiastolic Phase of Myocardial Contraction-Helical heart-Diastolic function

Introduction

Historically, the ventricular expansion process has not had the thorough analysis it deserves, the real meaning of diastolic filling being ignored in the physiological mechanism. In this regard, only systole has been given the category of being an active phase, with muscle contraction and energy consumption [1,2]. As expressed so far, how should we refer to diastolic filling? As cause or consequence of the expansion? As a result, would it be produced by venous pressure (vis a tergo) or by an active mechanism of myocardial suction? [3]. Venous pressure has been considered the cause of the opening of the atrioventricular valves. However, the maximum pressure occurring at the exit of the aorta and the pulmonary artery steadily decreases until it reaches minimum values at the entrance to the atria. In a system of conduits through which a viscous fluid circulates, such as the circulatory system, energy losses occur due to the friction of fluid particles against each other and of the fluid against the walls, due to its viscosity. This phenomenon is known as pressure loss, which is not constant along the circuit because it depends on the local diameter of the circuit and the local velocities of the circulating fluid. This pressure is a loss along the circuit, which translates into added resistance to the free circulation of the fluid [4].

Thus, venous pressure would be unviable as a cause of ventricular expansion, since, in addition, since it occurs in only 500ms, it would be incompatible with such an achievement. This minimum diastolic filling time, approximately 400ms if we discount the 100ms of the early diastolic phase (isovolumetric), implies considering the need to assess an aspiration mechanism, a ventricular suction. Here the necessary disquisition arises that each ventricular chamber, by fulfilling two energies, of expulsion and suction, is forced into an asynchrony to maintain a continuous circulatory cycle. Ventricular expansion thus results from the functional intersection between the expulsion and suction of each of the ventricular chambers, knowing that each ventricle operates with this functional duality through muscular contraction with energy expenditure. Thus, the circulatory system consists of a positive pressure responsible for moving blood through the arterial system and also of negative pressures to fill the ventricles, which requires asynchrony. If we did not consider active ventricular suction, the drop in venous pressure to negative values in the cardiac chambers would be illogical (Figure 1).

Figure 1: Diagram of the circulatory system with pressure values throughout its course. Pressures are expressed in mmHg.

Note*: LVs: Left Ventricle in systole; LA: left atrium; LVd: Left Ventricle in diastole; CP: capillary (pulmonary); RV: right ventricle; RA: right atrium; CS: capillary (systemic).

We must also conceptualize that the atria do not have the adequate morphology to develop adequate pressures that determine ventricular filling, also lacking valves that prevent blood backflow. Moreover, they contract at the end of diastole, when the ventricles already have two-thirds of their blood load, during period 3 of ventricular filling. Evidence of this fact is found in patients with atrial fibrillation, which demonstrates the lack of influence of the atria on cardiac filling. From this analysis, it is deduced that neither venous pressure nor atrial systole justify ventricular filling and that it is necessary to consider the need for intercalated energy, an impulse based on ventricular suction, which has been exhaustively investigated during this work.

Material and Methods

The endo and epicardial electrical activation sequence of the Left Ventricle (LV) has been studied by means of three-dimensional electroanatomic mapping (3D-EAM) with a Carto navigation and mapping system (Biosense Webster, California, USA) that allows a three-dimensional anatomical representation, with activation maps and electrical propagation. Isochronic and activation sequence maps were generated, correlating them with the surface ECG. Endo and epicardial ventricular activation maps were also produced, obtaining detailed high-density recordings with apical, lateral and basal views. The study was conducted at Presidente Perón Hospital (Buenos Aires Province, Argentina) including patients who provided their informed consent. The research was previously approved by the Institutional Ethics Committee. All patients were in sinus rhythm, with a normal QRS and did not have evident structural heart disease by Doppler echocardiography and in gamma camera stress and rest studies (Table 1) [3,5].

Table 1: Patient Characteristics.

IG: intervention group; CG: control group

Three-dimensional electroanatomic mapping was performed during the course of radiofrequency ablation for arrhythmias owing to probable abnormal occult epicardial pathways. Mapping was carried out at the onset of studies, followed by ablation maneuvers. No complications developed. The presence of abnormal pathways did not interfere with mapping, as during the whole procedure baseline sinus rhythm was preserved with normal QRS complexes, both in duration and morphology, without antegrade preexcitation. As the muscular structure of the LV is made up of an endocardial layer (descending segment) and an epicardial layer (left and ascending segments), two approaches were used to carry out mapping (Figure 2). The endocardial access was performed through a conventional atrial transseptal puncture. The epicardial access was obtained by means of a percutaneous approach in the pericardial cavity with an ablation catheter (Figure 3). Endo and epicardial mappings were performed consecutively and immediately and were later superimposed, synchronizing them by electrocardiographic timing. Thus, a simultaneous mapping of both surfaces was obtained. In addition, the propagation times of electrical activation through the myocardium were measured in milliseconds (ms) (Figure 2).

Figure 2: Site of the cardiac fulcrum in the continuous myocardium (cord model). PA: pulmonary artery; A: aorta. The right inset shows the threedimensional helical arrangement of the continuous myocardium. The histology shows the different orientation of the longitudinal fibers (ascending segment, AS) in relation to the descending (transverse fibers, DS) (bovine heart). Given the different anisotropic orientations of the fibers, this zone corresponds to the beginning of the opposite helical movement that produces myocardial torsion.

Figure 3: Epicardial Mapping.

Note*: 1: catheter located in the right atrium; 2: Endocavity catheter. 3: Catheter in pericardial space.

Until now, the theory of the continuous myocardium lacked an essential investigation, due to the absence of documentation on the electrophysiological mechanism that would support the mechanical activation sequence of the helical anatomical model. The advent of 3D-EAM managed to overcome this limitation, since it not only allows independent recording of the various ventricular zones, but also those of the endocardium and epicardium, either exclusively or integrated. We mapped the activation of the left ventricle on its endocavitary and epicardial surfaces according to the methodology described. Mapping was performed simultaneously with the surface ECG. This provided a unified temporal frame of reference, allowing on the one hand to correlate both records, and on the other hand to obtain a synchronized view of the simultaneous activation observed in various electroanatomical incidents. Percutaneous access technique. The Carto system was used for 3D-EAM to obtain voltage, activation and propagation maps. Epicardial mapping was done in the pericardial cavity through the left paraxiphoid space (Figure 3). A decapolar catheter in the coronary sinus and a quadripolar catheter in the bundle of His were placed as fluoroscopic reference. Once the epicardial recording of both ventricles was obtained, left ventricular intracavitary mapping was performed. The LV was accessed by transeptal puncture through the right femoral vein using standard technique Figure 3.

Results

Electrophysiological research on cardiac suction. One of the most debated aspects of the suction pump concept is its electrophysiological rationale, namely the alleged lack of correlation between the sequence of the mechanical activity proposed and the electrical activation observed. The recent advent of electrophysiological three-dimensional navigators has allowed the acquisition of highly accurate and detailed information on the activation sequence of the various cardiac structures, which has helped to clarify in our investigation the electrophysiological activation of the helical continuous myocardium. We have previously published the complete study on ventricular mapping (Figures 4 to 8) [6-11]. The central point of this specific research on cardiac suction, which we will discuss in this article, consists of the postulation that we have called the Protodiastolic Phase of Myocardial Contraction (PPMC) (classically isovolumic diastolic phase), which constitutes an active phenomenon generated by a late myocardial contraction that produces the lengthening of the ventricle, separating the base from the apex. This concept presents two apparent “inconsistencies” from classical mechanical pathophysiology.

1) Muscle contraction is always associated with ventricular chamber reduction. 2) Ventricular contraction and relaxation are classically considered to have an “en bloc” simultaneous performance throughout their course and not in successive phases (Figures 4-8).

Figure 4: Integrated endo-epicardial mapping.

The left panel shows: the mitral valve annulus (limited by pink dots), the left ventricular endocardium, the left ventricular septal endocardium and the left ventricular epicardium. The red zone in the blue vertical bar to the right of the panel indicates total cycle duration and the red zone within it, the activation moment corresponding to the activation graph on the left. The right panel shows the surface ECG. The red dot at peak QRS indicates the point of gated trigger. The green channels correspond to reference electrograms. The dotted vertical line shows QRS onset and the full line the present recording moment. The upper panel represents Torrent Guasp’s cord model.

Figure 5: A. Onset of Left Ventricular Activation: The left panel shows the depolarization of the interventricular septum, corresponding to the descending band. In the right panel, the ventricular epicardium (ascending band), has not been activated yet. B. Simultaneous Band Activation: Activation progresses in the left ventricular septum through the descending band (longitudinal activation) and simultaneously propagates to the epicardium (transverse activation) activating the ascending band.

Figure 6: A. Bidirectional apex and ascending band activation: The final activation of the septum is observed, progressing towards the apex, synchronously with the epicardial activation in the same direction. At the same time the epicardial activation is directed towards the base of the left ventricle. B. Activation Progression: Activation progresses in the same directions of the previous figure.

Figure 7: A. Late activation of the ascending band: At this moment, which corresponds to approximately 60% of QRS duration, the endocavitary activation (descending band) is already complete. The distal portion of the ascending (epicardial) band depolarizes later. This phenomenon correlates with the persistence of the band contraction in the initial phase of diastole. B. Final Activation: In the right panel, the projection was changed from left anterior oblique to left posterolateral, showing very late activation of the distal portion of the ascending band.

Figure 8: Chord Model Activation sequence (A-F) in the continuous myocardium according to our investigation. The propagation times are observed. The 25.8 milliseconds in B represent the delay of the stimulation to pass from the descending band in A to the ascending band in B (detailed in the black circle). In red: depolarization; in blue: zones already activated.

In order to investigate and clarify these controversial points, we have studied the sequence of left ventricular activation using high-resolution three-dimensional mapping. A very important finding of this investigation was that endocardial activation is fully completed when the surface QRS has barely reached 60% of its duration. The rest, therefore, corresponds to epicardial activation. This late stimulation (lasting around 80-100ms) at the epicardial level, corresponds to the apical loop ascending segment and results in its stiffening during the PPMC through an active process with energy consumption. According to recordings obtained by three-dimensional mapping, the electrical impulse propagates along the helical myocardium in order to achieve two opposite forces that facilitate ventricular torsion (helical movement). Transmission is longitudinal, eliciting shortening of the base-apex and radial (transverse) distance, with chamber narrowing and myocardium twisting, thus determining ventricular torsion (Figure 5). During the PPMC onset, the ascending band is contracting and the descending band is repolarizing. This late contraction of the ascending segment allows, in the PPMC, the mechanical process to achieve ventricular detorsion- lengthening and suction, generating the necessary pressure drop to draw in blood (Figure 9).

Figure 9: The endocardial activation ends in the area corresponding to the mitral annulus. Note that all the endocardial activation “occupies” approximately 60% of QRS duration (D line in the right panel). Epicardial activation has started earlier, but its completion occurs during the final portion of the QRS.

The basal loop (contraction of the right and left segments) determines ventricular narrowing, while contraction of the descending segment together with the ascending segment causes the shortening-torsion movement of systole. All these physiological processes are required for the ejection phase. In the continuity of cardiac activity, the contraction of the apical loop ascending segment, by providing ventricular lengthening, establishes the PPMC process, which generates intraventricular negative pressure (suction phase) through a “suction cup”-like or suck-up mechanism (Figure 9). Ventricular expansion, last cardiac movement, is produced during the diastolic relaxation phase (diastolic filling). During PPMC, there is a contraction of the ascending segment of the apical loop. As the walls that exert ventricular suction dilate due to muscle deterioration, the “aspiration mechanism” that allows suction becomes precarious, and through this concept, a different assessment of heart failure and its clinical severity can be established. The recoil of the left ventricle also causes the right ventricle to rise, promoting rapid and accelerated filling. The movement of the entire heart contributes to filling. As a result of this mechanism, the increased contractility of the left side increases the performance of the right side. Furthermore, when the mitral valve opens and wall stress increases with a decrease in wall thickness, the fibers lengthen, allowing the ventricle to fill rapidly [12]. The high filling rate at low pressures is explained by the suction phenomenon. This active mechanism of the myocardium on the diastolic effect opens up a broad panorama for surgical techniques for ventricular restoration, both in terms of the shape and volume and consequent function of the left ventricle. Within these concepts, cardiac function consists of three movements. Between systole (300ms) and diastole (400ms) there is a third contraction movement (100ms) which represents a link between the other two, generating the intermediate cardiac suction phase.

In this new model, the interrelationship between the cardiac phases becomes critical for the proper functioning of the heart:

1) Due to the movement it acquires in systole, the base of the heart is pushed downwards and the blood in the opposite direction (Newton’s principle of action and reaction). In diastole, on the other hand, the cardiac base projects upwards. This latter action increases blood velocity and helps to produce filling [13]. 2) Systole compresses both the elastic elements of the heart and its muscle fibers, to such an extent that even the natural tendency of the ventricles is towards expansion without external filling. In this way, together with the contraction of the ascending segment in the PPMC, negative intraventricular pressure or suction is facilitated. 3) Let us recall that in the traditional model filling is only determined by the venous pressure of the right heart. Actually, the difference between the periphery and the right atrium is too low to explain heart filling. Based on this “key doubt” of Torrent Guasp concerning the classical explanation, the concept of active suction pump was developed supported by the physio- muscular structure described in this investigation [14]. The last contracted areas of the myocardial apical loop ascending segment produce the negative pressure conditions to achieve blood suction from the atria to the ventricular chambers.

It is important to recall that the helical arrangement of the myocardium matches the anisotropy of directions adopted by the cardiac muscle fibers in their sequential depolarization, that we have verified with a very slight activation delay between the ascending and descending segments (Figure 8) [15]. The geometrical properties of the cardiac fibers have great importance in the ability to generate, through electrical propagation, the necessary forces for their function (Figure 2) [16]. The fibers of the descending segment on the anterior aspect of the LV, which run in depth through the mesocardium, crossing obliquely with the ascending segment at an angle of 75% are responsible for the opposite activation of the descending (endocardial) and ascending (epicardial) segments. The spatial orientation of myocardial fibers explains the torsion movement and functional efficiency of the heart throughout the cardiac cycle. The right and left segments make up the basal loop, which, attached at its origin to the anterior face of the cardiac fulcrum (myocardial support), is fundamentally made up of circular fibers in a descending direction [17,18]. At the anterior border of the LV these fibers become the descending segment with a subendocardial position. Upon reaching the apex, they abruptly change their orientation to form the ascending segment (right side of the septum and subepicardium of the LV) to insert into the cardiac fulcrum, mainly on its inferior face.

Discussion

Here a necessary reflective point opens: can the Right Ventricle (RV) have a suction phase despite having half the thickness of the LV? Let us recall that the relationship of pressure and resistance between the LV and RV is 6:1, that is, the RV is proportional to 15% of the LV. In the face of a lower resistance, the pulmonary valve in relation to the force to which it is subjected, opens before the aortic valve, which is fundamental in the complementarity of the ventricles in a dynamic interaction between ejection and suction [19,20]. Mean pressure in the venae cavae is between 0 and 2mmHg. Pulsations in the veins suggest right ventricular contractile phenomena, which correlates with the active period in the Right Ventricular Protodiastolic Phase of Myocardial Contraction (RVPPMC). This activity in the venae cavae resembles the pressure waves in the right atrium. As aortic valve closure is prior to that of the pulmonary valve, and tricuspid valve opening before that of the mitral valve, RVPPMC duration is obviously shorter than that of the Left Ventricular Protodiastolic Phase of Myocardial Contraction (LVPPMC). This phase lasts 30.8ms in the RV, while in the LV it lasts an average of 83ms, according to echocardiographic investigations we performed in control patients. The values of RVPPMC duration vary in the literature. A confirmation of this point is the increased blood velocity in the final segment of the venae cavae, because as the pressure drop in the circulatory system is constant reaching very low values in the venae cavae, this acceleration has to be related with RV suction in the RVPPMC. Thus, at the beginning of diastole, even negative values can be detected [21,22]. As explained, this phase is active and with energy consumption. Its action is analogous to the same phase in the LV. Aortic valve closure prior to that of the pulmonary valve represents a plunger effect of the LV more adequate in time to the moment in which the RVPPMC is produced. The suction phenomenon appears as a necessary element, as its lack in both ventricles would stop flow at the slightest difficulty (Figures 10-13). Thus, this investigation indicates that the ventricles cannot be studied independently, but rather, both the systemic and pulmonary circuits should be analyzed with the intervention of both chambers, exploring both impulse and suction and, what is even more important, their synchronization, whose causes could be due to both the interrelated sequence in muscle activation and pressure variations in the circuits.

Figure 10: Propagation sequence map with 3D electro anatomical mapping in patients As the pulmonary valve closes, the blood volume within the right ventricle remains constant. However, during this period, the interventricular septum at the level of the intraseptal band continues to contract. This causes a drop in right intraventricular pressure with the consequent subsequent suction of the systemic circuit.

Note*: S: septum.

Figure 11: Left intraventricular pressure curve during the LVPPMC. See the pressure drop until reaching negative values (red circle).

Figure 12: Right ventricle recording The drop in intraventricular pressure during the RVPPMC is observed in one patient (yellow circle).

Figure 13: Left intraventricular pressure with resynchronization therapy. A. Resynchronization device turned off. B. In the same patient, a drop in left ventricular diastolic pressure is observed after resynchronization is restarted. 1) The yellow circle points out the increase of systolic arterial pressure in B with respect to A. 2) The red circle shows the negative intraventricular pressure in B.

The blood circuit driven by the LV is longer, and several beats are necessary for a blood particle that flows from the LV to be suctioned by the RV, completing the cycle. The volume ejected by the RV must be the same as that ejected by the LV, but the number of beats needed to send blood from the RV to the left atrium is less than the number necessary to send blood from the LV to the right atrium. The volume of the LV-right atrium circuit is greater than the volume of the RV-left atrium circuit. The previous ventricular suction phase is coherent with the diastolic filling time of about 400ms. This suction in the PPMC, due to the low gradients attained at the atrial entry, must be considered the fundamental element for venous return in complementarity with the systolic impulse [23]. This is supported by the subatmospheric pressures (“depressions”) recorded in these chambers during the PPMC. The driving role of the atria (“atrial kick”) is minimal. Its power is 1% relative to that of the ventricle. Obviously, this low gradient is related with a need for active ventricular suction [2]. The spatial arrangement of the continuous helical myocardium clearly indicates that the propulsion is given by the ventricular cavity walls that define this structure. Formed by two loops, basal (right and left segments) and apical (descending and ascending segments) (Figure 2), the muscular unit they constitute are the walls of the ventricles, to which it provides propulsion power. It is not the ventricles, mere cavities, that display this action but their muscular walls that make up the helical continuity of the myocardium as a single mass and that give it its leading role. The atria are outside this morphology and therefore lack adequate walls to propel their contents; they have a reservoir function and act as decompression chambers for the sharp blows produced by the sudden closure of the atrioventricular valves.

If we step back to the primitive stage in the evolution of the circulatory system, we can clearly appreciate the phylogenetic hallmarks of the different species. In this process, the atria belong to the venous segment and the ventricles to the arterial segment; therefore, their origin and the fact that they lack a muscular wall that allows blood propulsion is determined [24,25]. Between the atria and the ventricles there is only connective tissue, allowing the easy separation of these chambers during dissection. This assertion coincides with Claudius Galen’s theory in the II century A.D. stating that the atria can be detached from the ventricles without any incision, simply separating them from their respective ventricles. This situation supports the integral evolutionary, anatomical and independent arrangement of the ventricles in relation to the atria. In the classical concept, there was only one active function in each ventricle, systole, with a positive pressure that determined it was the cause of venous return. This is not justified with what has been observed; on the contrary, venous pressure is fundamentally a consequence and not a cause of ventricular expansion, according to the values of the pressure gradient displayed by the venous circuit. This fact is supported by observing the moment in the PPMC in which the filling pressure, both in the systemic and pulmonary circuits, tends to have a suction action. The mechanical action of the heart is complex because it is the result of integrating its ejection, suction and filling properties in its ventricles, under different successive and concatenated phases through the continuous helical myocardium, which to fulfil its mechanical function presents a support, called the cardiac fulcrum.

The pressure of the circulatory circuit decreases from the aorta to the venous end. This drop in pressure determines a very low venous pressure, with a mean value between 0 and 2mmHg in the venae cavae, so it is expressed in cm of water. The low venous pressure at the entry of both ventricles cannot create the force that propels the blood to enter the ventricles, but through the active suction of these chambers. The ventricles, made up of resistant muscles, do not expand with low venous pressure and much less due to atrial contraction, with their very thin walls, which also lack an adequate structure to prevent blood backflow. Venous pressure is not the cause of ventricular expansion but its consequence. As deduced from our investigations, we must admit that blood entering the ventricles is the result of suction due to the contraction of both ventricular walls during the PPMC. In the LV, the components of the three-dimensional reduction of the heart (three-dimensional reduction of 15% in the left ventricular longitudinal and radial axes -anteroposterior and transverse-) together with the torsion-detorsion movement, interact synergistically achieving torsion-ejection and later detorsion-ventricular suction. The atrioventricular annulus contracts, the aortic annulus is slightly expanded, the mitral and aortic planes descend, and the outflow tract is kept open. The LVPPMC occurs after aortic valve closure. During this phase, the presence of a drop in intraventricular pressure has been documented until reaching negative values evidencing suction, both in human clinical and in experimental animal studies. A fluid moves along a tube in response to a pressure gradient.

Therefore, the pressure gradient must be greater than 10mmHg to generate flow, due to energy losses in the system. When the vascular duct lacks this gradient, flow ceases. This is called “critical closing pressure”. Blood pressure fluctuates around a mean value of 90 mmHg. Pulmonary pressures have an average of 22/8mmHg with a mean pressure of 13mmHg. On the other hand, the pressure difference between the pulmonary capillaries and the LA is 4-6mmHg. Thus, a low-pressure gradient allows the same amount of blood to pass through the pulmonary circuit as through the general circuit, which has a gradient of 90mmHg, due to the complementarity between ejection and suction energies [4]. In addition, the power of the left atrium is only 1% that of the LV, so noticeable effects as pump function cannot be expected from it. The left atrium distends in the face of a LV suction deficit, but no notable effects of flow impulse can be expected. Obviously, this low gradient could not generate a sudden ventricular filling without the need for active ventricular suction. Ventricular-septal interdependence. What we have seen in the electrophysiological study with a Carto navigation and mapping system is that endocavitary activation ends before the end of the QRS complex (Figure 7A); therefore, its continuity corresponds to the late activation of the distal portion of the ascending segment after semilunar valve closure, justifying the persistence of contraction during the isovolumic diastolic phase, the basis of the ventricular suction mechanism of both ventricles which we call PPMC. According to our echocardiographic investigation in patients without heart disease this stimulation lasts 83ms in the LV and about 30ms in the RV. Its epicenter occurs in the ascending segment of the apical loop with the result of producing lengthening of the septum during the PPMC, implying consequences in both ventricles. The echocardiographic work of Mora Llabata, et al., finds a difference of 88±7.1ms in the development of systolic distortion between the systolic and postsystolic phases, which coincides with the duration of the ascending segment activation in the LVPPMC found in our studies [26].

Post-systolic longitudinal strain, indicating the contraction involved in left ventricular detorsion, is basically produced in the septal segments and in the anterior basal region which correspond to the anatomical location of the ascending segment. The interventricular septum has a predominant value in myocardial function as its anatomical location is essential in biventricular interdependence. It consists of a ventral and a dorsal part. The first portion is made up of the descending segment, the intraseptal band (final segment of the muscle band), and the anterior septal band. The first two belong to the LV and the other to the RV. The posterior region of the septum is made up of the descending segment (dependence of the LV) and the posterior septal band, corresponding to the RV. In this way, septal contraction determines the PPMC in both ventricles, as this septum is a structural interdependence between both (Figures 14,15) [27].

Figure 14: The silicona model of the heart shows the contiguity between the descending and ascending segments in the folded heart (black circle) in the septum.

Note*: AS: ascending segment; DS: descending segment; RV: right ventricle; LV: left ventricle.

Figure 15: Microscopic view (right) of the interventricular septum medial segment in the human heart, clearly showing absence of transition circumferential fibers between the descending and ascending segments of the continuous myocardium. Also note that there is no fascia or anatomical structure located between the two fiber bundles. Moreover, in the macroscopic section (left), it can be seen how the sudden transition of the fiber angle change draws a line that can be perceived with the naked eye and that, in echocardiographic images, gives rise to the known medioseptal linear image generated by the acoustic interphase originating from by the abrupt change in angulation in this region of the septum.

This is possible due to myocardial fiber orientation, with longitudinal predominance in the final part of the ascending segment, which become progressively more oblique as they descend, preserving the spiral fibrillar conformation in the general structure. The fibers, being able to expand longitudinally, achieve an elongation effect and generate a drop in intraventricular pressure when the atrioventricular valves are closed, while the rest of the fibers are relaxed. This anatomical interdependence between both ventricles controlled by the septum, not only implies the LVPPMC but also that ofthe RV, which is a scarcely known situation. This contraction of the interventricular septum that persists after semilunar valve closure also causes a drop of intraventricular pressure in the RV (“depression”), with the remaining walls relaxed. The intraseptal band (final portion of the ascending segment), located between the anterior septal band and the descending segment, takes part in this mechanism. This is confirmed through echocardiography by demonstrating that postsystolic strain occurs later in the segments of the interventricular septum, which implies finding during the RVPPMC a subatmospheric pressure at the beginning of diastole estimated in about -2mmHg. In this regard, the transseptal gradient correlates with the degree of curvature that the septum can reach. The right heart interacts with the opposite left heart through the interventricular septum. This is not only an anatomical wall, but also has a functional aspect. The Bernheim effect describes septum bulging to the right side when there is overdistension of the left counterpart. Changes in the volume of one ventricular chamber lead to impairment of the other through the mechanism of diastolic ventricular interdependence. What is remarkable is that this diastolic ventricular interdependence is much greater in the case the pericardium remains open. Thus, with the incised pericardium, we have observed in cardiac surgeries that high right ventricular volumes are needed to generate an increase in left ventricular filling. On the other hand, if it remains closed, this increase in right volume-pressure correlates perfectly with the modifications on the left. The compromised septum distorts the apex-base approach movement that normally contributes to stroke volume.

Conclusion

The consequence of PPMC in both ventricles is a drop in intraventricular pressure, which implies generating the mechanical conditions for subsequent diastolic filling. Thus, this phase has myocardial contraction and energy consumption. This physiological situation in both ventricles is feasible, given that by sharing the interventricular septum, the chambers are subject to a process of anatomical and functional interdependence.

Acknowledgements

None.

Conflicts of Interest

None.

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