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Circulation. 1995;92:156-157

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(Circulation. 1995;92:156-157.)
© 1995 American Heart Association, Inc.


Articles

Two Hearts That Beat as One

Magdi H. Yacoub, FRCS

From the National Heart and Lung Institute, Harefield and Royal Brompton Hospitals, Harefield, Uxbridge, Middlesex, England.

Correspondence to Sir Magdi Yacoub, FRCS, British Heart Foundation Professor of Cardiothoracic Surgery, National Heart and Lung Institute, Harefield and Royal Brompton Hospitals, Harefield, Uxbridge, Middlesex, UK UB9 6JH.


Key Words: ventricles • Editorials • imaging • Fontan procedure • transposition of the great arteries


*    Introduction
up arrowTop
*Introduction
down arrowReferences
 
"Two souls with but a single thought, two hearts that beat as one" Maria Lovall (1803-1877), Ingomar the Barbarian

Although the right and left ventricles develop from the same primitive heart tube during morphogenesis, they evolve into two relatively independent structures with so many different characteristics that with some justification they may be regarded as two different organs. Despite that, they are closely linked physically, mechanically, and electrically and appear to "beat as one." This intimate ventricular–ventricular relation is believed to have important functional implications during physiological and pathological states.1 2 3 4 5 6 The article by Fogel and colleagues in this issue of Circulation is a welcome addition to the literature, as it addresses certain aspects of ventricular–ventricular interaction and raises many issues relating to the similarities and differences between the two ventricles, including an instantaneous pattern of wall motion as defined by new imaging techniques, their relation to congenital abnormalities, and different forms of semicorrective operations with resultant adaptation, remodeling, and/or damage.

The shape of each ventricle is genetically determined to suit its exact function.7 Thus, the left ventricle is "flask" shaped with the inlet and outlet sharing one orifice. This enables the ventricle to deliver a bolus of blood against high resistance.

In contrast, the right ventricle consists of a flattened tube wrapped around the left ventricle with separate inlet and outlet orifices and a presumed contraction pattern simulating peristalsis. Such an arrangement is suited for pumping blood against low resistance. The fiber orientation and internal organization of each ventricle result in a tightly controlled specific motion of the different components of the ventricular wall that is designed to optimize the work and minimize the wall stress and myocardial oxygen consumption.8 9 The functional potential of fiber orientation was recognized by William Harvey10 in 1628, who referred to earlier studies by Vesalius. Interest in the characterization of fiber orientation in postmortem specimens continues to this day.11 12 Recently, in vivo studies of instantaneous regional wall motion in humans became possible with the development of sophisticated imaging techniques. This involved high-speed biplane cineangiography after the insertion of intramyocardial radiopaque markers13 during cardiac transplantation and, more recently, through the use of magnetic resonance imaging and radio frequency tagging of specific points in the myocardium.14 15 The importance of a torsion movement of the left ventricle during systole was alluded to by Stenson in 1664,16 who noted the helical orientation of left ventricular fibers. Shortly afterward, Giovanni Alphonso Borelli, a student of Galileo, proposed that left ventricular ejection involved torsional deformation in a manner analagous to wringing out a wet towel.17 Recent imaging studies have confirmed the presence of left ventricular torsion and have served to characterize its location, direction, timing, and rate in different parts of the left ventricular wall; the significance of these findings is still not fully understood. Almost all available data regarding in vivo studies of wall motion in the normal heart relate to the left ventricle and virtually none relate to the normal right ventricle.

This functional integration of the two ventricles requires close interaction or "cross talk" throughout the cardiac cycle, during both systole and diastole. Like many of us who get along with a little help from our friends, the left ventricle contributes to the systolic function of the right. This was shown in several elegant studies2 that demonstrated that during normal sinus rhythm, left ventricular contraction slightly preceded right ventricular contraction (mean, 20 milliseconds), and left and right ventricular dp/dt recordings show single positive peaks that are coincident; however, during endocardial pacing of the right ventricular free wall, two systolic right ventricular dp/dt peaks were recorded with the second peak coinciding with the single systolic left ventricular dp/dt peak. Experimental studies have shown that alteration in the volume of one ventricle alters the compliance of the contralateral ventricle and that this effect is accentuated by the pericardium.1 Ventricular interdependence is important in understanding the cardiovascular response to sudden changes in ventricular volume and can explain left ventricular dysfunction in diseases that alter the systolic or diastolic load of the right ventricle, such as atrial septal defect, mitral stenosis, Ebstein anomaly, and pulmonary hypertension.1 4 Fogel and colleagues have extended our knowledge of ventricular interdependence to the field of complex congenital heart disease, particularly after radical semicorrective operations. In their study, they compared the pattern of ventricular contraction in the "single" right ventricle serving the systemic circulation after the Fontan operation for hypoplastic left heart syndrome (HLHS) with that after inflow repair of complete transposition of the great arteries. The authors found important differences in the pattern of contraction of these two types of "systemic" right ventricle when compared with each other or with a normal left ventricle. They speculated that the differences in the contraction pattern of the two types of right ventricle could be due to the absence of a left ventricle in the Fontan group. Although this may be true, at least in part, caution is needed in interpreting the results, as the right ventricle in HLHS is not a pure model of the single right ventricle due to the detrimental effects of the fibrosed, possibly infarcted left ventricle and the possible presence of coronary arterial lesion in HLHS.18 Similar difficulties could arise from comparing the pattern of contraction of the right ventricle serving the systemic circulation with that of a normal left ventricle due to the marked differences in shape and fiber orientation. As the examinations were by necessity recorded on isolated occasions during the postoperative period, they do not provide meaningful information about whether some of the changes observed, particularly the presence and direction of the torsion movement, represent intrinsic anatomic or functional features of the ventricle, an adapative process, or the result of perioperative damage to the myocardium. These issues need to be explored further. The use of imaging techniques to understand the inner functioning of each ventricle as well as ventricular interaction, particularly after surgical procedures, could help our understanding of the integrated cardiac action in health and disease and could have important implications in the optimization of the management of patients with congenital heart disease.


*    References
up arrowTop
up arrowIntroduction
*References
 
1. Bove AA, Stanmore WP. Ventricular interdependence. Cardiovasc Dis. 1981;23:365.

2. Feneley MP, Gavaghan TP, Baron DW, Branson JA, Roy PR, Morgan JJ. Contribution of left ventricular contraction to the generation of right ventricular systolic pressure in the human heart. Circulation. 1985;71:473-480.[Abstract/Free Full Text]

3. Moulopoulos SD, Sarcas A, Stamatelopoulos S, et al. Left ventricular performance during by-pass or distension of the right ventricle. Circ Res. 1965;17:484-491.[Abstract/Free Full Text]

4. Srojnic BB, Brecker SJD, Gibson DJ. Left ventricular filling characteristics in pulmonary hypertension: a new mode of ventricular interaction. Br Heart J. 1992;68:16-20.[Abstract/Free Full Text]

5. Ibrahim MM. Left ventricular function in rheumatic mitral stenosis: clinical echocardiographic study. Br Heart J.. 1979;42:514-520.[Abstract/Free Full Text]

6. Olivari MT, Fiorentini C, Polesi A, et al. Pulmonary hemodynamics and right ventricular function in hypertension. Circulation. 1978;57:1185-1190.[Abstract/Free Full Text]

7. Yacoub MH. The case for anatomic correction of transposition of the great arteries. J Thorac Cardiovasc Surg. 1979;78:3.[Medline] [Order article via Infotrieve]

8. Burns JW, Covell JW, Myers R, Ross J Jr. Comparison of directly measured left ventricular stress and stress calculated from geometric stress figures. Circ Res. 1971;18:611-621.

9. Waldman LK, Fung YC, Covell JW. Transmural myocardial deformation in the canine left ventricle: normal in vivo three dimensional finite strains. Circ Res. 1985;57:152-163.[Abstract/Free Full Text]

10. Harvey W. An anatomical disposition on the motion of the heart and blood in animals, 1628. In: Willis FA, Keys TE, eds. Cardiac Classics. London, England: Henry Kimpton; 1941:19-79.

11. Greenbaum RA, Ho SS, Gibson DG, Becker AE, Anderson RH. Left ventricular fibre architecture in man. Br Heart J. 1981;15:248-263.

12. Torrent-Guasp F. The Cardiac Muscle. Madrid, Spain: Foundation Juan; 1973.

13. Ingels NB Jr, Daughters GT, Stinsen EB, Alderman EL. Measurement of midwall myocardial dynamics in intact man by radiography of surgically implanted markers. Circulation. 1975:859.

14. Axel DL. Imaging of motion with special modulation of magnetisation. Radiology. 1989;1971:841.

15. Buchalter MB, Weiss JL, Rogers WJ, Zehroni EA, Weisfeldt ML, Beyar R, Shapiro EP. Quantification of left ventricular rotational deformation in normal humans using magnetic resonance imaging myocardial tagging. Circulation. 1990;81:1236-1244.[Abstract/Free Full Text]

16. Stenson N. De Musculis et Glandulis Observationum Specimen, cum Epistolis dua bos Anatomicis. Amsterdam, Netherlands: P le Grand; 1664:90.

17. Borelli GA. De Motue Animalium. 1680:T.xviii.

18. Sauer U, Gittenberger-de-Groot AC, Geishanson M. Coronary arteries in hypoplastic left heart syndrome: histopathological and histochemical study, implications for surgery. Circulation. 1988;78:86. Abstract.




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