Journal of ISSN: 2373-4396JCCR

Cardiology & Current Research
Volume 6 Issue 5 - 2016
Left Atrial Volume Index as a Clinical Marker for Atrial Fibrillation and Predictor of Cardiovascular Outcomes
Osmar Antonio Centurión*1, Nelson Javier Aquino-Martinez2 and Judith María de los Angeles Torales-Salinas2
1Department of Health Sciences’s Investigation, Sanatorio Metropolitano, Fernando de la Mora, Paraguay
2Cardiology Department, Clinic Hospital, Asunción National University, San Lorenzo, Paraguay
Received: September 29, 2016 | Published: October 07, 2016
*Corresponding author: Osmar Antonio Centurión, Professor of Medicine, Asuncion National University, Department of Health Sciences’s Investigation, Sanatorio Metropolitano, Teniente Ettiene 215 c/ Ruta Mariscal Estigarribia, Fernando de la Mora, Paraguay, Email:
Citation: Centurión OA, Aquino-Martinez NJ, Torales-Salinas JMLA (2016) Left Atrial Volume Index as a Clinical Marker for Atrial Fibrillation and Predictor of Cardiovascular Outcomes. J Cardiol Curr Res 6(5): 00223. DOI: 10.15406/jccr.2016.06.00223


The prevalence of AF increases with aging and with the severity of the heart disease reaching up to 40% in advanced cases. In patients with heart failure, AF is an independent predictor of morbidity and mortality increasing the risk of death and hospitalization. It is well known that the presence of atrial enlargement in patients with organic heart disease increases the chances to develop AF [1-5]. Left atrial (LA) enlargement measured by echocardiography is considered to be a useful tool in the evaluation of cardiovascular outcomes. Guidelines from the American Society of Echocardiography provide clarification as to which of the multiple methods to estimate LA size should be used in clinical practice. It has been demonstrated that LA volume and LA volume index provide a more accurate measure of LA size than conventional M-mode LA dimension [6,7]. The LA mechanical functionality can be described to be as a reservoir, a conduit, and a contractile function [8]. During ventricular systole and isovolumic relaxation, the LA functions as a reservoir that receives blood from pulmonary veins. Then, during the early phase of ventricular diastole, the LA operates as a conduit for transfer of blood into the left ventricle (LV) after mitral valve opening via a pressure gradient. In addition, the atrial kick or the contractile function of the LA serves to increase the LV stroke volume by approximately 20-30% [9]. When the diastolic function is normal, the relative contribution of the reservoir function of the LA to the LV filling is 40%, the conduit 35%, and the contractile function 25% [10]. The relative contribution of LA phasic function to LV filling is dependent upon the LV diastolic properties in a way that this LA booster pump function becomes more dominant in the setting of LV dysfunction [11,12]. When the LV relaxation is altered, the relative contribution of LA reservoir and contractile function increases and the conduit function decreases. However, as LV filling pressure progressively increases with advancing diastolic dysfunction, the LA serves predominantly as a conduit [10].

Several alterations are associated with LA remodeling and dilatation. The increase in prevalence of AF in older persons has been reported to be associated with degeneration of the atrial muscle in pathological studies. It was demonstrated that there is clear evidence in the human atrial muscle of age-related electrical uncoupling of the side-to-side connections between bundles, related to the proliferation of extensive collagenous tissue septa in intracellular spaces [13,14]. These age-induced changes include a reduction in the number of myocardial cells within the sinus node, a generalized loss of atrial myocardial fibers, as well as an increase in fibrosis which leads to an apparent loss of myocardial fiber continuity [15-17]. The LA remodeling and dilatation process will also occur in response to pressure and volume overload. LA enlargement due to pressure overload is usually secondary to increased LA afterload. High blood pressure increases LV end-diastolic pressure and induce LV diastolic dysfunction, which subsequently increases the LA pressure and causes stress on LA walls. The LA pressure overload induces pathophysiological changes, which causes structural and functional remodeling. These changes alter the electrophysiological properties of the atrial myocardium increasing atrial vulnerability and the predisposition to develop episodes of AF [18-22]. LA dilation is attributed to impairment of the diastolic blood flow from the LA to the LV due to the increased LV stiffness. It has been suggested that LA dilatation can also occur in response to pressure overload resulting from fibrosis and calcification of the LA, a condition known as stiff LA syndrome [23,24]. This entity causes a reduction of LA compliance, a marked increase in LA and pulmonary pressures, and right heart failure. Chronic volume overload associated with conditions with high output states can also contribute to generalized chamber enlargement [25,26]. Two-dimensional and tissue Doppler imaging at different phases of the cardiac cycle have been utilized in LA volume measurement and various LA functions. Interesting prospective results and outcomes from large population-based studies have established a relationship between M-mode antero-posterior LA diameter and the risk of developing AF [27,28]. For example, in the Framingham study, a 5-mm incremental increase in antero-posterior LA diameter was associated with a 39% increased risk for subsequent development of AF [27]. In the Cardiovascular Health Study, subjects in sinus rhythm with an antero-posterior LA diameter greater than 5 cm had approximately fourfold the risk of developing AF in the follow-up period [28]. LA volume index has been shown to predict AF in patients with cardiomyopathy, and also in first-diagnosed nonvalvular AF [29-32]. These studies have shown that LA volume index represents a superior measure over LA diameter for predicting cardiovascular outcomes and provided prognostic information that was incremental to clinical risk factors. Tenekecioglu E et al. [33] demonstrated in their investigation that the left atrium in the hypertensive group with AF was characterized by further enlargement when compared to the hypertensive group without AF [33]. While LA booster pump function was increased in hypertensive patients when compared to normotensive subjects, it was impaired in hypertensive subjects with AF as compared with hypertensive patients without AF [33]. These are interesting data since arterial hypertension causes an increase in LV wall stress that generates myocardial hypertrophy. Increased LV wall thickness elevates LV diastolic filling pressure inducing a fibro-degenerative process within the myocardium of the left chambers. This fibrosis constitutes a favorable substrate for reentrant arrhythmias. The occurrence of AF in hypertensive individuals may be associated with impairment of atrial contractility.

Patients with an enlarged LA and altered atrial myocardium tend to have increased load and wall stress with atrial myocardial impairment causing contractile dysfunction and a milieu for electrical conduction abnormalities within the atrial myocardium. LA volume index and function is a useful tool for monitoring cardiovascular risk and outcomes and for guiding medical therapy. Continuously evolving technology will enhance its utility and may prove to have an interesting impact in global health care.


  1. Pozzoli M, Cioffi G, Traversi E, Pinna GD, Cobelli F, et al. (1989) Predictors of primary atrial fibrillation and concomitant clinical and hemodynamic changes in patients with chronic heart failure: A prospective study in 344 patients with baseline sinus rhythm. J Am Coll Cardiol 32(1): 197-204.
  2. Dries DL, Exner DV, Gersh BJ, Domanski MJ, Waclawiw MA, et al. (1998) Atrial fibrillation is associated with an increased risk for mortality and heart failure progression in patients with asymptomatic and symptomatic left ventricular systolic dysfunction: A retrospective analysis of the SOLVD trials. J Am Coll Cardiol 32(3): 695-703.
  3. Carson PE, Johnson GR, Dunkman WB, Fletcher RD, Farrell L, et al. (1993) The influence of atrial fibrillation on prognosis in mild to moderate heart failure: The V-He FT studies. Circulation 87(6 suppl): V1102-V1110.
  4. Middlekauff HR, Stevenson WG, Stevenson LW (1991) Prognostic significance of atrial fibrillation in advance heart failure: A study of 390 patients. Circulation 84(1): 40-48.
  5. Mathew J, Hunsberger S, Fleg J, Mc Sherry, Williford, et al. (2000) Incidence, predictive factors, and prognostic significance of supraventricular tachyarrhythmias in congestive heart failure. CHEST 118(4): 914-922.
  6. Lester SJ, Ryan EW, Schiller NB, Foster E (1999) Best method in clinical practice and in research studies to determine left atrial size. Am J Cardiol 84(7): 829-832.
  7. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, et al. (2005) Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 18(12): 1440-1463.
  8. Pagel PS, Kehl F, Gare M, Hettrick DA, Kersten JR, et al. (2003) Mechanical function of the left atrium: new insights based on analysis of pressure-volume relations and Doppler echocardiography. Anesthesiology 98(4): 975-994.
  9. Mitchell JH, Shapiro W (1969) Atrial function and the hemodynamic consequences of atrial fibrillation in man. Am J Cardiol 23(4): 556-567.
  10. Prioli A, Marino P, Lanzoni L, Zardini P (1998) Increasing degrees of left ventricular filling impairment modulate left atrial function in humans. Am J Cardiol 82(6): 756-761.
  11. Appleton CP, Hatle LK, Popp RL (1988) Relation of transmitral flow velocity patterns to left ventricular diastolic function: new insights from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 12(2): 426-440.
  12. Thomas L, Levett K, Boyd A, Leung DY, Schiller NB, et al. (2002) Compensatory changes in atrial volumes with normal aging: is atrial enlargement inevitable? J Am Coll Cardiol 40(9): 1630-1635.
  13. Spach MS, Dober PC, Anderson PA (1989) Multiple regional differences in cellular properties that regulate repolarization and contraction in the right atrium of adult and newborn dogs. Circ Res 65(6): 1594-1611.
  14. Spach MS, Dober PC (1986) Relating extracellular potentials and their derivatives to anisotropic propagation at microscopic level in human cardiac muscle. Evidence for electrical uncoupling of side-to-side fiber connections with increasing age. Circ Res 58(3): 356-371.
  15. Lev M (1954) Aging changes in the human sinoatrial node. J Geront 9(1): 1-9.
  16. Davies MJ, Pomerance A (1972) Quantitative study of aging changes in the human sinoatrial node and internodal tracts. Br Heart J 34(2): 150-152.
  17. Hudson REB (1960) The human pacemarker and its pathology. Br Heart J 22(2): 153-167.
  18. Centurión OA, Isomoto S, Shimizu A, Konoe A, Kaibara M, et al. (2003) The effects of aging on atrial endocardial electrograms in patients with paroxysmal atrial fibrillation. Clin Cardiol 26(9): 435-438.
  19. Centurión OA, Shimizu A, Isomoto S, Konoe, Kaibara, et al. (2005) Influence of advancing age on fractionated right atrial endocardial electrograms. Am J Cardiol 96(2): 239-242.
  20. Centurión OA, Fukatani M, Konoe A, Tanigawa M, Shimizu A, et al. (1992) Different distribution of abnormal endocardial electrograms within the right atrium in patients with sick sinus syndrome. Br Heart J 68(6): 596-600.
  21. Centurión OA, Isomoto S, Fukatani M, Shimizu A, Konoe A, et al. (1993) Relationship between atrial conduction defects and fractionated atrial endocardial electrograms in patients with sick sinus syndrome. PACE 16(10): 2022-2033.
  22. Centurión OA, Shimizu A, Isomoto S, Konoe A, Hirata T, et al. (1994) Repetitive atrial firing and fragmented atrial activity elicited by extrastimuli in the sick sinus syndrome with and without abnormal atrial electrograms. Am J Med Sci 307(4): 247-254.
  23. Mehta S, Charbonneau F, Fitchett DH, Marpole DG, Patton R, et al. (1991) The clinical consequences of a stiff left atrium. Am Heart J 122(4 pt 1): 1184-1191.
  24. Pilote L, Huttner I, Marpole D, Sniderman A (1988) Stiff left atrial syndrome. Can J Cardiol 4(6): 255-257.
  25. Hoogsteen J, Hoogeveen A, Schaffers H, Wijn PF, van der Wall EE (2003) Left atrial and ventricular dimensions in highly trained cyclists. Int J Cardiovasc Imaging 19(3): 211-217.
  26. Lai ZY, Chang NC, Sai MC, Lin CS, Chang SH, et al. (1998) Left ventricular filling profiles and angiotensin system activity in elite baseball players. Int J Cardiol 67(2): 155-160.
  27. Vaziri SM, Larson MG, Benjamin EJ, Levy D (1994) Echocardiographic predictors of nonrheumatic atrial fibrillation. The Framingham Heart Study. Circulation 89(2): 724-730.
  28. Psaty BM, Manolio TA, Kuller LH, Kronmal, Cushman, et al. (1997) Incidence of and risk factors for atrial fibrillation in older adults. Circulation 96(7): 2455-2461.
  29. Tani T, Tanabe K, Ono M, Yamaguchi, Okada, et al. (2004) Left atrial volume and the risk of paroxysmal atrial fibrillation in patients with hypertrophic cardiomyopathy. J Am Soc Echocardiogr 17(6): 644-648.
  30. Losi MA, Betocchi S, Aversa M, Raffaella, Miranda, et al. (2004) Determinants of atrial fibrillation development in patients with hypertrophic cardiomyopathy. Am J Cardiol 94: 895-900.
  31. Tsang TS, Barnes ME, Bailey KR, Liebson, Montgomery, et al. (2001) Left atrial volume: important risk marker of incident atrial fibrillation in 1,655 older men and women. Mayo Clin Proc 76(5): 467-475.
  32. Tsang TS, Gersh BJ, Appleton CP, Tajik, Barnes, et al. (2002) Left ventricular diastolic dysfunction as a predictor of the first diagnosed nonvalvular atrial fibrillation in 840 elderly men and women. J Am Coll Cardiol 40(9): 1636-1644.
  33. Tenekecioglu E, Agca FV, Ozluk OA, Karaagac K, Demir S, et al. (2014) Disturbed left atrial function is associated with paroxysmal atrial fibrillation in Hypertension. Arq Bras Cardiol 102(3): 253-262.
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