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ECHOCARDIOGRAM AND ATRIAL FIBRILLATION


Authors: T. Ciocarlie, M. Balint, V. Moga, C. Tudoran, L. Vasiluta, Anca-Maria Pujo, Rodica Avram



Received for publication: 15th of July, 2013
Revised: 1st of August, 2013



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SUMMARY: (Hide the summary)

Atrial fibrillation is the most common sustained arrhythmia affecting humans. Pathology studies have found loss of atrial myocardium with fibrosis and fatty infiltration, but many similar changes can occur as a result of aging alone. I studied a number of 420 patients (p.) admitted in the Cardiology Department of the Emergency County Hospital Timișoara, 122p. with paroxysmal atrial fibrillation and 298p. with persistent/permanent atrial fibrillation, using  anamnesis,  ECG and echocardiography. We found that the difference between the paroxysmal and the persistent/permanent  atrial fibrillation was statistically  significant regarding the mitral stenosis and insufficiency, but not in relation with aortic insufficiency and left ventricle hypertrophy, suggesting the pathological relation between the mitral valve disease, the left atrium and the permanent atrial fibrillation. As we expected the majority of patients with paroxysmal atrial fibrillation have had a normal left atrium and most of the patients with persistent/permanent atrial fibrillation were found with a pathological  left atrium. But surprising finding was that even if there was a statistical significant difference between the patients with paroxysmal and persistent/permanent atrial fibrillation regarding the dimensions of the left atrium, we have not found a statistical difference between these two groups of patients regarding the presence of spontaneous contrast or of left atrial thrombus.


Key Words:

Atrial fibrillation, echocardiography, thrombus.

 


 

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INTRODUCTION 

Atrial fibrillation (AF) is the most common sustained arrhythmia affecting humans. Pathology studies have found loss of atrial myocardium with fibrosis and fatty infiltration, but many similar changes can occur  as a result of aging alone. Maintenance of AF may depend on reentry, with  multiple wavelets occurring simultaneously,   continuous   triggers, or  both. The initiation of AF in many patients may be caused by rapidly firing foci, typically in the pulmonary vein(s).

AF has a profound effect on morbidity and mortality among hundreds of thousands of patients and on health care costs in the United States (1). One report analyzed 3,806,000 patient hospital discharges in 1990 from 678 hospitals to determine  the frequency with which arrhythmia was  the  principal diagnosis (2). Approximately   1.5%  of all  hospital  discharges  listed arrhythmia as a principal diagnosis, and AF accounted for nearly 35% of the arrhythmias  noted. The epidemiology  of AF has changed substantially since the early part of the twentieth  century  primarily  because of the dramatic decrease in rheumatic fever and the longer life span of the population (3-8). The patient populations evaluated differ substantially. For example, two studies included patients admitted through the emergency department and one evaluated only outpatients.  Nonetheless, it is obvious that rheumatic heart disease plays a relatively minor role in the current etiology of atrial fibrillation in the Western world,  whereas hypertension and, to a lesser extent, coronary artery disease currently  are major etiologic factors in AF. The incidence of lone AF is quite variable and  is influenced  by the intensity  of the diagnostic workup, the definition of lone atrial fibrillation used, and the patient  population  studied.  Kannel and associates reported a 31% incidence of lone AF, but some of their patients  had  obvious  heart disease  identified  by an enlarged heart on chest radiography. Thus, these data are problematic. In contrast, Prystowsky and colleagues studied only patients who had no known etiologic factors for AF  and  normal  ventricular  function  identified  by echocardiography.   However, in  their  study, only outpatients were evaluated. It is clear that the prevalence and types of etiologic factors for AF depend on the setting in which AF is evaluated, including the country of origin.

Changes in etiology of atrial fibrillation may affect its course,  especially  the evolution  of paroxysmal  atrial fibrillation into established  atrial  fibrillation.  In a study involving  1,212 patients  from Denmark,  three time periods, 1940 through 1948, 1949 through 1957, and 1958 through 1967, were evaluated (9). Atherosclerotic heart disease was  present in 23%, 37%,  and  38% of patients, respectively; hypertensive heart disease was present in 8%, 7%, and 10% of patients, respectively; and rheumatic heart disease occurred in 27%, 17%, and 15% of patients, respectively. During follow-up, the transition rate from paroxysmal to established or permanent atrial fibrillation varied according to the etiology of the disease and was 27% among patients with atherosclerotic heart disease, 40% among patients  with hypertensive heart disease, and 66% among patients with rheumatic heart disease. Few data are given on the use of antiarrhythmic drugs to  prevent   transition to  established   atrial fibrillation. However, given the dates of the study, only quinidine  would  have been used with any frequency. These data suggest that the transition from paroxysmal to established atrial fibrillation is not inevitable, especially among patients without  rheumatic heart disease. It is quite possible that antiarrhythmic therapy may further decrease the number of patients with established atrial fibrillation.

The prevalence of AF increases with  age and is 0.5% for patients aged 50 to 59 years and 8.8% for those aged 80 to 89 years (10). Men are affected slightly more often than women. In   the Framingham  data,   excluding individuals  with rheumatic  heart  disease,  the 2-year incidence of development of AF was 0.04% and 0.00% for men and women, respectively, aged 30 to 39 years, and 4.6% and 3.6%, respectively,  for men and women aged 80 to 89 years (11). Thus, the number of patients who have  AF  will rise  pari passu  with the aging  of the population. In the first two decades of life, AF is relatively rare. When it is found in patients in this age group, it is usually associated with heart disease or the presence of an accessory pathway.

The incidence of atrial fibrillation increases with age, and the condition is especially prevalent among individuals aged 60 years or older. Thus, it is important, in attempts to identify the pathologic changes associated with atrial fibrillation,  to consider  changes  that are associated with the aging process in and of itself. Macroscopic and microscopic alterations in atrial tissue begin in the first year of life (12). By the fourth and fifth decades, small fat spots appear in the right atrium in the region of the AV node and septum. There is accentuation of the thickening of the plaques in later decades. In the left atrium, the endocardial thickening  is diffuse. With aging, increased thickening occurs, especially at the mitral  valve annulus. Calcification  and fatty infiltration may be present in the annulus. Histologic examination reveals   an  endothelial   lining, beneath   which is  a fibroelastic core. With aging, there is focal or diffuse proliferation of smooth muscle cells, elastic fibers, or both and, in some cases, collagen fibers. This process has been termed endocardial hypertrophy (12). In the fourth decade, hypertrophic and sclerotic changes occur in previously uninvolved portions of the right atrium, and in the fifth decade, atrophy of smooth muscle layers can be seen. Increased sclerotic changes occur in the sixth decade. By  the fourth  decade, the  entire  left atrium appears to be affected by hypertrophy and sclerosis, and collagen    replacement    is   frequent. The    changes associated   with  aging   result in  eventual   loss of myocardial fibers and an increase in fatty metamorphosis and connective tissue in the sinus node, the AV node, and the atrial approaches to these structures (12).

One study analyzed pathologic changes in the atria in 145 patients with AF and control patients (19). Etiologies were diverse and included conditions such as rheumatic fever, hypertension,   hyperthyroidism,   and  coronary artery disease. The author speculated that no specific histologic syndrome is associated with AF. In another study, lesions of the sinus node were evaluated in the hearts of 65 patients (20). The anatomy of the sinus node was compared with clinical data in a blinded manner. The sinus node was obviously damaged in 15 patients, and an established  arrhythmia,  usually  AF,  was seen  in 14 patients. The sinus node was normal in 49 patients, and AF had been present in 5 patients. The common association in this study between sinus nodal damage and a clinical history  of AF supports the idea that sick sinus syndrome is a panatrial disorder in many patients.

One of the most important pathologic studies of the atria of patients  with AF  was done  by Davies  and Pomerance (13). These authors analyzed the hearts of 100 patients with AF and grouped them into patients who had AF for less than 2 weeks before death and those who had AF for more than 1 month  before death. Among patients who had the longer-term  AF, cor pulmonale, rheumatic heart disease, and ischemic heart disease were the most frequently associated clinical conditions. In nearly 75% of cases of chronic AF, sinus node muscle loss, internodal tract muscle loss, and atrial dilation of some degree were present. Notably, left atrial appendage thrombosis was identified in 46 patients with long-term AF and cerebral infarction was identified in 19. However, only 3 of 19 patients with short-term  AF had left atrial thrombus  and  only 1 patient  had  cerebral  infarction. These    authors offered an important hypothesis concerning the origin of pathologic changes in the atria. They stated that while it is conventional to regard the fibrotic changes in the node and atria as the cause of atrial fibrillation, it is also possible that they result from the arrhythmia and consequent disordered function of the chambers (14). This prescient observation supports the current belief that AF begets  AF, therefore  making  it possible to retard or even prevent the development of permanent  AF in some patients by maintaining sinus rhythm, which may beget sinus rhythm.

An echocardiogram is an important test to obtain in patients with AF. It allows evaluation of atrial size, right and left ventricular function, and the presence of valvular lesions. Echocardiography, especially transesophageal echocardiography, has been valuable in investigating atrial function in patients with atrial fibrillation (15-19). Transesophageal echocardiography, but not transthoracic  echocardiography, can provide valuable information on the presence of atrial thrombi, typically in the left  atrial appendage. Atrial thrombi have been detected in  as   many as 15% of patients before cardioversion. It is important to note new thrombi can occur after successful  cardioversion and may cause embolic events (20). Thus, at least two mechanisms are possible for  thromboembolism after cardioversion: dislodgment of a preexisting thrombus and formation of a new thrombus after cardioversion.

 

MATERIAL AND METHOD

We studied a number of 420 patients (p.) admitted in the Cardiology  Department  of the Emergency County Hospital Timișoara, 122p. with  paroxysmal   atrial fibrillation  and 298p.  with persistent/permanent  atrial fibrillation, using anamnesis, ECG and echocardiography. The CHA2DS2-VASc risk score was also recorded in all the 420 p.

 

RESULTS

From  the  420 p., 122 had  paroxysmal   and  298 persistent/permanent  atrial fibrillation  (Figure 1). From the patients with paroxysmal atrial fibrillation, 46 were men and   76  women, and   from the  group   with persistent/permanent atrial fibrillation 154 were men and 144 women (p=0,009) (Figure 2).

Regarding the presence of valvular heart disease: 2 p. with paroxysmal and 22 with persistent/permanent atrial fibrillation were diagnosed with mitral stenosis (p=0.02), 4 and 24 with aortic insufficiency (p=0.08), and 54 with paroxysmal  and  206 with persistent/permanent were diagnosed with mitral insufficiency (p=0.0001).  54 p. with paroxysmal  and  105 with persistent/permanent atrial fibrillation  have had left ventricle hypertrophy on echocardiogram (p=0.096)  (Figure 3).

 

 

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Fig. 1. Type of atrial fibrillatio

 

 

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Fig. 2. Gender distribution

 

 

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Fig. 3. Type of atrial fibrillation and echocardiographic changes

 

 

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Fig. 4. Type of atrial fibrillation and ejection fraction

 

Regarding the left ventricle systolic function 52 p. with paroxysmal atrial fibrillation had an ejection fraction over 50%, 25 between 49-40%, 36 between 39-30% and 9 less than 30%. From the patients with persistent/permanent atrial fibrillation 21 had an ejection  fraction  over 50% (p=0.0001), 92  between 49-40% (p=0.031), 130 between  39-30%  (p=0.008) and  55 less than  30% (p=0.004) (Figure 4).

When we look at the left atrium, we found that 21 patients with paroxysmal atrial fibrillation had dilated left atrium, 14 spontaneous  contrast and  only  6 were diagnosed with  thrombus. From the group of p. with persistent  atrial fibrillation,  dilated left atrium was diagnosed in 87 (p=0.013), spontaneous contrast in 36 (p=1) and left atrium thrombus in 28p (p=0.16)  (Figure 5).

 

CONCLUSIONS AND DISCUSSION

From the 420 patients admitted with atrial fibrillation in the Cardiology Department in 2013, 29% were diagnosed with paroxysmal atrial fibrillation and more the two thirds - 71% with persistent/permanent atrial fibrillation. Almost two thirds of patients with paroxysmal atrial fibrillation were women,  but the men and women  were  evenly distributed in the group with persistent/permanent atrial fibrillation, with a p that was statistically significant.

If we look at the valvular heart disease, the difference between the paroxysmal and the persistent/permanent atrial fibrillation was statistically significant regarding the mitral stenosis and insufficiency, but not in relation with aortic insufficiency   and   left  ventricle hypertrophy, suggesting the pathological relation between the mitral valve disease, the left atrium and the permanent atrial fibrillation.

46% of patients with paroxysmal atrial fibrillation  have had an ejection fraction greater than 50%, but only 7% of the patients with persistent/permanent atrial fibrillation have had a normal systolic function. The difference between paroxysmal and persistent/permanent atrial fibrillation was also statistical  significant regarding the lower ejection in all the student groups: 40-49%, 30-39% and less than 30%. So almost half of the patients with paroxysmal  atrial fibrillation   have  had  a  normal  left ventricle systolic function and almost all the patients with persistent/permanent atrial fibrillation were recorded as having an ejection fraction lower than 50%, suggesting the clear relation the bidirectional relation between the left ventricle function and the atrial fibrillation.

As we  expected  the majority of  patients with paroxysmal atrial fibrillation have had a normal left atrium and most of the patients with persistent/permanent atrial fibrillation were found with a pathological left atrium. But surprising finding was that even if there was a statistical significant difference   between    the  patients   with paroxysmal and persistent/permanent atrial fibrillation regarding the dimensions of the left atrium, we have not found a statistical difference between these two group of patients regarding the presence of spontaneous contrast or of left atrium thrombus, suggesting, once again, that the decision for oral anticoagulation treatment should be based not on the time of atrial fibrillation, but exclusively on the presence or absence of the risk factors for stroke (like Congestive  Heart  Failure,  Hypertension,   Age, Diabetes Mellitus,  Stroke, Vascular Disease, Women) that were add in the CHA2DS2-VASc risk score.

 

References:

  1. Prystowsky EN, Benson DW, Fuster V, et al. Management of patients with atrial fibrillation: a statement for healthcare professionals from   the   Subcommittee   on   Electrocardiography   and   Electrophysiology,   American   Heart   Association.   Circulation 1996;93:1262-1277.
  2. Bialy D, Lehmann MH, Schumacher DN, et al. Hospitalization for arrhythmias in the United States: importance of atrial fibrillation. J Am Coll Cardiol 1992;19:41A.
  3. Parkinson J, Campbell M. Paroxysmal auricular fibrillation: a record of two hundred patients. QJM 1930;67-100.
  4. Kannel WB, Abbott RD, Savage DD, et al. Epidemiologic features of chronic atrial fibrillation: the Framingham study. N Engl J Med 1982;306:1018-1022.
  5. 13. Davidson E, Weinberger I, Rotenberg Z, et al. Atrial fibrillation: cause and time of onset. Arch Intern Med 1989;149:457-459.
  6. 14. Lok NS, Lau CP. Presentation and management of patients admitted with atrial fibrillation: a review of 291 cases in a regional hospital. Int J Cardiol 1995;48:271-278.
  7. 15. Prystowsky EN, Margiotti R, Fogel RI, et al. Atrial fibrillation with and without heart disease: clinical characteristics and proarrhythmia risk. Circulation 1996;94(8):I:191.
  8. 16. Godtfresen J. Atrial fibrillation: cause and prognosis a follow-up study of 1212 cases. In: Kulbertus HE, Olsson SB, Schlepper M, eds. Atrial fibrillation. Sweden: AB Hassle, 1982. 
  9. Einthoven W. Le telecardiogramme, Arch Internat Physiol 1908;4:132-164.
  10. 17. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke 1991;22:983-988.
  11. 18. Wolf PA, Abbott RD, Kannel WB: Atrial fibrillation: a major contributor to stroke in the elderly. The Framingham Study. Arch Intern Med 1987;147:1561-1564.
  12. Yater WM. Pathologic changes in auricular fibrillation and in allied arrhythmias. Arch Intern Med 1929;43:808-838.
  13. Davies MJ, Pomerance A. Pathology of atrial fibrillation in man. Br Heart J 1972;34:520-525.
  14. Davidson E, Weinberger I, Rotenberg Z, et al. Atrial fibrillation: cause and time of onset. Arch Intern Med 1989;149:457-459.
  15. Prystowsky EN. Management of atrial fibrillation: simplicity surrounded by controversy. Ann Intern Med 1997;126:244-246.
  16. Sanfilippo  AJ,  Abascal  VM,  Sheehan  M,  et  al.  Atrial  enlargement  as  a  consequence  of  atrial  fibrillation.  Circulation 1990;82:792-797.
  17. Gosselink AT, Grijns HJ, Hamer HPM, et al. Changes in left and right atrial size after cardioversion of atrial fibrillation: role of mitral valve disease. J Am Coll Cardiol 1993;22:1666-1672.
  18. Manning WJ, Silverman DI, Katz SE, et al. Impaired left atrial mechanical function after cardioversion: relation to the duration of atrial fibrillation. J Am Coll Cardiol 1994;23:1535-1540.
  19. Mitusch R, Garbe M, Schmucker G, et al. Relation of left atrial appendage function to the duration and reversibility of nonvalvular atrial fibrillation. Am J Cardiol 1995;75:944-947.
  20. Fatkin D, Kuchar DL, Thorburn CW, et al. Transesophageal echocardiography before and during direct current cardioversion of atrial  fibrillation:  evidence  for  atrial  stunning•    as  a  mechanism  of  thromboembolic  complications.  J  Am  Coll  Cardiol 1994;23:307-316.


Correspondence to:
Correspondence to: Tudor Ciocārlie, tudorfox@yahoo.com, University of Medicine and Pharmacy Victor Babeș Timișoara