DISCUSSION
In our study, basically; the facts that
- LA mechanics were disrupted in AR patients
- LA reservoir and LA conduit decreased as the severity of AR increased
- LA reservoir and LA conduit significantly decreased in severe AR
compared to mild and moderate AR were determined.
The grading of AR for the patient’s follow-up and planning the treatment
after the diagnosis of AR is critical. Patients with normal levels of LV
diameters and functions, and who are
asymptomatic
with mild and moderate AR do not need to be treated, and a
12-to-24-month echocardiographic follow-up period is suggested for them.
On the other hand, patients with normal LV functions, and who are
asymptomatic with severe aortic regurgitation are supposed to be
examined at a 6-month period. (8)
The grading of AR needs to be done with many clinical and
echocardiographic parameters, without separating them. Some of the
echocardiographic parameters are EROA, regurgitant volume, Jet/LVOT
ratio, VC, holodiastolic flow reversal, LV dilatation, and AR PHT.
Despite all of these parameters that are in use for the grading of AR,
an ultimate decision cannot be taken in some cases and the severity of
AR cannot be clarified. Each unit decrease in LA strain value was
demonstrated to increase the likelihood of the progress of pulmonary HT
in AR patients by 6%. (9) These data show the importance of the LA
mechanics in chronic AR. In our study, it was noticed that LA reservoir
and LA conduit significantly decreased in severe AR patients compared to
the patients with mild and moderate AR, and that LA reservoir and LA
conduit might contribute to the grading of AR.
Some of the parameters used for the grading of AR, and, especially AR
PHT value were associated with elevated LVEDP, and they were inversely
correlated. In other words, as LVEDP increases, AR PHT value decreases,
and the values below 200 ms are interpreted to be related to severe AR.
Elevated LVEDP present in AR is closely related to the LA mechanics, and
decreased LA strain is an independent predictor of elevated LVEDP. (10)
LA dimension might be considered to be an approximate indicator of LV
diastolic filling pressures. (11)
In healthy individuals, the left atrium is quite flexible in exposure to
rather low pressures; however, it becomes tense and stiff in case of
acute and chronic damage. (12,13,14). The left atrium is directly
exposed to LV vacuum pressure during diastole; therefore, in the absence
of LA
volume
overload, an enlarged left atrium is a strong indicator of elevated LV
filling pressure, which also explains the causality between LA
dilatation and negative results. (11)
LA reservoir is significantly associated with systolic performance
measurements such as ejection fraction and LV systolic volume index. In
other words, both diastolic (LVEDP) and systolic (LV systolic volume
index) LV variables are independent predictors of the LA reservoir. (15)
Besides, the LA reservoir presents more precise information than the LA
volume index and other Doppler dependent variables for the assessment of
LVEDP.
Severe chronic AR causes pressure and volume overload on the left
ventricle. According to LaPlace’s law, wall stress is about the
division of wall thickness by intraventricular pressure and the radius.
LV dilatation increases LV systolic wall stress, which is required for
obtaining the systolic pressure level similar to the one obtained at
normal ventricular diameter. Therefore, in chronic AR, both preload and
afterload increase simultaneously. LV systolic function is preserved
with LV dilatation and hypertrophy. The amount of regurgitant volume is
directly associated with volume overload, and it is directly
proportional with the severity of the leak. While mild AR causes volume
overload minimally, severe AR might result in progressive circles
dilatation due to massive volume overload. (1)
Extreme volume overload in AR causes the dysfunction of the myocardial
mechanics insidiously. (16) In compensated severe AR, extreme
volume overload is adjusted by eccentric hypertrophy, which includes
lengthened myofibrils. (17,18) In spite of elevated regurgitant volume,
diastolic adaptation is preserved by keeping the LV filling pressures at
normal or mildly-elevated levels with eccentric hypertrophy. Meanwhile,
EF is maintained at normal levels by balancing increased volume overload
with increased LV bulk. (19) Even though it was compensated, in mild and
moderate AR, it was demonstrated that global LV performance
significantly decreased despite normal EF values. (20) Thus, in order an
optimal surgical date to be determined, new indicators that would show
subclinical dysfunction are required. (16)
In decompensated AR, decompensation progresses due to increased
interstitial
fibrosis and decreased compliance, and pressure and volume increase
after LV systole. LV diastolic compliance decreases due to hypertrophy
and fibrosis, and it coexists with systolic function. This condition
causes high filling pressures and symptoms of heart failure.
At the stages of decompensation; left atrial, pulmonary capillary
wedge pressure, the pressures in the right heart and pulmonary artery
increase, and cardiac output begins to decrease firstly during exercise,
then during rest. Increased LA pressure is directly associated with
regurgitant volume, and it can be stated that this association is
continuous. Hence, in parallel with the facts we obtained with the LA
mechanics, it can be suggested that LA strain parameters might
contribute to the grading of AR.
When the pathophysiology of chronic AR is considered, it is not
surprising that elevated LVEDP and LA strain parameters, which increase
with the severity of AR, are affected. In our study, it was demonstrated
that among the patients whose diseases were classified as mild,
moderate, and severe AR, LA reservoir and LA conduit values of the
severe AR group significantly decreased compared to those of the mild
and moderate group. The decrease was not significant for the difference
between the mild and moderate. It is possible that LV compensatory
capacity is not sufficient due to severe LV overload, and as LVEDP
increases, it causes the LA mechanics and strain parameters to be
affected in time. When considered from this point of view, LA reservoir
and LA conduit parameters can provide a supplementary contribution to
and be illuminating for EKO parameters, which have been clinical and in
use for the grading of AR for a long time.
The fact that our study was monocentric and observational, that the
number of the patients was not sufficient and the fact that LVEDP could
not be calculated with invasive methods are some of the limitations of
our study. However, the fact that a group of patients whom could only be
rarely encountered in clinical practice like isolated AY were chosen,
the likelihood that a routinely-performed invasive procedure would
increase the complication risk in the present group of patients and some
ethical issues led to these limitations.
Polycentric
studies that can be carried out with a larger group of patients can help
us to obtain more precise facts on this issue.