DISCUSSION
In our study, basically; the facts that
  1. LA mechanics were disrupted in AR patients
  2. LA reservoir and LA conduit decreased as the severity of AR increased
  3. 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.