Hypothesis / aims of study
Detrusor contraction depends on outflow-resistance and a slowly (over many years) growing prostate demands an increase of detrusor contractility to maintain the ability to void. On the other hand, the uroflow-rate (urethral -flow controlling zone- distension) depends on detrusor voiding contraction strength. How differences in outflow resistance relate to differences in contraction in an individual is however remarkably little studied. One study reported test-retest differences of BOOI of plus or minus 14 of the BOOI (was ‘AG index’ at that time) and plus or minus 7 cmH2O for the outlet resistance quantifier URA, when a four -week interval was chosen. Variability of detrusor voiding contraction was however not included in this analysis and obvious differences of pressure zeroing procedures between patients and tests (as visible in the figures) were not considered.(1) Penile cuff pressure tests show a mean difference in maximum of isovolumetric contractions (as a measurement of contractility) of 4.0 ± 26 cm H2O in one study (PMID: 15371853) and -3.3 (32.0) cm H2O in another (PMID: 15371853). This testing does not directly account for the degree of outflow obstruction and, the correlation/association of maximum of isovolumic contraction with (maximum) of detrusor voiding contraction is not known. Furthermore, group mean values were reported but individual test-retest differences are more relevant. These studies nevertheless imply that short time differences in outflow resistance and voiding contraction are of relevance. The do however not clarify what contributes to the differences observed, and do not explain the balance between contraction and outflow resistance. (2) We present immediate and longer-term test-retest differences and how contraction varies with outflow resistance, both short time and longer time. We do this with the assumption that short time test-retest studies represent the variability of the combination of contraction and outflow obstruction, and the longer time may better represent if adaption of detrusor muscle to differences in outflow resistance occurs.
Study design, materials and methods
273 men with LUTS without relevant concomitant abnormalities had ICS standard UDS with pressure flow study (PFS). ICS-standard UDS used fluid filled catheters, external pressure transducers, levelled to the symphysis pubis of the patient, saline fill with a rate of 10% of expected capacity per minute and voiding in private when the patient reports a strong sensation of bladder filling. 190 men (70%) had immediate test and retest, frequently sitting-standing, but also for other reasons. The other 83 men had longer term test-retest interval 1 month -10y for all possible reasons (e.g., long term continued pharmacological treatment, but also after surgical des-obstruction). The PFS parameters URA and BOOI as a measure of urethral resistance (outflow obstruction) and Wmax and BCI as quantifiers of detrusor voiding contraction (and detrusor underactivity) are used after correction of flow (peak-) artefacts.
The differences (dif.) between first and second PFS are calculated by subtracting the second measurement result from the first. (e.g., Wmax2 – Wmax1= Wmaxdiff) these difference -values were plotted on X-Y graphs to show differences of (maximum of) voiding contraction versus differences in urethral resistance.
The figure shows (top row scatter-graphs) all URA differences with Wmax differences and (bottom row), the BOOI versus BCI differences, all with regression lines. Regression demonstrates that Wmax is ‘more independent’ of outflow resistance than BCI.
Correlation (all retests) of BOOIdif with URAdif is strong and significant (r.899, .000) and correlation of BCIdif with Wmax is weaker (r.493, .000). Correlation of URAdif with Wmax is absent (r.022, p723), correlation of BOOIdif with BCIdif is weak, however significant. (p.294, .000). Mean differences of long term and imtermediate (<5years) retests were not significantly different.
Interpretation of results
Analysis of both, regression and correlation shows that differences in outflow resistance have less influence on Wmax as a measure of contraction, than BCI. Wmax is not based on the same parameters as BOOI (and URA), while BCI is. Wmax appears more robust to grade contraction of the individual, because it is less sensitive to variations of BOO. Although Wmax (and BCI) have a tendency to increase with increasing grade of outflow obstruction the analysis of men with symptoms does not show evidence of compensation. It is not clear whether detrusor voiding contraction power/strength compensation occurs earlier in the development of pathophysiology (and or whether symptoms become bothersome when compensation is failing).