Diagnostic power of the noninvasive condom catheter method in patients eligible for transurethral resection of the prostate.

AIMS: The aim of this study was to determine the accuracy of the non-invasive condom catheter method for diagnosing B(ladder) O(utlet) O(bstruction) in patients eligible for T(rans)U(rethral) R(esection) of the P(rostate). METHODS: A group of 71 patients eligible for TURP on clinical grounds were invasively and non-invasively studied. On the basis of invasive pressure-flow studies they were stratified into obstructed, equivocal or unobstructed, according to the International Continence Society standard. Subsequently they were diagnosed non-invasively on the basis of a free flowrate measurement, or on the basis of the free flowrate measurement plus the isovolumetric bladder pressure measured with the condom catheter method. R(eceiver) O(perating) C(haracteristic)s were calculated. RESULTS: The A(rea) U(nder) the (RO)C for discriminating unobstructed/equivocal patients from obstructed patients was 0.68 in our population. This improved to 0.84 for the 50 patients in whom the isovolumetric bladder pressure was not underestimated by the non-invasive method. CONCLUSIONS: In our population of TURP patients, the low flowrates affected the accuracy of the condom method to a degree that it did not perform better than a free flowrate measurement, which performed remarkably well. By excluding measurements in which the condom pressure underestimated the isovolumetric bladder pressure this method may contribute to a more accurate, patient friendly diagnosis of BOO in these patients. In the present study this exclusion was done by comparison with an invasive pressure measurement. A practical non-invasive test would necessitate a non-invasive exclusion criterion, which might be based on the risetime of the condom pressure.

Longitudinal changes in isovolumetric bladder pressure in response to age-related prostate growth in 1,020 healthy male volunteers.

AIM: To non-invasively study if compensation and decompensation occurs in the urinary bladder of healthy male volunteers in response to benign prostatic enlargement (BPE) using the condom catheter method. METHODS: Between 2001 and 2010, 1,020 healthy male volunteers were included in a longitudinal study based on three non-invasive urodynamic examinations during a 5-year follow-up. Inclusion criteria were an informed consent, the ability to void in a normal standing position and a minimum free flow rate of 5.4 ml/sec. Study parameters were prostate volume (PV), maximum free urinary flow rate (Q(max)) and bladder contractility, quantified by the maximum isovolumetric bladder pressure, measured in the condom (P(cond.max)). Volunteers also completed the International Prostate Symptom Score Form (IPSS). RESULTS: Within limitations, the included volunteers had a flat age distribution between 38 and 72 years. This made it possible to combine longitudinal analysis in a 5-year observation interval, with cross sectional analysis in a 35-year age range. Longitudinal analysis showed that with increasing age, PV increased with 1.9% per year, whereas Qmax decreased with 1.1% per year. IPSS increased with 1.1% per year when volunteers were older than 55 years. P(cond.max) increased during the 5-year longitudinal follow-up, but not in the cross sectional analysis. CONCLUSIONS: The difference between cross sectional and longitudinal results of the P(cond.max) may have been caused by compensation of the urinary bladder resulting in a selection effect. This would imply that compensation is a relatively fast process, taking approximately 5 years.

Increased postvoid residual volume after measuring the isovolumetric bladder pressure using the noninvasive condom catheter method.

OBJECTIVE: To test, in an ongoing noninvasive longitudinal study in healthy men, whether the condom catheter method (a noninvasive urodynamic test to assess bladder function and bladder outlet obstruction) inhibits bladder function and whether this affects the reliability of the measured isovolumetric bladder pressure (P(ves.iso)). SUBJECTS AND METHODS: Subjects (754, aged 40-79 years) voided three times, i.e. one free void and two condom measurements. The postvoid residual volume (PVR) was measured after each void using transabdominal ultrasonography. The statistical significance of differences was tested using Wilcoxon rank test and the Mann-Whitney U-test. RESULTS: After free voiding the median (interquartile range) PVR was 18 (37) mL, and independent of the amount of fluid intake. In a subgroup of volunteers, when the free void was done last, the PVR was no different (P = 0.25), suggesting that the bladder did not become exhausted during the protocol. The PVR after two subsequent condom measurements was significantly higher than after free voiding, at 45 (78) and 57 (88) (both P < 0.05), independent of the number of interruptions in voiding. After supplementary fluid intake before the condom measurements, the PVR was double that with a normal fluid intake (P = 0.03). The median P(ves.iso) was 3 cmH(2)O higher in the second condom measurement than in the first (P < 0.05), although this small difference was not clinically relevant. CONCLUSIONS: The condom measurement is associated with a significantly higher PVR, partly caused by supplementary fluid intake. This effect was only temporary and did not affect the measured P(ves.iso).

Myocardial blood supply by left ventricle-to-coronary artery channel: an old idea revisited.

Coronary artery disease is one of the most important causes of death in Western society. Attempts to revascularize the coronary artery by myocardial retroperfusion, direct revascularization from the left ventricle, and bypass surgery have finally led to percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass grafting (CABG) as standard treatment for coronary artery disease. Direct revascularization from the left ventricle has already been studied in the late 1960s, but the idea was rejected because of a decrease in flow in combination with a failure of myocardial function. Recently, a left ventricle-to-coronary artery (LV-CA) stent has renewed interest as an alternative procedure when PTCA and CABG are no option. Animal studies showed a change in flow pattern from diastolic coronary inflow at baseline to systolic coronary inflow followed by diastolic regurgitive flow during direct ventricular sourcing, resulting in a coronary flow of 50-75% of baseline flow. Global myocardial function decreased in the same extent as the coronary flow suggesting perfusion-contraction matching. In a recent pilot study in the anaesthetized pig, direct revascularization after acute proximal coronary ligation resulted in sufficient blood supply to the outer layers of the myocardium, however, in the inner layers a metabolic disbalance occurred. Incorporation of a valve-like mechanism to minimize the diastolic regurgitive flow may be necessary to improve the performance of the LV-CA stent. In addition, further research should be done in chronic ischemic animal models in which the effect of the collateral circulation on myocardial perfusion and performance is an important issue.

Epinephrine in the heart: uptake and release, but no facilitation of norepinephrine release.

BACKGROUND: Several studies have suggested that epinephrine augments the release of norepinephrine from sympathetic nerve terminals through stimulation of presynaptic receptors, but evidence pertaining to this mechanism in the heart is scarce and conflicting. Using the microdialysis technique in the porcine heart, we investigated whether epinephrine, taken up by and released from cardiac sympathetic nerves, can increase norepinephrine concentrations in myocardial interstitial fluid (NE(MIF)) under basal conditions and during sympathetic activation. METHODS AND RESULTS: During intracoronary epinephrine infusion of 10, 50, and 100 ng/kg per minute under basal conditions, large increments in interstitial (from 0.31+/-0.05 up to 140+/-30 nmol/L) and coronary venous (from 0.16+/-0.08 up to 228+/-39 nmol/L) epinephrine concentrations were found, but NE(MIF) did not change. Left stellate ganglion stimulation increased NE(MIF) from 3.4+/-0.5 to 8.2+/-1.5 nmol/L, but again, this increase was not enhanced by concomitant intracoronary epinephrine infusion. Intracoronary infusion of tyramine resulted in a negligible increase in epinephrine concentration in myocardial interstitial fluid (EPI(MIF)), whereas 30 minutes after infusion of epinephrine an increase of 9.5 nmol/L in EPI(MIF) was observed, indicating that epinephrine is taken up by and released from cardiac sympathetic neurons. Although 68% to 78% of infused epinephrine was extracted over the heart, the ratio of interstitial to arterial epinephrine concentrations was only approximately 20%, increasing to 29% with neuronal reuptake inhibition. CONCLUSIONS: Our findings demonstrate epinephrine release from cardiac sympathetic neurons, but they do not provide evidence that epinephrine augments cardiac sympathoneural norepinephrine release under basal conditions or during sympathetic activation.

Urinary Bladder Contractility Revisited. Correlation of Noninvasively and Invasively Measured Contractility Parameters in Patients Eligible for Transurethral Resection of the Prostate.

OBJECTIVE: To validate a noninvasively estimated measure of urinary bladder contractility by correlating it with 3 existing invasive contractility parameters and to compare and correlate those invasive parameters. METHODS: A group of 74 patients, recruited in 3 different hospitals, and eligible for transurethral resection of the prostate on clinical grounds, were noninvasively studied preoperatively using the condom catheter method. The maximum condom pressure pcond.max measured during a mechanical interruption of flow rate was considered an estimate of urinary bladder contractility and compared to conventional contractility parameters calculated from preoperative (invasive) pressure-flow studies. RESULTS: The highest correlations were found between the invasive parameters. The correlation between the noninvasive parameter on the one hand and the invasive parameters on the other hand was lower, but mostly significant. In a number of patients, pcond.max underestimated the isovolumetric bladder pressure. The underestimated patients were more obstructed than those who were not underestimated and had a higher (invasively measured) contractility. When the underestimated patients were deselected, the correlation between the noninvasive pcond.max and the invasive parameters in the remaining 52 patients was higher. CONCLUSION: The 4 tested contractility parameters represent different aspects of urinary bladder contractility. Nevertheless, there was a significant correlation among them supporting the concept of a common basis, that is, detrusor contractility. The invasive contractility parameter bladder contractility index overestimated contractility in patients with lower urinary tract symptoms and/or benign prostatic enlargement. A modified parameter is suggested.

Myocardial blood supply through a direct left ventricle-coronary artery shunt is not aided by augmented coronary capacitance.

OBJECTIVES: Left ventricle-coronary artery shunting is proposed as an alternative means of myocardial revascularization when standard methods are not an option. During diastole, however, regurgitant coronary flow to the left ventricle decreases the efficacy of the left ventricle-coronary artery shunt. We investigated whether augmented coronary compliance would improve net forward shunt flow. METHODS: In 11 anesthetized pigs a specially designed stent was placed through the lateral wall of the left ventricle. Through an arterial graft, it was connected to the proximal left anterior descending coronary artery. A blind stump of the right internal thoracic artery (15 cm) was anastomosed to the distal left anterior descending coronary artery to serve as added coronary compliance chamber. Blood flow was measured in the coronary artery just distal from the left ventricle-coronary artery shunt, as well as in the shunt and in the compliance chamber entrance-exit. RESULTS: The left ventricle-coronary artery shunt decreased the net forward midcoronary flow to 53% +/- 18% (mean +/- SD) of native flow (8 +/- 4 vs 16 +/- 5 mL/min at baseline, P <.01). The augmented compliance did not significantly increase net forward coronary flow (61% +/- 25% of native flow, P <.01 vs baseline and P =.21 vs left ventricle-coronary artery shunt with normal compliance). The increase in systolic forward flow (53 +/- 23 vs 37 +/- 19 mL/min with normal compliance) was accompanied by a similar increase in diastolic regurgitant flow (-26 +/- 20 vs -16 +/- 16 mL/min). CONCLUSION: In healthy pigs a left ventricle-coronary artery shunt decreased net forward coronary flow to 53% +/- 18% of native flow. Augmentation of coronary artery compliance did not improve shunt performance.

Transmural differences in myocardial function and metabolism during direct left ventricular to coronary artery sourcing.

BACKGROUND: We investigated the hypothesis that in the absence of collateral circulation, a left ventricle-coronary artery (LV-CA) bypass will maintain normal LV wall function and metabolism transmurally, both at rest and during stress, when the left anterior descending coronary artery (LAD) is acutely occluded proximally. METHODS: In 18 anesthetized pigs (74 +/- 7 kg, mean +/- standard deviation), a covered stent was placed transmurally in the lateral wall of the beating LV and connected to the proximal LAD via an arterial graft. Subepicardial and subendocardial segmental shortening as well as interstitial lactate and glucose concentrations were measured regionally by sonomicrometry and microdialysis, respectively. RESULTS: When the LAD was occluded proximally, direct left ventricular sourcing decreased the net LAD flow to 64 +/- 25% of the native flow (n = 18, all animals). In the subepicardium, systolic shortening (SS) decreased to 87 +/- 18% of baseline (p = 0.124), with the appearance of minor postsystolic shortening (PSS), and minor changes in interstitial lactate and glucose levels. In the subendocardium, in contrast, SS decreased to 54 +/- 20% (p = 0.001). Marked PSS concurred with a sixfold increase in lactate (p = 0.008), and a 65 +/- 31% decrease in glucose (p = 0.003), indicating subendocardial anaerobic metabolism. Stress induced by infusion of dobutamine increased lactate and decreased glucose concentration in the subepicardium to subendocardial levels, indicating transmural anaerobic metabolism. CONCLUSIONS: In the anesthetized pig, direct sourcing by a LV-CA bypass distal to an acute coronary occlusion resulted in a 36% decrease in net forward coronary flow, subendocardial anaerobic metabolism, and loss of subendocardial contractile function at rest. These adverse effects extended into the subepicardium when the heart was stressed.

Exogenous angiotensin II does not facilitate norepinephrine release in the heart.

Studies on the effect of angiotensin II on norepinephrine release from sympathetic nerve terminals through stimulation of presynaptic angiotensin II type 1 receptors are equivocal. Furthermore, evidence that angiotensin II activates the cardiac sympathetic nervous system in vivo is scarce or indirect. In the intact porcine heart, we investigated whether angiotensin II increases norepinephrine concentrations in the myocardial interstitial fluid (NE(MIF)) under basal conditions and during sympathetic activation and whether it enhances exocytotic and nonexocytotic ischemia-induced norepinephrine release. In 27 anesthetized pigs, NE(MIF) was measured in the left ventricular myocardium using the microdialysis technique. Local infusion of angiotensin II into the left anterior descending coronary artery (LAD) at consecutive rates of 0.05, 0.5, and 5 ng/kg per minute did not affect NE(MIF), LAD flow, left ventricular dP/dt(max), and arterial pressure despite large increments in coronary arterial and venous angiotensin II concentrations. In the presence of neuronal reuptake inhibition and alpha-adrenergic receptor blockade, left stellate ganglion stimulation increased NE(MIF) from 2.7+/-0.3 to 7.3+/-1.2 before, and from 2.3+/-0.4 to 6.9+/-1.3 nmol/L during, infusion of 0.5 ng/kg per minute angiotensin II. Sixty minutes of 70% LAD flow reduction caused a progressive increase in NE(MIF) from 0.9+/-0.1 to 16+/-6 nmol/L, which was not enhanced by concomitant infusion of 0.5 ng/kg per minute angiotensin II. In conclusion, we did not observe any facilitation of cardiac norepinephrine release by angiotensin II under basal conditions and during either physiological (ganglion stimulation) or pathophysiological (acute ischemia) sympathetic activation. Hence, angiotensin II is not a local mediator of cardiac sympathetic activity in the in vivo porcine heart.