Blood-brain barrier disruption by low-frequency ultrasound.
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Biomedical subjects
Publications and source records attributed to Georg Bachmann.
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OBJECTIVE: To compare three-dimensional (3D) power Doppler ultrasonography (PDUS) with contrast enhanced magnetic resonance imaging (MRI) in their capability to visualize synovial vascularity in inflamed wrists of patients with rheumatoid arthritis (RA). METHODS: Nine patients with RA showing clinically active arthritis of the wrist as determined by tenderness and swelling were examined by contrast enhanced MRI and 3D PDUS. Vascularity close to and inside the joint capsule was visualized by conventional power Doppler mode. In a region with high Doppler signal intensity (=region of interest/ROI) a 3D blood vessel tree was obtained by a free-hand sweep. 3D images were evaluated with regard to the number of blood vessels in the intra- and peri-articular region. MRI examinations were performed using a 1.5 T Scanner. In MRI, time resolved coronal contrast enhanced T1-weighted sequences with fat suppression were acquired during an 8 min period to assess tissue enhancement. Relative enhancement was calculated and compared to 3D PDUS findings. RESULTS: A 3D vascular tree consisting of peri- and intra-articular blood vessels could be demonstrated in the same anatomical ROI in which an increased gadolinium enhancement was measured by MRI in all examined RA patients. The number of penetrating vessels into the joint capsule, the number of intra-articular vessels and a semiquantitative estimation of the strength of blood flow were used to generate a 3D score for the intensity of synovial vascularity. CONCLUSION: When compared with clinical symptoms and the gold standard dynamic MRI, 3D PDUS is a reliable imaging technique for assessing synovial vascularity in inflamed wrists of RA patients.
BACKGROUND AND PURPOSE: Ultrasound-accelerated thrombolysis is a promising approach toward acute stroke treatment. In previous in vitro studies, we demonstrated enhanced thrombus destruction induced by 20-kHz ultrasound. However, little is known about biological interactions of low-frequency ultrasound with brain tissue. The aim of this in vivo MRI study was to assess safety aspects of transcranial low-frequency ultrasound in rats. METHODS: The cranium of 33 male Wistar rats was sonificated for 20 minutes (20-kHz continuous wave). Power output was varied between 0 and 2.6 W/cm2. Tympanal and rectal temperature was monitored. Diffusion-weighted imaging and T2-weighted imaging was performed before and 4 hours, 24 hours, and 5 days after sonification. Apparent diffusion coefficients (ADCs) and T2 relaxation time (T2-RT) were measured in regions of interest in the cortex and the basal ganglia. The animals were euthanized for histological evaluation thereafter. RESULTS: Tympanal temperature increased significantly during insonation with 1.1 and 2.6 W/cm2. ADCs decreased significantly at 0.5 and 1.1 W/cm2, indicating cytotoxic edema. T2-RT increased significantly in the 0.5 and 1.1 W/cm2 group, consistent with vasogenic edema. No changes were detectable in the low-power output group (0.2 W/cm2). After sonification with 2.6 W/cm2, a significant loss of neurons could be detected on histopathology. Furthermore, 3 animals developed circumscript cortical lesions that could be identified as parenchymal necrosis. CONCLUSIONS: Low-frequency ultrasound caused vasogenic and cytotoxic brain edema and intracerebral necrosis in a dose-dependent fashion. This study indicates therapeutic low-frequency ultrasound as being potentially harmful and underlines the necessity of careful evaluation in further animal models.
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OBJECTIVE: The purpose of this study was to assess the individual and combined usefulness of MRI techniques in cases of acute pulmonary embolism and to compare the usefulness of these techniques with that of 16-MDCT. SUBJECTS AND METHODS: Sixty-two patients with symptoms indicating acute pulmonary embolism underwent an MRI protocol that progressed from real-time MRI through MR perfusion imaging to MR angiography. The results were compared with those of 16-MDCT, which was the reference standard. Thoracic incidental diagnoses other than pulmonary embolism also were sought with CT and MRI. RESULTS: Pulmonary embolism was diagnosed with CT in 19 patients for totals of 90 lobar, 245 segmental, and 434 subsegmental arteries. On a per-patient basis, the sensitivities of real-time MRI, MR angiography, MR perfusion imaging, and the combined protocol were 85%, 77%, 100%, and 100%, respectively. The specificities were 98%, 100%, 91%, and 93%. The kappa values in a comparison of the MR techniques with CT were 0.89, 0.87, 0.86, and 0.9. On a per-embolus basis, the sensitivities of real-time MRI, MR angiography, and MR perfusion imaging for lobar pulmonary embolism were 79%, 62%, and 100%. The sensitivities for segmental pulmonary embolism were 86%, 83%, and 97%, respectively. MR perfusion imaging had a sensitivity of 93% for subsegmental pulmonary embolism. Eight of nine incidental findings revealed on CT were also subsequently diagnosed with real-time MRI. MRI failed to reveal a case of emphysema. Mean MRI examination time was 9 minutes 56 seconds. CONCLUSION: The combined MR protocol is both reliable and sensitive in comparison with 16-MDCT in the diagnosis of pulmonary embolism. MR perfusion imaging is sensitive for the detection of pulmonary embolism, whereas real-time MR and MR angiography are specific.
OBJECTIVE: The purpose of this study was to prospectively assess the feasibility and quality of combined MRI examinations consisting of thoracic MRI for suspected pulmonary embolism (PE) and MR venography for deep vein thrombosis (DVT), to assess the diagnostic yield of a combined examination for detecting thromboembolism compared with each component alone, and to retrospectively assess the concordance of duplex sonography and MR venography. SUBJECTS AND METHODS: Two hundred twenty-one consecutive patients (119 men, 102 women; mean age, 51 years; range, 31-86 years) with suspected PE were examined using a multitechnique thoracic MRI protocol (real-time MRI using true fast imaging with steady-state precession [FISP], perfusion MRI, and MR angiography) followed by stepping-table MR venography. RESULTS: Two hundred twenty-one thoracic MRI examinations were performed. Two hundred eighteen MR venography examinations were scheduled, of which five (2.3%) were not performed for clinical or technical reasons and six were not performed after negative thoracic MRI. Among 207 combined examinations, PE was diagnosed in 76 and DVT in 78 examinations. Thirteen patients without PE showed DVT; thus, MR venography detected 17% additional cases of thromboembolism. Agreement with duplex sonography was good at the upper leg (kappa = 0.87-0.89) but moderate at the pelvis (kappa = 0.59-0.65). CONCLUSION: A combined "one-stop-shopping" MRI approach for PE and DVT was routinely feasible and detected 17% more cases of thromboembolism compared with separate examinations. MRI may be considered a second-line technique to avoid contraindications to CT but also a primary comprehensive technique for diagnosing thromboembolism.
BACKGROUND: Based on a newly developed model of reversible superior sagittal sinus (SSS) thrombosis in the rat, we investigated the effect of thrombolytic and anticoagulant treatment on recanalization, brain parenchymal changes, and motor deficits. METHODS: Thrombosis of the SSS was induced by topical application of ferric chloride. Occlusion was confirmed by magnetic resonance angiography (MRA). Six hours after operation, single treatment with 10 mg recombinant tissue plasminogen activator (rtPA)/kg and 6 mg abciximab/kg or subcutaneous injection of 450 IU/kg enoxaparin twice daily was started, each group containing 10 rats. Follow-up MRI with T2- and diffusion-weighted images was performed on the first, second, and seventh postoperative day. RESULTS: Control and enoxaparin-treated animals developed diffuse brain edema without infarction or intracerebral bleeding. This was indicated by an increase of T2 relaxation time and a decrease of the apparent diffusion coefficient in the parasagittal and lateral cortex. In these groups, the degree of recanalization after 7 days was comparable (48% versus 52%). Enoxaparin-treated animals showed significant amelioration of functional deficits. Clinical outcome was best in the abciximab-treated group, with a residual sinus occlusion of 36% after 1 week. Highest recanalization was achieved by lysis with rtPA (85%). CONCLUSIONS: Enoxaparin treatment in rats with cerebral venous thrombosis significantly influences clinical outcome. However, it has no effect on recanalization. GPIIb/IIIa antagonists and rtPA accelerate thrombolysis. They may represent an alternative in treatment of cerebral venous thrombosis.
OBJECTIVE: The causes of cerebral sinus and vein occlusion and the accompanying parenchymal changes remain largely unexplained. The clinical variability and low incidence of the disease complicate systematic clinical investigations. Animal studies are indispensable; however, existing animal models of sinus thrombosis do not allow for long-term follow-up studies and are not suitable for pharmacological recanalization because sinus thrombosis is induced by ligation and injection of thrombogenic substances and does not resemble sinus thrombosis in humans. METHODS: We induced thrombosis of the superior sagittal sinus (SSS) by careful topical application of ferric chloride onto the SSS of rats, leading to highly reproducible occlusions. Magnetic resonance imaging was performed immediately after initiation of thrombosis and on postoperative Days 1, 2, and 7. Diffusion- and T2-weighted images allowed for calculation of the apparent diffusion coefficient and T2 relaxation time. Vascular status was assessed by venous magnetic resonance angiography. Neurological deficits were assessed with the rotarod test. RESULTS: Seven days after induction of thrombosis, partial recanalization (50.7% of the SSS remaining occluded) was accompanied by a resolution of early generalized changes of the apparent diffusion coefficient and of T2 relaxation time, indicating edema of the entire brain parenchyma. Compared with sham-treated animals, clinical skills in the experimental group improved over time, which was statistically independent from the degree of recanalization. Histopathological analysis revealed no signs of cerebral infarction. CONCLUSION: This is the first animal model of SSS thrombosis that offers the possibility to investigate pathophysiological aspects of the disease as well as the influence of therapy on the nature of disease progression.
BACKGROUND AND PURPOSE: Investigating focal cerebral ischemia requires animal models that are relevant to human stroke. Complications and side effects are common among these models. The present study describes potential pitfalls in 3 techniques for middle cerebral artery occlusion (MCAO) in rats using magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA). METHODS: Rats were subjected to temporary MCAO for 90 minutes using the suture technique (group I; n=10) or to permanent MCAO using the suture technique (group II; n=10) or the macrosphere technique (group III; n=10). Clinical evaluation was performed after 3 hours and 24 hours. After 24 hours, animals underwent MRI and MRA to determine lesion size and the intracranial vascular status. RESULTS: Hemispheric lesion volume was significantly smaller in group I (14.6%) compared with groups II (35.2%; P<0.01) and III (21.3%; P<0.05). Two animals (1 each in group II and III) did not demonstrate neurological deficits and had no lesion on MRI and a patent MCA main stem on MRA. Subarachnoid hemorrhage was detected in 2 animals (1 each in group I and II). MRA indicated a patent MCA main stem in 2 animals (group II), although both rats displayed neurological deficits. Hypothalamic infarction with subsequent pathological hyperthermia was detected in all animals in group II and in 1 rat in group III. CONCLUSIONS: Model failures occurred frequently in all groups. MRI and MRA helps to identify animals that need to be excluded from experimental stroke studies.
BACKGROUND AND PURPOSE: Cardiac surgery carries a high risk of neurological complications; therefore, these patients would be an appropriate target population for neuroprotective strategies. In this study, we evaluated postoperative diffusion-weighted imaging (DWI) as a potential surrogate marker for brain embolism and its relationship to neurobiochemical markers of brain injury. METHODS: Of a total of 45 consecutive patients undergoing aortic valve replacement, 37 completed preoperative and postoperative MRI. At the time of the MRI studies, serum S100beta and neuron-specific enolase concentrations were determined. Preexisting T2 and postoperative DWI lesion volumes were quantified. All patients had a blinded neurological examination before and after operation. RESULTS: New perioperative DWI lesions were present in 14 patients (38%), of whom only 3 developed focal neurological deficits. Eighteen small lesions were found in the white matter or vascular border zones in all but 2 patients with territorial stroke. The appearance of new DWI lesions correlated with age, pre-existing T2 lesion volume, and postoperative S100beta concentrations on days 2 to 4 after surgery. In a forward stepwise canonical discrimination model, only T2 lesion volume was selected as a relevant variable. CONCLUSIONS: The incidence of postoperative DWI lesions in aortic valve replacement is high, and a suitable marker for neuroprotective trials would be a reduction in the number of such lesions. The volume of preexisting T2 lesions is related to the development of perioperative DWI lesions.
Arteriogenesis has been associated with the presence of monocytes/macrophages within the collateral vessel wall. Induced macrophage migration in vivo is driven by the binding of monocyte chemoattractant protein-1 (MCP-1, or CCL2 in the new nomenclature) to the CCR2-chemokine receptor on macrophages. To determine whether the CCL2-CCR2 signaling pathway is involved in the accumulation of macrophages in growing collateral vessels, we used mice that are deficient in CCR2 in a model of experimental arterial occlusion and collateral vessel growth. In an in vitro CCL2-driven chemotaxis assay, mononuclear cells isolated from wild-type BALB/c mice exhibited CCL2 concentration-dependent migration, whereas this migration was abolished in cells from CCR2(-/-) mice on a BALB/c genetic background. In vivo, blood flow recovery as measured by laser Doppler (LDI) and MRI (MRI) was impaired in CCR2(-/-) mice on either the BALB/c or C57BL/6 genetic backgrounds. Three weeks after femoral artery ligation, LDI perfusion ratio of operated versus nonoperated distal hindlimb in BALB/c wild-type mice increased to 0.45+/-0.06 and in CCR2(-/-) animals only to 0.21+/-0.03 (P<0.01). In C57BL/6 mice, ratio increased to 0.96+/-0.09 and 0.85+/-0.08 (P<0.05), respectively. MRI at 3 weeks (0.76+/-0.06 versus 0.62+/-0.01; P<0.05) and hemoglobin oxygen saturation measurements confirmed these findings. Active foot movement score significantly decreased and gastrocnemius muscle atrophy was significantly greater in CCR2(-/-) mice. Morphometric analysis showed a lesser increase in collateral vessel diameters in CCR2(-/-) mice. Importantly, the number of invaded monocytes/macrophages in the perivascular space of collateral arteries of CCR2(-/-) animals was dramatically reduced in comparison to wild-type mice. In conclusion, our results demonstrate that the CCR2 signaling pathway is essential for efficient collateral artery growth.
PURPOSE: To evaluate the feasibility of using time-of-flight (TOF) imaging to directly measure hindlimb blood flow in a mouse model of peripheral vascular disease. MATERIALS AND METHODS: Four tubes were imaged simultaneously (diameters = 0.39 mm, 0.59 mm, and two at 1.46 mm) with a 1.0 mM copper sulfate solution for 19 flow velocities. In vivo measurements were performed in the hindlimbs of three mouse strains-C57BL/6 (N = 5), BALB/c (N = 5), and 129S2/Sv (N = 5)-three weeks after femoral artery ligation with a calibration standard. RESULTS: The flow phantom showed that the intensity was linear (r2 = 0.92) over the pertinent blood flow velocities in the mouse hindlimbs. Measurements of the blood flow in the distal hindlimbs in different strains of mice (combination of both the venous and arterial flows) were obtained 21 days after right-sided femoral artery occlusion. The results showed that under similar conditions of anesthesia and temperature, SV129 mice on the nonligated side had the highest flows (0.50 +/- 0.07 mL/minute), followed by C57BL/6 (0.28 +/- 0.04 mL/minute) and BALB/c (0.23 +/- 0.05 mL/minute), P < 0.02. The ligated side measurements (SV129, 0.31 +/- 0.05 mL/minute (P = 0.02); C57BL/6, 0.21 +/- 0.02 mL/minute (P = 0.13); and BALB/c, 0.12 +/- 0.02 mL/minute (P= 0.06)) showed a trend in BALB/c and C57BL/6 and significant differences in SV129 for incomplete recovery three weeks after surgery, compared to the nonligated side. CONCLUSION: Two-dimensional TOF imaging permits quantitative in vivo measurements of hindlimb blood flow in a mouse model of peripheral vascular disease without the need of contrast injection, offering advantages of serial imaging not limited by tissue penetration.
The in vivo detection of growing collateral vessels following arterial occlusion is difficult in small animals. We have addressed the feasibility of performing high resolution time-of-flight angiograms to monitor the growth of collateral vessels after femoral artery occlusion in mice. We will also present a low-pass quadrature birdcage coil construction with a sufficient signal-to-noise ratio to produce high resolution. After a 4-month recovery period a C57BL/6 mouse with a surgical occlusion of the right femoral artery was used to assess the image quality and time requirements to produce magnetic resonance angiograms sufficient to assess collateral artery development using a two-dimensional gradient echo sequence. At a resolution of 100 x 100 x 100 microm and a matrix size of 256 x 128 x 256 for a 2.56 cm isometric volume, three scans were performed with one, two and four repetitions resulting in signal-to-noise ratios for the femoral artery proximal to the ligation site of 58, 126 and 194, respectively. Five C57BL/6 mice were additionally measured 4 weeks after occlusion using two repetitions and the visual collateral vessels were assessed for number and location: 2.0 +/- 1.2 in quadriceps muscle, 0.6 +/- 0.5 in adductor (deep adductor vessel), 0.0 +/- 0.0 in adductor (surface adductor vessels). The results showed a significant difference, two-sided t-test, p < 0.05, in number of vessels in all the locations. We have shown that this method can be utilized to elucidate the contribution of collateral vessels to arterial flow.
Magnetic resonance imaging (MRI) provides insights into the dynamics of focal cerebral ischemia. Usually, experimental stroke is induced outside the magnet bore, preventing investigators from acquiring pre-ischemic images for later pixel-by-pixel comparisons and from studying the earliest changes in the hyperacute phase of ischemia. Herein, we introduce a new and easy to apply in-bore occlusion protocol based on the intraarterial embolization of ceramic macrospheres. PE-50 tubing, filled with saline and six macrospheres (0.315-0.355 mm in diameter), was placed into the internal carotid artery (ICA) of anesthetized Sprague-Dawley rats. The animals were transferred into an MRI scanner (7.0 T) and baseline diffusion-weighted imaging (DWI) and T2-imaging was performed. Then the macrospheres were injected into the internal artery to occlude the MCA. Post-ischemic DWI and T2-imaging was started immediately thereafter. The apparent diffusion coefficient (ADC) (a marker for cytotoxic brain edema) and T2-relaxation time (a marker for vasogenic brain edema) were determined in the ischemic lesions and compared to the unaffected hemisphere. ADC significantly declined within the first 5-10 min after stroke onset. T2-relaxation time increased as early as at the first T2-imaging time-point (20-35 min after embolization). After 150 min of ischemia, the lesions covered 18.0 +/- 7.4% of the hemispheres. The model failed in one out of nine animals (11%). This model allows MR-imaging from the initial minutes after permanent middle cerebral artery (MCA) occlusion. It does not permit reperfusion. This technique might provide information about the pathophysiological processes in the hyperacute phase of stroke.
STUDY OBJECTIVES: The functional impact of pulmonary vein (PV) stenosis on pulmonary perfusion after radiofrequency ablation (RFA) for atrial fibrillation (AF) has not been systematically evaluated previously. Therefore, we correlated magnetic resonance (MR) pulmonary perfusion imaging with single-photon emission CT (SPECT) perfusion and with the degree of PV stenosis (PVS) apparent on MR angiography (MRA) after RF ablation. SETTING: Joint radiology-cardiology collaborative magnetic resonance unit at the Kerckhoff Heart Center. DESIGN AND PATIENTS: This was a cohort study of 110 patients who were routinely examined by MRA after RFA for AF, whereby 51 patients with a PV diameter reduction of > 25% or with clinical symptoms (ie, dyspnea and cough) were enrolled into the study. Patients were examined at follow-up by MR perfusion imaging and MRA, and the results were compared to those from patients who underwent SPECT scanning and from a control group of 26 untreated patients. Twelve patients underwent PVS dilatation as well as 22 sequential follow-up examinations. METHODS: Pulmonary perfusion was evaluated using a dynamic contrast-enhanced three-dimensional MR perfusion sequence (1.5 T, 2.5-s temporal resolution, and 0.05 cm spatial resolution), and high-resolution, contrast-enhanced MRA was performed to measure PV diameter. PV dilatation was performed using an angioplasty catheter that was 8 to 10 mm in diameter. RESULTS: The localization and extent of perfusion defects measured by MRI or SPECT scanning were precisely matched. MR perfusion imaging detected 20 of 21 perfusion defects (sensitivity, 95.2%; specificity, 100%). PVSs and perfusion deficits correlated closely and showed the following threshold: perfusion decreased substantially in PVs 6 mm in diameter. After PVS dilatation, perfusion was restored partially after weeks, and complete normalization was seen in 4 of 12 patients (33%). CONCLUSIONS: PVSs caused severe perfusion deficits, which were reliably demonstrated by MR perfusion imaging. Clinical symptoms correlated better with MR perfusion than they did with MRA. The combination with MRA to assess underlying PVS allowed a "one-stop-shopping" MRI procedure to be carried out. The results led to alterations of RFA techniques, and therefore MRA and MR perfusion imaging may be beneficial in patient follow-up and in evaluating new ablation techniques.
The feasibility and diagnostic value of real-time magnetic resonance imaging (RT-MRI) for the diagnosis of acute pulmonary embolism (PE) was evaluated by comparing RT-MRI and magnetic resonance angiography (MRA). In 39 consecutive patients with suspected PE real-time true fast imaging with steady-state precession (TrueFisp) was prospectively compared with contrast-enhanced MRA on a 1.5-T MR scanner. The TrueFisp sequence used allowed acquisition of T2-weighted images at 0.4 s per image so that the pulmonary vasculature could be visualized in three orientations in <3 min without the need for breath holding or contrast media application. Results of additional scintigraphic pulmonary perfusion examinations were available from 17 patients. All 39 primary RT examinations (100%) and 30 of 39 MRA examinations (77%) were of diagnostic quality. The reasons underlying failure to achieve diagnostic quality for MRA were breathing artifacts among dyspneic patients in all 9 cases. Compared with MRA, the sensitivities and specificities of RT sequences for PE were 93 and 100% (per examination), 96 and 100% (lobar artery PE), and 97 and 100% (segmental artery PE), respectively. Compared with scintigraphy, the sensitivity and specificity of RT-MRI were 83 and 100%, respectively. The MRA reached 100% sensitivity and specificity in this subgroup. The RT-MRI proved to be very robust and undisturbed by respiratory movements and patient cooperation. Its image quality assured fast diagnostic examinations, and its sensitivity and specificity, compared with MRA and scintigraphy, were sufficient to allow the diagnosis of acute central, lobar, and segmental PE; therefore, the emergency diagnosis of PE using RT-MRI is feasible and reliable.
OBJECTIVES: The purpose of the present study was to evaluate whether magnetic resonance (MR) planimetry of the aortic valve area (AVA) may prove to be a reliable, non-invasive diagnostic tool in the assessment of aortic valve stenosis, and how the results compare with current diagnostic standards. BACKGROUND: Current standard techniques for assessing the severity of aortic stenosis include transthoracic and transesophageal echocardiography (TEE) as well as transvalvular pressure measurements during cardiac catheterization. METHODS: Forty consecutive patients underwent cardiac catheterization, TEE, and MR. The AVA was estimated by direct planimetry (MR, TEE) or calculated indirectly via the peak systolic transvalvular gradient (catheter). Pressure gradients from cardiac catheterization and Doppler echocardiography were also compared. RESULTS: By MR, the mean AVA(max) was 0.91 +/- 0.25 cm(2); by TEE, AVA(max) was 0.89 +/- 0.28 cm(2); and by catheter, the AVA was calculated as 0.64 +/- 0.26 cm(2). Mean absolute differences in AVA were 0.02 cm(2) for MR versus TEE, 0.27 cm(2) for MR versus catheter, and 0.25 cm(2) for TEE versus catheter. Correlations for AVA(max) were r = 0.96 between MR and TEE, r = 0.47 between TEE and catheter, and r = 0.44 between MR and catheter. The correlation between Doppler and catheter gradients was r = 0.71. CONCLUSIONS: Magnetic resonance planimetry of the AVA correlates well with TEE and less well with the catheter-derived AVA. Invasive and Doppler pressure correlated less well than those obtained from planimetric techniques. Magnetic resonance planimetry of the AVA may provide an accurate, non-invasive, well-tolerated alternative to invasive techniques and transthoracic echocardiography in the assessment of aortic stenosis.
BACKGROUND: Radiofrequency catheter ablation (RFCA) is a promising intervention to treat atrial fibrillation. However, pulmonary vein (PV) stenosis after RFCA has been reported. The aim of this study was to investigate the incidence and time course of pulmonary vein stenosis after RFCA within a period of 3 months. Contrast-enhanced magnetic resonance angiography (MRA) was used to visualize pulmonary veins and was compared with radiographic angiography. METHODS AND RESULTS: Forty-six consecutive patients with symptomatic paroxysmal atrial fibrillation had RFCA in the orifice of 138 pulmonary veins. Comparison of diameters measured in 44 untreated vessels either by radiographic angiography or with MRA established the reliability of MRA (r=0.934). MRA measurements revealed an incidence of relevant diameter reductions of > or =25% or stenosis of > or =50% after RFCA of 25 of 138 (18.1%) treated vessels 1 day and/or 3 months after ablation. A progression of diameter reduction after RFCA was observed in 8.3% (maximum 75%), whereas a regression was observed in 6.3% of treated PVs. Ablation at a radial angle of >180 degrees of a pulmonary vein orifice increased the risk of diameter reduction significantly compared with ablation at a radial angle < or =180 degrees (P=0.002). CONCLUSIONS: The occurrence and progression of PV stenosis is a potential significant complication of RFCA in the orifice of pulmonary veins. These findings may have an impact on the technical performance of this intervention. In addition, long-term studies will be necessary to evaluate lumen reduction over time. MRA is a noninvasive, reproducible imaging modality for this purpose.