Systemic-to-pulmonary Collateral Flow Research Articles

Reduced scan time and superior image quality with 3D flow MRI compared to 4D flow MRI for hemodynamic evaluation of the Fontan pathway

Long scan times prohibit a widespread clinical applicability of 4D flow MRI in Fontan patients. As pulsatility in the Fontan pathway is minimal during the cardiac cycle, acquiring non-ECG gated 3D flow MRI may result in a reduction of scan time while accurately obtaining time-averaged clinical parameters in comparison with 2D and 4D flow MRI. Thirty-two Fontan patients prospectively underwent 2D (reference), 3D and 4D flow MRI of the Fontan pathway. Multiple clinical parameters were assessed from time-averaged flow rates, including the right-to-left pulmonary flow distribution (main endpoint) and systemic-to-pulmonary collateral flow (SPCF). A ten-fold reduction in scan time was achieved [4D flow 15.9 min (SD 2.7 min) and 3D flow 1.6 min (SD 7.8 s), p < 0.001] with a superior signal-to-noise ratio [mean ratio of SNRs 1.7 (0.8), p < 0.001] and vessel sharpness [mean ratio 1.2 (0.4), p = 0.01] with 3D flow. Compared to 2D flow, good–excellent agreement was shown for mean flow rates (ICC 0.82–0.96) and right-to-left pulmonary flow distribution (ICC 0.97). SPCF derived from 3D flow showed good agreement with that from 4D flow (ICC 0.86). 3D flow MRI allows for obtaining time-averaged flow rates and derived clinical parameters in the Fontan pathway with good–excellent agreement with 2D and 4D flow, but with a tenfold reduction in scan time and significantly improved image quality compared to 4D flow.

Systemic-to-Pulmonary Collateral Flow Correlates with Clinical Condition Late After the Fontan Procedure.

In the Fontan circulation, there is a substantial degree of systemic-to-pulmonary collateral flow (SPCF), which can be measured by cardiac magnetic resonance (CMR). However, the correlation between the degree of SPCF and long-term outcomes is not fully understood. We retrospectively studied 321 patients who underwent the Fontan procedure and CMR at a single center. Using CMR, we calculated SPCF as pulmonary blood flow - systemic blood flow. %SPCF was defined as SPCF ÷ pulmonary blood flow. The mean age of patients at CMR was 14.3 ± 7.5years. The average %SPCF was 13.0% ± 11.0%. With a multivariate analysis, %SPCF was significantly correlated with time (i.e., the longer the time period since the Fontan procedure, the lower the %SPCF) (p = 0.006), previous total anomalous pulmonary vein drainage (p = 0.007), a low pulmonary artery index (Nakata index) before the Fontan procedure (p = 0.04), and older age at the time of the Fontan procedure (p = 0.002). Regarding the findings after the Fontan procedure, %SPCF was significantly correlated with ventricular end-diastolic volume (p < 0.001), ventricular end-systolic volume (p < 0.001), central venous pressure (p < 0.001), plasma brain natriuretic peptide concentration (p < 0.001), hemoptysis (p = 0.009), and poor New York Heart Association functional class (p = 0.007). SPCF was correlated with clinical condition after the Fontan procedure. The importance of sufficient growth of the pulmonary vascular bed should be emphasized because the development of SPCF is believed to result from the poor condition of the pulmonary circulation.

The Impact of Systemic-to-Pulmonary Collateral Flow (SPCF) in Patients after Bidirectional Cavopulmonary Connection (BCPC) or Fontan Operation Assessed with 4D Flow MRI

The Impact of Systemic-to-Pulmonary Collateral Flow (SPCF) in Patients after Bidirectional Cavopulmonary Connection (BCPC) or Fontan Operation Assessed with 4D Flow MRI

Favorable Effects of Oxygen Inhalation in Patients After Bidirectional Glenn Procedure as Assessed by Cardiovascular Magnetic Resonance Flow Measurement.

Home oxygen therapy (HOT) is used to adapt patients to the bidirectional Glenn (BDG) physiology. However, the precise cardiovascular effect of oxygen inhalation is still unknown. We used phase-contrast MRI to evaluate the cardiovascular effects of oxygen inhalation in young patients with BDG physiology. The 56 sessions of cardiac MRI were performed in 36 patients with BDG circulation. Oxygen saturation (SpO2) and heart rate (HR) were monitored under both room air and nasal 100% oxygen inhalation, and the blood flow volumes of the ascending aorta (AA), superior vena cava (SVC), and inferior vena cava (IVC) were measured by phase-contrast MRI. Systemic-to-pulmonary collateral flow (SPCF) volumes were calculated by subtracting the sum of flow volumes through the SVC and IVC from the flow volume through the AA, and used for further comparative examination. Under nasal oxygen inhalation, SpO2significantly increased from 82% to 89%, while HR decreased from 115 to 110 beats/min. AA (5.0 vs. 4.9 L·min(-1)·m(-2)), SVC (1.85 vs. 1.77 L·min(-1)·m(-2)), and systemic blood flow volume (=SVC+IVC) significantly decreased (3.60 vs. 3.46 L·min(-1)·m(-2)). In contrast, SPCF and the pulmonary-to-systemic blood flow ratio (Qp/Qs) remained unchanged. Oxygen inhalation improved arterial blood oxygenation and lowered HR in patients with BDG circulation without an increase in Qp/Qs. HOT would be protective of the cardiovascular system in patients with BDG circulation. (Circ J 2016; 80: 1378-1385).

Effect of Inhaled Nitric Oxide on Blood Flow Dynamics in Patients After the Fontan Procedure Using Cardiovascular Magnetic Resonance Flow Measurements.

Invasive hemodynamic studies have shown that nitric oxide (NO), a selective pulmonary vasodilator, can lower pulmonary vascular resistance in Fontan patients. Because oximetry-derived flow quantification may be unreliable, we sought to detect changes in blood flow within the Fontan circulation after inhalation of NO using cardiovascular magnetic resonance (CMR). Thirty-three patients (mean age 12.8 ± 7.0 years) after the Fontan procedure underwent CMR as part of their routine clinical assessment. Standard two-dimensional blood flow measurements were performed in the Fontan tunnel, superior vena cava (SVC) and ascending aorta (AAO) before and after inhalation of 40 ppm NO for 8-10 min. Systemic-to-pulmonary collateral (SPC) flow was calculated as AAO - (SVC + tunnel). Heart rate (82 ± 18 to 81 ± 18 bpm; p = 0.31) and transcutaneous oxygen saturations (93 ± 4 to 94 ± 3 %; p = 0.13) did not change under NO inhalation. AAO flow (3.23 ± 0.72 to 3.12 ± 0.79 l/min/m(2); p = 0.08) decreased, tunnel flow (1.58 ± 0.40 to 1.65 ± 0.46 l/min/m(2); p = 0.032) increased, and SVC flow (1.01 ± 0.39 to 1.02 ± 0.40 l/min/m(2); p = 0.50) remained unchanged resulting in higher total caval flow (Qs) (2.59 ± 0.58 to 2.67 ± 0.68 l/min/m(2); p = 0.038). SPC flow decreased significantly from 0.64 ± 0.52 to 0.45 ± 0.51 l/min/m(2) (p = 0.002) and resulted in a significant decrement of the Qp/Qs ratio (1.23 ± 0.23 to 1.15 ± 0.23; p = 0.001). Inhalation of NO in Fontan patients results in significant changes in pulmonary and systemic blood flow. The reduction in SPC flow is accompanied by a net increase in effective systemic blood flow suggesting beneficial effects of pulmonary vasodilators on cardiac output, tissue perfusion and exercise capacity.

Quantification of Systemic-to-Pulmonary Artery Collateral Flow

Abnormal vascular connections between systemic arteries and the pulmonary vascular bed—systemic-to-pulmonary collateral (SPC) vessels—manifest in patients with a variety of congenital and acquired heart disease. These vessels, which originate from branches off the brachiocephalic arteries, chest wall arteries, and the descending aorta, vary markedly in size, number, course, and distribution. Although the precise mechanisms that lead to development of SPCs are incompletely understood, hypoxemia, diminished global or regional pulmonary blood flow, and nonpulsatile flow in the pulmonary arteries are some of the commonly cited contributors.1 Indeed, SPCs are frequently encountered in patients with cardiac anomalies that include ≥1 of these abnormalities such as severe forms of tetralogy of Fallot and functional single ventricle (FSV). In the latter group, the clinical importance of SPCs and their optimal management have been topics of intense debate for >2 decades.2–6 Article see p 218 The physiology of SPC flow involves both beneficial and deleterious effects.1,2 SPCs can augment blood flow to hypoperfused lung segments, improve gas exchange, and potentially inhibit the development of pulmonary arteriovenous malformations in patients in whom hepatic venous flow does not reach the pulmonary circulation. In contrast, like other shunts, SPC flow is inherently inefficient because relatively highly oxygenated blood returns to the pulmonary circulation and potentially competes with the more efficient antegrade flow to the lungs through the native pulmonary arteries. Consequently, SPC flow results in volume load on the FSV, which can lead to ventricular dilatation and dysfunction, atrioventricular valve regurgitation, and heart failure symptoms. Other deleterious effects of excessive SPCs include flow energy loss,7 exuberant blood flow returning through the pulmonary veins to the surgical field during cardiopulmonary bypass, respiratory distress, pulmonary hypertension, and hemoptysis.8 In patients with FSV, the hemodynamic burden from SPCs has been the topic …

Flow-sensitive four-dimensional magnetic resonance imaging facilitates the quantitative analysis of systemic-to-pulmonary collateral flow in patients with univentricular hearts

Background Systemic-to-pulmonary collateral flow (SPCF) may constitute a risk factor for increased morbidity and mortality in patients with single-ventricle physiology (SV). However, clinical research is limited by the complexity of multi-site two-dimensional (2D) cardiovascular magnetic resonance (CMR) flow assessment. We sought to validate four-dimensional flow (4D-flow) for concise quantification of SPCF in patients with SV. Methods 29 patients with SV physiology prospectively underwent CMR (1.5T) to quantify SPCF (n=14 bidirectional cavopulmonary connection [BCPC], age 2.9±1.3 years; and n=15 Fontan, 14.4±5.9 years) and 20 healthy volunteers (age, 28.7±13.1 years) served as controls. Five 2D-flow measurements (ascending aorta, superior/inferior caval veins, right/left pulmonary arteries) were performed and SPCF (=aortic minus caval flows) was calculated and compared with 4D-flow measurements and calculations. Additionally, 4D-flow measurements were used to calculate SPCF as pulmonary venous minus pulmonary arterial flow. Results The comparison between 4D-flow and 2D-flow showed good Bland-Altman agreement for all individual vessels (mean bias, 0.05±0.24 l/min/m2), calculated SPCF (-0.02 ±0.18 l/min/m2), low intra and inter-observer variance (ICC>0.95[0.91-0.97]) and significantly shorter 4D-flow acquisition-time (12:34min/17:28min,p<0.01). 4D-flow in patients versus controls revealed (1) good agreement between systemic versus pulmonary estimator for SPFC; (2) significant SPCF in patients (BCPC 0.79±0.45 l/min/ m2; Fontan 0.62±0.82 l/min/m2) and not in controls (0.01+0.16 l/min/m2) and (3) inverse relation of right/ left pulmonary artery perfusion and right/left SPCF (Pearson=-0.47,p=0.01). Conclusions

Correction

HomeCirculation: Cardiovascular ImagingVol. 3, No. 1Correction Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBCorrection Originally published1 Jan 2010https://doi.org/10.1161/HCI.0b013e3181cc5045Circulation: Cardiovascular Imaging. 2010;3:e1In the article by Whitehead et al., “Noninvasive Quantification of Systemic-to-Pulmonary Collateral Flow: A Major Source of Inefficiency in Patients With Superior Cavopulmonary Connections,” which appeared in the September 2009 issue of the Journal (Circulation: Cardiovascular Imaging 2009;2:405-411), the following correction must be made.During the copyediting of this article, the term SCPC (superior cavopulmonary connection) was incorrectly changed to SPCF (systemic-to-pulmonary collateral flow) throughout the article.Equation 1 was also incorrect and should read: equationDownload figureThis error has been corrected in the current online version of the article (http://circimaging.ahajournals.org/cgi/content/full/2/5/405). The publisher regrets the error. Previous Back to top Next FiguresReferencesRelatedDetails January 2010Vol 3, Issue 1 Advertisement Article InformationMetrics https://doi.org/10.1161/HCI.0b013e3181cc5045 Originally publishedJanuary 1, 2010 PDF download Advertisement

Noninvasive Quantification of Systemic-to-Pulmonary Collateral Flow

Background— Systemic-to-pulmonary collateral flow (SPCF) is common in single-ventricle patients with superior cavopulmonary connections (SCPC). Because no validated method to quantify SPCF exists, neither its hemodynamic burden nor its clinical impact can be systematically evaluated. We hypothesize that (1) the difference in total ascending aortic (Ao) and caval flow (superior vena cava [SVC]+inferior vena cava [IVC]) and (2) the difference between pulmonary vein and pulmonary artery flow (PV−PA) provide 2 independent estimators of SPCF. Methods and Results— We measured Ao, SVC, IVC, right (RPA) and left (LPA) PA, and left (LPV) and right (RPV) PV flows in 17 patients with SCPC during routine cardiac MRI studies using through-plane phase-contrast velocity mapping. Two independent measures of SPCF were obtained: model 1, Ao−(SVC+IVC); and model 2, (LPV−LPA)+(RPV−RPA). Values were normalized to body surface area, Ao, and PV, and comparisons were made using linear regression and Bland-Altman analysis. SPCF ranged from 0.2 to 1.4 L/min for model 1 and 0.2 to 1.6 L/min for model 2, for an average indexed SPCF of 0.5 to 2.8 L/min/m 2 : 11% to 53% (mean, 37%) of Ao and 19% to 77% (mean, 54%) of PV. The mean difference between model 1 and model 2 was 0.01 L/min ( P =0.40; 2-SD range, −0.45 to 0.47 L/min). Conclusions— We present a noninvasive method for SPCF quantification in patients with SCPC. It should provide an important clinical tool in treating these patients. Furthermore, we show that SPCF is a significant hemodynamic burden in many patients with bidirectional Glenn shunt physiology. Future investigations will allow objective study of the impact of collateral flow on outcome.