Gadolinium-enhanced three-dimensional magnetic resonance angiography of pulmonary and systemic venous anomalies.

OBJECTIVE: The goal of this study was to evaluate the diagnostic value of gadolinium (Gd)-enhanced three-dimensional (3D) magnetic resonance angiography (MRA) in patients with congenital and acquired anomalies of the pulmonary and systemic veins. BACKGROUND: Gadolinium-enhanced 3D MRA is a fast magnetic resonance imaging technique that has shown great promise in the evaluation of large and medium-sized arteries. However, its application to venous anomalies has not been studied in detail. METHODS: The study retrospectively analyzed all patients who underwent Gd-enhanced 3D MRA examination from January 1998 through January 2001, were diagnosed with anomalies of the pulmonary or systemic veins and had additional diagnostic data available for comparison with the MRA findings. RESULTS: Sixty-one patients (age 1 day to 60 years) were included. Image acquisition was completed in 29 +/- 6.9 s. Pulmonary venous anomalies were found in 37 patients, systemic venous anomalies in 17 patients and both pulmonary and systemic venous anomalies in 7 patients. Compared with available diagnostic information by other modalities, all known or suspected venous anomalies were imaged by 3D MRA. In three patients, catheterization did not detect anomalies of the pulmonary veins that were subsequently diagnosed by MRA. The 3D MRA diagnoses were followed by 10 interventional catheterization procedures and 15 operations. In 74% of patients, 3D MRA either diagnosed previously unsuspected venous anomalies (28%) or added new clinically important information (46%). The mechanism of pulmonary vein compression in eight patients was determined by MRA but not by other imaging modalities. Using a five-level grading system for MRA image quality (1 = nondiagnostic; 5 = excellent), the average grade was 4.6 +/- 0.6, with a 0.28 +/- 0.6 mean grade difference between two independent observers. CONCLUSIONS: Gadolinium-enhanced 3D MRA is capable of rapidly and accurately diagnosing a wide spectrum of pulmonary and systemic venous anomalies and is a useful noninvasive alternative to diagnostic catheterization.     

Exercising pulmonary blood flow in mitral stenosis with anomalous pulmonary venous connection.

Exercising pulmonary blood flow was estimated from indicator-dilution curves in a patient with the infrequent combination of rheumatic mitral stenosis and anomalous pulmonary venous connection from the left lung. During supine exercise against progressively increasing external workloads, the proportion of flow to each lung remained nearly constant. The pulmonary vascular resistance was highest in the left lung, which emptied into the low-pressure systemic vein. Although right and left atrial pressures differed markedly during supine exercise, the proportion of pulmonary blood flow shunted to the systemic venous sytem remained essentially unchanged.     

Alternate pathways of thyroid hormone metabolism.

The major thyroid hormone (TH) secreted by the thyroid gland is thyroxine (T(4)). Triiodothyronine (T(3)), formed chiefly by deiodination of T(4), is the active hormone at the nuclear receptor, and it is generally accepted that deiodination is the major pathway regulating T(3) bioavailability in mammalian tissues. The alternate pathways, sulfation and glucuronidation of the phenolic hydroxyl group of iodothyronines, the oxidative deamination and decarboxylation of the alanine side chain to form iodothyroacetic acids, and ether link cleavage provide additional mechanisms for regulating the supply of active hormone. Sulfation may play a general role in regulation of iodothyronine metabolism, since sulfation of T(4) and T(3) markedly accelerates deiodination to the inactive metabolites, reverse triiodothyronine (rT(3)) and T(2). Sulfoconjugation is prominent during intrauterine development, particularly in the precocial species in the last trimester including humans and sheep, where it may serve both to regulate the supply of T(3), via sulfation followed by deiodination, and to facilitate maternal-fetal exchange of sulfated iodothyronines (e.g., 3,3'-diiodothyronine sulfate [T(2)S]). The resulting low serum T(3) may be important for normal fetal development in the late gestation. The possibility that T(2)S or its derivative, transferred from the fetus and appearing in maternal serum or urine, can serve as a marker of fetal thyroid function is being studied. Glucuronidation of TH often precedes biliary-fecal excretion of hormone. In rats, stimulation of glucuronidation by various drugs and toxins may lead to lower T(4) and T(3) levels, provocation of thyrotropin (TSH) secretion, and goiter. In man, drug induced stimulation of glucuronidation is limited to T(4), and does not usually compromise normal thyroid function. However, in hypothyroid subjects, higher doses of TH may be required to maintain euthyroidism when these drugs are given. In addition, glucuronidates and sulfated iodothyronines can be hydrolyzed to their precursors in gastrointestinal tract and various tissues. Thus, these conjugates can serve as a reservoir for biologically active iodothyronines (e.g., T(4), T(3), or T(2)). The acetic acid derivatives of T(4), tetrac and triac, are minor products in normal thyroid physiology. However, triac has a different pattern of receptor affinity than T(3), binding preferentially to the beta receptor. This makes it useful in the treatment of the syndrome of resistance to thyroid hormone action, where the typical mutation affects only the beta receptor. Thus, adequate binding to certain mutated beta receptors can be achieved without excessive stimulation of alpha receptors, which predominate in the heart. Ether link cleavage of TH is also a minor pathway in normal subjects. However, this pathway may become important during infections, when augmented TH breakdown by ether-link cleavage (ELC) may assist in bactericidal activity. There is a recent claim that decarboxylated derivates of thyronines, that is, monoiodothyronamine (T(1)am) and thyronamine (T(0)am), may be biologically important and have actions different from those of TH. Further information on these interesting derivatives is awaited.     

Changes in pulmonary venous flow pattern during early neonatal life.

OBJECTIVE--To investigate serial changes in the pattern of flow in the pulmonary vein during the early neonatal period. METHODS--Pulsed Doppler echocardiography was used to measure flow in the right upper pulmonary vein in 26 normal newborn infants. Peak flow velocity during systole (S) and diastole (D) and flow velocity at indents between the systolic and diastolic fraction (O) and between the diastolic and systolic fraction (X) were measured 1, 4-8, 24, and 96 hours after birth. The heart rate and diameter of the ductus arteriosus were measured simultaneously. RESULTS--Continuous and phasic high flow velocity waveforms were seen 1 and 4-8 hours after birth. The mean (SD) peak flow velocities of X, S, O, and D an hour after birth were 35.2 (13.6) cm/s, 73.1 (23.1) cm/s, 58.5 (20.5) cm/s, and 81.5 (19.2) cm/s respectively. There were significant decreases in X, S, O, and D by 24 hours of age (p < 0.01 v 1 hour after birth) to 8.1 (10.3) cm/s, 52.8 (18.0) cm/s, 38.6 (14.5) cm/s, and 54.4 (11.2) cm/s respectively. These results indicate intermittent flow in the pulmonary vein, with flow stopping between diastole and systole. These flow velocities, X, S, O, and D, correlated well with the diameter of the ductus arteriosus (r = 0.80 v X, r = 0.62 v S, r = 0.63 v O, r = 0.75 v D). CONCLUSION--This serial study showed changes in normal pulmonary vein flow patterns during the early neonatal period. The continuous and high flow velocity waveform that was seen immediately after birth resembled the pattern of pulmonary vein flow seen in congenital pulmonary stenosis and in cases of acute volume overload. This waveform may reflect a sudden increase in pulmonary circulatory volume with additional left to right shunting through the ductus arteriosus in relatively hypoplastic pulmonary veins.     

The pulmonary venous systolic flow pulse--its origin and relationship to left atrial pressure.

OBJECTIVES: The purpose of this study was to determine the origin of the pulmonary venous systolic flow pulse using wave-intensity analysis to separate forward- and backward-going waves. BACKGROUND: The mechanism of the pulmonary venous systolic flow pulse is unclear and could be a "suction effect" due to a fall in atrial pressure (backward-going wave) or a "pushing effect" due to forward-propagation of right ventricular (RV) pressure (forward-going wave). METHODS: In eight patients during coronary surgery, pulmonary venous flow (flow probe), velocity (microsensor) and pressure (micromanometer) were recorded. We calculated wave intensity (dP x dU) as change in pulmonary venous pressure (dP) times change in velocity (dU) at 5 ms intervals. When dP x dU > 0 there is a net forward-going wave and when dP x dU < 0 there is a net backward-going wave. RESULTS: Systolic pulmonary venous flow was biphasic. When flow accelerated in early systole (S1), pulmonary venous pressure was falling, and, therefore, dP x dU was negative, -0.6 +/- 0.2 (x +/- SE) W/m2, indicating a net backward-going wave. When flow accelerated in late systole (S2), pressure was rising, and, therefore, dP x dU was positive, 0.3 +/- 0.1 W/m2, indicating a net forward-going wave. CONCLUSIONS: Pulmonary venous flow acceleration in S1 was attributed to a net backward-going wave secondary to a fall in atrial pressure. However, flow acceleration in S2 was attributed to a net forward-going wave, consistent with propagation of the RV systolic pressure pulse across the lungs. Pulmonary vein systolic flow pattern, therefore, appears to be determined by right- as well as left-sided cardiac events.     

Endothelial interactions of neutrophils under flow in chronic obstructive pulmonary disease.

It is generally accepted that the neutrophil is central to the pathogenesis of chronic obstructive pulmonary disease (COPD). Enhanced endothelial interactions of this cell may contribute to the susceptibility of smokers who develop the disease; however, these interactions have not previously been studied in COPD. The aim of the current study was to determine whether enhanced endothelial interactions of neutrophils from smokers are a predisposing factor for the development of COPD. Endothelial interactions under flow and adhesion molecule expression of peripheral blood neutrophils were compared between seven never-smokers (NS), seven healthy smokers (HS), 11 COPD patients with severe alpha1-antitrypsin deficiency (PiZ) and neutrophils from 11 COPD patients without the deficiency (PiM). Total adhesive and migratory responses (per mm2 endothelium per 10(6) neutrophils) were significantly greater in the PiM group (mean+/-se 704.2+/-57.9 versus 509.3+/-48.8 in the PiZ group, 499.3+/-40.1 in the HS and 491.2+/-33.7 in the NS). This corresponded with increased macrophage antigen-1 (CD11b) expression on stimulated neutrophils in the PiM group compared with the PiZ group (mean+/-se relative fluorescence intensity 1.4+/-0.1 versus 1.1+/-0.1). In conclusion, the enhanced endothelial interaction of neutrophils from smokers who have developed chronic obstructive pulmonary disease in the presence of normal levels of alpha1-antitrypsin deficiency, but not in those with severe alpha(1)-antitrypsin deficiency, suggests that this is a predisposing factor for the development of the disease, and upregulation of macrophage antigen-1 may be responsible.     

Prominent pulmonary venous flow mimicking mitral regurgitation

The present case highlights a potential pitfall in assessing mitral regurgitation severity due to the presence of similar colored prominent pulmonary vein signals in the left atrium during color Doppler examination.     

Abnormalities of pulmonary venous flow in patients with lone atrial fibrillation.

AIMS: Mechanisms underlying lone atrial fibrillation (LAF) are poorly defined. We sought to investigate indices of left atrial (LA) function in patients with recurrent LAF, in comparison with that in healthy subjects. METHODS AND RESULTS: Investigations were performed in 42 patients aged 51.8 +/- 8.7 at least 30 days after the last episode of LAF and in 38 healthy controls. Each subject underwent echocardiographic evaluation including left ventricular parameters and LA function indices. LA ejection fraction served as a measure of LA systolic performance, and acceleration (SAT) and deceleration time (SDT) of systolic phase of pulmonary venous flow (PVF) corresponded to LA relaxation and compliance, respectively. Patients with LAF showed significantly lower values of SAT (179.1 +/- 63.2 vs. 199.2 +/- 45.1 ms, P < 0.02) and higher values of SDT (250.8 +/- 81.6 vs. 211.7 +/- 57.3 ms, P < 0.01) when compared with controls. No significant differences were found with respect to other measured parameters. The combination of SAT < 185 ms and SDT > 239 ms showed a positive predictive value of 92% in the identification of patients prone to LAF. CONCLUSION: This study suggests that (i) patients with LAF have abnormalities of the systolic phase of PVF and (ii) Doppler estimation of PVF seems to be very valuable in the evaluation of patients with LAF.     

Abnormalities in jugular venous flow velocity in pulmonary hypertension

Doppler recordings of jugular venous flow velocity previously performed in this laboratory in patients with pulmonary hypertension had shown variations from the normal dominant systolic flow (SF) greater than diastolic flow (DF), to SF = DF, SF less than DF or DF alone. The mechanisms underlying these flow alterations were studied in 25 patients and correlated with hemodynamics. The patients with abnormal flow patterns had increased right atrial V-wave pressures. This was associated with an increased right ventricular early diastolic pressure. The incidence of clinical heart failure was higher in patients with SF less than DF or DF alone (8 of 11) compared with 5 of 10 patients with SF = DF. Thus, in patients with pulmonary hypertension, the abnormal jugular venous flow patterns appear to be caused by both an increased DF velocity and a decrease in SF velocity. Because the right atrial V-wave pressures were similar in patients with both SF = DF and SF less than DF or DF alone and the incidence of heart failure was higher in the latter, the decrease in SF must be a later phenomenon. Serial observations confirmed this temporal sequence. The applicability of these observations to bedside evaluation of patients with pulmonary hypertension is emphasized.     

Mechanism of pulmonary venous pressure and flow waves

Summary The pulmonary venous systolic flow wave has been attributed both to left heart phenomena, such as left atrial relaxation and descent of the mitral annulus, and to propagation of the pulmonary artery pressure pulse through the pulmonary bed from the right ventricle. In this study we hypothesized that all waves in the pulmonary veins originate in the left heart, and that the gross wave features observed in measurements can be explained simply by wave propagation and reflection. A mathematical model of the pulmonary vein was developed; the pulmonary vein was modeled as a lossless transmission line and the pulmonary bed by a three-element lumped parameter model accounting for viscous losses, compliance, and inertia. We assumed that all pulsations originate in the left atrium (LA), the pressure in the pulmonary bed being constant. The model was validated using pulmonary vein pressure and flow recorded 1 cm proximal to the junction of the vein with the left atrium during aortocoronary bypass surgery. For a pressure drop of 6 mmHg across the pulmonary bed, we found a transit time from the left atrium to the pulmonary bed ofτ ≈ 150ms, a compliance of the pulmonary bed ofC ≈ 0.4ml/mmHg, and an inertance of the pulmonary bed of 1.1mmHgs²/ml. The pulse wave velocity of the pulmonary vein was estimated to bec ≈ 1 m/s. Waves, however, travel both towards the left atrium and towards the pulmonary bed. Waves traveling towards the left atrium are attributed to the reflections caused by the mismatch of impedance of line (pulmonary vein) and load (pulmonary bed). Wave intensity analysis was used to identify a period in systole of net wave propagation towards the left atrium for both measurements and model. The linear separation technique was used to split the pressure into one component traveling from the left atrium to the pulmonary bed and a reflected component propagating from the pulmonary bed to the left atrium. The peak of the reflected pressure wave corresponded well with the positive peak in wave intensity in systole. We conclude that the gross features of the pressure and flow waves in the pulmonary vein can be explained in the following manner: the waves originate in the LA and travel towards the pulmonary bed, where reflections give rise to waves traveling back to the LA. Although the gross features of the measured pressure were captured well by the model predicted pressure, there was still some discrepancy between the two. Thus, other factors initiating or influencing waves traveling towards the LA cannot be excluded.