60 research outputs found

    Pulmonary intravascular blood volume changes through the cardiac cycle in healthy volunteers studied by cardiovascular magnetic resonance measurements of arterial and venous flow

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    BACKGROUND: This study aims to present a novel method for using cardiovascular magnetic resonance (CMR) to non-invasively quantify the variation in pulmonary blood volume throughout the cardiac cycle in humans. METHODS: 10 healthy volunteers (7 males, 3 female, age range 21-32 years) were studied. The blood flow in the pulmonary artery and all pulmonary veins was quantified during free breathing using phase contrast velocity encoded CMR. The difference in flow between the pulmonary artery and the pulmonary veins was integrated to calculate the change in pulmonary blood volume throughout the cardiac cycle. RESULTS: The stroke volumes in the pulmonary artery and the sum of the pulmonary veins were (mean +/- SEM) 103 +/- 6 ml and 95 +/- 6 ml, respectively. The pulmonary blood volume variation (PBVV) was 48 +/- 5 ml, and the PBVV expressed as percent of the pulmonary artery stroke volume was 46 +/- 3%. The maximum increase in pulmonary blood volume occurred 310 +/- 12 ms after the R-wave from the ECG (32 +/- 2% of the cardiac cycle). PBVV did not correlate to change in cross-sectional area in the pulmonary artery (R2 = 0.03, p = 0.66). CONCLUSION: It is feasible to non-invasively quantify the change in pulmonary blood volume during the cardiac cycle in humans using CMR. The average pulmonary blood volume variation in healthy volunteers was approximately 50 ml and this was approximately 50% of the stroke volume. Further studies are needed to assess the utility of the pulmonary blood volume variation as a measure for identifying cardiac and pulmonary vascular disease

    Quantification of left and right atrial kinetic energy using four-dimensional intracardiac magnetic resonance imaging flow measurements

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    Kinetic energy (KE) of atrial blood has been postulated as a possible contributor to ventricular filling. Therefore, we aimed to quantify the left and right atrial blood KE using cardiac magnetic resonance (CMR). Fifteen healthy volunteers underwent CMR at 3T, including a four-dimensional phase contrast flow sequence. Mean left atrial (LA) KE was lower than right atrial (RA) KE (1.1±0.1 mJ vs 1.7±0.1 mJ, P<0.01). Three KE peaks were seen in both atria; one in ventricular systole, one during early ventricular diastole, and one during atrial contraction. The systolic LA peak was significantly smaller than the RA peak (P<0.001), and the early diastolic LA peak was larger than the RA peak (P<0.05). Rotational flow contained 46 ± 7% of total KE, and conserved energy better than non-rotational flow did. The KE increase in early diastole was higher in the LA (P<0.001). Systolic KE correlated with the combination of atrial volume and systolic velocity of the atrioventricular plane displacement (R2=0.57 for LA and R2=0.64 for RA). Early diastolic KE of the LA correlated with LV mass (R2=0.28), however no such correlation was found in the right heart. This suggests that LA KE increases during early ventricular diastole due to LV elastic recoil, indicating that LV filling is dependent on diastolic suction. RV relaxation does not seem to contribute to atrial KE. Instead, atrial KE generated during ventricular systole may be conserved in a hydraulic "flywheel" and transferred to the RV through helical flow, which may contribute to RV filling

    Myocardium at risk by magnetic resonance imaging: head-to-head comparison of T2-weighted imaging and early gadolinium enhanced steady state free precession

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    AIMS: To determine the myocardial salvage index, the extent of infarction needs to be related to the myocardium at risk (MaR). Thus, the ability to assess both infarct size and MaR is of central clinical and scientific importance. The aim of the present study was to explore the relationship between T2-weighted cardiac magnetic resonance (CMR) and contrast-enhanced steady-state free precession (CE-SSFP) CMR for the determination of MaR in patients with acute myocardial infarction. METHODS AND RESULTS: Twenty-one prospectively included patients with first-time ST-elevation myocardial infarction underwent CMR 1 week after primary percutaneous coronary intervention. For the assessment of MaR, T2-weighted images were acquired before and CE-SSFP images were acquired after the injection of a gadolinium-based contrast agent. For the assessment of infarct size, late gadolinium enhancement images were acquired. The MaR by T2-weighted imaging and CE-SSFP was 29 ± 11 and 32 ± 12% of the left ventricle, respectively. Thus, the MaR with T2-weighted imaging was slightly smaller than that by CE-SSFP (-3.0 ± 4.0%; P < 0.01). There was a significant correlation between the two MaR measures (r(2)= 0.89, P < 0.01), independent of the time after contrast agent administration at which the CE-SSFP was commenced (2-8 min). CONCLUSION: There is a good agreement between the MaR assessed by T2-weighted imaging and that assessed by CE-SSFP in patients with reperfused acute myocardial infarction 1 week after the acute event. Thus, both methods can be used to determine MaR and myocardial salvage at this point in time
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