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Biomedical subjects

M Saeed

Publications and source records attributed to M Saeed.

At least 19 recordsLinked to original sources
PubMed1995

Effects of iopromide on vasoactive peptides and allergy-mediated substances in healthy volunteers.

RATIONALE AND OBJECTIVES: Little information is available about the direct action of angiographic contrast media on vasoactive peptides and allergy-mediated substances in humans. This study defined the acute effects of iopromide, a nonionic contrast medium (370 mg/mL iodine), on vasoactive peptides, allergy-mediated substances, and hemodynamic parameters in healthy volunteers. METHODS: Pulmonary digital subtraction angiography was performed in seven healthy volunteers with no cardiovascular or pulmonary disease. Iopromide was administered as a total volume of 100 mL through a 7-Fr catheter inserted in the right femoral vein. The injected volumes and duration of injection (15-20 mL/second) were kept constant. The following hemodynamic parameters were monitored continuously: results of electrocardiogram, heart rate, and phasic and mean pulmonary arterial and peripheral arterial pressures. Blood samples were obtained before and 3 to 5 minutes after injection of contrast media to determine the concentrations of the following vasoactive peptides: renin, angiotensin I-converting enzyme, angiotensin II, aldosterone, atrial natriuretic peptide, antidiuretic hormone, cyclic guanosine monophosphate, and myoglobin; and to allergy-mediated substances such as tryptase, eosinophil protein X, and eosinophil cationic protein, using radioimmunoassay techniques. RESULTS: Iopromide substantially increased atrial natriuretic peptide (48.8 +/- 8.9 to 85.8 +/- 13.0) and antidiuretic hormone (3.4 +/- 0.3 to 4.6 +/- 0.5) levels, whereas renin decreased (0.9 +/- 0.1 to 0.8 +/- 0.2) slightly but not significantly. Iopromide did not induce substantial changes in the other vasoactive peptides or in allergy-mediated substances after the contrast medium was injected. Similarly, cardiovascular parameters (heart rate, pulmonary and systemic blood pressures, and results of electrocardiogram) also remained unchanged after contrast injection. CONCLUSION: Iopromide caused no appreciable hemodynamic alterations associated with the changes in atrial natriuretic peptide and antidiuretic hormone and no evidence of allergy-mediated reactions in all volunteers.

Adult↗
PubMed1995

Coronary artery stenosis: detection with contrast-enhanced MR imaging in dogs.

PURPOSE: To monitor with fast gradient-echo magnetic resonance (MR) imaging the dynamics of gadolinium benzyloxypropionictetraacetate (gadobenate) dimeglumine on myocardial signal intensity in dogs with critical left circumflex coronary artery stenosis. MATERIALS AND METHODS: Fast gradient-echo MR images were acquired in a short axis of the left ventricle. Two bolus injections of 0.05 mmol/kg gadobenate dimeglumine were administered in the basal state after stenosis and after infusion of 0.5 mg/kg dipyridamole. RESULTS: In the basal state, there was an equivalent increase in signal intensity of normal and hypoperfused myocardium during the first pass. Dipyridamole increased left anterior descending flow (287% +/- 36; P < .05) and decreased left circumflex flow (65% +/- 14; P < .05). The magnitude of signal intensity increase during the second bolus in the hypoperfused region was less than that of normal myocardium (P < .05). Contrast-enhanced images showed the hypoperfused region as smaller than the postmortem measurement (43.8% +/- 3.3; P < .05). CONCLUSION: Contrast-enhanced fast MR imaging in the vasodilated state allows detection of hypoperfused myocardium in the presence of critical coronary stenosis.

Animals↗
PubMed1995

Rheumatoid arthritis of the craniocervical region by MR imaging: detection and characterization.

OBJECTIVE: The purpose of our study was to evaluate the potential of contrast-enhanced MR imaging to detect and to characterize craniocervical rheumatoid arthritis in a large population group, to compare MR imaging with clinical and conventional radiographic findings, and to examine the relationship between the histopathologic and MR imaging findings in seven patients. SUBJECTS AND METHODS: We performed contrast-enhanced MR imaging using T2-weighted gradient-echo sequences and T1-weighted spin-echo sequences in 136 patients with rheumatoid arthritis. Sequential T1-weighted images were obtained before, 3 min after, and 15 min after injection of contrast material. Plain films were acquired in all patients. Serologic status and neurologic status were determined in each patient within 2 days of MR imaging. Patients were categorized into one of four groups, depending upon whether they had joint effusion, hypervascular pannus, hypovascular pannus, or fibrous pannus according to signal patterns on contrast-enhanced MR images. Signal intensity was measured to assess the enhancement of synovial hypertrophy, joint capsule, joint effusion, and the various stages of pannus tissue. Histologic specimens were obtained from seven patients and were correlated with MR imaging findings. RESULTS: Acute and chronic synovitis were differentiated with contrast-enhanced MR imaging as follows: joint effusion (n = 29), hypervascular pannus (n = 54), hypovascular pannus tissue (n = 8), and fibrous pannus (n = 22). Signal intensity differed significantly among the four groups on contrast-enhanced T1-weighted images. In 59 patients with effusion or hypervascular pannus tissue, atlantoaxial subluxation was diagnosed with plain films. Patients with negative findings on radiographic studies (n = 20) had joint effusion, hypervascular pannus tissue, hypovascular pannus formation, or fibrous pannus tissue on MR imaging studies. Cord compression was found in 10% of all cases and isolated sac compression in 16%. Neurologic findings showed no correlation with MR imaging features. CONCLUSION: Contrast-enhanced T1-weighted spin-echo MR imaging can discriminate between joint effusion and various forms of pannus in patients with rheumatoid arthritis of the craniocervical region. MR imaging also can detect joint effusion and pannus tissue in patients with negative radiographic findings. No relationship between MR imaging findings and clinical symptoms were found. Tissue enhancement and histopathologic findings correlated in a limited number of autopsies.

Acute Disease↗
PubMed1995

The developing role of magnetic resonance contrast media in the detection of ischemic heart disease.

Recent developments in magnetic resonance (MR) imaging have opened up new avenues in the investigation of cardiovascular physiology. Inherent signal intensity of any tissue on MR images depends largely on proton concentration as well as longitudinal (T1) and transverse (T2) relaxation times. Myocardial contrast can be manipulated by using specific MR pulse sequences which are selectively sensitive to differences in any one of these parameters. Paramagnetic metal complexes are used as contrast media in MR imaging to enhance the inherent contrast. Contrast media in MR imaging are not directly visible but change the magnetic properties of other nuclei in close proximity, such as those of the water hydrogen. The signal of water can be altered by the contrast medium in different ways, either by changing the relaxation times or through bulb susceptibility effects, or both. The role of MR contrast media for quantitative characterization of ischemic heart disease has advanced considerably in the past 10 years. Conventional MR imaging techniques following the administration of contrast media are useful for identifying and sizing myocardial infarctions and for distinguishing between occlusive and reperfused myocardial infarctions as well as reversible (stunned) and irreversible injuries. Recent results suggest that contrast-enhanced MR imaging can also be used to identify dead cells in reperfused ischemically injured myocardium. The recently developed fast MR imaging techniques, with the aid of MR contrast media as a perfusion indicator, may be useful in estimating regional myocardial perfusion and blood volume. The assessment of capillary circulation or myocardial perfusion may be used for evaluating the extent of hypoperfusion and treatment efficacy. Experimental and clinical perfusion studies indicate that perfusion-sensitive MR imaging detects compromised myocardium (area at risk). Combining myocardial perfusion imaging with the anatomic and functional information provided by other MR imaging sequences could make MR imaging a comprehensive noninvasive technique for the evaluation of ischemic heart disease.

Animals↗
PubMed1994

Reperfused myocardial infarctions on T1- and susceptibility-enhanced MRI: evidence for loss of compartmentalization of contrast media.

The purpose of this study was to characterize the contrast caused by a susceptibility MRI contrast agents, on spin echo T2-weighted imaging of reperfused myocardial infarction. Our interest in this model focused on the expected requirement that such agents be compartmentalized in the tissue to cause signal loss on spin echo images, a condition which may not be present in reperfused infarcted myocardium. Accordingly, nine rats were subjected to 2 h of left coronary artery occlusion followed by 3 +/- 0.5 h of reperfusion prior to administration of contrast media. Three sets of MR images were acquired: (a) baseline axial images at the midventricle, both T1-weighted (TR/TE = 300/20) and T2-weighted (TR/TE = 1500/60); (b) T1-weighted images after administering a T1-enhancing agent, Gd-DTPA-BMA (0.2 mmol/kg), to document that contrast media is delivered to the reperfused infarction; and (c) T2-weighted images after administering the susceptibility agent, Dy-DTPA-BMA (1.0 mmol/kg). Gadolinium-enhanced T1 images depicted reperfused infarction as regions with greatly enhanced signal intensity compared with uninfarcted myocardium, indicating that contrast agent was delivered to the infarcted zone. Dysprosium-enhanced T2 images depicted the injury as a region of persistent signal intensity relative to depletion of signal in normal myocardium, consistent with failure of the contrast agent to cause signal loss. Similar infarction sizes were observed for unenhanced T2-weighted images (33 +/- 5%), gadolinium-enhanced T1-weighted images (36 +/- 5%) and postmortem staining (30 +/- 6%); strong correlations (r > 0.9) were noted in comparisons of these data.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Inversion recovery EPI of bolus transit in rat myocardium using intravascular and extravascular gadolinium-based MR contrast media: dose effects on peak signal enhancement.

Inversion recovery gradient recalled echo planar imaging (TI/TR/TE = 700/2000/10 ms) was used to dynamically monitor the first pass of an intravascular (GdDOTA-polylysine) and an extravascular (GdDTPA-BMA) contrast agent through normal rat myocardium. It was found that myocardial enhancement increased with dose of the intravascular agent to a limiting value of approximately 50% of fully relaxed intensity, consistent with enhancement of 40% of myocardial water content during the first pass. Larger doses produced no further increase in peak response. On the other hand, the extravascular agent caused incrementally increased enhancement throughout the dose range examined to a final value of 68 +/- 2% of fully relaxed intensity. The profile of dose dependence for both agents was inconsistent with monoexponential T1 relaxation. It was concluded that: (a) compartmentalization of myocardial water combined with restricted myocardial water diffusion limits the peak response during bolus transit; (b) extraction of the extravascular agent during transit elevates the peak response over that obtained from agent confined to the vascular volume; and (c) models that assume simple monoexponential T1 relaxation to derive time-density curves do not adequately describe the relationship between changes in signal intensity, R1 and contrast concentration.

Albumins↗
PubMed1994

The use of contrast-enhanced magnetic resonance imaging to define ischemic injury after reperfusion. Comparison in normal and hypertrophied hearts.

RATIONALE AND OBJECTIVES: Magnetic resonance imaging (MRI) was used to demonstrate the infarction size in reperfused ischemic myocardium of normal and hypertrophied hearts, and to test the hypothesis that hypertrophied hearts manifest greater susceptibility to ischemia. METHODS: Normal rats (n = 11) and rats subjected to left ventricular hypertrophy (LVH) by aortic banding (n = 13) were studied. After 7 weeks, the left coronary artery was occluded for 25 minutes and reperfused for 1 hour before MRI. Electrocardiogram-gated spin-echo images were acquired before and after administration of 0.3 mmol/kg gadoteridol. To quantify the hyperintense area demarcated by gadoteridol, 3 transaxial images were acquired at different levels. Jeopardy and infarcted areas were measured in the same three slices postmortem using blue dye and triphenyltetrazolium chloride (TTC) stain, respectively. RESULTS: Before administration, there was no significant difference in signal intensity between nonischemic (0.42 +/- 0.03 arbitrary units) and ischemic (0.41 +/- 0.03) myocardium in either group. After gadoteridol injection, signal intensity of the reperfused injured region was higher than that of nonischemic myocardium (1.48 +/- 0.16 vs. 0.72 +/- 0.06, P < .05). Magnetic resonance delineation of the hyperintense area persisted for at least 30 minutes. The size of the hyperintense area was larger in LVH than in control hearts (25 +/- 5% vs. 7 +/- 3% of LV surface area, P < .05) and did relate closely to the area of myocardial infarction (r = .97), but not with the jeopardy area (r = .42). On TTC staining, the infarction size also was significantly greater in LVH than in normal group (18 +/- 5% vs. 5 +/- 2% of LV surface area, P < .05). The jeopardy areas of normal and LVH hearts showed no significant difference (46 +/- 2% vs. 47 +/- 3%). CONCLUSION: Magnetic resonance imaging confirms the concept that reperfused myocardial injury is larger in LVH than normal hearts after brief coronary occlusion. Contrast-enhanced MRI can define the size of reperfused myocardial injury. Thus, MRI is a suitable technique to assess conditions accentuating ischemic injury.

Animals↗
PubMed1994

Identification of myocardial reperfusion with echo planar magnetic resonance imaging. Discrimination between occlusive and reperfused infarctions.

BACKGROUND: The current treatment of many cases of acute myocardial infarction involves the use of thrombolytic agents. Evaluation of this therapy requires determination of the success of reperfusion and assessment of the presence and extent of infarction in the reperfused territory. The present study was designed to simulate in rat models several possible outcomes of reperfusion therapy: (1) successful reperfusion and absence of myocardial infarction, (2) successful reperfusion and presence of myocardial infarction, and (3) unsuccessful reperfusion. The usefulness of contrast-enhanced fast magnetic resonance (MR) imaging in defining the success of reperfusion was investigated. The dynamic effects were examined of low and high doses of gadolinium-BOPTA/dimeglumine (Gd-BOPTA/dimeg) on myocardial signal using MR inversion recovery echo planar imaging (IR-EPI) and gradient recalled echo planar imaging (GR-EPI), respectively. METHODS AND RESULTS: Rats were subjected to one of the following regimens: reperfused reversible myocardial injury (n = 9), reperfused irreversible myocardial injury (n = 9), and occlusive infarction (n = 9). MR echo planar images were acquired every 1 or 2 seconds before, during, and after administration of Gd-BOPTA/dimeg. In all groups, normal myocardial signal was sharply increased on IR-EPI and decreased on GR-EPI at the peak of the bolus, followed by a gradual decline to baseline. In animals subjected to reperfused reversible myocardial injury, normal and previously ischemic regions were indistinguishable during and after the passage of Gd-BOPTA/dimeg. On the other hand, enhancement of reperfused irreversibly injured myocardium was delayed but increased steadily to a higher level than normal myocardium on IR-EPI. The reperfused irreversibly injured myocardium was identified on IR-EPI as a zone of high signal (hot spot). On GR-EPI, signal loss in reperfused irreversibly injured myocardium was significantly less compared with normally perfused myocardium. In animals with occlusive infarctions, there was no change in signal intensity over the ischemic region on either IR-EPI or GR-EPI. Occlusive infarction was identified as zones of either low (cold spot) or high (hot spot) signal compared with normal myocardium, depending on MR pulse sequence and dose of the contrast medium. CONCLUSIONS: The transit of Gd-BOPTA/dimeg monitored by fast MR imaging techniques can be used to distinguish between reperfused reversibly and reperfused irreversibly injured myocardium and between occlusive and reperfused infarctions.

Animals↗
PubMed1993

Comparison of T1-enhancing and magnetic susceptibility magnetic resonance contrast agents for demarcation of the jeopardy area in experimental myocardial infarction.

RATIONALE AND OBJECTIVES: This study compared the areas demarcated by a T1-enhancing agent, Gd-DTPA-BMA, and a magnetic susceptibility agent, Dy-DTPA-BMA, with 201thallium autoradiography (indicator of perfusion) and postmortem histochemical staining with triphenyltetrazolium chloride (TTC)(indicator of infarction). METHODS: Thirteen rats were subjected to coronary artery occlusion for 3 to 4 hours before acquisition of four sets of electrocardiogram-gated spin-echo magnetic resonance (MR) images: T1-weighted images before and after 0.2 mmol/kg Gd-DTPA-BMA; and T2-weighted images before and after 0.3 mmol/kg Dy-DTPA-BMA. After MR imaging, intravenous 201thallium delineated the area of decreased myocardial perfusion. At autopsy, TTC staining delineated the area of myocardial infarction. RESULTS: A myocardial region in the distribution of the occluded artery was delinated as a hyperintense area ("hot-spot") by Dy-DTPA-BMA and as a hypointense area ("cold-spot") by Gd-DTPA-BMA. The hyperintense area demarcated by Dy-DTPA-BMA (51 +/- 3% of the area of the midequitorial slice of the left ventricle) showed a closer relationship to the area of decreased myocardial perfusion (jeopardized area) (46 +/- 3%), determined by 201thallium autoradiography, than the area of myocardial infarction (36 +/- 4%), determined by histochemical staining. However, the hypointense area demarcated by Gd-DTPA-BMA (29 +/- 2%) did not relate as closely to the area of decreased myocardial perfusion (slope = 0.54) or the area of myocardial infarction (r = 0.46). CONCLUSIONS: The abnormal myocardial area delineated by the magnetic susceptibility agent showed a closer relationship to the area of deficient myocardial perfusion (jeopardy area) after coronary occlusion than that defined by T1-enhancing contrast media.

Animals↗
PubMed1993

Effects of concurrent oral administration of monensin and selenium on some haematological and biochemical parameters in broiler chickens.

Monensin and selenium (sodium selenite) at different toxic levels were administered orally to the broiler chickens for variable periods. A depression in haematological parameters and biochemical ones such as alanine and aspartate aminotransferase, serum total protein and cholesterol were recorded in acute and subacute toxicosis of these substances. The present experiments led to the conclusion that concurrent administration of selenium and monensin at toxic levels resulted in exasperated toxic response in broiler chickens which in turn had been produced by embellishment of toxicosis inducing properties of both examined substances.

Administration, Oral↗
PubMed1992

Effect of cilazapril on regional left ventricular wall thickness and chamber dimension following acute myocardial infarction: in vivo assessment using MRI.

The primary goal of the current study was to assess in situ, using magnetic resonance imaging, the effect of a new angiotensin-converting enzyme inhibitor, cilazapril, in reducing left ventricular remodeling after acute myocardial infarction. Three groups of animals were investigated: (1) sham-operated rats (n = 19); (2) infarcted rats receiving no treatment (n = 23); and (3) infarcted rats receiving cilazapril (100 mg/L drinking water, n = 20). Treatment with cilazapril began on the third day postocclusion and continued for 3 to 4 months. Myocardial infarction was produced by ligation of the left coronary artery, and electrocardiographic (ECG)-gated short-axis images were acquired 3 to 4 months later. Sham-operated animals were subjected to the same procedure but the left coronary artery was not ligated. From the image acquired in the middle of the left ventricle (equatorial slice), left ventricular wall thicknesses, chamber diameters, and surface area measurements of the cavities were determined. At autopsy examination, infarct size and tissue water content were determined. The results demonstrate that magnetic resonance imaging has the potential to assess in situ the alterations of left ventricular dimensions and mass after acute myocardial infarction and can be used to document the influence of therapeutic interventions. Cilazapril provided protection against the deleterious remodeling changes such as ventricular dilation and wall thinning consequent to acute myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Delineation of acute myocardial infarction with dysprosium DTPA-BMA: influence of dose of magnetic susceptibility contrast medium.

OBJECTIVES: The contrast enhancement of acutely infarcted myocardium produced by the nonionic magnetic susceptibility-enhancing agent dysprosium diethylenetriamine pentaacetic acid-bis-methylamide (DyDTPA-BMA [S-043 Injection]) was assessed in the current study to establish the lowest dose that would yield optimal contrast between normal and acutely infarcted myocardium. BACKGROUND: Magnetic susceptibility contrast agents enhance differences between normal and ischemic tissue by reducing the signal of the normally perfused tissue to which they distribute. METHODS: Acute myocardial infarctions were produced by ligation of the left coronary artery. At 3 to 4 h after occlusion, a dose of 0.1, 0.3 or 0.5 mmol/kg of DyDTPA-BMA was injected intravenously into eight rats each in group 1, 2 or 3, respectively; a fourth group of seven rats served as a control group. Nuclear magnetic resonance (NMR) transverse relaxation time (T2)-weighted images (electrocardiographically gated to every 5th beat, echo delay time [TE] = 60 ms) were acquired before and for 1 h after administration of contrast agent. RESULTS: Images obtained before the injection of contrast agent showed moderate differences in signal intensity between normal and infarcted myocardium (p < 0.05). The contrast enhancement and the duration of delineation between infarcted and normal myocardium produced by this agent were dose dependent. At doses of 0.1, 0.3 and 0.5 mmol/kg, DyDTPA-BMA produced signal loss in normal myocardium: 63 +/- 5%, 41 +/- 4% and 28 +/- 4% of the baseline values, respectively, without any significant reduction in signal intensity of the infarcted region. The reduction in signal of normal myocardium and delineation of the infarct persisted for 5 min at a dose of 0.1 mmol/kg, for 20 min at a dose of 0.3 mmol/kg and for 40 min at a dose of 0.5 mmol/kg. No change in signal intensity or signal intensity ratio between normal and infarcted myocardium was observed in the control group during the same observation period. CONCLUSIONS: These results suggest that low doses of this agent, comparable to those of longitudinal relaxation time (T1)-enhancing agents, can delineate acutely infarcted myocardium. A dose of 0.3 mmol/kg of DyDTPA-BMA (S-043 Injection) provides reasonably persistent demarcation of acute myocardial infarction. Because this dose dramatically suppresses the NMR signal of normal myocardium, it shows the infarcted region as a region of high intensity (bright spot) on NMR images.

Animals↗
PubMed1992

Preservation of high-energy phosphate reserves in a cat model of post-ischemic myocardial dysfunction.

Brief episodes of myocardial ischemia are known to cause reversible depression of regional myocardial contraction after reperfusion. One of the mechanisms of this persistent regional dysfunction has been proposed to be depletion of high-energy phosphate compounds. Eight cats were prepared with a reversible snare occluder around the left anterior descending artery (LAD); a surface coil sutured to the epicardial surface over the LAD territory for measurement of 31-phosphorus (31P) magnetic resonance spectroscopy (MRS) spectra; and a pair of ultrasonic crystals implanted in the mid-myocardium for measurement of regional segment length shortening. The baseline value of percent segment length shortening (%SS) was 12.8 +/- 1.4%. Increased afterload did not significantly alter high-energy phosphate levels or %SS. All animals exhibited passive systolic bulging during occlusion (-8.4 +/- 3.6% systolic shortening) as well as reduced phosphocreatine (PRc, 30 +/- 3% of control) and increased inorganic phosphorus (Pi) (239 +/- 18%), but there was no change in adenosine triphosphate (ATP). During reflow, %SS did not completely recover (4.0 +/- 2.9%, P less than .05 versus baseline). PCr and Pi returned to control levels during the first 30 minutes of reperfusion. Increased afterload had no significant effect on high-energy phosphates or %SS in stunned hearts. These findings indicate a lack of correlation between recovery of high-energy phosphate stores and regional myocardial contractility in stunned myocardium. High-energy phosphate reserves are preserved in stunned myocardium and are unlikely to be a direct cause of myocardial dysfunction.

Animals↗
PubMed1992

Real-time dynamics of an extravascular magnetic resonance contrast medium in acutely infarcted myocardium using inversion recovery and gradient-recalled echo-planar imaging.

RATIONALE AND OBJECTIVES: The purposes of this study are to evaluate the first-pass profile of gadolinium-BOPTA/Dimeg (Gd-BOPTA/Dimeg) during its transit through hearts subjected to acute myocardial infarction, and to delineate these infarcted regions by the use of ultrafast magnetic resonance imaging (MRI). METHODS: Regional ischemia was induced in anesthetized rats by occluding the left coronary artery. Imaging parameters for single shot EPI included TE, 10 mseconds; AT, 33 mseconds; and 64 x 64-pixel matrix. Consecutive images were obtained every 1 to 2 seconds over a 30-second period. After approximately two images, Gd-BOPTA/Dimeg was injected intravenously (0.05 and 0.25 mmol/kg). RESULTS: Gd-BOPTA/Dimeg (0.05 mmol/kg), with inversion recovery EPI, produced a substantial increase in signal intensity of right and then left ventricular blood. Normally perfused myocardium also was enhanced, but not the acutely infarcted region. Clear delineation of the infarcted region as negatively enhanced "cold spots" persisted for at least 20 seconds. Gd-BOPTA/Dimeg (0.25 mmol/kg) with standard gradient-recalled EPI produced a different profile of signal intensity changes. Signal intensities of ventricular blood and normal myocardium were greatly reduced, leaving the infarcted zone as a positively enhanced "hot spot." Delineation of the infarcted region persisted for 6 to 8 seconds. The infarcted zone detected with MRI corresponded to that observed at autopsy. CONCLUSIONS: Regions of acute myocardial infarction can be detected as negatively enhanced "cold spots" or positively enhanced "hot spots" by studying the first-pass dynamics of Gd-BOPTA/Dimeg through hearts with regional ischemia by use of single shot EPI.

Animals↗
PubMed1992

Measurement of blood flow and perfusion in the cardiovascular system.

Complete evaluation of cardiovascular disease by a single imaging technique requires measurement of bulk flow in blood vessels and estimation of relative or ideally absolute perfusion at the tissue level. Magnetic resonance (MR) measurement of blood flow in arteries and veins has been done using the velocity-encoded phase cine gradient echo technique. This technique has been applied with cine MR to measure normal and pathologically high velocities. Measurement of relative perfusion in the myocardium has used the intravenous injection of T1 relaxation enhancing and magnetic susceptibility MR contrast media with rapid image acquisition using echoplanar imaging. MR images (MRIs) acquired during steady-state distribution or during the first passage of these contrast media have depicted ischemic myocardial regions.

Animals↗