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Biomedical subjects

M Saeed

Publications and source records attributed to M Saeed.

At least 127 records · Page 7Linked to original sources
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↗
PubMed1992

Reperfusion and irreversible myocardial injury: identification with a nonionic MR imaging contrast medium.

The potential of a new nonionic gadolinium complex--gadodiamide injection--to (a) allow distinction between reperfused and occlusive infarction and (b) enable differentiation between reperfused reversible and irreversible myocardial injury was investigated. Three groups of rats were used: 10 with reversibly reperfused myocardial injury, 10 with irreversibly reperfused injury, and 10 with occlusive infarction. Before administration of contrast material, there was no significant difference in signal intensity between normal and injured regions on T1-weighted images. After administration of gadodiamide injection (0.2 mmol/kg), the reversibly injured myocardium was indistinguishable from normal myocardium, while the reperfused irreversibly injured zone showed prominent and homogeneous enhancement. Occlusive infarcts showed three zones of differential enhancement consisting of normal, periinfarction, and infarction regions. Gadodiamide injection provides differential enhancement in reversibly reperfused, irreversibly reperfused, and occlusive infarcts. Thus, it may be useful as a marker of reperfusion and extent of infarction after thrombolytic therapy.

Animals↗
PubMed1992

Hemodynamic effects of bolus injection of gadodiamide injection and gadopentetate dimeglumine as contrast media at MR imaging in rats.

The trend to administer contrast agents for magnetic resonance (MR) imaging by rapid injection and to use higher doses necessitates additional safety assessments with regard to potential hemodynamic effects. The current study was designed to evaluate the hemodynamic effects or rapid injection of increasing doses of gadodiamide injection (gadolinium diethylenetriaminepentaacetic acid bismethylamide) and gadopentetate dimeglumine. Each animal received incremental doses (0.1, 0.3, and 0.5 mmol/kg) of either contrast agent via the left jugular vein as a rapid bolus (1-2 seconds). Gadodiamide injection caused no hemodynamic alterations; however, gadopentetate dimeglumine caused dose-dependent cardiodepressive effects. At a dose of 0.5 mmol/kg, gadopentetate dimeglumine transiently decreased left ventricular end-systolic pressure by 25%, systolic arterial pressure by 34%, and positive peak differential quotient of pressure change against time by 43% of preinjection values. All hemodynamic parameters returned to baseline in the first 3-5 minutes.

Animals↗
PubMed1992

Amelioration of cardiodepressive effects of gadopentetate dimeglumine with addition of ionic calcium.

Doses of gadopentetate dimeglumine of 0.1-0.5 mmol/kg cause cardiodepressive effects when injected as a rapid central bolus into the left jugular vein. This study evaluated the hemodynamic effects of this magnetic resonance imaging contrast medium with and without calcium supplementation in a rat model. Also, the potential of gadopentetate dimeglumine to bind ionized serum calcium was investigated in vitro. Addition of calcium ions resulted in dose-dependent attenuation of the hemodynamic depression induced by gadopentetate dimeglumine alone. The cardiodepressive response was negated for a 0.1-mmol/kg dose of the contrast agent by addition of 6 mumol/kg of calcium, for a 0.3-mmol/kg dose by addition of 12 mumol/kg of calcium, and for a 0.5-mmol/kg dose by addition of 18 mumol/kg of calcium. Concentrations of 2 and 4 mmol/L of gadopentetate dimeglumine were found to bind 5.1% and 10.1% of the ionized calcium in rat serum under in vitro conditions, respectively.

Animals↗
PubMed1991

Myocardial infarction: assessment with an intravascular MR contrast medium. Work in progress.

The effect of a new intravascular magnetic resonance (MR) contrast medium (gadolinium diethylenetriaminepentaacetic acid [DTPA] polylysine) was evaluated in acute, subacute, and chronic myocardial infarctions in rats. Signal intensity (SI) was measured before and after intravenous administration of Gd-DTPA polylysine. Before administration of contrast material, chronic infarctions had lower SI than normal myocardium. With Gd-DTPA polylysine, three zones were identified in acute and subacute stages of myocardial infarction, but in the chronic stage, images demonstrated two zones. In acute and subacute infarctions, Gd-DTPA polylysine produced greater enhancement (over 60 minutes) in the peri-infarction zone than in the normal or infarcted myocardium. In chronic infarctions, Gd-DTPA polylysine had no discernible effect on the SI of the central infarction zone. Overall, it caused no significant hemodynamic effects. MR imaging with Gd-DTPA polylysine produced differential tissue enhancement in myocardial infarctions, which varied according to the age of the infarction.

Animals↗
PubMed1991

Occlusive and reperfused myocardial infarcts: MR imaging differentiation with nonionic Gd-DTPA-BMA.

To increase the time during which effective contrast exists between normal and infarcted myocardium, a high dose (0.6 mmol/kg) of the nonionic contrast medium gadolinium diethylenetriaminepentaacetic acid bismethylamide (Gd-DTPA-BMA) was used to distinguish between occlusive and reperfused myocardial infarctions in rats. After administration of Gd-DTPA-BMA, there was clear and persistent demarcation of both occlusive and reperfused infarcts on T1-weighted MR images. In occlusive infarcts, normal, infarcted, and periinfarcted myocardium could be identified. High signal intensity was evident for 60 minutes in a band straddling the border between infarcted and normal myocardium, namely, the periinfarction zone. In the reperfused infarct, normal and infarcted myocardium could be identified. The reperfused zone was immediately enhanced after injection of Gd-DTPA-BMA. A differential pattern of enhancement between occlusive and reperfused myocardial infarcts was evident for 1 hour. Thus, Gd-DTPA-BMA has the potential to allow (a) depiction of occlusive and reperfused acute myocardial infarcts, (b) documentation of reperfusion of myocardial infarction, and (c) distinction between occlusive and reperfused infarction.

Animals↗
PubMed1991

MRI in ischemic heart disease: expansion of the current capabilities with MR contrast.

Magnetic resonance imaging (MRI) has been used to identify acute and chronic myocardial infarctions and the complications of myocardial infarctions. Studies in animals have shown high accuracy in the quantification of the volume (mass) of acute myocardial infarctions. However, the role of MRI in ischemic heart disease has been limited by the inability to detect noninfarctional myocardial ischemia or to reliably indicate relative myocardial perfusion. Studies in animal models of various myocardial ischemic events have shown that these aims can be addressed using MR contrast media. The effect of MR contrast media on regional myocardial signal intensity is complex and determined by several factors, including: (1) the type of contrast medium; (2) the dose of the contrast medium; (3) the T1- or T2-weighting of the imaging sequence; and (4) the type of imaging technique applied (spin echo, gradient echo, or echoplanar). This article describes some of the potential applications of MR contrast media in ischemic heart disease and the several factors that interact to cause the regional myocardial signal alterations induced by MR contrast media.

Animals↗