Physiological basis of myocardial contrast enhancement in fast magnetic resonance images of 2-day-old reperfused canine infarcts.

BACKGROUND Contrast-enhanced fast magnetic resonance (MR) images of acute, reperfused human infarcts demonstrate regions of hypoenhancement and hyperenhancement. The relations between the spatial extent and time course of these enhancement patterns to myocardial risk, infarct, and no-reflow regions have not been well characterized. METHODS AND RESULTS The proximal left anterior descending coronary artery was occluded in 11 closed-chest dogs for 90 minutes followed by 2 days of reperfusion. Regional blood flow was determined by use of radioactive microspheres. The animals were studied at the 2-day time point with contrast-enhanced fast MRI (Signa 1.5 T, General Electric). Thioflavin-S was administered to demarcate no-reflow regions. The hearts were then excised, sectioned into five base-to-apex slices, stained with 2,3,5-triphenyltetrazolium chloride (TTC), and photographed under room light (for TTC) and ultraviolet light (for thioflavin). The spatial extents of thioflavin-negative, TTC-negative, and risk regions were compared planimetrically with MRI hypoenhanced and hyperenhanced regions. The spatial locations of subendocardial hypoenhancement in MR images correlated closely with those of thioflavin-negative regions. Microsphere blood flow in these regions was significantly reduced compared with remote regions (0.37 +/- 0.09 versus 0.88 +/- 0.10 mL/min per gram, respectively, P < .001) and with baseline (0.37 +/- 0.09 versus 0.87 +/- 0.15 mL/min per gram, P < .01). The spatial extent of hyperenhancement was smaller than the risk region (r = .64, slope = 0.48, P < .001) but highly correlated with TTC-negative regions and were, on average, 12% larger (r = .93, slope = 1.12, P = .035). CONCLUSIONS In contrast-enhanced MR images of 2-day-old reperfused canine infarcts, myocardial regions of hypoenhancement are related to the no-reflow phenomenon. Approximately 90% of the myocardium within hyperenhanced regions is nonviable.

[1]  E. Atalar,et al.  Regional heterogeneity of human myocardial infarcts demonstrated by contrast-enhanced MRI. Potential mechanisms. , 1995, Circulation.

[2]  E. McVeigh,et al.  A magnetization‐driven gradient echo pulse sequence for the study of myocardial perfusion , 1995, Magnetic resonance in medicine.

[3]  R. Judd,et al.  Effects of Myocardial Water Exchange on T1 Enhancement during Bolus Administration of MR Contrast Agents , 1995, Magnetic resonance in medicine.

[4]  C. Higgins,et al.  Inversion recovery EPI of bolus transit in rat myocardium using intravascular and extravascular gadolinium‐based MR contrast media: Dose effects on peak signal enhancement , 1994, Magnetic resonance in medicine.

[5]  Maythem Saeed,et al.  Reperfused myocardial infarctions on T1‐ and susceptibility‐enhanced MRI: Evidence for loss of compartmentalization of contrast media , 1994, Magnetic resonance in medicine.

[6]  K. Uğurbil,et al.  Contrast‐enhanced first pass myocardial perfusion imaging: Correlation between myocardial blood flow in dogs at rest and during hyperemia , 1993, Magnetic resonance in medicine.

[7]  K. Bailey,et al.  Immediate angioplasty compared with the administration of a thrombolytic agent followed by conservative treatment for myocardial infarction. The Mayo Coronary Care Unit and Catheterization Laboratory Groups. , 1993, The New England journal of medicine.

[8]  M. Moseley,et al.  Echo-planar MR imaging of normal and ischemic myocardium with gadodiamide injection. , 1993, Radiology.

[9]  A de Roos,et al.  Usefulness of ultrafast magnetic resonance imaging in healed myocardial infarction. , 1992, The American journal of cardiology.

[10]  C B Higgins,et al.  Reperfusion and irreversible myocardial injury: identification with a nonionic MR imaging contrast medium. , 1992, Radiology.

[11]  E. Ritman,et al.  In Vivo Relation of Intramyocardial Blood Volume to Myocardial Perfusion: Evidence Supporting Microvascular Site for Autoregulation , 1992, Circulation.

[12]  C. Sotak,et al.  Dependence of MR signal intensity on Gd tissue concentration over a broad dose range , 1991, Magnetic resonance in medicine.

[13]  F. Klocke,et al.  First‐Pass Entry of Nonionic Contrast Agent Into the Myocardial Extravascular Space: Effects on Radiographic Estimates of Transit Time and Blood Volume , 1991, Circulation.

[14]  R. Edelman,et al.  First-pass nuclear magnetic resonance imaging studies using gadolinium-DTPA in patients with coronary artery disease. , 1991, Journal of the American College of Cardiology.

[15]  W J Manning,et al.  Factors in myocardial “Perfusion” imaging with ultrafast MRI and Gd‐DTPA administration , 1991, Magnetic resonance in medicine.

[16]  D Chien,et al.  0.3‐second flash mri of the human heart , 1990, Magnetic resonance in medicine.

[17]  R. Jennings,et al.  Development of cell injury in sustained acute ischemia. , 1990, Circulation.

[18]  L. Becker,et al.  Progressive impairment of regional myocardial perfusion after initial restoration of postischemic blood flow. , 1989, Circulation.

[19]  M E Moseley,et al.  Assessment of myocardial salvage after ischemia and reperfusion using magnetic resonance imaging and spectroscopy. , 1989, Circulation.

[20]  C. Higgins,et al.  Occlusive and reperfused myocardial infarcts: differentiation with Mn-DPDP--enhanced MR imaging. , 1989, Radiology.

[21]  R. Peshock,et al.  Gadolinium-DTPA-enhanced nuclear magnetic resonance imaging of reperfused myocardium: identification of the myocardial bed at risk. , 1988, Journal of the American College of Cardiology.

[22]  A. M. Skene,et al.  TRIAL OF TISSUE PLASMINOGEN ACTIVATOR FOR MORTALITY REDUCTION IN ACUTE MYOCARDIAL INFARCTION Anglo-Scandinavian Study of Early Thrombolysis (ASSET) , 1988, The Lancet.

[23]  Dwight E. Peake,et al.  Thrombolysis in myocardial infarction (TIMI) trial: Phase I. A comparison between intravenous tissue plasminogen activator and intravenous streptokinase , 1988 .

[24]  R Roberts,et al.  Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: A comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge. , 1987, Circulation.

[25]  R. Peshock,et al.  Magnetic resonance imaging of acute myocardial infarction: gadolinium diethylenetriamine pentaacetic acid as a marker of reperfusion. , 1986, Circulation.

[26]  G L Wolf,et al.  Relaxation of water protons in the intra‐ and extracellular regions of blood containing Gd(DTPA) , 1986, Magnetic resonance in medicine.

[27]  D Tscholakoff,et al.  Occlusive and reperfused myocardial infarcts: effect of Gd-DTPA on ECG-gated MR imaging. , 1986, Radiology.

[28]  Gruppo Italiano per lo Studio della Soprawivenza nell'Inf Miocardico..  EFFECTIVENESS OF INTRAVENOUS THROMBOLYTIC TREATMENT IN ACUTE MYOCARDIAL INFARCTION , 1986, The Lancet.

[29]  M. Fishbein,et al.  Early phase acute myocardial infarct size quantification: validation of the triphenyl tetrazolium chloride tissue enzyme staining technique. , 1981, American heart journal.

[30]  Seymour Geisser,et al.  Statistical Principles in Experimental Design , 1963 .

[31]  F. Plum.  Handbook of Physiology. , 1960 .