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Objective: Cardiac magnetic resonance imaging (MRI) at 3.0 T has recently become available and potentially provides a significant improvement of tissue contrast in T1-weighted imaging techniques relying on Gd-based contrast enhancement. Imaging at high-field strength may be especially advantageous for methods relying on strong T1-weighting and imaging after contrast material administration. The aim of this study was to compare cardiac delayed enhancement (DE) MRI at 3.0 T and 1.5 T with respect to image quality, signal-to-noise ratio (SNR), and contrast-to-noise ratio (CNR) between infarcted and normal myocardium., Materials and Methods: Forty consecutive patients with history of myocardial infarction were examined at 3.0 T (n = 20) or at 1.5 T (n = 20). Myocardial function was assessed using cine steady-state-free-precession (SSFP) sequences (TR 3.1 milliseconds, TE 1.6 milliseconds, flip angle 70 degrees , and a matrix of 168 x 256 at 1.5 T and TR 3.4 milliseconds, TE 1.7 milliseconds, flip angle 50 degrees and a matrix of 168 x 256 at 3.0 T), acquired in long- and short-axes views. DE images were obtained 15 minutes after the administration of 0.15 mmol of Gd-DTPA/kg body weight using a segmented inversion recovery prepared gradient echo sequence at 1.5 T (TR 9.6 milliseconds, TE 4.4 milliseconds, flip angle 25 degrees , matrix 160 x 256, bandwidth 140 Hertz/pixel) and at 3.0 T (TR 9.8 milliseconds, TE 4.3 milliseconds, flip angle 30 degrees , matrix 150 x 256, bandwidth 140 Hertz/pixel). For image analysis, standardized SNR and CNR measurements were performed in infarcted and remote myocardial regions. Two independent observers rated image quality on a 4-point scale (0 = poor image quality, 1 = sufficient image quality, 2 = good image quality, 3 = excellent image quality)., Results: High diagnostic image quality was obtained in all patients. Rating of mean image quality was 2.2 +/- 0.8 at 1.5 T and 2.5 +/- 0.6 at 3.0 T (P = 0.012) for observer 1 and 2.2 +/- 0.7 at 1.5 T and 2.6 +/- 0.6 at 3.0 T (P = 0.003) for observer 2, respectively. Interobserver agreement was good (kappa = 0.68 at 1.5 T and 0.78 at 3.0 T). SNR measurements yielded a mean SNR of 37.8 +/- 13.9/22.9 +/- 6.0 in infarcted myocardium (P < 0.001) and 5.6 +/- 2.2/5.9 +/- 2.4 in normal myocardium (P = 0.45) at 3.0 T/1.5 T, respectively. CNR measurements revealed mean values of 32.4 +/- 13.0/16.7 +/- 5.4 (P< 0.001) at 3.0 T/1.5 T, respectively., Conclusions: Delayed enhancement MRI at 3.0 T is feasible and provides superior image quality compared with 1.5 T. Furthermore, using identical contrast doses, increased SNR and CNR values were recorded at 3.0 T.

Background: In patients with acute myocardial infarction (AMI), activated platelets and altered haemostatic/fibrinolytic systems with and without thrombolytic therapy are known. Platelets thereby interact with neutrophils, stimulated endothelial cells and with monocytes leading to adverse effects on further myocardial damage. Thrombolysis in these patients is still hampered by procoagulant effects favoring early reocclusion. The additional treatment with a GPIIb/IIIa antagonist aimed to minimize early reocclusion thus improving the present therapeutic regimen., Methods: In 38 patients with AMI, we investigated the effects of a thrombolytic regimen with half reteplase (r-PA) dose plus abciximab vs. full dose r-PA on membrane-bound adhesion molecules (CD41, CD42b, CD40, CD40L) expressed on platelets, neutrophils and monocytes as well as on soluble platelet-selectin as interaction and activation markers of these cells., Results: The combination group had significantly (p < 0.05) lower sP-selectin levels over 48 h vs. the group treated with full dose r-PA. After 3 h, the percentage of CD41 and CD42b positive monocytes and granulocytes as well as the percentage of CD40 positive granulocytes and the percentage of CD40L positive monocytes markedly (p < 0.01, p < 0.05) decreased in the combination group vs. data at admission compared with the r-PA group indicating less leukocyte-patelet adhesion., Conclusions: The thrombolytic regimen with half dose r-PA and abciximab had a benefical influence on platelet activation and induced a more marked decrease of platelet-monocyte, and in part, platelet-granulocyte aggregates compared with the r-PA regimen. This could contribute to a probably lesser monocyte activation state with favourable effects on monocyte-endothelial adhesion and a consecutively possible influence of myocardial damage, a reduction of the additionally acute local inflammatory processes and a reduction of adherence of platelet-granulocyte aggregates to subendothelium.

In patients with acute myocardial infarction treated with thrombolytics, platelet activation as well as alterations of the hemostatic and fibrinolytic systems have been described favoring early infarct-related artery reocclusion. We investigated the effects of a newer thrombolytic regimen with half-dose double-bolus reteplase (2 x 5 IU, 20 patients) combined with abciximab versus full-dose reteplase (2 x 10 IU, 18 patients) on the fibrinolytic and the hemostatic system in patients with acute ST-segment elevation (in the electrocardiogram) myocardial infarction. The thrombolytic regimen with half-dose reteplase in combination with abciximab caused in vivo a lower systemic plasminemia and a lower paradoxical activation of the contact phase of the coagulation system (measured as activated factor XII); a lower paradoxical thrombin activation/generation; and a lesser extent of fibrinogen breakdown compared with the reteplase regimen. These results could be, at least in part, a possible explanation for the observed significantly lower rates of reinfarction until 7 days after enrollment and of recurrent ischemia in the combination group in the Global Use of Strategies to Open Occluded Coronary Arteries V (GUSTO V) trial.

Patients with subacute myocardial infarction were studied to detect regions of ischemic injury but with preserved myocardial function combining different MRI techniques. On a 1.5-T imaging system 27 patients were examined 7-14 days after acute myocardial infarction. The imaging protocol included T2-weighted fast spin-echo imaging, a cine fast low-angle shot (FLASH) 2D technique to determine regional function at rest, and a first pass as well as late contrast enhancement perfusion study injecting 0.1 mmol/kg Gd-DTPA. Preserved function was compared with the transmural extent of first-pass perfusion phenomena, increased T2 signal intensity (SI), and late contrast enhancement. Semi-quantitative first-pass perfusion parameters were correlated with quantitative myocardial wall thickening (MWT) and degree of coronary artery stenosis. Indicating ischemic injury increased T2 SI and late enhancement was present in 29 and 26% of segments. Preserved function was found predominantly in segments with non-transmural late enhancement (112 of 338 segments with late enhancement) and transmural increase of T2 SI (129 of 386 segments with increased T2 SI). A high-grade perfusion deficit was detected in 4% of all segments and regularly associated with markedly decreased systolic function. Correlation of first-pass perfusion parameters was observed with MWT (r=0.50-0.90, p<0.001) but not with the degree of coronary artery stenosis. Our data suggest that preserved function was detected in non-transmural myocardial infarction demonstrated by non-transmural late enhancement and increase of T2 SI.

Objectives: Thrombolytic therapy in patients with acute myocardial infarction is hampered by bleeding complications and procoagulant effects favoring early reocclusion. TNK-tPA was shown in vitro to have considerable fibrin specificity. We investigated the effects of tenecteplase (TNK-tPA) and alteplase (rt-PA) on the haemostasis and fibrinolytic system., Methods and Results: We enrolled 30 patients with AMI into the study. Twenty patients received front-loaded rt-PA up to 100 mg; 10 patients were given TNK-tPA in a single bolus up to 50 mg. All patients received aspirin and intravenous heparin. During the first 2 days, the following parameters were repetitively determined: thrombin-antithrombin III complexes (TAT), antithrombin III (ATIII), prothrombin fragment F 1 + 2 (F 1 + 2), kallikrein-like activity (KK), activated factor XII (FXIIa), plasmin alpha 2-antiplasmin complexes (PAP), fibrinogen, D-dimers (DD), tissue-type plasminogen activator (t-PA). A total of 75 healthy persons served as control group. TAT increased significantly after rt-PA but not after TNK-tPA (3 h: 38.1 +/- 29.4 versus 10.5 +/- 4.2 microg/l; p < 0.01), indicating paradoxical thrombin activation. F 1 + 2 increased transiently after rt-PA but not after TNK-tPA. Fibrinogen was significantly lower after rt-PA versus TNK-tPA (3 h: 163 +/- 27 versus 380 +/- 54 mg/dl; p < 0.05). KK activities in the rt-PA group were significantly (p < 0.01) increased over 48 h versus TNK-tPA. PAP and D-dimers were lower over the time course of 48 h in the tenecteplase group versus rt-PA., Conclusions: This study indicates that tenecteplase has higher fibrin specificity not only in vitro but also in vivo versus alteplase. TNK-tPA consecutively has no paradoxical systemic procoagulant effect due to the lower extent of activation of the kallikrein-factor XII system than alteplase., (Copyright 2002 Elsevier Science Ltd.)

Purpose: Increased T2 signal intensity (SI) can be regularly observed in myocardial infarction. However, there are controversial reports about the relationship of elevated T2 SI to myocardial viability and some authors propose that high T2 SI serves as a sign of irreversible myocardial injury. This study investigates increased T2 SI compared to myocardial function in patients with reperfused subacute myocardial infarction. Preserved function was used as criterion for viability., Methods: Ten healthy volunteers and 17 patients with myocardial infarction and patent infarct related coronary artery were examined on a 1.5 T Magnetom Vision system (Siemens). For T2-weighted MR imaging a breath-hold STIR sequence with dark-blood preparation was used. Cine FLASH 2D imaging was applied to assess myocardial function. Signal-to-noise (S/N) in STIR T2 images was measured in normal and infarcted regions and subsequently identified by two independent observers. Based on a 20 segment model of the left ventricle findings were compared to regional myocardial function., Results: Elevated STIR T2 SI was found in all 17 patients and observed in 27% (204/754) of segments. S/N of normal myocardium was 5.1 +/- 0.7 in volunteers and 4.9 +/- 0.8 in patients (P = NS). Infarcted myocardium presented with significantly increased S/N 12.8 +/- 1.9 (P < 0.0001). Significant transmural elevation of T2 SI was noted in 32% of segments with preserved systolic function., Conclusion: Increased STIR T2 SI can be observed transmurally in post-ischemic myocardial regions with preserved function. It therefore cannot be used as an exclusive marker for the non-viable region.

This study was undertaken to compare the effects of reteplase and alteplase regimens on hemostasis and fibrinolysis in acute myocardial infarction (AMI). Thrombolytic treatment in patients with AMI is hampered by paradoxical procoagulant effects that favor early reocclusion. In vivo data comparing this effect and the fibrin specificity of double-bolus reteplase and front-loaded alteplase regimens are not available. In a prospective, randomized study, 50 patients with AMI were either treated with double bolus (10 + 10 U) reteplase or with front-loaded alteplase (up to 100 mg) within 6 hours of symptom onset. Thirty apparently healthy persons served as controls. Molecular markers of coagulation and fibrinolysis were serially examined for up to 5 days. Paradoxical thrombin activation at 3 hours after initiation of therapy was comparable between reteplase and alteplase. Reteplase (65 +/- 5 U/L) and alteplase (72 +/- 8 U/L) caused significantly elevated kallikrein activity at 3 hours after adminstration (p <0.01 vs controls 30 +/- 1 U/L). Fibrin specificity was less for reteplase (p <0.05) with a decrease in fibrinogen at 3 hours to 122 +/- 27 mg/dl versus 224 +/- 28 mg/dl for alteplase (p <0.01 and p <0.05 vs controls). D-Dimer levels at 3 hours were higher (p <0.05) after reteplase (5,459 +/- 611 ng/ml) versus alteplase (3,445 +/- 679 ng/ml) (both p <0.01 vs controls 243 +/- 17 ng/ml). Plasmin generation (plasmin-antiplasmin complexes) was significantly (p <0.01) increased at 3 hours with both regimens to 27,079 +/- 3,964 microg/L (reteplase) and 19,522 +/- 2,381 microg/L (alteplase). The data from 3 hours after start of thrombolytic therapy proved less marked fibrin specificity of the reteplase regimen (in vivo) compared with front-loaded alteplase. Both regimens have a moderate procoagulant effect without differences in activation of the kallikrein system.

Background: Thrombolytic therapy in patients with acute myocardial infarction (AMI) is hampered by procoagulant effects. In vitro studies have indicated that plasmin stimulation activates the kallikrein-contact-phase system, resulting in thrombin activation. This prospective comparative study was designed to examine the procoagulant effects of streptokinase or alteplase in AMI., Methods and Results: Sixty-one patients with AMI received 1.5 million U of streptokinase or front-loaded alteplase (up to 100 mg) and systemic heparin. Twenty-four patients with AMI and no thrombolytic therapy and 30 control subjects were examined for comparison. Molecular markers of thrombin, plasmin activation, and coagulation activities were determined before therapy and serially for up to 10 days. Moderate thrombin (initial thrombin-antithrombin [TAT] complex 18+/-5 versus 4+/-0.3 microg/L, P<0.05) and kallikrein (up to 45+/-4 versus 30+/-1 U/L at 3 hours, P<0.01) activation occurs in patients with AMI. D-Dimers are increased (P<0.01), and plasmin is stimulated (P<0.01). Streptokinase and alteplase increase TAT to 50+/-17 and 51+/-18 microg/L at 3 hours and to 50+/-17 and 33+/-14 microg/L at 6 hours, respectively (P<0.01). Kallikrein activity is elevated (P<0. 01) to 76+/-5 and 71+/-7 U/L at 3 hours and 64+/-6 and 47+/-5 U/L by streptokinase and alteplase, respectively, at 6 hours. Reductions in fibrinogen and increases in D-dimers and plasmin-antiplasmin complexes are more marked (P<0.05 and 0.01) after streptokinase versus alteplase. Correlations were found among TAT, kallikrein activity, and plasmin activation (P<0.01)., Conclusions: The data indicate a more marked procoagulant action of the streptokinase regimen compared with front-loaded alteplase, thus supporting the hypothesis of a plasmin-mediated kallikrein activation with consecutive procoagulant action in vivo.

Objectives: We sought to examine whether the disturbed fibrinolytic system in patients with an acute coronary syndrome is associated with a reduced endothelial fibrinolytic capacity., Background: Intracoronary thrombus formation is a frequent finding in acute coronary syndromes. Systemic alterations of coagulation and fibrinolysis are known to occur, but possible disturbances of endothelial fibrinolytic function have not been investigated., Methods: We compared 42 patients with an acute coronary syndrome (acute myocardial infarction in 11 and unstable angina pectoris in 31) with 25 patients with stable angina. Venous blood was sampled serially for determination of markers of the fibrinolytic system and of hypercoagulability from admission to day 10. An occlusion test to determine the maximal endothelial tissue-type plasminogen activator (t-PA) release was also performed., Results: Both on day 0 and day 10, patients with an acute coronary syndrome had a marked elevation of t-PA mass concentration (mean value +/- SEM 14.4 +/- 1.6 [day 0], 18.9 +/- 2.5 ng/ml [day 10]) and of plasminogen activator inhibitor (PAI) (9.4 +/- 2.2 [day 0], 11.3 +/- 2.6 AU/liter [day 10], p < 0.05 vs. patients with stable angina). There was also a hypercoagulative state with elevated thrombin activity and increased D-dimers (p < 0.05 vs. patients with stable angina). Maximal endothelial t-PA release was initially reduced (p < 0.05 vs. patients with stable angina) to 2.3 +/- 0.9 ng/ml, but levels recovered during follow-up to 4.4 +/- 1.4 ng/ml (vs. 5.7 +/- 1.5 ng/ml in patients with stable angina)., Conclusions: Despite the known prolonged systemic alteration of fibrinolysis in acute coronary syndromes, endothelial fibrinolytic capacity is reduced only during the acute phase and becomes normalized during follow-up, and thus is linked more to intravascular thrombus formation than to steady state levels of markers of the fibrinolytic system.

Purpose: With the advent of fast pulse sequences, MR imaging of myocardial function and perfusion in ischaemic heart disease has become possible. Prior studies examined either myocardial perfusion or systolic wall motion. We intended to establish an examination procedure to simultaneously investigate regional myocardial motility and perfusion in patients 7-14 days after myocardial infarction., Methods: A Turbo-FLASH 2D sequence was optimised to maximise image contrast between normal and malperfused myocardium after Gd-injection using a calculation model basing on the Bloch equation. Calculated values for trigger delay TD, inversion time TI and flip angle alpha were confirmed in a Gd-phantom and healthy volunteers. Subsequently, myocardial motility was studied (cine FLASH 2D sequence) and in slice positions with reduced wall thickening first pass and post contrast studies after 2-10 minutes were performed using the optimised Turbo-FLASH sequence., Results: First pass SI-differences of normal compared to malperfused myocardium vary in relation to TD, TI and alpha in a relevant degree. Reduced myocardial motility was found with a sensitivity of 81% and specificity of 96%. Pathological perfusion patterns were detectable in all of these patients., Conclusions: A combined examination of motility and perfusion is possible by means of MRI and information about the status of postinfarct myocardium can be obtained.