Natural time course of myocardial infarction at delayed enhancement magnetic resonance.

The case reported, who suffered prolonged coronary occlusion, was evaluated by repeated MRI images in the acute, subacute and chronic phase. Scans showed hemorrhagic myocardial infarction and massive endothelial injury and its evolution over time.

Cardiogenic shock developing in the coronary care unit in patients with ST-elevation myocardial infarction.

INTRODUCTION: A relevant proportion of patients with ST-segment elevation myocardial infarction may develop cardiogenic shock after presentation, and the identification of these patients would be very important in order to improve their outcome. The aim of the current study was to identify, among patients in the BLITZ-1, the clinical predictors, and describe the outcome of patients who developed cardiogenic shock during hospitalization. METHODS: The study was a nationwide survey of patients admitted to a coronary care units for an acute myocardial infarction with or without ST-segment elevation myocardial infarction in October 2001. The 30-day follow-up was conducted by hospital visits and concerned major cardiac events occurred from hospital discharge. RESULTS: A total of 1345 patients presenting with ST-segment elevation myocardial infarction or left bundle branch block/pacemaker were included in this analysis. A total of 97 patients (7.2%) had cardiogenic shock, 26 patients at presentation, whereas 71 patients (73.2%) developed shock during hospital stay. Mortality was 71.8% among patients who developed cardiogenic shock during hospitalization as compared with 65.4% among those who were already in shock upon admission (P = 0.54). By multivariable analysis, we identified Killip class more than 1, lower systolic blood pressure at presentation, older age, unsuccessful reperfusion and diabetes as independent predictors of developing shock during hospitalization. CONCLUSION: The present study shows that the largest proportion of cardiogenic shock complicating ST-segment elevation myocardial infarction is observed after initial hospitalization, particularly in patients with Killip class more than 1, low systolic blood pressure at presentation and advanced age. The identification of these patients may help in preventing this complication by more aggressive pharmacological therapies, mechanical haemodynamic support, as well as coronary revascularization.

Myocardial late gadolinium enhancement in specific cardiomyopathies by cardiovascular magnetic resonance: a preliminary experience.

Late gadolinium enhancement cardiovascular magnetic resonance (CMR) can visualize myocardial interstitial abnormalities. The aim of this study was to assess whether regions of abnormal myocardium can also be visualized by late enhancement gadolinium CMR in the specific cardiomyopathies. A retrospective review of all referrals for gadolinium CMR with specific cardiomyopathy over 20 months. Nine patients with different specific cardiomyopathies were identified. Late enhancement was demonstrated in all patients, with a mean signal intensity of 390 +/- 220% compared with normal regions. The distribution pattern of late enhancement was unlike the subendocardial late enhancement related to coronary territories found in myocardial infarction. The affected areas included papillary muscles (sarcoid), the mid-myocardium (Anderson-Fabry disease, glycogen storage disease, myocarditis, Becker muscular dystrophy) and the global sub-endocardium (systemic sclerosis, Loeffler's endocarditis, amyloid, Churg-Strauss). Focal myocardial late gadolinium enhancement is found in the specific cardiomyopathies, and the pattern is distinct from that seen in infarction. Further systematic studies are warranted to assess whether the pattern and extent of late enhancement may aid diagnosis and prognostic assessment.

Quantification of myocardial perfusion using dynamic 64-detector computed tomography.

OBJECTIVES: The purpose of this study was to determine the ability of dynamic 64 slice multidetector computed tomography (d-MDCT) to provide an accurate measurement of myocardial blood flow (MBF) during first-pass d-MDCT using semiquantitative and quantitative analysis methods. MATERIALS AND METHODS: Six dogs with a moderate to severe left-anterior descending artery stenosis underwent adenosine (0.14 mL . kg-1 . min-1) stress d-MDCT imaging according to the following imaging protocol: iopamidol 10 mL/s for 3 seconds, 8 mm x 4 collimation, 400 milliseconds gantry rotation time, 120 kV, and 60 mAs. Images were reconstructed at 1-second intervals. Regions of interest were drawn in the LAD and remote territories, and time-attenuation curves were constructed. Myocardial perfusion was analyzed using a model-based deconvolution method and 2 upslope methods and compared with the microsphere MBF measurements. RESULTS: The myocardial upslope-to-LV-upslope and myocardial upslope-to-LV-max ratio strongly correlated with MBF (R2 = 0.92, P < 0.0001 and R2 = 0.87, P < 0.0001, respectively). Absolute MBF derived by model-based deconvolution analysis modestly overestimated MBF compared with microsphere MBF (3.0 +/- 2.5 mL . g-1 . min-1 vs. 2.6 +/- 2.7 mL . g-1 . min-1, respectively). Overall, MDCT-derived MBF strongly correlated with microspheres (R = 0.91, P < 0.0001, mean difference: 0.45 mL . g-1 . min-1, P = NS). CONCLUSIONS: d-MDCT MBF measurements using upslope and model-based deconvolution methods correlate well with microsphere MBF. These methods may become clinically applicable in conjunction with coronary angiography and next generation MDCT scanners with larger detector arrays and full cardiac coverage.

Morphologic validation of reperfused hemorrhagic myocardial infarction by cardiovascular magnetic resonance.

The purposes of this study were to assess the ex vivo cardiovascular magnetic resonance (CMR) signals of pathologically proved hemorrhagic myocardial infarction (MI) and to correlate these with in vivo CMR findings. Late gadolinium hypoenhancement within a hyperenhanced area in reperfused acute MI is ascribed to severe microvascular obstruction. The hearts of 2 patients, who died from cardiogenic shock after acute MIs and who had undergone coronary recanalization and in vivo CMR, were examined by T(2) and T(1) late enhancement sequences as well as by gross and histologic investigation. Four corresponding short-axis slices of each cardiac specimen from the base to the left ventricular apex were selected to assess the extent of MI and hemorrhage and were compared with the in vivo T(2) and late enhancement CMR scans. On pathologic examination, the extent of MI was 57 +/- 30% and 44 +/- 24%, and the extent of hemorrhage was 23 +/- 13% and 19 +/- 8% of the left ventricular area, respectively, showing progressive increases from the base to the apex. The low-signal intensity areas observed by ex vivo T(2) CMR strongly correlated with the hemorrhage quantified on histology (R = 0.93, p = 0.0007). Using ex vivo late gadolinium sequences, bright areas surrounded by thin dark rims, consistent with magnetic susceptibility effects, were detected, corresponding with hemorrhage. On in vivo CMR images, low-signal intensity and hyperintense areas with peripheral susceptibility artifacts were observed within the MI core on T(2) and late gadolinium sequences, respectively. In conclusion, in reperfused MI, CMR hypointense T(2) signal and susceptibility effects within the late gadolinium hypoenhanced areas are consistent with interstitial hemorrhage due to irreversible vascular injury, as proved by pathologic study.

Contrast-enhanced cardiovascular magnetic resonance in primary and ischemic dilated cardiomyopathy.

OBJECTIVES: Differentiation between primary dilated cardiomyopathy and ischemic cardiomyopathy has an important clinical significance. Contrast-enhanced cardiovascular magnetic resonance can play a role in this task, identifying myocardial scarring or fibrosis as presence of delayed enhancement. The aim of the present study was to evaluate the diagnostic potential of contrast-enhanced cardiovascular magnetic resonance in differentiating dilated cardiomyopathy from ischemic cardiomyopathy. METHODS: Contrast-enhanced cardiovascular magnetic resonance was performed in 100 patients with left ventricular dilatation and reduced systolic function: 24 had normal coronary arteries (dilated cardiomyopathy group) and 76 had significant coronary artery disease (ischemic cardiomyopathy group), with or without previous myocardial infarction. RESULTS: In the dilated cardiomyopathy group, only seven (29%) patients showed delayed enhancement and its pattern was characterized by mid-wall, patchy or diffuse location. All patients with ischemic cardiomyopathy and prior myocardial infarction (54 subjects) showed delayed enhancement with subendocardial (n = 4) or transmural (n = 50) extension. Among the 22 patients with ischemic cardiomyopathy but without previous myocardial infarction, 13 (59%) showed either subendocardial (n = 4) or transmural (n = 9) delayed enhancement. CONCLUSIONS: Patterns of delayed enhancement are different in dilated cardiomyopathy and ischemic cardiomyopathy, reflecting the presence of scarring or various degrees of fibrosis in left ventricular myocardium. The presence of subendocardial or transmural delayed enhancement at contrast-enhanced cardiovascular magnetic resonance allowed distinction between dilated cardiomyopathy and ischemic cardiomyopathy with high sensitivity (88%) and specificity (100%). Integration of cardiovascular magnetic resonance results with angiographic information can be useful in the identification of pathogenic mechanisms underlying left ventricular dysfunction.

Multidetector computed tomography myocardial perfusion imaging during adenosine stress.

OBJECTIVES: The purpose of this study is to validate the accuracy of multidetector computed tomography (MDCT) to measure differences in regional myocardial perfusion during adenosine stress in a canine model of left anterior descending (LAD) artery stenosis, during first-pass, contrast-enhanced helical MDCT. BACKGROUND: Myocardial perfusion imaging by MDCT may have significant implications in the diagnosis and treatment of coronary artery disease. METHODS: Eight dogs were prepared with a LAD stenosis, and contrast-enhanced MDCT imaging was performed 5 min into adenosine infusion (0.14 to 0.21 mg/kg/min). Images were analyzed using a semiautomated approach to define the regional signal density (SD) ratio (myocardial SD/left ventricular blood pool SD) in stenosed and remote territories, and then compared with microsphere myocardial blood flow (MBF) measurements. RESULTS: Mean MBF in stenosed versus remote territories was 1.37 +/- 0.46 ml/g/min and 1.29 +/- 0.48 ml/g/min at baseline (p = NS) and 2.54 +/- 0.93 ml/g/min and 8.94 +/- 5.74 ml/g/min during adenosine infusion, respectively (p < 0.05). Myocardial SD was 92.3 +/- 39.5 HU in stenosed versus 180.4 +/- 41.9 HU in remote territories (p < 0.001). There was a significant linear association of the SD ratio with MBF in the stenosed territory (R = 0.98, p = 0.001) and between regional myocardial SD ratio and MBF <8 ml/g/min, slope = 0.035, SE = 0.007, p < 0.0001. Overall, there was a significant non-linear relationship over the range of flows studied (LR chi-square [2 degrees of freedom] = 31.8, p < 0.0001). CONCLUSIONS: Adenosine-augmented MDCT myocardial perfusion imaging provides semiquantitative measurements of myocardial perfusion during first-pass MDCT imaging in a canine model of LAD stenosis.

Contrast-enhanced multidetector computed tomography viability imaging after myocardial infarction: characterization of myocyte death, microvascular obstruction, and chronic scar.

BACKGROUND: The ability to distinguish dysfunctional but viable myocardium from nonviable tissue has important prognostic implications after myocardial infarction. The purpose of this study was to validate the accuracy of contrast-enhanced multidetector computed tomography (MDCT) for quantifying myocardial necrosis, microvascular obstruction, and chronic scar after occlusion/reperfusion myocardial infarction. METHODS AND RESULTS: Ten dogs and 7 pigs underwent balloon occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion. Contrast-enhanced (Visipaque, 150 mL, 325 mg/mL) MDCT (0.5 mm x 32 slice) was performed before occlusion and 90 minutes (canine) or 8 weeks (porcine) after reperfusion. MDCT images were analyzed to define infarct size/extent and microvascular obstruction and compared with postmortem myocardial staining (triphenyltetrazolium chloride) and microsphere blood flow measurements. Acute and chronic infarcts by MDCT were characterized by hyperenhancement, whereas regions of microvascular obstruction were characterized by hypoenhancement. MDCT infarct volume compared well with triphenyltetrazolium chloride staining (acute infarcts 21.1+/-7.2% versus 20.4+/-7.4%, mean difference 0.7%; chronic infarcts 4.15+/-1.93% versus 4.92+/-2.06%, mean difference -0.76%) and accurately reflected morphology and the transmural extent of injury in all animals. Peak hyperenhancement of infarcted regions occurred approximately 5 minutes after contrast injection. MDCT-derived regions of microvascular obstruction were also identified accurately in acute studies and correlated with reduced flow regions as measured by microsphere blood flow. CONCLUSIONS: The spatial extent of acute and healed myocardial infarction can be determined and quantified accurately with contrast-enhanced MDCT. This feature, combined with existing high-resolution MDCT coronary angiography, may have important implications for the comprehensive assessment of cardiovascular disease.