Differentiation between fresh and old left ventricular thrombi by deformation imaging.

BACKGROUND: Noninvasive echocardiographic differentiation between old and fresh left ventricular thrombi after myocardial infarction would be of clinical importance to estimate the risk for embolization and the necessity of anticoagulation. METHODS AND RESULTS: Fifty-two patients, aged 41 to 87 years, with a thrombus after myocardial infarction were included in this 2-part study: In substudy-I, 20 patients, 10 each with a definite diagnosis of fresh or old thrombus, were included. In the subsequent prospective substudy-II, 32 consecutive patients with an incident thrombus after myocardial infarction but unknown thrombus age were started on phenprocoumon and followed for 6 months. Data on medical history, standard echocardiography, strain-rate (SR) imaging and magnetic resonance tomography were analyzed. In substudy-I, analysis of thrombus deformation revealed the most rapid change in SR during the isovolumetric relaxation period when cavity pressure decreases rapidly. Fresh (range: 5-27 days) and old thrombi (4-26 months) could be discriminated without overlap by peak SR during the isovolumetric relaxation period, using a cutoff value of 1 s(-1). Applying this threshold value in substudy-II, 17 thrombi were echocardiographically classified as fresh (=SR ≥1 s(-1)) and 15 as old. After 6 months in the fresh thrombus group, 16 of 17 thrombi had disappeared (94%), and in 1 patient the thrombus size was diminished by >50% (now presenting an old thrombus SR pattern). In contrast, 14 of the 15 old thrombi remained unchanged in size and deformation (1 thrombus disappeared). CONCLUSIONS: Fresh and old intracavitary thrombi can be reliably differentiated by deformation imaging. In fresh thrombi, anticoagulation with phenprocoumon results in thrombus resolution in most patients.

Echocardiographic quantification of regional deformation helps to distinguish isolated left ventricular non-compaction from dilated cardiomyopathy.

AIMS: Pronounced trabeculation is presented in both left ventricular non-compaction (LVNC) and dilated cardiomyopathy (DCM), which sometimes makes the differentiation difficult. We hypothesized that echocardiographic deformation analysis would help to differentiate these two cardiomyopathies. METHODS AND RESULTS: We investigated 15 patients with LVNC (9 males; 42 ± 9 years), 15 age- and gender-matched DCM patients, and 15 healthy controls. The echocardiographic diagnosis of LVNC was confirmed by magnetic resonance imaging. In all subjects standard echocardiography and tissue Doppler imaging (TDI) to study regional LV deformation were carried out. No statistical difference was observed in standard echocardiographic parameters between LVNC and DCM patients. Compared with controls, both patient groups showed significantly reduced annular displacements (septal: controls 14 ± 2 mm vs. DCM 6 ± 3 mm vs. LVNC 7 ± 3 mm) and reduced strain values of the LV segments. A characteristic deformation pattern with significantly higher values in the LV base compared with the apex was observed in patients with LVNC by deformation measurements with TDI. This gradient was found particularly in the lateral and inferior wall but spared the anteroseptal wall; non-compaction was not found in basal segments throughout the ventricle and also spared the anteroseptal midventricular wall. In DCM the strain and strain rate values were homogeneously reduced in all LV segments. CONCLUSION: A special regional deformation pattern (preserved deformation in basal segments of LVNC) seems to be of major diagnostic help for the definite differential diagnosis of LVNC and DCM.

Remodeling of the infarct territory in the time course of infarct healing in humans.

OBJECT: To analyze the remodeling processes of the infarct territory in the time course of infarct healing. MATERIALS AND METHODS: Serial late enhancement (LE) studies were performed in 30 patients following reperfused myocardial infarction (MI) in the first and second week post-MI and after 3 months. To characterize infarct remodeling over time, the following variables were derived and analyzed in a blinded fashion: Infarct size (IS, in mm(3)), maximum infarct thickness (IT(max), mm), mean infarct thickness (IT(mean), mm) and the variability of infarct thickness (VIT=IT(max)/IT(mean)). Further, a new parameter for the assessment of infarct remodeling, the infarct extent (IE, mm(2)) was computed. IE quantifies IS in two dimensions along the heart's circumferential and longitudinal directions. IS was divided by the IE to obtain IT(mean). RESULTS: Overall infarct thickness was highly variable. Infarct shrinkage due to infarct thinning and IE reduction was found in the first months of healing. IS, IT(mean) and IT(max) significantly decreased during follow-up. There was a less consistent change of the IE: IE decreased in 75% of all infarcts from the first week up to 3 months post-MI, whereas 25% of infarcts expanded. Infarct thinning was found in almost all patients (92%), hence occurring in patients with infarct expansion and in patients without infarct expansion. CONCLUSION: Infarct thinning and-to a lesser extent-IE reduction, contribute to infarct shrinkage in the time course of infarct healing. Infarct thinning may occur without infarct expansion.

23Na MRI combined with contrast-enhanced 1H MRI provides in vivo characterization of infarct healing.

Although (23)Na MRI has been shown to delineate acute myocardial infarction (MI), the time course of in vivo (23)Na MRI during infarct healing remains unknown. In this study (23)Na MRI was combined with contrast-enhanced (CE) (1)H MRI to noninvasively characterize infarct healing in vivo. Serial in vivo 3D (23)Na MRI and (1)H MRI were performed for up to 9 weeks postinfarction in 10 dogs. Radioactive microspheres were used to measure myocardial perfusion, and Hematoxylin-Eosin (H&E) and Masson's trichrome (MT) staining were used to assess interstitial cell infiltrate and collagen content. In vivo (23)Na MRI accurately delineated infarct size up to day 5 postinfarction in comparison with (1)H MRI (8.9% +/- 8.1% vs. 8.6% +/- 7.9% on day 1 postinfarction, P = NS; and 6.3% +/- 6.2% vs. 6.2% +/- 6.2% on days 4/5 postinfarction, P = NS). The in vivo (23)Na MRI signal intensity, expressed as the signal intensity ratio of infarcted tissue vs. noninfarcted tissue (MI/R) peaked on day 1 of infarction (2.04 +/- 0.23) but decreased significantly to 1.27 at 9 weeks postinfarction (P < 0.05) due to granulation tissue infiltrate and collagen deposition. To confirm the MI/R decrease during scar formation ex vivo, we performed (23)Na MRI in 12 rats on day 3 post-MI (N = 5) and after 6 weeks (N = 7). H&E and Picrosirius Red staining confirmed granulation tissue infiltrate on day 3 and scar formation after 6 weeks. MI/R decreased significantly from 1.91 +/- 0.45 on day 3 post-MI to 1.3 +/- 0.09 after 6 weeks. Thus, in vivo (23)Na MRI accurately delineates infarct size up to day 5 postinfarction. In vivo (23)Na MRI signal intensity decreases during infarct healing as a result of the underlying infarct healing process.

Time course of 23Na signal intensity after myocardial infarction in humans.

Experimental studies demonstrated persistently increased 23Na content in nonviable myocardium post-myocardial infarction (MI). We hypothesized that nonviable myocardium in humans would show elevated 23Na content at all stages of infarct development, and therefore could be imaged with 23Na MRI. Ten patients were examined on days 4, 14, and 90 after infarction, and five of these patients participated in a 12-month follow-up. Double angulated short-axis cardiac 23Na images were obtained with the use of a 23Na surface coil and an ECG-triggered, 3D gradient-echo sequence. 1H T2-weighted imaging (N = 9) was performed on days 4, 14, and 90. Wall motion was assessed by cine MRI, and the infarct size was determined by late enhancement on day 90. The 23Na signal intensity (SI) of infarcted myocardium was expressed as the percentage increase over 23Na SI of noninfarcted myocardium. All of the patients showed an area of elevated SI on 23Na and 1H T2-weighted images that correlated with wall motion abnormalities and late enhancement. 23Na SI was highest on day 4. It then decreased until day 90, but remained elevated (39% +/- 18%, 31% +/- 17%, 28% +/- 13% on days 4, 14, and 90, respectively, P = 0.001). No further decrease was found 1 year after infarction (25% +/- 7%, P = 0.89 vs. day 90). 1H T2-weighted SI decreased between days 4 and 14, but on day 90 only six of nine patients had a residual elevated SI. Thus, 23Na SI is elevated in nonviable infarction at all time points following MI, and 23Na MRI may become a suitable technique for imaging nonviable myocardium in humans.

Infarct resorption, compensatory hypertrophy, and differing patterns of ventricular remodeling following myocardial infarctions of varying size.

OBJECTIVES: We sought to identify advantages of contrast-enhanced magnetic resonance imaging (MRI) in studying postinfarction ventricular remodeling. BACKGROUND: Although sequential measurements of ventricular volumes, internal dimensions, and total ventricular mass have provided important insights into postinfarction left ventricular remodeling, it has not been possible to define serial, directionally opposite changes in resorption of infarcted tissue and hypertrophy of viable myocardium and effects of these changes on commonly used indices of remodeling. METHODS: Using gadolinium-enhanced MRI, the time course and geometry of changes in infarcted and noninfarcted regions were assessed serially in dogs subjected to coronary occlusion for 45 min, 90 min, or permanently. RESULTS: Infarct mass decreased progressively between three days and four to eight weeks following coronary occlusion; terminal values averaged 24 +/- 3% of those at three days. Radial infarct thickness also decreased progressively, whereas changes in circumferential and longitudinal extent of infarction were variable. The ability to define the circumferential endocardial and epicardial extents of infarction allowed radial thinning without epicardial expansion to be distinguished from true infarct expansion. The mass of noninfarcted myocardium increased by 15 +/- 2% following 90-min or permanent occlusion. However, the time course of growth of noninfarcted myocardium differed systematically from that of infarct resorption. Measurements of total ventricular mass frequently failed to reflect concurrent changes in infarcted and noninfarcted regions. Reperfusion accelerated infarct resorption. Histologic reductions in nucleus-to-cytoplasm ratios corresponded with increases in noninfarcted ventricular mass. CONCLUSIONS: Concurrent directionally opposite changes in infarcted and noninfarcted myocardium can be defined serially, noninvasively, and with high spatial resolution and full ventricular coverage following myocardial infarction.