Search

Aims: The autopsy rate worldwide is alarmingly low (0-15%). Mortality statistics are important, and it is, therefore, essential to perform autopsies in a sufficient proportion of deaths. The imaging autopsy, non-invasive, or minimally invasive autopsy (MIA) can be used as an alternative to the conventional autopsy in an attempt to improve postmortem diagnostics by increasing the number of postmortem procedures. The aim of this study was to determine the diagnostic accuracy of postmortem magnetic resonance imaging (MRI), computed tomography (CT), and CT-guided biopsy for the detection of acute and chronic myocardial ischaemia., Methods and Results: We included 100 consecutive adult patients who died in hospital, and for whom next-of-kin gave permission to perform both conventional autopsy and MIA. The MIA consists of unenhanced total-body MRI and CT followed by CT-guided biopsies. Conventional autopsy was used as reference standard. We calculated sensitivity and specificity and receiver operating characteristics curves for CT and MRI as the stand-alone test or combined with biopsy for detection of acute and chronic myocardial infarction (MI). Sensitivity and specificity of MRI with biopsies for acute MI was 0.97 and 0.95, respectively and 0.90 and 0.75, respectively for chronic MI. MRI without biopsies showed a high specificity (acute: 0.92; chronic: 1.00), but low sensitivity (acute: 0.50; chronic: 0.35). CT (total Agatston calcium score) had a good diagnostic value for chronic MI [area under curve (AUC) 0.74, 95% confidence interval (CI) 0.64-0.84], but not for acute MI (AUC 0.60, 95% CI 0.48-0.72)., Conclusion: We found that the combination of MRI with biopsies had high sensitivity and specificity for the detection of acute and chronic myocardial ischaemia.

Despite early revascularization, remodeling and dysfunction of the left ventricle (LV) after acute myocardial infarction (AMI) remain important therapeutic targets. Intermittent pacing therapy (IPT) of the LV can limit infarct size, when applied during early reperfusion. However, the effects of IPT on post-AMI LV remodeling and infarct healing are unknown. We therefore investigated the effects of IPT on global LV remodeling and infarct geometry in swine with a 3-day old AMI. For this purpose, fifteen pigs underwent 2 h ligation of the left circumflex coronary artery followed by reperfusion. An epicardial pacing lead was implanted in the peri-infarct zone. After three days, global LV remodeling and infarct geometry were assessed using magnetic resonance imaging (MRI). Animals were stratified into MI control and IPT groups. Thirty-five days post-AMI, follow-up MRI was obtained and myofibroblast content, markers of extracellular matrix (ECM) turnover and Wnt/frizzled signaling in infarct and non-infarct control tissue were studied. Results showed that IPT had no significant effect on global LV remodeling, function or infarct mass, but modulated infarct healing. In MI control pigs, infarct mass reduction was principally due to a 26.2 ± 4.4% reduction in infarct thickness (P ≤ 0.05), whereas in IPT pigs it was mainly due to a 35.7 ± 4.5% decrease in the number of infarct segments (P ≤ 0.05), with no significant change in infarct thickness. Myofibroblast content of the infarct zone was higher in IPT (10.9 ± 2.1%) compared to MI control (5.4 ± 1.6%; P ≤ 0.05). Higher myofibroblast presence did not coincide with alterations in expression of genes involved in ECM turnover or Wnt/frizzled signaling at 5 weeks follow-up. Taken together, IPT limited infarct expansion and altered infarct composition, showing that IPT influences remodeling of the infarct zone, likely by increasing regional myofibroblast content.

Background: Our current understanding is that left ventricular (LV) remodeling after acute myocardial infarction (AMI) is caused by expansion of the infarcted myocardium with thinning of the wall and eccentric hypertrophy of the remote myocardium. To study the geometric changes in the remodeling process after reperfused AMI we used cardiac magnetic resonance imaging (CMR)., Methods: Nine juvenile swine underwent a 120-min occlusion of the left circumflex coronary artery followed by reperfusion. CMR was performed at 3 and 36 days post-infarction. Global and regional LV remodeling was assessed including geometric changes of infarcted and remote myocardium; infarct longitudinal length (mm), mean circumferential length (mm), total infarct surface (mm(2)), end-diastolic wall thickness (EDWT) (mm) and transmural extent of infarction (TEI)., Results: From 3 days to 36 days post-infarction end-diastolic volume increased by 43% (p<0.01). Infarct mass decreased by 36% (p<0.01), mainly by reduction of EDWT with 26%, while mean infarct circumferential length and longitudinal infarct length did not change. Remote myocardial mass increased by 23%, which was the result of an increase in its circumferential length from 95 ± 10 mm to 113 ± 11 mm (p<0.01), with no change in its EDWT. In contrast, EDWT in the infarct, peri-infarct and border zone decreased., Conclusions: Contrary to the widely held view the present, using CMR measurements, shows that post-infarction remodeling was not associated with expansion of the infarcted myocardium. These findings suggest that eccentric hypertrophy of the remote myocardium, but not expansion of the infarct region, is responsible for left ventricular dilatation after AMI., (© 2013.)

Regeneration of infarcted myocardium by injecting stem cells has been proposed to prevent heart failure. We studied the i.c. administration of human umbilical cord blood stem cells (USSC) in a porcine model of myocardial infarction (MI) and reperfusion. In 15 swine, MI was induced by balloon-occlusion of the left circumflex coronary artery (LCX) for 2 h followed by reperfusion. Five swine served as healthy controls. One week later, magnetic resonance imaging (MRI) was performed to assess left ventricular (LV) function and infarct size. Then, under immune suppression, 6 of the 12 surviving MI swine received intracoronary injection of approximately 10(8) human USSC in the LCX while the other MI-swine received medium. Four weeks later all swine underwent follow-up MRI, and were sacrificed for histology. One week after MI, end-diastolic volume (92+/-3 mL) and LV mass (75+/-2 g) were larger, while ejection fraction (42+/-2%) was smaller than in healthy control (68+/-3 mL, 66+/-3 g and 55+/-3%, all P<0.05). Regional wall thickening (-7+/-2%) in the LCX area became akinetic. No difference in global and regional LV function at 5 weeks was observed between MI animals receiving USSC or medium. Infarct size after USSC treatment was significantly larger (20+/-3 g vs. 8+/-2 g, P<0.05). USSC survived only in the infarct border zone at 5 weeks and did not express cardiomyocyte or endothelial markers. Histology showed that intracoronary injection of USSC caused micro infarctions by obstructing blood vessels. In swine with a 1 week old MI, injection of USSC via the intracoronary route does not improve LV function 4 weeks later.

Aims: Magnetic resonance imaging (MRI) has been proposed as a tool to track iron oxide-labelled cells within myocardial infarction (MI). However, infarct reperfusion aggravates microvascular obstruction (MO) and causes haemorrhage. We hypothesized that haemorrhagic MI causes magnetic susceptibility-induced signal voids that may interfere with iron oxide-labelled cell detection., Methods and Results: Pigs (n = 23) underwent 2 h occlusion of the left circumflex artery. Cine, T2*-weighted, perfusion, and delayed enhancement MRI scans were performed at 1 and 5 weeks, followed by ex vivo high-resolution scanning. At 1 week, MO was observed in 17 out of 21 animals. Signal voids were observed on T2*-weighted scans in five out of eight animals, comprising 24 +/- 22% of the infarct area. A linear correlation was found between area of MO and signal voids (R2 = 0.87; P = 0.002). At 5 weeks, MO was observed in two out of 13 animals. Signal voids were identified in three out of seven animals. Ex vivo scanning showed signal voids on T2*-weighted scanning in all animals because of the presence of haemorrhage, as confirmed by histology. Signal voids interfered with the detection of iron oxide-labelled cells ex vivo (n = 21 injections)., Conclusion: Haemorrhage in reperfused MI produces MRI signal voids, which may hamper tracking of iron oxide-labelled cells.

Unlabelled: The effects of reperfusion on early and late infarct size and left ventricular wall characteristics were studied by performing cine-magnetic resonance imaging, first-pass perfusion, and delayed enhancement imaging in 22 patients at five days and five months after successful primary angioplasty for first acute myocardial infarction. Infarct size, end-diastolic wall thickness, and segmental wall thickening were quantified, and the extent of microvascular obstruction (MO) was evaluated qualitatively. Infarct size decreased by 31%. Segments without MO had early increased wall thickness and late partially normalized wall thickening. Segments with MO showed late wall thinning and no functional recovery at five months., Objectives: We aimed to study the effects of early successful primary angioplasty for ST-segment elevation acute myocardial infarction (AMI) on early and late infarct size and left ventricular (LV) wall characteristics., Background: Early reperfusion treatment for AMI preserves LV function, but the effects on early and late infarct size, end-diastolic wall thickness (EDWT), and segmental wall thickening (SWT) are not well known., Methods: In 22 patients with successful primary angioplasty for first AMI, cine-magnetic resonance imaging (MRI), first-pass perfusion, and delayed-enhancement imaging was performed at five days and five months. The extent of microvascular obstruction (MO) was evaluated on perfusion images. Infarct shrinkage was defined as the difference between the volume of delayed-enhancement at five days and five months. The EDWT and SWT were quantified on cine-MRI., Results: Infarct shrinkage occurred to the same extent in small and large infarctions [r = 0.92; p < 0.001], with a mean decrease of 31% (35 +/- 21 g to 24 +/- 17 g). Dysfunctional segments without MO had an increased EDWT at five days compared with remote myocardium (9.2 +/- 1.7 mm vs. 8.4 +/- 1.7 mm; p < 0.001). At five months, EDWT in these segments became comparable to the thickness of remote myocardium (7.8 +/- 1.6 mm vs. 7.6 +/- 1.4 mm; p = 0.60), and SWT improved (21 +/- 15% to 40 +/- 24%; p < 0.001) but remained impaired (40 +/- 24% vs. 71 +/- 29%; p < 0.001). Segments with MO demonstrated wall thinning at five months (6.4 +/- 1.3 mm vs. 7.6 +/- 1.4 mm; p = 0.006) and no significant recovery in SWT (12 +/- 14% to 17 +/- 20%; p = 0.15)., Conclusions: Infarct size decreased by 31%. Segments without MO had early increased wall thickness and late partial functional recovery. Segments with MO showed late wall thinning and no functional recovery at five months.

Aims: To study recovery of segmental wall thickening (SWT), ejection fraction (EF), and end-systolic volume (ESV) after acute myocardial infarction (AMI) in patients who underwent primary stenting with drug-eluting stents. Additionally, to evaluate the predictive value of magnetic resonance imaging (MRI)-based myocardial perfusion and delayed enhancement (DE) imaging., Methods and Results: Twenty-two patients underwent cine-MRI, first-pass perfusion, and DE imaging 5 days after successful placement of a drug-eluting stent in the infarct-related coronary artery. Regional myocardial perfusion and the transmural extent of DE were evaluated. A per patient perfusion score was calculated and consisted of a summation of all segmental scores. Myocardial infarct size was quantified by measuring the volume of DE. At 5 months after AMI, cine-MRI was performed and SWT, EF, and ESV were quantified. EF increased from 48+/-11 to 55+/-9% (P<0.01). SWT at 5 months was inversely related to baseline segmental DE scores (P<0.001) and segmental perfusion scores (P<0.001). EF and ESV at 5 months were related to acute infarct size (R(2)=0.65; P<0.001 and R(2)=0.78; P<0.001, respectively) and the calculated perfusion score (R(2)=0.23; P=0.02 and R(2)=0.14; P=0.09, respectively) at baseline., Conclusion: Marked recovery of left ventricular function was observed in patients receiving a drug-eluting stent for AMI. DE imaging appears to be a better prognosticator than perfusion imaging.