Infarct Mass Research Articles

Relationship Between Myocardial Reperfusion, Infarct Size, and Mortality: The INFUSE-AMI (Intracoronary Abciximab and Aspiration Thrombectomy in Patients With Large Anterior Myocardial Infarction) Trial

This study sought to compare infarct size (IS) measured by magnetic resonance imaging in patients with successful (myocardial blush grade [MBG] 2/3) versus unsuccessful (MBG 0/1) microcirculatory reperfusion in the INFUSE-AMI (Intracoronary Abciximab and Aspiration Thrombectomy in Patients With Large Anterior Myocardial Infarction) trial. Successful microcirculatory reperfusion, defined angiographically by MBG 2 or 3, is associated with improved outcomes in patients with ST-segment elevation myocardial infarction. The precise mechanism underlying this association is not well defined. The INFUSE-AMI trial randomized 452 patients with anterior ST-segment elevation myocardial infarction to intracoronary bolus abciximab delivered locally at the infarct lesion versus no abciximab, and to manual thrombus aspiration versus no aspiration. The primary endpoint was IS (percentage of left ventricular mass) at 30 days. MBG 2/3 was achieved in 367 patients (81.4%). IS was significantly lower in patients with MBG 2/3 than in those with MBG 0/1 (median: 16.7% [interquartile range (IQR): 7.0 to 22.7] vs. 19.5% [IQR: 11.1 to 29.2]; p = 0.002). Intracoronary abciximab further reduced IS in patients with MBG 2/3 (median: 14.4% [IQR: 5.4 to 20.9] vs. 17.4% [IQR: 10.5 to 23.8]; p = 0.01). MBG 2/3 was associated with ∼30% reduction in infarct mass (p = 0.002) and ∼90% reduction in microvascular obstruction on day 5. Ejection fraction was higher with MBG 2/3 at 30 days: median: 50.3% (IQR: 43.8 to 57.8) versus 46.9% (IQR: 37.5 to 54.0); p = 0.004. At 30 days, the rate of death was significantly lower (1.7% vs. 8.3%; p = 0.0008) in the MBG 2/3 group. MBG 2/3 occurs in 80% of ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention and is associated with smaller infarct size, less microvascular obstruction, improved ejection fraction, and significantly lower 30-day mortality. (Intracoronary Abciximab and Aspiration Thrombectomy in Patients With Large Anterior Myocardial Infarction [INFUSE-AMI]; NCT00976521).

1039Time after contrast injection is crucial to determine infarct transmurality and myocardial functional recovery after an acute myocardial infarction

Background: In acute myocardial infarction (MI), contrast hyperenhancement include infarcted myocardium (late enhancement), and area at risk (early enhancement). There is no information about the optimal timing to differentiate these 2 time periods in order to better determine infarct size. Aims: To determine whether the time after contrast injection influences the size of hyperenhancement in acute and chronic MI, and the time that better predicts infarct size and functional recovery.9 Table Table Methods: Subjects were evaluated using CMR the first week (n= 60) and 3 months (n = 47) after an STEMI percutaneously revascularized. Short-axis cine views (SSFP sequences) were performed to quantify volumes, ejection fraction and determine the wall motion score index (WMSI). Inversion-recovery single-shot true fast imaging with steady-state precession (ss-IR) and segmented inversion-recovery gradient-echo (seg-IR) sequences were used. SS-IR was acquired 1, 3, 5, 7, 10, 15, 20, and 25 min after administration of 0.2 mmol/kg Gd-DTPA to analyze dynamic changes. Seg-IR was acquired starting at 10 min after contrast and were used for comparison to ss-IR. Inversion time was properly adjusted to null normal myocardium. All images were blinded, randomized, and measured for hyperenhancement volumes. Results: In acute MI, there was a significant decrease in infarct mass over time (p = 0.005). Hyperenhancement volume was maximum 3 min after contrast injection and stable after 20 min. Nevertheless, infarct mass remained constant over time in chronic MI (p = 0.886). Mean infarct size in acute and chronic MI by seg-IR was 24 ± 16 g and 12 ± 8 g respectively with excellent correlation to ss-IR (r = 0.96 and r = 0.98 p < 0.001). Depending on the imaging time for LGE, the transmurality index also changed, and thus, the number of patient with a transmural infarction (>75%) decreased over time (Table). A transmural infarction (>75%) at 25th min better predicted the absence of improvement in the WMSI, a lower number of segments that recovers function, a higher increase in left ventricular volumes and a lower ejection fraction compared to the transmurality assessed 10th minutes after. (Table). Conclusions: There is a change in infarct mass over time in acute but not in chronic MI, with a maximum volume 3 min after contrast injection. Infarct transmurality 25th min after contrast injection better predicts infarct size and functional recovery at follow-up.

093 RECIPROCAL ECG CHANGE IN ST-ELEVATION MYOCARDIAL INFARCTION IS ASSOCIATED WITH AREA AT RISK AND MYOCARDIAL SALVAGE FOLLOWING REVASCULARIZATION

<h3>Background</h3> ST elevation acute myocardial infarction (STEMI) is frequently associated with reciprocal ST depression in the contralateral ECG leads. The ECG remains a primary diagnostic factor in the hyperacute treatment of myocardial infarction. There has been longstanding debate over the relevance of reciprocal ECG changes in STEMI. CMR can retrospectively determine myocardial area at risk (AAR), namely, the area of myocardium that is susceptible to infarction prior to opening the infarct-related artery. T2-weighted (T2w) imaging can be combined with measures of infarction by late gadolinium enhanced (LGE) imaging to derive myocardial salvage, a measure with established prognostic relevance. We hypothesised that reciprocal ECG change reflects larger AAR as defined by CMR. <h3>Methods</h3> Patients after primary percutaneous coronary intervention for first STEMI underwent CMR at 1.5 T within 3 days of reperfusion. Presenting ECGs were assessed for presence or absence of reciprocal change, defined as ≥1 mm ST depression in ≥2 inferior leads for anterior STEMI, or ≥2 anterior leads for inferior STEMI. Patients with posterior ECG changes were excluded from analysis. Infarcted tissue was defined as hyperenhancement ≥2 SDs above remote myocardium on LGE imaging. AAR was defined on T2w images, defined as the mass of myocardium with signal intensity ≥2 SD above remote, normalised to LV myocardial mass (figure&nbsp;1). Myocardial salvage was calculated as (AAR mass—infarct mass), and myocardial salvage index as (myocardial salvage/AAR mass). <h3>Results</h3> Thirty-five patients had ECGs and images suitable for analysis. There were no significant differences in patient demographics (table&nbsp;1). Patients with reciprocal ECG changes had significantly higher AAR than those without (42.3% vs 23.6%, p&lt;0.001), myocardial salvage (17 g vs 2 g, p&lt;0.001) and myocardial salvage index (40% vs 7%, p&lt;0.001). Infarct size was not significantly different between patients with and without reciprocal ECG changes (25.6 g vs 27.4 g, p=0.8), nor was ejection fraction (43% vs 45%, p=0.5) or LV end diastolic volume (173 ml vs 174 ml, p=0.9). <h3>Conclusions</h3> Patients with STEMI presenting with reciprocal ECG changes have significantly larger AAR, and significantly higher myocardial salvage and salvage index than those without. Reciprocal ECG changes may be a marker of larger volumes of myocardium at risk, and may also denote patients with larger potential for salvage with revascularization. There was no relationship to infarct size, presumably as other factors, such as time to revascularization and TIMI flow post-procedure will influence the degree of myocardium infarcted. Data are shown as mean±SEM or n (%). There were no significant differences between the groups (p≥0.1 for all).

Coronary Wave Energy

Revascularization after acute coronary syndromes provides prognostic benefit, provided that the subtended myocardium is viable. The microcirculation and contractility of the subtended myocardium affect propagation of coronary flow, which can be characterized by wave intensity analysis. The study objective was to determine in acute coronary syndromes whether early wave intensity analysis-derived microcirculatory (backward) expansion wave energy predicts late viability, defined by functional recovery. Thirty-one patients (58±11 years) were enrolled after non-ST elevation myocardial infarction. Regional left ventricular function and late-gadolinium enhancement were assessed by cardiac magnetic resonance imaging, before and 3 months after revascularization. The backward-traveling (microcirculatory) expansion wave was derived from wave intensity analysis of phasic coronary pressure and velocity in the infarct-related artery, whereas mean values were used to calculate hyperemic microvascular resistance. Twelve-hour troponin T, left ventricular ejection fraction, and percentage late-gadolinium enhancement mass were 1.35±1.21 µg/L, 56±11%, and 8.4±6.0%, respectively. The infarct-related artery backward-traveling (microcirculatory) expansion wave was inversely correlated with late-gadolinium enhancement infarct mass (r=-0.81; P<0.0001) and strongly predicted regional left ventricular recovery (r=0.68; P=0.001). By receiver operating characteristic analysis, a backward-traveling (microcirculatory) expansion wave threshold of 2.8 W m(-2) s(-2)×10(5) predicted functional recovery with sensitivity and specificity of 0.91 and 0.82 (AUC 0.88). Hyperemic microvascular resistance correlated with late-gadolinium enhancement mass (r=0.48; P=0.03) but not left ventricular recovery (r=-0.34; P=0.07). The microcirculation-derived backward expansion wave is a new index that correlates with the magnitude and location of infarction, which may allow for the prediction of functional myocardial recovery. Coronary wave intensity analysis may facilitate myocardial viability assessment during cardiac catheterization.

Qualitative analysis of the elliptical centric technique and the TRICKS technique

This study evaluated the usefulness of time resolved imaging of contrast kinetics (TRICKS) magnetic resonance angiography (MRA) and elliptical centric MRA according to the type of cerebral disease. From February 2010 to January 2012, elliptical centric MRA and TRICKS MRA images were acquired from 50 normal individuals and 50 patients with cerebral diseases by using 3.0-Tesla magnetic resonance imaging (MRI) equipment. The images were analyzed qualitatively by examining areas such as the presence or absence of artifacts on the images, the distinctness of boundaries of blood vessels, accurate representation of the lesions, and the subtraction level. In addition, the sensitivity, specificity, positive prediction rate, negative prediction rate and accuracy were assessed by comparing the diagnostic efficacy of the two techniques. The results revealed TRICKS MRA to have superior image quality to elliptical centric MRA. Regarding each disease, TRICKS MRA showed higher diagnostic efficacy for artery venous malformation (AVM) and middle cerebral artery (MCA) bypass patients whereas elliptical centric MRA was more suitable for patients with brain tumors, cerebral infarction, cerebral stenosis or sinus mass.

Clinical parameters associated with myocardial hemorrhage in reperfused acute myocardial infarction — a cardiovascular MR study

Background Late reperfusion of acutely ischemic myocardium may result in intramyocardial hemorrhage that has been described as a contributor t or eperfusion injury. In patients with reperfused acute myocardial infarction (MI), the presence of myocardial hemorrhage can be detected by T2*-weighted cardiovascular magnetic resonance (CMR). This study aimed to identify clinical parameters associated with myocardial hemorrhage. Methods Thirty patients underwent CMR three days after acute reperfused MI including cine, hemorrhage-sensitive T2*weighted imaging, early (2-5 minutes post contrast) and late gadolinium enhancement (LGE) imaging for microvascular obstruction (MO) and necrosis, respectively. The extent of MO was measured on both early and late post-contrast images. Stepwise logistic regression analysis was performed to identify associations of clinical parameters with the presence of hemorrhage. The parameters tested were age, gender, risk factors, left ventricular (LV) volume and function, the extent of MO on early post-contrast images, the extent of MO on LGE images, the extent of infarc tion, time from the onset of pain to reperfusion, culprit artery, blood pressure, heart rate, TIMI flow, use of a thrombolytic agent, use of thrombo-aspiration devices, maximum value of troponin T and creatine kinase (CK), LDL, and HbA1c. LV volume was indexed by body surface area and infarct mass and MO mass were indexed by LV myocardial mass. Results Out of 30 patients, 19 patients showed MO and 18 of this group also showed hemorrhage. Indexed LV enddiastolic volume, the indexed MO mass on LGE images, the indexed infarction mass, maximum CK and troponin T were related to the presence of hemorrhage. The indexed infarct mass was the strongest predictor of the presence of hemorrhage (estimated regression coefficient 0.241(SE .095), p=0.011). Conclusions The presence of hemorrhage is associated with larger LV end-diastolic volume, larger infarct size, greater MO on LGE images, higher CK and troponin T value with infarct mass being the strongest predictor. These findings indicate that myocardial hemorrhage is strongly associated with the extent of myocardial damage in reperfused acut eM I. However, this study was limited by the small sample size. Future studies with larger sample size could provide more definitive conclusions.

Reciprocal ECG change in ST-elevation myocardial infarction is associated with area at risk and myocardial salvage following revascularization

Background ST elevation acute myocardial infarction (STEMI) is frequently associated with reciprocal ST depression in the contralateral ECG leads. The ECG remains a primary diagnostic factor in the hyperacute treatment of AMI. There has been longstanding debate over the relevance of reciprocal ECG changes in AMI. CMR can retrospectively determine myocardial area at risk (AAR), namely, the area of myocardium that is susceptible to infarction prior to opening the infarct-related artery. T2-weighted (T2w) imaging can be combined with measures of infarction by late gadolinium enhanced (LGE) imaging to derive myocardial salvage, a measure with established prognostic relevance. We hypothesised that reciprocal ECG change reflects larger AAR as defined by CMR. Methods Patients after primary percutaneous coronary intervention for first STEMI underwent CMR at 1.5T within 3 days of reperfusion. Presenting ECGs were assessed for presence or absence of reciprocal change, defined as ≥1mm ST depression in ≥2 inferior leads for anterior STEMI, or ≥2 anterior leads for inferior STEMI. Patients with posterior ECG changes were excluded from analysis. Infarcted tissue was defined as hyperenhancement ≥2 standard deviations (SD) above remote myocardium on LGE imaging. AAR was defined on T2w images, defined as the mass of myocardium with signal intensity ≥2 SD above remote, normalized to LV myocardial mass. Myocardial salvage was calculated as (AAR mass infarct mass), and myocardial salvage index as (myocardial salvage / AAR mass). Results Thirty-five patients had ECGs and images suitable for analysis. There were no significant differences in patient demographics (Table 1). Patients with reciprocal ECG changes had significantly higher AAR than those without (42.3% vs. 23.6%, p<0.001), myocardial salvage (17g vs 2g, p<0.001) and myocardial salvage index (40% vs. 7%, p<0.001). Infarct size was not significantly different between patients with and without reciprocal ECG changes (25.6g vs. 27.4g, p=0.8), nor was ejection fraction (43% vs. 45%, p=0.5) or LV end diastolic volume (173ml vs. 174ml, p=0.9). Conclusions Patients with STEMI presenting with reciprocal ECG changes have significantly larger AAR, and significantly higher myocardial salvage and salvage index than those without. Reciprocal ECG changes may be a marker of larger volumes of myocardium at risk, and may also denote patients with larger potential for salvage with revascularization. There was no relationship to infarct size, presumably as other factors, such as time to revascularization and TIMI flow post-procedure will influence the degree of myocardium infarcted.

Late Cardiac Remodeling After Primary Percutaneous Coronary Intervention

Primary percutaneous coronary intervention (PPCI) preserves function and improves survival. The late effects of PPCI on left ventricular remodeling, however, have not yet been investigated on cardiac magnetic resonance imaging (CMRI). Twenty-five patients with acute myocardial infarction (AMI) treated with PPCI underwent CMRI within 10 days, at 4 months and at 5 years. Left ventricular ejection fraction (LVEF), end-diastolic volume (EDV) and end-systolic volume were quantified on cine images. Infarct mass and transmural extent of infarction were quantified on contrast-enhanced imaging. In all patients EDV increased significantly in the early phase (192 ± 40 ml to 211 ± 49 ml, P ≤ 0.01) and LVEF improved significantly (42 ± 9% to 46 ± 9%, P=0.02). In the late phase (>4 months) no significant changes were observed (LVEF 44 ± 9%, P=0.07; EDV 216 ± 68 ml, P=0.38). Three different groups could be identified. One-third (32%) had no dilatation at all; one-third (32%) had limited dilatation at 4 months without progression later; and 36% had progressive dilatation both at 4 months and at late follow-up. This third group had an average increase in EDV of 20% in the acute phase followed by an additional 13%. The strongest predictor for progressive dilatation was infarct mass. Even in the era of PPCI for AMI followed by optimal medical therapy, one-third of patients had progressive dilatation, which was best predicted by infarct mass.

The allometric model in chronic myocardial infarction

BackgroundAn allometric relationship between different electrocardiogram (ECG) parameters and infarcted ventricular mass was assessed in a myocardial infarction (MI) model in New Zealand rabbits.MethodsA total of fifteen animals were used, out of which ten underwent left anterior descending coronary artery ligation to induce infarction (7–35% area). Myocardial infarction (MI) evolved and stabilized during a three month-period, after which, rabbits were sacrificed and the injured area was histologically confirmed. Right before sacrifice, ECGs were obtained to correlate several of its parameters to the infarcted mass. The latter was normalized after combining data from planimetry measurements and heart weight. The following ECG parameters were studied: RR and PR intervals, P-wave duration (PD), QRS duration (QRSD) and amplitude (QRSA), Q-wave (QA), R-wave (RA) and S-wave (SA) amplitudes, T-wave peak amplitude (TA), the interval from the peak to the end of the T-wave (TPE), ST-segment deviation (STA), QT interval (QT), corrected QT and JT intervals. Corrected QT was analyzed with different correction formulae, i.e., Bazett (QTB), Framingham (QTFRA), Fridericia (QTFRI), Hodge (QTHO) and Matsunaga (QTMA) and compared thereafter. The former variables and infarcted ventricular mass were then fitted to the allometric equation in terms of deviation from normality, in turn derived after ECGs in 5 healthy rabbits.ResultsSix variables (JT, QTB, QA, SA, TA and STA) presented statistical differences among leads. QT showed the best allometric fit (r = 0.78), followed by TA (r = 0.77), STA (r = 0.75), QTFRA (r = 0.72), TPE (r = 0.69), QTFRI (r = 0.68) and QTMA (r = 0.68). Corrected QT’s (QTFRA, QTFRI and QTMA) performed worse than the uncorrected counterpart (QT), the former scaling allometrically with similar goodness of fits.ConclusionsQT, TA, STA and TPE could possibly be used to assess infarction extent in an old MI event through the allometric model as a first approach. Moreover, the TPE also produced a good allometric scaling, leading to the potential existence of promising allometric indexes to diagnose malignant arrhythmias.

133 Coronary wave intensity: a novel invasive tool for predicting myocardial viability following acute coronary syndromes

IntroductionWave intensity analysis (WIA) uses simultaneous changes in intracoronary pressure and flow to characterise energy transfer within the coronary circulation. In normal hearts, flow is predominantly driven by a microcirculatory-derived,...

Intracoronary Abciximab and Aspiration Thrombectomy in Patients With Large Anterior Myocardial Infarction

Thrombus embolization during percutaneous coronary intervention (PCI) in ST-segment elevation myocardial infarction (STEMI) is common and results in suboptimal myocardial perfusion and increased infarct size. Two strategies proposed to reduce distal embolization and improve outcomes after primary PCI are bolus intracoronary abciximab and manual aspiration thrombectomy. To determine whether bolus intracoronary abciximab, manual aspiration thrombectomy, or both reduce infarct size in high-risk patients with STEMI. Between November 28, 2009, and December 2, 2011, 452 patients presenting at 37 sites in 6 countries within 4 hours of STEMI due to proximal or mid left anterior descending artery occlusion undergoing primary PCI with bivalirudin anticoagulation were randomized in an open-label, 2 x 2 factorial design to bolus intracoronary abciximab delivered locally at the infarct lesion site vs no abciximab and to manual aspiration thrombectomy vs no thrombectomy. A 0.25-mg/kg bolus of abciximab was administered at the site of the infarct lesion via a local drug delivery catheter. Manual aspiration thrombectomy was performed with a 6 F aspiration catheter. Primary end point: infarct size (percentage of total left ventricular mass) at 30 days assessed by cardiac magnetic resonance imaging (cMRI) in the abciximab vs no abciximab groups (pooled across the aspiration randomization); major secondary end point: 30-day infarct size in the aspiration vs no aspiration groups (pooled across the abciximab randomization). Evaluable cMRI results at 30 days were present in 181 and 172 patients randomized to intracoronary abciximab vs no abciximab, respectively, and in 174 and 179 patients randomized to manual aspiration vs no aspiration, respectively. Patients randomized to intracoronary abciximab compared with no abciximab had a significant reduction in 30-day infarct size (median, 15.1%; interquartile range [IQR], 6.8%-22.7%; n = 181, vs 17.9% [IQR, 10.3%-25.4%]; n = 172; P = .03). Patients randomized to intracoronary abciximab also had a significant reduction in absolute infarct mass (median, 18.7 g [IQR, 7.4-31.3 g]; n = 184, vs 24.0 g [IQR, 12.1-34.2 g]; n = 175; P = .03) but not abnormal wall motion score (median, 7.0 [IQR, 2.0-10.0]; n = 188, vs 8.0 [IQR, 3.0-10.0]; n = 184; P = .08). Patients randomized to aspiration thrombectomy vs no aspiration had no significant difference in infarct size at 30 days (median, 17.0% [IQR, 9.0%-22.8%]; n = 174, vs 17.3% [IQR, 7.1%-25.5%]; n = 179; P = .51), absolute infarct mass (median, 20.3 g [IQR, 9.7-31.7 g]; n = 178, vs 21.0 g [IQR, 9.1-34.1 g]; n = 181; P = .36), or abnormal wall motion score (median, 7.5 [IQR, 2.0-10.0]; n = 186, vs 7.5 [IQR, 2.0-10.0]; n = 186; P = .89). In patients with large anterior STEMI presenting early after symptom onset and undergoing primary PCI with bivalirudin anticoagulation, infarct size at 30 days was significantly reduced by bolus intracoronary abciximab delivered to the infarct lesion site but not by manual aspiration thrombectomy. clinicaltrials.gov Identifier: NCT00976521.

High-concentration versus titrated oxygen therapy in ST-elevation myocardial infarction: A pilot randomized controlled trial

The optimal approach to oxygen therapy in ST-elevation myocardial infarction (STEMI) is uncertain. A randomized controlled trial was undertaken in which 136 patients presenting with their first STEMI uncomplicated by cardiogenic shock or marked hypoxia were randomized to receive high-concentration (6 L/min via medium concentration mask) or titrated oxygen (to achieve oxygen saturation 93%-96%) for 6 hours after presentation. The main outcome variables were 30-day mortality and infarct size assessed by troponin T level at 72 hours. Secondary outcomes included a meta-analysis of mortality data from this study and previous randomized controlled trials, and infarct size was assessed by magnetic resonance imaging at 4 to 6 weeks. There were 1 of 68 and 2 of 68 deaths in the high-concentration and titrated oxygen groups, respectively; a meta-analysis including these data with those from the 2 previous studies showed an odds ratio for mortality of high-concentration oxygen compared with room air or titrated oxygen of 2.2 (95% CI 0.8-6.0). There was no significant difference between high-concentration versus titrated oxygen in troponin T (ratio of mean levels 0.74, 95% CI 0.50-1.1, P = .14), infarct mass (mean difference -0.8 g, 95% CI -7.6 to 6.1, P = .82), or percent infarct mass (mean difference -0.6%, 95% CI -5.6 to 4.5, P = .83). This study found no evidence of benefit or harm from high-concentration compared with titrated oxygen in initially uncomplicated STEMI. However, our estimates have wide CIs, and as a result, large randomized controlled trials are required to resolve the clinical uncertainty.

Effect of erythropoietin as an adjunct to primary percutaneous coronary intervention: a randomised controlled clinical trial

ObjectiveThe acute administration of high-dose erythropoietin (EPO) on reperfusing ischaemic myocardium has been reported to halve myocardial infarct (MI) size in preclinical studies, but its effect in ST elevation myocardial...

Role of Noninvasive Imaging in the Diagnosis of Cardiac Allograft Vasculopathy

Cardiac allograft vasculopathy (CAV) is common, with a prevalence of 52% at 10 years after transplantation, and represents a leading cause of death beyond the first year, responsible for approximately 15% of deaths annually.1 It is characterized by diffuse and concentric intimal proliferation, typically involving the intramural as well as epicardial coronary arteries. Its diagnosis is difficult to establish clinically because of denervation of the transplanted heart. Consequently, it presents late with silent myocardial infarction, progressive heart failure, or arrhythmic sudden death.2 Screening is therefore required for its early detection. Although coronary intravascular ultrasound (IVUS) is considered the gold-standard technique for detecting the anatomic features of CAV (Table 1), its broad clinical use in this context is limited by cost and lack of widespread expertise, and its evaluation is limited to epicardial vessels.3 Coronary angiography, performed annually or biannually, remains the most common clinical screening method.4 However, because of the diffuse nature of CAV with a lack of normal reference segments and the relatively late occurring luminal narrowing, the sensitivity of angiography is as low as 30% when compared with IVUS (Figure 1).5 As a result, complications frequently occur before disease is evident angiographically.6 Furthermore, angiography is associated with significant albeit uncommon complications (overall complication rate, 7.4/1000 procedures, including rates of 0.65/1000, 1.6/1000, and 0.72/1000 for cerebrovascular accidents, vascular complications, and death, respectively), is disliked by transplant recipients, is costly, and repeated studies are associated with an important cumulative radiation dose.7 View this table: Table 1. Stanford Classification of CAV Severity on IVUS Figure 1. Invasive assessment of cardiac allograft vasculopathy (CAV) in a patient with severe disease, highlighting the limited sensitivity of conventional coronary angiography. Although no left anterior descending (LAD) flow-limiting stenoses are seen on angiography ( A ), intravascular ultrasound ( B ) shows significant intimal thickening, measuring up to …

651 A novel method for automatic quantification of myocardial infarct mass

651 A novel method for automatic quantification of myocardial infarct mass

Jejunal diverticulum with ectopic pancreatic mucosa: Was it really a Meckel's diverticulum?

We report the case of a 72-year-old man who underwent surgery for a jejunal intussusception caused by an infarcted mass on the antimesenteric surface of the small bowel approximately 90 cm from the duodenojejunal flexure. The specimen was reported as an infarcted diverticulum containing heterotopic pancreatic mucosa in keeping with infarcted Meckel's diverticulum. We initially wished to establish when the term "Meckel's diverticulum" should be used. The anatomical site in the present case argues against this being a Meckel's diverticulum, a remnant from the mid-gut loop. Non-Meckelian diverticula are usually acquired and often multiple and generally occur on the mesenteric border of the bowel. It is rare for them to contain ectopic mucosa. The diverticulum in our patient thus has features which suggest it may have been congenital. We believe our patient had a rare occurrence of a congenital, but non-Meckelian, diverticulum with associated ectopic epithelium.

Prediction of Life-Threatening Arrhythmic Events in Patients With Chronic Myocardial Infarction by Contrast-Enhanced CMR

We hypothesized that infarct transmurality assessed with late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) predicts arrhythmic events in patients with chronic myocardial infarction. Patients with decreased left ventricular function due to chronic myocardial infarction are at increased risk for life-threatening arrhythmias related to infarcted tissue. LGE-CMR accurately detects infarct morphology. We prospectively enrolled 52 patients with chronic myocardial infarction referred for primary preventive implantable cardioverter-defibrillator (ICD) implantation following MADIT (Multicenter Automatic Defibrillator Implantation Trial) study criteria. Using LGE-CMR, left ventricular volumes, function, and infarct morphology were assessed including calculation of total and relative infarct mass, infarct border, infarct border zone, and infarct transmurality. Patients were followed for 1,235 ± 341 days. The primary combined endpoint including appropriate device therapy (ICD discharge or antitachycardia pacing) or death from cardiac cause occurred in 16 individuals resulting in an annual event rate of 4.7%. Six patients received an appropriate shock, 7 patients received recurrent appropriate antitachycardia pacing for sustained ventricular tachycardia, and 3 patients died of cardiac cause. There was a significant association to relative infarct mass (38 ± 8% vs. 28 ± 14%, p = 0.02), infarct transmurality (24 ± 8 g vs. 16 ± 12 g, p = 0.02), and relative infarct transmurality (RIT) (63 ± 12% vs. 48 ± 23%, p = 0.01). In separate logistic regression models, no variable emerged as significant when combined with RIT. As a single effect, RIT emerged as a predictor of the primary endpoint (p = 0.02). A RIT cutoff at 43% resulted in a sensitivity of 88%, a specificity of 50%, a positive predictive value of 44%, and a negative predictive value of 90%. In patients with chronic myocardial infarction scheduled for primary preventive ICD implantation, infarct transmurality as defined by LGE-CMR identifies a subgroup with increased risk for life-threatening arrhythmias and cardiac death.

Influence of left ventricular hypertrophy on infarct size and left ventricular ejection fraction in ST-elevation myocardial infarction

Left ventricular hypertrophy (LVH) predisposes to larger infarct size, which may be underestimated by the left ventricular ejection fraction (LVEF) due to supranormal systolic performance often present in patients with LVH. The aim of the study was to compare infarct size and LVEF in patients with ST-segment elevation myocardial infarction (STEMI) and increased left ventricular mass on cardiac magnetic resonance (CMR). The study included unselected group of 52 patients (61±11 years, 69% male) with first STEMI who had CMR after median 5 days from the onset of the event. Left ventricular hypertrophy (LVH) was defined as left ventricular mass index exceeding 95th percentile of references values for age and gender. Infarct size was assessed with means of late gadolinium enhancement (LGE). LVH was found in 16 patients (31%). In comparison to the rest of the group, patients with LVH had higher absolute and relative infarct mass (p=0.002 and p=0.02, respectively). LVH was related to higher prevalence of microvascular obstruction and myocardial haemorrhage and higher number of LV segments with transmural necrosis (p=0.02, p=0.01 and p=0.01, respectively). Despite marked difference in the infarct size between both studied subgroups there was no difference in LVEF and mean number of dysfunctional LV segments. Patients with LVH undergoing STEMI have larger infarct size underestimated by the LV systolic performance in comparison to patients without LVH.

Influence of infarct healing on left ventricular remodeling in patients with acute st-segment elevation myocardial infarction

Background Infarct healing is a complex process consisting in replacement of necrotic tissue with fibrotic scar. Animal studies indicate that this process is highly anisotropic showing different patterns, which may ultimately influence left ventricular (LV) remodeling. Study aim: to investigate the influence of infarct healing on post-infarction LV remodeling in patients with acute ST-segment elevation myocardial infarction (MI). Methods Seventy-eight patients with acute ST-segment elevation MI treated by percutaneous coronary intervention within 12-hour from symptoms onset were studied by cardiovascular magnetic resonance (CMR) within oneweek (baseline) and at four-month (follow-up) after MI. Cine CMR was used to assess LV volumes, mass and function. Early and late post-gadolinium 3-dimensional T1-weighted inversion-recovery segmented gradientecho CMR in short and long-axis directions was utilized to depict microvascular obstruction (MO) and myocardial necrosis/fibrosis, respectively. On late post-contrast short-axis images, the following parameters were measured: infarct mass, infarct-wall thickness, infarctthickness (ie, radial extent of infarction), infarct transmurality and circumferential infarct length (CIL). Longitudinal infarct length (LIL) was derived on longaxis late post-contrast images. Infarct-surface was calculated multiplying CIL by slice thickness (ie, 5 mm). Results Infarct size was 25±19g (19±12% of LV) at baseline and 13 ±9g (12±8% of LV) at follow-up (p<0.001), yielding an infarct size reduction of 45±17%. Non-infarcted myocardium tended to decrease during follow-up (p=0.051). Infarct resorption was more pronounced in the radial direction (31±15%) than circumferential (10±14%) or longitudinal (10±11%) ones (p<0.001). Infarct-surface reduction was 10±16% (range -26% to 53%), and 14 patients increased infarct-surface during follow-up (-12±6%) indicating chronic infarct expansion. Infarct-wall thinning was positively and strongly related to the infarct-thickness reduction (r=0.76, p<0.001) but not to overall MI shrinkage or to infarct-surface reduction. At multivariable linear regression analysis, the increase of infarct-surface during follow-up was independently associated to increase of LV end-diastolic volume during follow-up (Beta-coefficient=0.358, p=0.020) even after correction for baseline infarct size, MO extent, infarct-thickness reduction and LIL reduction. Conclusions Infarct healing is an anisotropic process occurring preferentially along the radial direction and playing a crucial role in post-infarction LV remodeling. Indeed, the degree of infarct radial resorption is strongly related to the infarct-wall thinning whereas the increase of infarct surface during follow-up (ie, chronic infarct expansion) is an independent predictor of adverse LV remodeling.

Left Atrial Appendage Anatomical Analysis Using Segmented Three-Dimensional Cardiac CT: A Comparison of Patients with Paroxysmal and Persistent Atrial Fibrillation

MVO. Late MVO also correlated best with infarct mass (r= 0.639) and non viable mass (r= 0.7) on CMR at day 90. Conclusion: Late MVO is the strongest predictor of left ventricular remodelling and infarct size following STEMI. Thismethod is a better predictor than novel semiquantitativeassessmentof infarct regionmyocardialblood flow. doi:10.1016/j.hlc.2011.05.444