Assessment Of Myocardial Infarct Size Research Articles

Estimating the extent of myocardial damage in patients with STEMI using the DETERMINE score

BackgroundRecently, a simple ECG score (DETERMINE score) has been proposed for estimating myocardial scar in patients with ischaemic cardiomyopathy. We sought to evaluate the usefulness of the DETERMINE score for...

Evaluating the possible role of mitochondrial ATP-sensitive potassium channels in the cardioprotective effects of morin in the isolated rat heart

AimsDuring heart ischemia, the lack of oxygen in the myocardial cells causes pH and ion disturbances and cell death through opening mitochondrial permeability transition pores (mPTP). Considering the inhibitory effects of mitochondrial ATP-dependent potassium channels (mt-KATP) on these pores and anti-ischemic effects of morin, we hypothesized that it may exert its positive effects via activating mt-KATP as well as its anti-oxidative effects. Main methodsIsolated rat hearts were perfused by Krebs-Henseleit solution enriched with the morin (0.25, 0.5 and 1 mg/L) or 5-hydroxydecanoate (5-HD, a mt-KATP blocker;100 μM) or both as needed 5 min before starting regional ischemia till the first 10 min of the reperfusion period. The reperfusion was developed with Krebs-Henseleit solution 60 or 120 min respectively for biochemical evaluations (lactate dehydrogenase and malondialdehyde level) or the assessment of myocardial infarct size. During the experiments, hemodynamic functions were recorded and cardiac arrhythmias were determined. Key findingsOur findings demonstrated that morin reduced the infarct size. Also, morin perfusion could remarkably prevent the malondialdehyde over-production during ischemia. Total ventricular ectopic beats had the same significant changes as the malondialdehyde level, in both ischemia and reperfusion phases. Morin could also relatively improve the ischemia-induced hemodynamic dysfunction. All mentioned protective effects of morin were reversed by concomitant perfusion of 5-HD. SignificanceMorin has protective effects against ischemic hearts through anti-oxidative effects. It also suggests a link between the cardioprotective effects of morin and mt-KATP. However, additional studies are required to prove this preliminary hypothesis.

MicroRNA-138 attenuates myocardial ischemia reperfusion injury through inhibiting mitochondria-mediated apoptosis by targeting HIF1-α.

Myocardial ischemia-reperfusion (I/R) injury is considered to have a detrimental role in coronary heart disease, which is considered to be the leading cause of death worldwide. However, the molecular mechanism involved in the progression of myocardial I/R injury is still unclear. The current study aimed to investigate the expression and function of microRNA (miR)-138 in the process of myocardial I/R injury. First, miR-138 expression levels were analyzed both in myocardium with I/R injury and control myocardium using reverse transcription-quantitative polymerase chain reaction analysis. Then, the relationship between the levels of miR-138 and hypoxia-inducible factor (HIF)1-α was also investigated using a luciferase reporter assay. Assessment of myocardial infarct size, measurements of serum myocardial enzymes and electron microscopy analysis were all utilized to analyse the effect of miR-138 on myocardial I/R injury. The authors of current study also used western blotting to examine the expression levels of the mitochondrial fission-related proteins dynamin-1-like protein and mitochondrial fission 1 protein. It was found that miR-138 is downregulated and HIF1-α is upregulated after myocardial ischemia reperfusion injury. Overexpression of miR-138 reduced myocardial I/R injury-induced infarct sizes and myocardial enzyme levels, and it also inhibited the expression of proteins related to mitochondrial morphology and myocardial I/R-induced mitochondrial apoptosis by targeting HIF1-α. Taken together, these findings provide a novel insight into the molecular mechanism of miR-138 and HIF1-α in the progression of myocardial I/R injury. miR-138 has the potential to become a promising therapeutic target for treating myocardial I/R injury.

Myocardial Infarct Size by CMR in Clinical Cardioprotection Studies: Insights From Randomized Controlled Trials

ObjectivesThe aim of this study was to review randomized controlled trials (RCTs) using cardiac magnetic resonance (CMR) to assess myocardial infarct (MI) size in reperfused patients with ST-segment elevation myocardial infarction (STEMI). BackgroundThere is limited guidance on the use of CMR in clinical cardioprotection RCTs in patients with STEMI treated by primary percutaneous coronary intervention. MethodsAll RCTs in which CMR was used to quantify MI size in patients with STEMI treated with primary percutaneous coronary intervention were identified and reviewed. ResultsSixty-two RCTs (10,570 patients, January 2006 to November 2016) were included. One-third did not report CMR vendor or scanner strength, the contrast agent and dose used, and the MI size quantification technique. Gadopentetate dimeglumine was most commonly used, followed by gadoterate meglumine and gadobutrol at 0.20 mmol/kg each, with late gadolinium enhancement acquired at 10 min; in most RCTs, MI size was quantified manually, followed by the 5 standard deviation threshold; dropout rates were 9% for acute CMR only and 16% for paired acute and follow-up scans. Weighted mean acute and chronic MI sizes (≤12 h, initial TIMI [Thrombolysis in Myocardial Infarction] flow grade 0 to 3) from the control arms were 21 ± 14% and 15 ± 11% of the left ventricle, respectively, and could be used for future sample-size calculations. Pre-selecting patients most likely to benefit from the cardioprotective therapy (≤6 h, initial TIMI flow grade 0 or 1) reduced sample size by one-third. Other suggested recommendations for standardizing CMR in future RCTs included gadobutrol at 0.15 mmol/kg with late gadolinium enhancement at 15 min, manual or 6-SD threshold for MI quantification, performing acute CMR at 3 to 5 days and follow-up CMR at 6 months, and adequate reporting of the acquisition and analysis of CMR. ConclusionsThere is significant heterogeneity in RCT design using CMR in patients with STEMI. The authors provide recommendations for standardizing the assessment of MI size using CMR in future clinical cardioprotection RCTs.

Impact of cardiac-specific expression of CD39 on myocardial infarct size in mice

AimsPrior work suggests that ischemic preconditioning increases the level of CD39 in the heart and contributes to cardiac protection. Therefore, we examined if targeted cardiac expression of CD39 protects against myocardial injury. Main methodsMice with cardiac-specific expression of human CD39 (αMHC/hCD39-Tg) were generated, characterized and subjected to left coronary artery ischemia-reperfusion injury and infarct size at 24h following injury quantified. Key findingsαMHC/hCD39-Tg mice have increased in cardiac ATPase and ADPase activity compared to WT littermates. The increased activity in αMHC/hCD39-mice was inhibited by the CD39 antagonist sodium polyoxotungstate (POM-1). Measurement of basal cardiac function by echocardiography revealed that αMHC/hCD39-Tg mice have a lower resting heart rate and increased stroke volume. In response to myocardial ischemia, systolic and diastolic function was better preserved in αMHC/hCD39-Tg compared to WT mice. Comparison of Tau also revealed preserved cardiac relaxation during ischemia in αMHC/hCD39-Tg hearts. Assessment of myocardial infarct size in response to 60min of ischemia and 24h of reperfusion demonstrated a significant reduction in infarct size in αMHC/hCD39-Tg hearts. Analysis of isolated cardiomyocytes revealed no basal difference in calcium transients between WT and αMHC/hCD39-Tg cardiomyocytes. However, in response to isoproterenol stimulation, there was a trend toward lower calcium transients in αMHC/hCD39 cardiomyocytes suggesting less calcium accumulation in response to metabolic stress. SignificanceCardiac-specific expression of CD39 reduces myocardial dysfunction and infarct size following ischemia-reperfusion injury. Increasing nucleotidase expression in the heart may be a novel approach to protect the heart from ischemic injury.

FADS2 Overexpression Increases Cardiovascular Risk and Ischemic Injury in Mice

Alterations in the polyunsaturated fatty acid (PUFA) composition of myocardial phospholipids have been reported in various forms of cardiac pathology for over 25 years. The pattern of PUFA redistribution is remarkably consistent across diverse etiologies and experimental models, manifesting primarily as a proportional loss of the essential PUFA linoleic acid (LA) paralleled by reciprocal increases in long‐chain highly unsaturated arachidonic (AA) and/or docosahexaenoic acids (DHA). Epidemiological studies have linked a similar pattern in serum phospholipids to elevated cardiometabolic risk and single nucleotide polymorphisms in the FADS2 gene encoding delta‐6 desaturase, the rate‐limiting enzyme in the conversion of essential PUFAs into AA and DHA. To determine if FADS2 was capable of promoting tissue phospholipid PUFA remodeling and a pathogenic cardiac phenotype in the absence of preexisting disease, we generated mice with global transgenic overexpression of FADS2 and evaluated their cardiac phenotype across 8 backcrossed (FVB) generations. FADS2‐tg mice exhibit moderate elevation of D6D protein expression in liver compared to wild‐type FVB (WT) mice, but nearly undetectable levels in heart from both genotypes. Despite this, hearts from FADS2‐tg mice exhibit significant elevations in phospholipid D6D product/precursor PUFA ratios (e.g., AA/LA), which parallel similar patterns in serum, liver and muscle. Compared to WT, FADS2‐tg mice develop significantly greater left ventricular end‐diastolic and end‐systolic dimensions by echocardiography at 2–4 months of age (27% and 93%, respectively), which results in a moderate (23%), but significant decrease in fractional shortening (P < 0.01). This is associated with greater levels of phosphorylated extracellular regulated kinase 1/2 expression and the pro‐hypertrophic AA‐derived eicosanoid 12‐hydroxyeicosatetraenoic acid, but no gross changes in tissue morphology or fibrosis. This phenotype does not appear to progress with age, but FADS2‐tg mice also develop moderate hyperlipidemia, glucose intolerance, and early mortality compared to WT, suggesting a more complex cardio‐metabolic phenotype. To evaluate the tolerance of FADS2‐tg hearts to pathogenic metabolic stress, hearts were isolated and Langendorff perfused for a 45/120 min protocol of global ischemia/reperfusion ex vivo, followed by assessment of myocardial infarct size by conventional triphenyltetrazolium chloride staining. Interestingly, preliminary results indicate that FADS2‐tg hearts exhibit ~15% greater infarcts following I/R compared to WT (P < 0.05; N = 4–5/group). Taken together, these studies implicate FADS2 and perhaps tissue phospholipid PUFA composition as important modulators of cardiovascular risk, consistent with epidemiological evidence from FADS2 haplotypes and serum PUFA profiling studies in humans. The possible mechanisms underlying this link are currently being explored in FADS2‐tg mice and other genetic models in our laboratory.Support or Funding InformationThese studies were supported by grants from the NHLBI and the American Heart Association to AJC.

Assessment of myocardial infarct size with body surface potential mapping: validation against contrast-enhanced cardiac magnetic resonance imaging.

Assessment of myocardial infarct (MI) size is important for therapeutic and prognostic reasons. We used body surface potential mapping (BSPM) to evaluate whether single-lead electrocardiographic variables can assess MI size. We performed BSPM with 120 leads covering the front and back chest (plus limb leads) on 57 patients at different phases of MI: acutely, during healing, and in the chronic phase. Final MI size was determined by contrast-enhanced cardiac magnetic resonance imaging (DE-CMR) and correlated with various computed depolarization- and repolarization-phase BSPM variables. We also calculated correlations between BSPM variables and enzymatic MI size (peak CK-MBm). BSPM variables reflecting the Q- and R wave showed strong correlations with MI size at all stages of MI. R width performed the best, showing its strongest correlation with MI size on the upper right back, there representing the width of the "reciprocal Q wave" (r = 0.64-0.71 for DE-CMR, r = 0.57-0.64 for CK-MBm, P < 0.0001). Repolarization-phase variables showed only weak correlations with MI size in the acute phase, but these correlations improved during MI healing. T-wave variables and the QRSSTT integral showed their best correlations with DE-CMR defined MI size on the precordial area, at best r = -0.57, P < 0.0001 in the chronic phase. The best performing BSPM variables could differentiate between large and small infarcts at all stages of MI. Computed, single-lead electrocardiographic variables can estimate the final infarct size at all stages of MI, and differentiate large infarcts from small.

Rapid assessment of myocardial infarct size in rodents using multi-slice inversion recovery late gadolinium enhancement CMR at 9.4T.

BackgroundMyocardial infarction (MI) can be readily assessed using late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR). Inversion recovery (IR) sequences provide the highest contrast between enhanced infarct areas and healthy myocardium. Applying such methods to small animals is challenging due to rapid respiratory and cardiac rates relative to T1 relaxation.MethodsHere we present a fast and robust protocol for assessing LGE in small animals using a multi-slice IR gradient echo sequence for efficient assessment of LGE. An additional Look-Locker sequence was used to assess the optimum inversion point on an individual basis and to determine most appropriate gating points for both rat and mouse. The technique was applied to two preclinical scenarios: i) an acute (2 hour) reperfused model of MI in rats and ii) mice 2 days following non-reperfused MI.ResultsLGE images from all animals revealed clear areas of enhancement allowing for easy volume segmentation. Typical inversion times required to null healthy myocardium in rats were between 300-450 ms equivalent to 2-3 R-waves and ~330 ms in mice, typically 3 R-waves following inversion. Data from rats was also validated against triphenyltetrazolium chloride staining and revealed close agreement for infarct size.ConclusionThe LGE protocol presented provides a reliable method for acquiring images of high contrast and quality without excessive scan times, enabling higher throughput in experimental studies requiring reliable assessment of MI.

Assessment of myocardial infarct size and left ventricular function following acute myocardial infarction by cardiovascular magnetic resonance: A comparison of treatment with thrombolysis versus primary percutaneous coronary intervention

Introduction Primary percutaneous coronary intervention (PPCI) is considered the optimum reperfusion strategy in the treatment of acute myocardial infarction (AMI). However, there remains some debate surrounding the benefits of PPCI over the early administration of thrombolytic therapy. In the UK, so called door to needle times for thrombolysis are generally less than 30 minutes and therefore, may decrease the reported benefits of delayed PPCI.

Head‐to‐head comparison between delayed enhancement and percent infarct mapping for assessment of myocardial infarct size in a canine model

To compare a novel method, percent-infarct-mapping (PIM), with conventional delayed enhancement (DE) of contrast for accurate myocardial viability assessment. Contrary to signal intensity (SI), the longitudinal relaxation-rate enhancement (DeltaR1) is an intrinsic parameter linearly proportional to the concentration of contrast agent (CA). Determining DeltaR1 voxel-by-voxel, after administering an infarct-avid CA, allows determination of per-voxel percentage of infarcted tissue. The feasibility of generating PIM is demonstrated in canine reperfused infarction using an infarct-avid, persistent-CA (PCA), (Gd)(ABE-DTTA). PIM is compared to the DE method using Gd(DTPA), and both to triphenyltetrazolium chloride (TTC) staining histochemistry. In six dogs, 48 hours following closed-chest, 180-minute coronary occlusion, DE imaging was carried out. PCA was administered immediately thereafter. Pixel-by-pixel R1 maps of the entire left ventricle (LV) were generated 48 hours after PCA using inversion-recovery with multiple inversion times. R1, DeltaR1, and percent-infarct values were calculated voxel-by-voxel. Significant correlations (P < 0.01, R >or= 0.8) were obtained for percent-infarct-per-slice (PIS) determined by DE or PIM vs. those from corresponding TTC-stained slices. Compared to TTC, DE overestimated PIS by 32 +/- 18%. PIM underestimated PIS by 2.5 +/- 4.9%. Infarction fraction overestimation was 29 +/- 6% of LV by DE, but only 1.0 +/- 2.3% by PIM. Errors with PIM were significantly smaller than those with DE. Infarct area determined by signal intensity was similarly overestimated whether using Gd(DTPA) or Gd(ABE-DTTA). The DeltaR1-based PIM method is highly reproducible and more accurate than DE for quantifying myocardial viability in vivo.

Assessment of Acute Reperfused Myocardial Infarction with Delayed Enhancement 64-MDCT

The purpose of this study was to evaluate the utility of delayed enhancement 64-MDCT in the assessment of myocardial infarct size in a porcine model of acute reperfused myocardial infarction. CT can be used for noninvasive assessment of coronary artery stenosis, but to our knowledge, evaluation of myocardial viability in the subacute phase of acute myocardial infarction has not been validated. We performed delayed enhancement imaging on six domestic swine 5 days after reperfused acute myocardial infarction and assessed the relation between delayed enhancement patterns in vivo and the extent of viable and nonviable myocardium at postmortem histochemical analysis. Delayed enhancement imaging with 64-MDCT can be used for accurate assessment of the size of reperfused acute myocardial infarcts.

Multislice Computed Tomography and Magnetic Resonance Imaging for the Assessment of Reperfused Acute Myocardial Infarction

We evaluated the accuracy of in vivo delayed-enhancement multislice computed tomography (DE-MSCT) and delayed-enhancement magnetic resonance imaging (DE-MRI) for the assessment of myocardial infarct size using postmortem triphenyltetrazolium chloride (TTC) pathology as standard of reference. The diagnostic value of DE-MSCT for the assessment of acute reperfused myocardial infarction is currently unclear. In 10 domestic pigs (25 to 30 kg), the circumflex coronary artery was balloon-occluded for 2 h followed by reperfusion. After 5 days (3 to 7 days), DE-MRI (1.5-T) was performed 15 min after administration of 0.2 mmol/kg gadolinium-DTPA using an inversion recovery gradient echo technique. On the same day, DE-MSCT (64-slice) was performed 15 min after administration of 1 gI/kg of iodinated contrast material. One day after imaging, hearts were excised, sectioned in 8 mm short-axis slices, and stained with TTC. Infarct size was defined as the hyperenhanced area on DE-MSCT and DE-MRI images and the TTC-negative area on TTC pathology slices. Infarct size was expressed as percentage of total slice area. Infarct size determined by DE-MSCT and DE-MRI showed a good correlation with infarct size assessed with TTC pathology (R2 = 0.96 [p < 0.001] and R(2) = 0.93 [p < 0.001], respectively). The correlation between DE-MSCT and DE-MRI was also good (R2 = 0.96; p < 0.001). The relative difference in CT attenuation value of infarcted myocardium compared to remote myocardium was 191 +/- 18%. The relative MR signal intensity between infarcted myocardium and remote myocardium was 554 +/- 156%. We demonstrated that DE-MSCT can assess acute reperfused myocardial infarction in good agreement with in vivo DE-MRI and TTC pathology.

Differences in Reperfusion Length Following 30 Minutes of Ischemia in the Rabbit Influence Infarct Size, as Measured by Triphenyltetrazolium Chloride Staining

Assessment of myocardial infarct size in acute experimental models is usually done by triphenyltetrazolium-chloride (TTC) staining. A certain period of reperfusion is mandatory for discrimination of the infarct zone, especially after relatively short ischemic periods. However, it is unclear what the optimal reperfusion time is for full delineation of the infarct following 30 min of myocardial ischemia in the rabbit. This study compares infarct size, assessed by TTC, in anesthetized open-chest rabbits subjected to 30 min of coronary artery occlusion followed by either 2 (n=14)v4 (n=14) (protocol 1), or 3 (n=8)v6 (n=7) h of reperfusion (protocol 2). Area at risk was assessed by blue dye and necrotic zone by TTC staining. Protocol 1: heart rate and mean blood pressure were comparable in both groups throughout the protocol. Regional myocardial blood flows in both the ischemic and non-ischemic zones during ischemia and after 2 h of reperfusion were comparable between the groups. Regional myocardial blood flow in the post-ischemic zone deteriorated between 2 and 4 h (1.11±0.15v0.58±0.09 ml/min/g, respectively;P=0.0004) of reperfusion. The size of the area at risk was comparable (0.31±0.03v0.33±0.03 of the LV weight in the 2 and 4 h reperfusion groups). However, the ratio of the necrotic zone to the ischemic zone at risk was 63% larger in the 4 compared to the 2 h of reperfusion group (0.31±0.04v0.19±0.03, respectively,P=0.02). Analysis of covariance performed on the weight of tissue that developed necrosis and the weight of ischemic zone at risk revealed a significant effect of the reperfusion time (P=0.014). Protocol 2: there was no difference in infarct size between rabbits subjected to three (0.38±0.05 of the area at risk)v6 h (0.41±0.07) of reperfusion (P=0.72). Analysis of covariance performed on the weight of tissue that developed necrosis and the weight of ischemic zone at risk did not reveal a significant effect of the reperfusion time. Infarct size as assessed by TTC following 30 min of myocardial ischemia, is smaller when measured 2 h after reperfusion than after 4 h of reperfusion. At least 3 h of reperfusion is needed to delineate infarct size by tetrazolium staining following 30 min of ischemia.

Non-invasive assessment of ventricular damage in rats with myocardial infarction

The aim was to evaluate whether two dimensional echocardiographic/Doppler (echo/Doppler) techniques could be used to detect left ventricular damage rapidly, accurately, and non-invasively in rats with a myocardial infarction. Female Wistar rats were initially subjected to either a sham operation or surgery to induce a myocardial infarct by ligating the left main coronary artery. Following a minimum of six weeks to recover from the surgery, all rats were re-anaesthetised and cardiac and stroke indexes were determined at similar heart rates, using echo/Doppler techniques. Postmortem histological assessment of myocardial infarct size was compared with the non-invasive detection of left ventricular wall motion abnormalities, left ventricular dilatation, and the presence of a left ventricular aneurysm found in the living animal. Rats with myocardial infarction (n = 8) showed a 33(SEM 4)% reduction (p < 0.01) in cardiac index (due to a 33% reduction in stroke index) when compared to their non-infarcted counterparts (n = 5). In addition, a significant correlation (r = 0.84; n = 25; p < 0.01) was found between the assessment of left ventricular damage via non-invasive echo/Doppler measurements and the histological determination of infarct size. These results support the conclusion that two dimensional echo/Doppler techniques can be used to estimate rapidly and non-invasively the degree of left ventricular damage produced in living rats with myocardial infarction when compared to non-infarcted controls.

Quantitation of acute myocardial infarct size by nuclear magnetic resonance imaging

Nuclear magnetic resonance (NMR) imaging has shown potential in the detection and characterisation of acute myocardial infarction in humans. This study was performed to evaluate the capability of NMR imaging in the measurement of infarct size in patients with recent myocardial infarction. Electrocardiograpic (ECG)-gated spinecho NMR imaging was performed in 26 patients a mean of 9 ± 3 days (range 5 to 20) after infarction. The imaging technique used provided single-slice, spin-echo (time to echo [TE] = 60 ms) images of the left ventricle in its true short axis, allowing direct correlation of NMR infarct location and size with the region of severe hypokinesia on left ventriculography.In all 20 patients with complete NMR studies, infarct location was correctly identified by using specific, objective criteria. The correlation between the mean infarct volume (29 ± 11 ml) and the quantitated left ventricular hypokinetic segment (7.1 ± 4.0 cm) was good (r = 0.84, p = 0.0002), suggesting that NMR imaging of the heart may have a role in the noninvasive assessment of myocardial infarct size in patients.

Infarct sizing by scintigraphic techniques and nuclear magnetic resonance imaging

Assessment of myocardial infarct size is the cornerstone in the evaluation of interventions designed to salvage myocardium, such as thrombolytic therapy and urgent coronary angioplasty. Enzymatic methods have probably the highest accuracy but can only be used in the very early phase of infarction. The electrocardiogram allows a reasonable estimate of infarct size, but its confidence limits are wide, and in inferior wall infarction the estimates are unreliable. In recent years, radionuclide techniques have been successfully used to identify, localize and determine infarct size in the course of acute myocardial infarction. These scintigraphic measurements have provided important diagnostic, therapeutic and prognostic information based on the extent of myocardial damage. Nuclear magnetic resonance imaging, particularly with contrast enhancement, is one of the methods that have the greatest potential in accurately delineating myocardial infarct size. Nuclear medicine procedures, on the other hand, employ more biologically oriented tracers and offer promise in view of their ability to monitor biochemical alterations as an effect of therapy in the course of myocardial infarction.

Assessment of myocardial infarct size by means of T 2-weighted 1H nuclear magnetic resonance imaging

Proton ( 1H) nuclear magnetic resonance (NMR) imaging is thought to depict zones of recent myocardial infarction in contrast to noninfarcted myocardium. This is related to T 2 increases in infarct zones that have been verified previously by relaxometry measurements in excised myocardial samples. Accordingly the present study was undertaken to evaluate a 1H NMR imaging method to optimize T 2 contrast and measure infarct size in a high-field imaging system (1.5 T). To accomplish this, NMR images were acquired every other R wave with echo times of 30 and 100 msec. The first echo image was used for myocardial border definition and the second echo image, which highlighted the myocardial infarction, for infarct border definition. This T 2-weighted approach yielded a significant correlation between infarct size by NMR and pathologic methods. However, NMR imaging tended to overestimate infarct size, and the NMR image depicted abnormal signal well beyond the extent of the pathology-determined infarct. There was a significant relationship between NMR-imaged infarct size and myocardial mass with microsphere-determined reduction in blood flow of 25% or more. These data suggest that T 2-weighted NMR imaging depicts not only infarct but also some reversibly injured myocardium.

Assessment of myocardial infarct size by serial changes in serum cardiac myosin light chain II in dogs.

The relationship between myocardial infarct size and serum levels of cardiac myosin light chain II (LC II; 20000 daltons) was studied in 24 dogs with left anterior descending coronary artery occlusion. LC II in the serum was measured by the radioimmunoassay which we have recently developed. In our assay, 0.1--5.0 ng of LC II were effectively measurable. Serum LC II levels rose rapidly and stayed elevated long after coronary occlusion. Infarct size was determined by gross inspection. In 24 dogs, infarct size ranged from 0.3 to 41.7 per cent of left ventricular weight. LC II release was calculated by the formula of Shell and associates. Regression analysis showed good correlation between infarct size and LC II release (r = 0.78). Infarct size also correlated with maximal LC II level (r = 0.77), and LC II level 24 hours after coronary occlusion (r = 0.69). Detection of circulating LC II is a useful method since it can be applied to the diagnosis of acute myocardial infarction at the early as well as late stage and infarct size can be assessed by analysis of serum LC II levels.

Quantitative assessment of myocardial infarct size from serial determinations of serum creatine phosphokinase activity: significance of previous infarction for the cardiac function and prognosis.

In 50 patients with acute myocardial infarction (16 patients with previous infarction and 34 patients without), total creatine phosphokinase (CPK) released which represents infarct size was calculated from the serial change of serum CPK activity by the method of Sobel improved by Norris, and related it to the presence or absence of heart failure, the ejection fraction and one-year-mortality. If the patients with previous myocardial infarction were excluded, mean total CPK released in 10 patients with heart failure (1428 ± 200.4 IU/ml in Group II) was significantly larger (P<0.01) than that in 24 patients without heart failure (735.3 ± 83.6 IU/ml in Group I). However, in patients with previous myocardial infarction there was no significant difference in infarct size between these two groups (Groups I and II) indicating that the complication of heart failure does not directly relate to the size of the recent infarction but in large extent to the presence of prior infarction. The ejection fraction was obtained in 15 patients who had left ventriculography. Both of two patients with prior myocardial infarction in these 15 patients showed smaller ejection fraction than the predicted values myocardial infarction could contribute to impaired cardiac function as well as the recently occured infarction. One-year-mortality in Group II (37.5%) was higher than that of Group I (7.4%). In four patients with prior infarction who died within one year after the onset, mean total CPK released (275.3 IU/ml) was significantly smaller than that in three patients without prior infarction (899.0 IU/ml). These results strongly suggest that the patients with previous myocardial infarction are often complicated with heart failure and have poor prognosis even with comparatively small infarction and also demonstrate the substantially large contribution of the reduced contractility resulting from the previous myocardial infarction to the impaired cardiac function.