Effect of transplantation of bone marrow stem cells on myocardial infarction size in a rabbit model

BACKGROUND:

Intravenous transplantation has been regarded as a most safe method in stem cell therapies. There is evidence showing the homing of bone marrow stem cells (BMSCs) into the injured sites, and thus these cells can be used in the treatment of acute myocardial infarction (MI). This study aimed to investigate the effect of intravenous and epicardial transplantion of BMSCs on myocardial infarction size in a rabbit model.

METHODS:

A total of 60 New Zealand rabbits were randomly divided into three groups: control group, epicardium group (group I) and ear vein group (group II). The BMSCs were collected from the tibial plateau in group I and group II, cultured and labeled. In the three groups, rabbits underwent thoracotomy and ligation of the middle left anterior descending artery. The elevation of ST segment >0.2 mV lasting for 30 minutes on the lead II and III of electrocardiogram suggested successful introduction of myocardial infarction. Two weeks after myocardial infarction, rabbits in group I were treated with autogenous BMSCs at the infarct region and those in group II received intravenous transplantation of BMSCs. In the control group, rabbits were treated with PBS following thoracotomy. Four weeks after myocardial infarction, the heart was collected from all rabbits and the infarct size was calculated. The heart was cut into sections followed by HE staining and calculation of infarct size with an image system.

RESULTS:

In groups I and II, the infarct size was significantly reduced after transplantation with BMSCs when compared with the control group (P<0.05). However, there was no significant difference in the infarct size between groups I and II (P>0.05).

CONCLUSION:

Transplantation of BMSCs has therapeutic effect on MI. Moreover, epicardial and intravenous transplantation of BMSCs has comparable therapeutic efficacy on myocardial infarction.KEY WORDS: Bone marrow stem cells, Acute myocardial infarction, Epicardial transplantation, Intravenous transplantation, Infarct size, Rabbit     

Differentiating type 1 and 2 acute myocardial infarctions using the N-terminal pro B-type natriuretic peptide/cardiac troponin T ratio

Purpose

Differentiation of type 1 (T1MI) from type 2 myocardial infarction (T2MI) is important as recommended treatments for each differ. Patients with T2MI may have more/earlier cardiac wall stress resulting in an increased N-terminal pro B-type natriuretic peptide (NT-proBNP)/cTnT generation 5 ratio (cTnT Gen 5).

Effects of ramipril on ventricular arrhythmia after myocardial infarction in rabbits

BACKGROUND:

Ventricular arrhythmia (VA) is one of the most common complications of myocardial infarction (MI), and ventricular tachycardia and fibrillation are the main causes for sudden cardiac death. This study aimed to explore the effect of ramipril on the occurrence of VA and its mechanism after MI in rabbits.

METHODS:

Twenty-four New Zealand rabbits purchased from the Wuhan Laboratory Animal Research Center were divided into three groups: sham-operated (SHAM) group (n=8), MI group (n=8) and MI with ramipril (RAM) group (n=8). Rabbits in the SHAM group received a median sternotomy without ligation of the left ventricular coronary artery. Rabbits in the MI and RAM groups received a median sternotomy followed by ligation of the left coronary artery. The successful anterior MI was confirmed by elevation of the ST segment with more than 0.2 mV in lead II and III. After MI, rabbits in the RAM group were fed with intragastric ramipril (1 mg/kg per day) for 12 weeks. Before and 12 weeks after MI in the three groups, ventricular tachycardia or fibrillation (VT/VF) episodes and MAP in cadiocytes of the epicardium, mid-myocardium and endocardium were recorded by a multichannel physiograph. Student''s t test and ANOVA were used for statistical analysis.

RESULTS:

VT/VF episodes were decreased more markedly in the RAM group than in the MI group after 12 weeks (2.6±0.8 vs. 12.4±2.9, P<0.05). Twelve weeks after MI, the duration of repolarization for 90% (APD₉₀) of three-tier ventricular myocytes in the MI group was longer than that before MI (258.2±21.1 vs. 230.1±23.2, 278.0±23.8 vs. 245.8±25.4, 242.6±22.7 vs. 227.0±21.7, P<0.05). However, the APD₉₀ was not significantly different at 12 weeks before and after MI in the RAM group (P>0.05). Moreover, the transmural dispersion of repolarization (TDR) was increased more markedly 12 weeks after MI in the MI group than in the SHAM and RAM groups (36.2±10.2 vs. 18.7±6.2, 24.9±8.7, P<0.05). But the TDR was not significantly different between the RAM and SHAM groups (18.7±6.2 vs. 24.9±8.7, P>0.05).

CONCLUSION:

Ramipril may reduce the incidence of malignant ventricular arrhythmia via improvement of transmembrance repolarization heterogeneity after MI.KEY WORDS: Myocardial infarction, Ventricular arrhythmia, Monophasic action potential duration, Transmural dispersion of repolarization, Ramipril, Rabbits     

Rehabilitation status three months after first-time myocardial infarction

Objective

To describe the rehabilitation status three months after first-time myocardial infarction (MI) to identify focus areas for long-term cardiac rehabilitation (CR) in general practice.

Design

Population-based cross-sectional study.

Setting and subjects

Patients with first-time MI in 2009 from the Central Denmark Region. Data were obtained from patient questionnaires and from registers.

Results

Of the 1288 eligible patients, 908 (70.5%) responded. The mean (SD) age was 67.1 (11.7) years and 626 (68.9%) were men. Overall, 287 (31.6%) of the patients lived alone and 398 (45.4%) had less than 10 years of education. Upwards of half (58.5%) of the patients stated that they had participated in hospital-based rehabilitation shortly after admission. A total of 262 (29.2%) were identified with anxiety or depressive disorder or both, according to the Hospital Anxiety and Depression Scale. Of these, 78 (29.8%) reported that they had participated in psychosocial support, and 55 (21.0%) used antidepressants. One in five patients smoked three months after MI although nearly half of the smokers had stopped after the MI. Regarding cardioprotective drugs, 714 (78.6%) used aspirin, 694 (76.4%) clopidogrel, 756 (83.3%) statins, and 735 (81.0%) beta-blockers.

Conclusion

After three months, there is a considerable potential for further rehabilitation of MI patients. In particular, the long-term CR should focus on mental health, smoking cessation, and cardioprotective drugs.Key Words: Depression, drug therapy, family practice, myocardial infarction, rehabilitation, smokingThe rehabilitation status three months after myocardial infarction and before long-term rehabilitation in general practice is unknown.

• Approximately 60% of the patients stated that they had received some kind of cardiac rehabilitation during the first three months after discharge.
• There is a considerable potential for further rehabilitation focusing on mental health, smoking cessation, and cardioprotective drugs.

     

Effect of spironolactone on cardiac remodeling after acute myocardial infarction

BACKGROUND:

Few studies have reported the effect of aldosterone receptor antagonist (ARA) on myocardial remodeling after acute myocardial infarction (AMI). This study was undertaken to investigate the preventive effect of ARA on myocardial remodeling after AMI.

METHODS:

A total of 616 patients who had been admitted into the CCU of the First Affiliated Hospital of Harbin Medical University from January 2008 to January 2010 were studied prospectively. Only 528 patients were observed completely, including 266 of the control group and 262 of the treatment group. There was no statistical difference in age, gender, medical history, admission situation, and treatment between the two groups (P>0.05). The preventive effects of spironolactone on cardiac remodeling, left ventricular function, renal function and blood levels of potassium were evaluated by echocardiography, serum potassium and serum creatinine at one-month and one-year follow-up.

RESULTS:

The echocardiography indicators such as LVESD, LVEDD, LVEF, LAD-ML and LAD-SI were significantly improved in the treatment group compared with the control group at one year (P<0.05). In the treatment group, LVESD, LVEDD, LVPWT, LVEF, LAD-ML and LAD-SI were more significantly improved at one year than one month (P<0.05, P=0.007 to LVEF), and in the control group LVEF was more significantly improved at one year than one month (P=0.0277). There were no significant differences in serum potassium and serum creatinine levels between the two groups.

CONCLUSION:

On the basis of conventional treatment, the early combination of low-dose spironolactone (20 mg/d) could inhibit cardiac remodeling at late stage and prevent heart failure.KEY WORDS: Myocardial infarction, acute, Ventricular remodeling, Atrial remodeling, Aldosterone, Aldosterone blockade, Spironolactone, Cardiac function, Prognosis     

Cardiovascular magnetic resonance of scar and ischemia burden early after acute ST elevation and non-ST elevation myocardial infarction

Background

The acute coronary syndrome diagnosis includes different classifications of myocardial infarction, which have been shown to differ in their pathology, as well as their early and late prognosis. These differences may relate to the underlying extent of infarction and/or residual myocardial ischemia. The study aim was to compare scar and ischemia mass between acute non-ST elevation myocardial infarction (NSTEMI), ST-elevation MI with Q-wave formation (Q-STEMI) and ST-elevation MI without Q-wave formation (Non-Q STEMI) in-vivo, using cardiovascular magnetic resonance (CMR).

Methods and results

This was a prospective cohort study of twenty five consecutive patients with NSTEMI, 25 patients with thrombolysed Q-STEMI and 25 patients with thrombolysed Non-Q STEMI. Myocardial function (cine imaging), ischemia (adenosine stress first pass myocardial perfusion) and scar (late gadolinium enhancement) were assessed by CMR 2–6 days after presentation and before any invasive revascularisation procedure. All subjects gave written informed consent and ethical committee approval was obtained. Scar mass was highest in Q-STEMI, followed by Non-Q STEMI and NSTEMI (24.1%, 15.2% and 3.8% of LV mass, respectively; p < 0.0001). Ischemia mass showed the reverse trend and was lowest in Q-STEMI, followed by Non-Q STEMI and NSTEMI (6.9%, 14.7% and 19.9% of LV mass, respectively; p = 0.012). The combined mass of scar and ischemia was similar between the three groups (p = 0.17). The ratio of scar to ischemia was 3.5, 1.0 and 0.2 for Q-STEMI, Non-Q STEMI and NSTEMI, respectively.

Conclusion

Prior to revascularisation, the ratio of scar to ischemia differs between NSTEMI, Non-Q STEMI and Q-STEMI, whilst the combined scar and ischemia mass is similar between these three types of MI. These results provide in-vivo confirmation of the diverse pathophysiology of different types of acute myocardial infarction and may explain their divergent early and late prognosis.     

Usefulness of synthesized 18-lead electrocardiography in the diagnosis of ST-elevation myocardial infarction: A pilot study

Objective

This was a pilot retrospective case-series study performed to investigate whether synthesized 18-lead electrocardiogram (ECG) could improve the accuracy of infarction site diagnosis in patients presenting with ST-elevation myocardial infarction (STEMI).

Expressions of SOCS-1 and SOCS-3 in the myocardium of patients with sudden cardiac death

BACKGROUND:

As the regulators of cytokines, suppressors of cytokine signaling (SOCS) play an important role in the inflammation reaction. Some studies found that SOCS-1 and SOCS-3 were involved in the pathogenesis of some inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease. But the expressions of SOCS in coronary heart disease have not yet been reported. This study aimed to investigate the expression and clinical significance of SOCS-1 and SOCS-3 in the myocardium of patients with sudden cardiac death (SCD).

METHODS:

Myocardial autopsy specimens were collected from 24 patients at the Forensic Medicine Department of Sun Yat-Sen University, Guangzhou, China between 2005 and 2006. Of them, 9 patients had autopsy findings consistent with coronary atherosclerosis (non-myocardial infarction) leading to SCD (non-MI group), 7 died of acute myocardial infaction (MI group), and 8 died from traffic accidents and trauma (control group). The expressions of SOCS-1 mRNA and SOCS-3 mRNA in the myocardium of the non-MI, MI and control groups were detected using RT-PCR. The levels of SOCS-1 and SOCS-3 proteins were detected using immunohistochemistry. Statistical analyses were performed using SPSS version 13.0 software and the data were analyzed by ANOVA.

RESULTS:

The expressions of SOCS-1 mRNA and SOCS-3 mRNA in the non-MI and MI groups were significantly higher than those in the control group[(0.788±0.101), (0.741±0.111) vs. (0.436±0.044), (P<0.01); (0.841±0.092), (0.776±0.070) vs. (0.454±0.076), (P<0.01)] respectively. The antibody-positive cells of SOCS-1 protein in the myocardium of the non-MI and MI groups were significantly higher than those in the myocardium of the control group[(320.00±48.48), (347.14±70.88) vs. (42.50±10.35), (P<0.01)] respectively. The antibody-positive cells of SOCS-3 protein in the myocardium of the non-MI and MI groups were significantly higher than those in the myocardium of the control group[(381.11±59.25) vs. (40.00±10.69), (P<0.01)] and[(332.86±111.91) vs. (40.00±10.69), (P=0.001)].

CONCLUSION:

The expressions of SOCS-1 and SOCS-3 in the myocardium of patients with SCD from coronary heart disease are significantly increased and contribute to the pathogenesis of SCD.KEY WORDS: Sudden cardiac death, Myocardial infarction, Suppressor of cytokine signaling-1, Suppressor of cytokine signaling-3     

A potential diagnostic pitfall in acute chest pain: Massive pulmonary embolism mimicking acute STEMI

Background

Pulmonary embolism (PE) represents a clinical challenge for clinicians because of nonspecific presentations, including dyspnea, chest pain, and tachycardia. The immediate 12-lead electrocardiogram (ECG) is commonly used to facilitate differential diagnosis of acute chest pain. Although relative rare, massive pulmonary embolism could induce ST segment elevation and mimic acute myocardial infarction.

Serum uric acid in patients with acute ST-elevation myocardial infarction

BACKGROUND:

Few studies investigated serum uric acid levels in patients with acute Stelevation myocardial infarction (STEMI). The study was to assess the clinical value of serum uric acid levels in patients with acute ST-elevation myocardial infarction (STEMI).

METHODS:

Totally 502 consecutive patients with STEMI were retrospectively studied from January 2005 to December 2010. The level of serum lipid, echocardiographic data and in-hospital major adverse cardiovascular events (MACE) in patients with hyperuricemia (n=119) were compared with those in patients without hyperuricemia (n=383). The relationship between the level of serum uric acid and the degree of diseased coronary artery was analyzed. All data were analyzed with SPSS version 17.0 software for Student’s t test, the Chi-square test and Pearson’s correlation coefficient analysis.

RESULTS:

Serum uric acid level was positively correlated with serum triglyceride level. Hyperlipidemia was more common in hyperuricemia patients than in non-hyperuricemia patients (43.7% vs. 33.7%, P=0.047), and serum triglyceride level was significantly higher in hyperuricemia patients (2.11±1.24 vs. 1.78±1.38, P=0.014). But no significant association was observed between serum uric acid level and one or more diseased vessels (P>0.05). Left ventricular end-diastolic diameter (LVEDd) was larger in hyperuricemia patients than in non-hyperuricemia patients (53.52±6.19 vs. 52.18±4.89, P=0.041). The higher rate of left systolic dysfunction and diastolic dysfunction was discovered in hyperuricemia patients (36.4% vs. 15.1%, P<0.001; 68.2% vs. 55.8%, P=0.023). Also, hyperuricemia patients were more likely to have in-hospital MACE (P<0.05).

CONCLUSIONS:

Serum uric acid level is positively correlated with serum triglyceride level, but not with the severity of coronary artery disease. Hyperuricemia patients with STEMI tend to have a higher rate of left systolic dysfunction and diastolic dysfunction and more likely to have more in hospital MACE.KEY WORDS: Acute ST-elevation myocardial infarction, Serum uric acid, Triglyceride, Coronary angiography, Echocardiography, Left ventricular systolic dysfunction, Left ventricular diastolic dysfunction, Major adverse cardiovascular events     

ST elevation measurements differ in patients with inferior myocardial infarction and right ventricular infarction

Purpose

Few studies specify the methods used to measure ST-segment elevation (STE). We therefore assessed differences in electrocardiography results depending on STE measurement methods for patients with inferior acute myocardial infarction (MI) and right ventricular infarction.

Methods

This study was a retrospective analysis. The STE group consisted of 88 patients consecutively admitted to the emergency department with inferior ST elevation MI associated with occlusion of right coronary artery or left circumflex coronary artery who underwent primary percutaneous coronary intervention. The control group consisted of 109 patients with non-ST elevation MI who had occlusion of right coronary artery or left circumflex coronary artery and underwent percutaneous coronary intervention. Measurements were performed at the J point and 60 milliseconds later for limb lead and right precordial V₄ lead (V4R). The criterion of at least 1-mm STE in 2 consecutive leads was applied, and the diagnostic accuracy of V4R was calculated.

Results

In the STE group, the measurements 60 milliseconds after the J point were significantly higher than measurements at the J point at the II, III, aVF, and V4R leads. In the control group, only the measurements at lead I differed significantly. There was a 5% difference in diagnostic sensitivity depending on the measuring points in the STE group, a 1% to 3% difference in the control group, and a 10% to 11% difference at the V4R lead.

Conclusion

In patients with inferior MI, STE depends on the method of measurement, indicating a need for the standardization of measurements.     

Long-term prognostic importance of diabetes after a myocardial infarction depends on left ventricular systolic function

OBJECTIVE

This study was performed to understand how left ventricular function modulates the prognostic importance of diabetes after myocardial infarction (MI).

RESEARCH DESIGN AND METHODS

Consecutively hospitalized MI patients screened for three clinical trials were followed for a median of 7 years. Multivariable Cox regression models were used to assess the risk of mortality associated with diabetes, and the importance of diabetes was examined independently within defined left ventricular ejection fraction (LVEF) subgroups.

RESULTS

A total of 16,912 patients were included; 1,819 (11%) had diabetes. Diabetes and 15% unit depression in LVEF were of similar prognostic importance: hazard ratios (HRs) were 1.45 (95% CI 1.37–1.54) and 1.41 (1.37–1.45) for diabetes and LVEF depression, respectively. LVEF modified the outcomes associated with diabetes, with HRs being 1.29 (1.19–1.40) and 1.61 (1.49–1.74) in patients with LVEF <40% and LVEF ≥40%, respectively (P = 0.03).

CONCLUSIONS

Patients within the higher LVEF categories have a greater mortality risk attributable to diabetes than patients within the lower LVEF categories.Diabetic patients without myocardial infarction (MI) and MI patients without diabetes have a high and equally adverse long-term risk of cardiovascular death compared with the general population (1,2). As well as diabetes, the presence of systolic dysfunction and heart failure are major risk factors for mortality after MI. A recent study suggested that diabetes may be regarded as a risk equivalent to low left ventricular ejection fraction (LVEF) and that ordinary LVEF risk stratification may not be valid in these patients (3). This study was performed to further clarify their interrelationship.     

Infarct evolution in man studied in patients with first-time coronary occlusion in comparison to different species - implications for assessment of myocardial salvage

Background

The time course of infarct evolution, i.e. how fast myocardial infarction (MI) develops during coronary artery occlusion, is well known for several species, whereas no direct evidence exists on the evolution of MI size normalized to myocardium at risk (MaR) in man. Despite the lack of direct evidence, current literature often refers to the "golden hour" as the time during which myocardial salvage can be accomplished by reperfusion therapy. Therefore, the aim of the present study was to investigate how duration of myocardial ischemia affects infarct evolution in man in relation to previous animal data. Consecutive patients with clinical signs of acute myocardial ischemia were screened and considered for enrollment. Particular care was taken to assure uniformity of the patients enrolled with regard to old MI, success of revascularization, collateral flow, release of biochemical markers prior to intervention etc. Sixteen patients were ultimately included in the study. Myocardium at risk was assessed acutely by acute Myocardial Perfusion Single photon emission computed tomography (MPS) and by T2 imaging (T2-STIR) cardiovascular magnetic resonance (CMR) after one week in 10 of the 16 patients. Infarct size was measured by late gadolinium enhancement (LGE) at one week.

Results

The time to reach 50% MI of the MaR (T₅₀) was significantly shorter in pigs (37 min), rats (41 min) and dogs (181 min) compared to humans (288 min). There was no significant difference in T₅₀ when using MPS compared to T2-STIR (p = 0.53) for assessment of MaR (288 ± 23 min vs 310 ± 22 min, T₅₀ ± standard error). The transmural extent of MI increased progressively as the duration of ischemia increased (R² = 0.56, p < 0.001).

Conclusion

This is the first study to provide direct evidence of the time course of acute myocardial infarct evolution in relation to MaR in man with first-time MI. Infarct evolution in man is significantly slower than in pigs, rats and dogs. Furthermore, infarct evolution assessments in man are similar when using MPS acutely and T2-STIR one week later for determination of MaR, which significantly facilitates future clinical trials of cardioprotective therapies in acute coronary syndrome by the use of CMR.     

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

Background

Myocardial 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.

Methods

Here 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.

Results

LGE 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.

Conclusion

The 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.     

Clinical and procedural predictors of no-reflow in patients with acute myocardial infarction after primary percutaneous coronary intervention

BACKGROUND:

The treatment of acute myocardial infarction (AMI) is thought to restore antegrade blood flow in the infarct-related artery (IRA) and minimize ischemic damage to the myocardium as soon as possible. The present study aimed to identify possible clinical predictors for no-reflow in patients with AMI after primary percutaneous coronary intervention (PCI).

METHODS:

A total of 312 consecutive patients with AMI who had been treated from January 2008 to December 2010 at the Cardiology Department of East Hospital, Tongji University School of Medicine were enrolled in this study. Inclusion criteria were: (i) patients underwent successfully primary PCI within 12 hours after the appearance of symptoms; or (ii) patients with ischemic chest pain for more than 12 hours after a successful primary PCI within 24 hours after appearance of symptoms. Exculsion criteria were: (i) coronary artery spasm; (ii) diameter stenosis of the culprit lesion was <50% and coronary blood flow was normal; (iii) patients with severe left main coronary or multivessel disease, who had to require emergency revascularization. According to thrombolysis in myocardial infarction (TIMI), the patients were divided into a reflow group and a no-reflow group. The clinical data, angiography findings and surgical data were compared between the two groups. Univariate and multivariate logistic regressions were used to determine the predictors for no-reflow.

RESULTS:

Fifty-four (17.3%) of the patients developed NR phenomenon after primary PCI. Univariate analysis showed that age, time from onset to reperfusion, systolic blood pressure (SBP) on admission, Killip class of myocardial infarction, intra-aortic balloon pump (IABP) use before primary PCI, TIMI flow grade before primary PCI, type of occlusion, thrombus burden on baseline angiography, target lesion length, reference luminal diameter and method of reperfusion were correlated with no-reflow (P<0.05 for all). Multiple logistic regression analysis identified that age >65 years [OR=1.470, 95% confidence interval (CI) 1.460–1.490, P=0.007], long time from onset to reperfusion >6 hours (OR=1.270, 95%CI 1.160–1.400, P=0.001), low SBP on admission <100 mmHg (OR=1.910, 95%CI 1.018–3.896, P=0.004), IABP use before PCI (OR= 1.949, 95%CI 1.168–3.253, P=0.011), low (≤1) TIMI flow grade before primary PCI (OR=1.100, 95%CI 1.080–1.250, P<0.001), high thrombus burden (OR=1.600, 95%CI 1.470–2.760, P=0.030), and long target lesion (OR=1.948, 95%CI 1.908–1.990, P=0.019) on angiography were independent predictors of no-reflow.

CONCLUSION:

The occurrence of no-reflow after primary PCI for acute myocardial infarction can predict clinical, angiographic and procedural features.KEY WORDS: Acute myocardial infarction, No-reflow phenomenon, Percutaneous coronary intervention, Thrombus     

Highly automatic quantification of myocardial oedema in patients with acute myocardial infarction using bright blood T2-weighted CMR

Background

T2-weighted cardiovascular magnetic resonance (CMR) is clinically-useful for imaging the ischemic area-at-risk and amount of salvageable myocardium in patients with acute myocardial infarction (MI). However, to date, quantification of oedema is user-defined and potentially subjective.

Methods

We describe a highly automatic framework for quantifying myocardial oedema from bright blood T2-weighted CMR in patients with acute MI. Our approach retains user input (i.e. clinical judgment) to confirm the presence of oedema on an image which is then subjected to an automatic analysis. The new method was tested on 25 consecutive acute MI patients who had a CMR within 48 hours of hospital admission. Left ventricular wall boundaries were delineated automatically by variational level set methods followed by automatic detection of myocardial oedema by fitting a Rayleigh-Gaussian mixture statistical model. These data were compared with results from manual segmentation of the left ventricular wall and oedema, the current standard approach.

Results

The mean perpendicular distances between automatically detected left ventricular boundaries and corresponding manual delineated boundaries were in the range of 1-2 mm. Dice similarity coefficients for agreement (0=no agreement, 1=perfect agreement) between manual delineation and automatic segmentation of the left ventricular wall boundaries and oedema regions were 0.86 and 0.74, respectively.

Conclusion

Compared to standard manual approaches, the new highly automatic method for estimating myocardial oedema is accurate and straightforward. It has potential as a generic software tool for physicians to use in clinical practice.     

Incidence and prevalence of unrecognized myocardial infarction in people with diabetes: a substudy of the Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycemia in Diabetes (RECORD) study

OBJECTIVE

To examine the prevalence and incidence of unrecognized myocardial infarction in a contemporary population with type 2 diabetes.

RESEARCH DESIGN AND METHODS

We performed a retrospective analysis of the electrocardiograms (ECGs) recorded at baseline and after 2 years for the first 1,004 type 2 diabetic individuals to be randomized in the Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycemia in Diabetes (RECORD) study.

RESULTS

ECGs suitable for analysis were obtained from 669 participants. The prevalence of unrecognized Q-wave myocardial infarction at baseline was 1.9% (n = 13). The incidence of unrecognized Q-wave myocardial infarction at the end of 2 years of follow-up was 1.5/1,000-person-years (n = 2). One-third (13 of 39) of prevalent and one-quarter (2 of 8) of incident myocardial infarctions were unrecognized.

CONCLUSIONS

Although the prevalence and incidence of myocardial infarction was low, unrecognized Q-wave myocardial infarctions made up a substantial proportion of all events.Although usually accompanied by typical symptoms, some myocardial infarctions (MIs) are not clinically recognized. Unrecognized MIs are thought to be important because there is some evidence that they carry a similar prognosis to recognized MIs (1–3). People with diabetes are considered to be more at risk for unrecognized MIs than those without diabetes, but few data have directly addressed this issue. Consequently, we examined the prevalence and incidence of clinically unrecognized MI in a contemporary population with type 2 diabetes enrolled in the Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycemia in Diabetes (RECORD) study.     

Cardiovascular magnetic resonance of the myocardium at risk in acute reperfused myocardial infarction: comparison of T2-weighted imaging versus the circumferential endocardial extent of late gadolinium enhancement with transmural projection

Background

In the situation of acute coronary occlusion, the myocardium supplied by the occluded vessel is subject to ischemia and is referred to as the myocardium at risk (MaR). Single photon emission computed tomography has previously been used for quantitative assessment of the MaR. It is, however, associated with considerable logistic challenges for employment in clinical routine. Recently, T2-weighted cardiovascular magnetic resonance (CMR) has been introduced as a new method for assessing MaR several days after the acute event. Furthermore, it has been suggested that the endocardial extent of infarction as assessed by late gadolinium enhanced (LGE) CMR can also be used to quantify the MaR. Hence, we sought to assess the ability of endocardial extent of infarction by LGE CMR to predict MaR as compared to T2-weighted imaging.

Methods

Thirty-seven patients with early reperfused first-time ST-segment elevation myocardial infarction underwent CMR imaging within the first week after percutaneous coronary intervention. The ability of endocardial extent of infarction by LGE CMR to assess MaR was evaluated using T2-weighted imaging as the reference method.

Results

MaR determined with T2-weighted imaging (34 ± 10%) was significantly higher (p < 0.001) compared to the MaR determined with endocardial extent of infarction (23 ± 12%). There was a weak correlation between the two methods (r² = 0.17, p = 0.002) with a bias of -11 ± 12%. Myocardial salvage determined with T2-weighted imaging (58 ± 22%) was significantly higher (p < 0.001) compared to myocardial salvage determined with endocardial extent of infarction (45 ± 23%). No MaR could be determined by endocardial extent of infarction in two patients with aborted myocardial infarction.

Conclusions

This study demonstrated that the endocardial extent of infarction as assessed by LGE CMR underestimates MaR in comparison to T2-weighted imaging, especially in patients with early reperfusion and aborted myocardial infarction.     

Oxygenation-sensitive CMR for assessing vasodilator-induced changes of myocardial oxygenation

Background

As myocardial oxygenation may serve as a marker for ischemia and microvascular dysfunction, it could be clinically useful to have a non-invasive measure of changes in myocardial oxygenation. However, the impact of induced blood flow changes on oxygenation is not well understood. We used oxygenation-sensitive CMR to assess the relations between myocardial oxygenation and coronary sinus blood oxygen saturation (SvO₂) and coronary blood flow in a dog model in which hyperemia was induced by intracoronary administration of vasodilators.

Results

During administration of acetylcholine and adenosine, CMR signal intensity correlated linearly with simultaneously measured SvO₂ (r² = 0.74, P < 0.001). Both SvO₂ and CMR signal intensity were exponentially related to coronary blood flow, with SvO2 approaching 87%.

Conclusions

Myocardial oxygenation as assessed with oxygenation-sensitive CMR imaging is linearly related to SvO₂ and is exponentially related to vasodilator-induced increases of blood flow. Oxygenation-sensitive CMR may be useful to assess ischemia and microvascular function in patients. Its clinical utility should be evaluated.     

Efficacy of a new mutated recombinant tissue-type plasminogen activator in beagles with acute coronary artery thrombi

BACKGROUND:

Development of new coronary thrombolytic agents is hot in the market. A new drug, mutated recombinant tissue-type plasminogen activator (rtPAm), is the product of mutation of tPA by changing binding loci with plasminogen activator inhibitor (PAI)-1 to reduce the degradation. In vitro test has demonstrated that the activity of rtPAm is much higher than rtPA in the absence of PAI. The present study is to observe the efficacy of mutated recombinant tissue-type plasminogen activator (rtPAm) in coronary thrombolytic therapy.

METHODS:

A total of 30 adult beagles were equally divided into 5 groups after thrombi: vehicle group, urokinase group, rtPAm low-dose group, rtPAm medium-dose group, and rtPAm high-dose group. Thrombolytic effect and myocardial infarction were observed after thrombolytic therapy.

RESULTS:

In the urokinase group, time to reperfusion was (15.8±3.8) minutes. TIMI 2 flow was demonstrated in 4 beagles, TIMI 3 flow in 2, and re-occlusion in 4 after 90 minutes respectively. In the low-dose rtPAm group, time to reperfusion was (15±4.5) minutes; TIMI 2 flow was demonstrated in 2 beagles, TIMI 3 flow in 4, and re-occlusion in 2 after 90 minutes. In the high-dose rtPAm group, time to reperfusion was (7.5±2.6) minutes. None of the beagles showed re-occlusion after 90 minutes. The infarction areas were (2.1+0.9)% in the medium-dose rtPAm group and (0.7+0.4)% in the high-dose rtPAm group, which decreased significantly than those in the low-dose rtPAm group. The aggregation rate in the medium-dose and high-dose rtPAm groups decreased significantly than that in the urokinase group.

CONCLUSION:

rtPAm may serve as a thrombolytic agent with platelet-targeted fibrinolysis and antiplatelet aggregation activities.KEY WORDS: Urokinase, RtPA, Thrombi, D-dime, Platelet aggregation