Presence Of Myocardial Necrosis Research Articles

State-of-the-Art of Myocardial Perfusion by CMR: A Practical View.

Ischemic heart disease (IHD) outstands among diseases threatening public health. Essential for its management are the continuous advances in medical and interventional therapies, although a prompt and accurate diagnosis and prognostic stratification are equally important. Besides information on the anatomy of coronary arteries, well covered nowadays by invasive and non-invasive angiographic techniques, there are also other components of the disease with clinical impact, as the presence of myocardial necrosis, the extent of pump function impairment, and the presence and extent of inducible myocardial ischemia, that must be considered in every patient. Cardiovascular Magnetic Resonance (CMR) is a multiparametric diagnostic imaging technique that provides reliable information on these issues. Regarding the detection and grading of inducible ischemia in particular, the technique has been widely adopted in the form of myocardial perfusion sequences under vasodilator stress, which is the subject of this review. While the analysis of images is conventionally performed by visual inspection of dynamic first-pass studies, with the inherent dependency on the operator capability, the recent introduction of a reliable application of quantitative perfusion (QP) represents a significant advance in the field. QP is based on a dual-sequence strategy for conversion of signal intensities into contrast agent concentration units and includes a full automatization of processes such as myocardial blood flow (MBF) calculation (in mL/min/g), generation of a pixel-wise flow mapping, myocardial segmentation, based on machine learning, and allocation of MBF values to myocardial segments. The acquisition of this protocol during induced vasodilation and at rest gives values of stress/rest MBF (in mL/min/g) and myocardial perfusion reserve (MPR), both global and per segment. Dual-sequence QP has been successfully validated against different reference methods, and its prognostic value has been shown in large longitudinal studies. The fact of the whole process being automated, without operator interaction, permits to conceive new interesting scenarios of integration of CMR into systems of entirely automated diagnostic workflow in patients with IHD.

MiRNA-29 aggravates myocardial infarction via inhibiting the PI3K/mTOR/HIF1α/VEGF pathway.

Introduction: MI is defined by the presence of myocardial necrosis, which is caused by acute and persistent ischemia and hypoxia of the coronary artery. In recent years, its incidence rate has been on the rise in China.Methods: GSE34198, GSE97320 and GSE141512 datasets were download for DEG analysis. KEGG pathway analysis, GO analysis, GSEA and PPI network construction were performed. Later, target genes of candidate miRNAs were predicted. Next, echocardiography was conducted to detect the effects of miR-29 on left ventricular structure and cardiac function in vivo, and H&E staining was adopted to study the effects of miR-29 on angiogenesis and fibrosis in vivo. Furthermore, Western blotting was employed to investigate the effects of miR-29 inhibition on the expressions of proteins related to the PI3K\\mTOR\\ HIF-1α\\VEGF pathway.Results: There were 162 DEGs involved in MI. GO analysis revealed that inflammatory responses, negative regulation of apoptosis and innate immune response were the main enriched biological processes. KEGG analysis manifested that DEGs were mainly enriched in the PI3K/Akt signaling pathway, and GSEA demonstrated that they were mainly enriched in the PI3K/Akt/mTOR, HIF and VEGF pathways. Moreover, target gene prediction showed that miR-29 was lowly expressed in MI. According to Masson's trichrome staining, miR-29 inhibition promoted angiogenesis, reduced fibrosis, and increased the protein expressions of p-PI3K, p-mTOR, HIF-1α, and VEGF.Conclusions: MiR-29 may play an important role in the growth and development of MI. After inhibition of miR-29, the PI3K/mTOR/HIF-1α/VEGF pathway is activated to alleviate MI.

The Case for Takotsubo Cardiomyopathy (Syndrome) as a Variant of Acute Myocardial Infarction

The Case for Takotsubo Cardiomyopathy (Syndrome) as a Variant of Acute Myocardial Infarction

The utility of troponin measurement to detect myocardial infarction: review of the current findings

Myocardial infarction (MI) is defined by the presence of myocardial necrosis in combination with clinical evidence of myocardial ischemia. Cardiac troponins are regulatory proteins within the myocardium that are released into the circulation when damage to the myocyte has occurred. Therefore, serum troponin is an exquisitely sensitive marker of myocardial injury and is necessary for establishing the diagnosis of MI. High-sensitivity troponin assays are improving the diagnostic accuracy and rapid detection of myocardial infarction. The early identification of MI is vital for the institution of anti-thrombotic therapy to limit myocardial damage and preserve cardiac function. Troponin has both diagnostic and prognostic significance in the setting of acute coronary syndrome (ACS). Increased troponin levels in the absence of ACS should prompt an evaluation for an alternative, non-thrombotic mechanism of troponin elevation and direct management at the underlying cause. This review describes the role of troponin in the evaluation of patients with suspected myocardial infarction.

Prevalence of first-pass myocardial perfusion defects detected by contrast-enhanced dual-source CT in patients with non-ST segment elevation acute coronary syndromes

To investigate the prevalence and diagnostic value of first-pass myocardial perfusion defects (PD) visualised by contrast-enhanced multidetector computed tomography (MDCT) in patients admitted for a first acute coronary syndrome (ACS). Thirty-eight patients with non-ST segment elevation myocardial infarction (NSTEMI) or unstable angina (UA) and scheduled for percutaneous coronary intervention underwent dual-source CT immediately before catheterisation. CT images were analysed for the presence of any PD by using a 17-segment model. Results were compared with peak cardiac troponin-I (cTnI) and angiography findings. PD were seen in 21 of the 24 patients with NSTEMI (median peak cTnI level 7.07 ng/mL; range 0.72-37.07 ng/mL) and in 2 of 14 patients with UA. PD corresponded with the territory of the infarct-related artery in 20 out of 22 patients. In a patient-based analysis, sensitivity, specificity, negative and positive predictive values of any PD for predicting NSTEMI were 88%, 86%, 80% and 91%. Per culprit artery, the respective values were 86%, 75%, 80% and 83%. In patients with non-ST segment elevation ACS, first-pass myocardial PD in contrast-enhanced MDCT correlate closely with the presence of myocardial necrosis, as determined by increases in cTnI levels.

Detection of coronary artery lesions and myocardial necrosis by magnetic resonance in systemic necrotizing vasculitides

Myocardium and coronary arteries can occasionally be affected in patients with systemic necrotizing vasculitides; however, such involvement has not been systematically assessed using cardiovascular magnetic resonance imaging (MRI). Magnetic resonance angiography and contrast-enhanced MRI were applied for the assessment of coronary arteries (the left anterior descending [LAD], left circumflex [LCx], and right coronary artery [RCA]) and myocardium, respectively, in 39 patients with vasculitis who were asymptomatic for cardiac disease (16 with microscopic polyangiitis [MPA], 11 with Wegener's granulomatosis [WG], 9 with Churg-Strauss syndrome [CSS], and 3 with polyarteritis nodosa [PAN]). Data were compared with age-matched disease-control patients with rheumatoid arthritis (n = 20) or systemic lupus erythematosus (n = 13), and with healthy control individuals with normal coronaries (n = 40). Patients with MPA, WG, and PAN (but not with CSS) were found to display significantly increased maximal diameters of coronary arteries compared with healthy controls (for MPA and WG; P < 0.001 for LAD and RCA, and P < 0.01 for LCx) and with both disease-control groups (for only MPA; P < 0.01 for LAD and RCA, and P < 0.05 for LCx). Fusiform coronary aneurysms were detected in patients with MPA (4/16) and PAN (2/3), whereas coronary ectasias were evident in patients with MPA (14/16) and WG (2/11). The presence of myocardial necrosis (by assessment of late gadolinium-enhanced images) was identified only in patients with MPA (2/16) and CSS (3/8 studied). Cardiovascular MRI assessment of patients with systemic vasculitis revealed coronary ectatic disease in the majority of patients with MPA and PAN, as well as in several patients with WG. Myocardial necrosis can be detected in MPA and CSS.

Extension of myocardial necrosis differently affects MIBG retention in heart failure caused by ischaemic heart disease or by dilated cardiomyopathy

This study aims to investigate the relationship between cardiac sympathetic nervous function (CSNF) and myocardial perfusion/function in patients with heart failure (HF) due to dilated cardiomyopathy (DCM) or ischaemic heart disease (CAD). Twenty patients (10 DCM, 10 CAD, 17 males, age 69+/-5 years) with NYHA class IIIb HF were studied. CSNF was evaluated by early/delayed (123)I-metaiodobenzylguanidine (MIBG) uptake and regional washout (WO). Myocardial perfusion and function were evaluated by (99m)Tc-tetrofosmin gated single-photon emission tomography (G-SPECT) using a 20-segment model for 400 segments. In each segment, regional MIBG WO was computed as (count density in early images-count density in delayed images/count density in early images)x100. DCM and CAD showed similar summed rest perfusion score (6.7+/-5 vs 9.5+/-5, p=NS) and mean ejection fraction values (29+/-7% vs 30+/-9%, p=NS). By contrast, the summed thickening score was higher in DCM than in CAD patients (26+/-7 vs 17+/-6, p<0.05). QGS analysis identified akinesis/dyskinesis in 129/137 (94%) severely hypoperfused segments which were considered as damaged. According to the underlying aetiology of HF, marked differences in regional MIBG WO were observed. In fact, within the CAD group, regional MIBG WO was lower in reference than in damaged segments (38+/-21% vs 46+/-19%, p<0.05). By contrast, in DCM patients, regional MIBG WO was faster in reference than in damaged segments (49+/-18% vs 41+/-30%, p<0.05). When the two groups were directly compared, regional MIBG WO from damaged areas was similar irrespective of the underlying disease, while it was faster in DCM than in CAD patients from reference segments. These data confirm the hypothesis that the presence of myocardial necrosis in HF due to CAD and the consequent loss of neuronal endings cause alterations in regional MIBG WO different from those observed in DCM.

Radionuclide Imaging in Patients with Ischemic Heart Failure

Nuclear imaging procedures are well-established diagnostic tools in clinical cardiology, providing noninvasive information about myocardial perfusion, cardiac function and metabolism. Scintigraphic parameters provide relevant information that aids in everyday clinical decision making for referring physicians. In patients with coronary artery disease, the presence of myocardial necrosis, postischemic stunning and hibernation can determine left ventricular dysfunction leading to ischemic heart failure. The prognosis of these patients is still poor and the long-term results of medical management remain discouraging. It is now well established that ventricular dysfunction is often a reversible process and ventricular function may improve following myocardial revascularization. Patients with extensive areas of hibernation treated medically have a worse prognosis as compared to those who undergo revascularization with a similar extent of viable myocardium. Therefore, an accurate non-invasive assessment of myocardial viability with the preoperative differentiation between hibernation and stunning and irreversibly necrotic tissue is important for clinical decision-making to select patients candidates for revascularization. Radionuclide imaging techniques evaluating myocardial perfusion, cell membrane integrity, ventricular function and cardiac metabolism have demonstrated clinical utility in the assessment of myocardial viability and in predicting improvement of ventricular function and prognosis after coronary revascularization. Keywords: radionuclide cardiac imaging, ischemic heart failure, myocardial viability

Differentiation of myocardial ischemia and necrosis by technetium 99m glucaric acid kinetics

Background. Current clinical approaches may not always be helpful in the early differentiation of necrotic tissue from ischemic viable myocardium in patients with acute myocardial infarction. Tc-99m-glucaric acid is a carbohydrate ligand that may permit differentiation of necrosis from ischemia. However, the myocardial kinetics of Tc-99m-glucaric acid have not been well defined early after myocardial injury. The aim of this study was to evaluate the effect of necrosis in comparison to postischemic injury alone on the kinetics of Tc-99m-glucaric acid with the use of an isolated perfused rat heart model. Methods and Results. Three groups of hearts were studied: group I: control (n = 6); group II: postischemia (15 minutes of no flow with complete reperfusion, n = 6); and group III: necrosis (90 minutes of no flow to induce necrosis with complete reperfusion, n = 6). Tc-99m-glucaric acid (1.3 ± 0.6) mCi/L of buffer) was perfused for 30 minutes to evaluate tracer accumulation. Then tracer-free buffer was perfused for 45 minutes to evaluate clearance. The peak accumulation relative to the control group mean was significantly increased ( p < 0.01) in group III (necrosis) (254% ± 75%) compared with control (100% ± 10%) and compared with postischemia (108% ± 26%). On kinetic data analysis, the monoexponential clearance rate constant (k c) was significantly reduced with necrosis (control: k c = 20.2 ± 14.0 × 10 −4) sec −1; postischemia: k c = 22.3 ± 15.2 × 10 −4 sec −1; and necrosis: k c = 1.2 ± 0.3 × 10 −4 sec −1; p < 0.05). A retention fraction was calculated from the activity after 45 minutes of clearance corrected for the peak activity for each group. The necrotic group had significant myocardial retention in comparison to control and postischemia (control: 12% ± 8%; postischemia: 14% ± 16%); necrosis: 64% ± 10%; p < 0.01). Conclusions. The accumulation and retention of Tc-99m-glucaric acid is markedly increased in the presence of myocardial necrosis in comparison to control and postischemic myocardial injury. In this model, Tc-99m-glucaric acid is capable of defining the presence of necrotic myocardial injury in comparison to postischemic injury alone. This agent may have potential application for the early differentiation of ischemic from necrotic myocardium in acute myocardial infarction.

938-56 Myocardial Contrast Echocardiography: What is the Meaning of Regional Perfusion Abnormalities After Release of Temporary Coronary Occlusions?

Myocardial contrast echocardiography (MCE) has been used to demonstrate regional perfusion abnormalities (RPA) in the presence of coronary occlusions, severe coronary stenosis, and myocardial infarctions (MI). We have observed such abnormalities following the release of a temporary occlusion in the absence of MI. To further define this, we studied 54 open-chest dogs. Temporary coronary occlusions were performed (Group A = 15 minutes; Group B = 30 to 360 minutes), followed by release of the occlusions and by the administration of dobutamine IV (10 μg/kg/min). Myocardial contrast echocardiography was performed with aortic root injections of sonicated albumin (Albunex ® ) during occlusion and following reperfusion with and without dobutamine. Postmortem TTC staining (+ stain = viable myocardiuml was used to determine the presence/absence of MI All Group A dogs (n = 14) showed no evidence of MI. In Group B (n = 40), 14 dogs showed no evidence of MI, whereas the other 26 did (12 papillary muscle, 7 subendocardial, and 7 transmural). The presence of RPA in all groups is shown below: Occlusion Reperfusion Reperfusion+ Dobutamine Group A 13/14 2/14 2/14 Group B 35/40 17/39 20/39 • No MI 11/14 7/13 8/13 • Papillary MI 10/12 3/12 5/12 • Subendocardial MI 7/7 3/7 3/7 • Transmural MI 7/7 4/7 4/7 In conclusion, the presence of a RPA following the release of coronary occlusions most likely indicates abnormal coronary reserve rather than the presence of myocardial necrosis.

Assessment of chest pain by nuclear cardiology techniques.

This article reviews the nuclear cardiology techniques which can be used to assess chest pain. Nuclear techniques can potentially give valuable information on the location and extent of myocardial perfusion abnormalities, the assessment of myocardial viability, and/or presence of myocardial necrosis and the effects, both regional and global, of myocardial ischemia on myocardial function. The article reviews specific tests available and their indications and indicates the usefulness of these techniques for the clinician managing myocardial ischemia.

Multiparametric approach to diagnosis of non-Q-wave acute myocardial infarction

The present study investigated whether the lack of enzyme increase is reason enough to exclude necrosis in patients with ischemic heart disease who develop electrocardiographic sustained ST-T changes in the absence of Q waves. In 15 consecutive patients with angina who developed sustained ST-T changes during hospitalization, the presence of myocardial necrosis was investigated by a prospective multiparametric approach. Serum enzymes and myoglobin, pyrophosphate uptake, 2-dimensional echocardiography, perfusion scintigraphy, left ventriculography and coronary angiography were evaluated. According to creatine kinase and creatine kinase-MB peak at twice the upper normal value, the diagnosis of acute myocardial infarction applied only to 40% of patients. However, myoglobin was positive in 80% and a perfusion defect could be documented by an electrocardiographic gated microsphere technique in 100% of patients. The positivity of myoglobin increased to 100% and of creatine kinase and creatine kinase-MB to 87 and 60%, respectively, when a peak value twice the individual lowest value was considered for positivity. The 100% presence of perfusion defects associated with the high prevalence of both positive pyrophosphate uptake (87%) and regional dyssynergies (87 and 73%, respectively, by left ventriculography and echocardiography) strongly suggest that sustained (≥7 days) ST-T changes in this population were indicative of myocardial necrosis. Thus, by conventional enzymatic approach, diagnosis of non-Q-wave infarction can be missed in a sizable number of patients and present important clinical implications.

Survival after resuscitation from out-of-hospital ventricular fibrillation.

During the first three years in operating a comprehensive system for the management of out-of-hospital medical emergencies, 146 patients were resuscitated from ventricular fibrillation, hospitalized, and discharged home. The diagnosis of acute transmural myocardial infarction associated with the episode of ventricular fibrillation was confirmed in only 17% of the patients. The presence of myocardial necrosis, based on either evidence of new transmural infarction or LDH-isoenzyme criteria was established in 49.5% of the patients. During the follow-up period, averaging 418 days, 43 of the 146 patients died. Thirty-four of the 43 deaths occurred suddenly outside the hospital. Patients whose aborted sudden cardiac death was associated with acute transmural infarction had a mortality rate of 14% after two years of follow-up. In contrast, patients without evidence of acute myocardial necrosis had a high mortality rate — 47% at two years. It is concluded that: 1) out-of-hospital ventricular fibrillation is common and treatable; 2) the phenomenon of sudden cardiac death should not be equated with acute myocardial infarction; 3) patients resuscitated from ventricular fibrillation without associated acute myocardial infarction are prone to sudden death — most likely from ventricular fibrillation.

Serum Enzymes in Experimental Myocardial Infarcts

THERE IS no known accurate technique of clinical quantitation of myocardial infarct size.1During the past decade practical methods of measuring the serum values of certain enzymes, present in abnormally elevated levels in the presence of myocardial necrosis, have been applied widely as diagnostic tests for the presence of myocardial infarction. The reliability of the correlation of infarct size with the magnitude of serum enzyme elevation has not been precisely established. A method based on myocardial distribution of intravenously administered radioactive rubidium (86Rb) has been used recently to quantitate the size of experimentally produced myocardial infarcts. In the present study the elevation of the serum glutamic oxaloacetic transaminase (SGOT), lactic dehydrogenase (LDH), and heat stable lactic dehydrogenase (LDH) following coronary artery ligation was assessed in relation to myocardial infarct size as determined by macroscopic examination (dissection) at autopsy and by the radioactive rubidium distribution technique Methods Myocardial infarcts