Relevant bibliographies by topics / Myocardium

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Myocardium'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 August 2024

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Journal articles on the topic "Myocardium"

1

A. Meenakshi, Martin, and Erik G. Seth. "Protective role of TAT-HSP70 after myocardial I/R injury." American Journal of BioMedicine 5, no. 3 (September 22, 2017): 279–84. http://dx.doi.org/10.18081/2333-5106/015-04/289-294.

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Myocardial ischemia reperfusion injury I/R adversely affects cardiac function. Heat shock proteins (HSPs) are a highly conserved family of proteins with diverse functions expressed by all cells exposed to environmental stress including myocardila injury. We investigated release of small constitutive heat shock proteins (HSPs) from mouse myocardium and the effects of TAT-HSP70 after myocardial I/R via occluding the left coronary artery (LAD). The results support the hypothesis that elevated HSPs in myocardium after ischemia and reperfusion and contributes to the inflammatory mechanism of myocardial functional injury. Further investigation of the significance of HSPs accumulation to the evolution of myocardial injury.
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Brown, TA. "Hibernating myocardium." American Journal of Critical Care 10, no. 2 (March 1, 2001): 84–91. http://dx.doi.org/10.4037/ajcc2001.10.2.84.

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According to estimates, up to 50% of patients with coronary artery disease and impaired left ventricular function have areas of viable myocardium. This dysfunctional, yet viable myocardial tissue, which can improve functionally after myocardial oxygen supply is reestablished, has been called hibernating myocardium. The possible pathophysiological mechanism that leads to hibernating myocardium is controversial: is the phenomenon due to persistent ischemia or is it the result of repetitive episodes of ischemia and reperfusion, such as myocardial stunning? Regardless of the mechanism, the presence of viable myocardial tissue indicates that structural and biochemical cellular changes occur, and the recovery of left ventricular function after revascularization depends on the severity and extent of these changes. Whether these changes reflect a long-lasting state of cellular dedifferentiation, an adaptive process that is reversible, or eventually lead to cellular degeneration has not been determined. Perhaps early detection of hibernating myocardial tissue via noninvasive imaging techniques used to assess contractile response, integrity of the cellular membrane, myocardial metabolism, and myocardial blood flow and subsequent early coronary revascularization may prevent infarction and deterioration in left ventricular function. Knowledge that reversible changes and areas of viable myocardium can occur in patients with left ventricular dysfunction will assist healthcare providers in the care and management of patients with hibernating myocardium.
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Lee, C. Y., Amar Singh, Kevin J. Lee, Roy D. Goldfarb, and Min-Fu Tsan. "Correlation between myocardial glutathione content and extent of ischemia-reperfusion injury." Proceedings, annual meeting, Electron Microscopy Society of America 47 (August 6, 1989): 1068–69. http://dx.doi.org/10.1017/s0424820100157322.

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Considerable evidence suggests that myocardial injury may occur during reperfusion of the ischemic myocardium. Reactive oxygen species are generated during reperfusion which may play an important role in the genesis of myocardial reperfusion injury. Glutathione (GSH) is an important antioxidant in the heart. A decrease in myocardial GSH content has been observed during ischemia and reperfusion of the ischemic myocardiijm. We hypothesized that this depletion of GSH may be detrimental to the ability of the ischemic myocardium to protect itself against reactive oxygen species during reperfusion.In this study, anesthetized open chest pigs were subjected to coronary occlusion for 45 minutes and 2 hours reperfusion. Myocardial GSH was experimentally depleted by pretreatment with buthionine sulfoximine (BSO), a potent inhibitor of cellular GSH synthesis, and was augmented by intravenous administration of GSH. For ultrastructural study multiple subepicardial biopsies 3 mm deep were taken from myocardium supplied by the occluded artery. The biopsies were processed by routine procedures. Thin sections were stained with uranyl acetate and lead citrate and examined with a Philip EM 300 electron microscope.
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Baran, I., B. Ozdemir, S. Gullulu, AA Kaderli, T. Senturk, and A. Aydinlar. "Prognostic Value of Viable Myocardium in Patients with Non-Q-wave and Q-wave Myocardial Infarction." Journal of International Medical Research 33, no. 5 (September 2005): 574–82. http://dx.doi.org/10.1177/147323000503300513.

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This study assessed the amount and prognostic value of myocardial viability in patients with non-Q-wave myocardial infarction (NQMI) and Q-wave myocardial infarction (QMI). A total of 175 patients with MI and an ejection fraction ≤ 45% underwent dobutamine stress echocardiography. On the basis of clinical criteria and myocardial viability, 110 patients were revascularized. The amount of viable myocardium and the clinical outcome were compared in the NQMI and QMI groups. Patients with NQMI exhibited a larger amount of viable myocardium compared with those with QMI. The mortality rate was 6% in patients with NQMI with viable myocardium and subsequent revascularization, 33% in patients with NQMI without viable myocardium or revascularization, 27% in patients with QMI with viable myocardium and subsequent revascularization, and 33% in patients with QMI without viable myocardium or revascularization. In conclusion, our data suggest that patients with NQMI and viable myocardium have the best prognosis after revascularization.
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Abdrahmanova, A. I., N. B. Amirov, and N. A. Cibulkin. "Application of Perfusion Single Photon Emission Computed Tomography of the Myocardium in Pain-Free Myocardial Ischemia." Russian Archives of Internal Medicine 10, no. 5 (October 9, 2020): 340–47. http://dx.doi.org/10.20514/2226-6704-2020-10-5-340-347.

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This literature review provides data on the use of single-photon emission computed tomography of myocardium in silent myocardial ischemia. The presence of silent myocardial ischemia increases the risk of cardiovascular complications several times and may be the first manifestation of coronary heart disease. Assessing the state of morphofunctional processes in the myocardium is the main goal of diagnostic imaging using singlephoton emission computed tomography of the myocardium. This allows to get three-dimensional image of left ventricle with information about distribution of perfusion volume across myocardium, makes it possible to more accurately differentiate such condition as silent myocardial ischemia. Conducting single-photon emission computed tomography in ECG synchronization mode allows you to visualize the kinetics of the myocardial walls in different phases of the cardiac cycle and thereby simultaneously assess the functional state of the left ventricular myocardium. Indicators of contractile function of the left ventricular myocardium in areas of transient hypoperfusion can be predictors of cardiac events after myocardial infarction and independent predictors of perioperative cardiac events in patients undergoing cardiac surgery. Performing single-photon emission computed tomography in ECG-synchronization mode allows visualizing kinetics of myocardial walls in different phases of cardiac cycle and thereby simultaneously assessing functional state of left ventricle myocardium. In combination with physical exercise and pharmacological tests, it helps to identify coronary stenosis among patients with silent myocardial ischemia. Perfusion single-photon emission computed tomography of myocardium is a necessary tool for stratification and assessment of prognosis of cardiac diseases in asymptomatic patients.
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Ristic, Andjelka, Milorad Damjanovic, Branislav Baskot, and Radomir Matunovic. "Stunned myocardium." Vojnosanitetski pregled 62, no. 2 (2005): 165–69. http://dx.doi.org/10.2298/vsp0502165r.

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Background. Stunned myocardium is a state of delayed recovery of regional contractility after a transient period of ischemia followed by reperfusion. Case report. A 67-year-old patient was admitted to our hospital with acute anterior myocardial infarction, and treated using percutaneous transluminal coronary angioplasty (PTCA) within acute disease stage. Reversible myocardial dysfunction persisted after ischemia following the return of normal perfusion. Abnormal resting wall motion with augmentation of contractility at low and high doses of dobutamine characterizes the stunned myocardium and reflects the normal blood flow reserve, characteristic for these postischemic, reperfused segments. SPECT (Single Photon Emission Computerized Tomography) with Tc 99 and dipyradamole showed normalization of perfusion defects in the apical region. Theree months after the infarction and PTCA, contractility was almost completely recovered. Conclusion. Stunned myocardium recovery lasted from few weeks to few months. Control ultrasonography as well as SPECT showed normalization of systolic function of the left ventricle in the viable segments registered at previous examinations.
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Chen, Harn-Shen, Jia Jia, Hou-Fen Su, Hong-Da Lin, Jaw-Wen Chen, Shing-Jong Lin, Jia-Ying Yang, Hui-Chin Lai, Ruben Mestril, and Ping H. Wang. "Downregulation of the constitutively expressed Hsc70 in diabetic myocardium is mediated by insulin deficiency." Journal of Endocrinology 190, no. 2 (August 2006): 433–40. http://dx.doi.org/10.1677/joe.1.06692.

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The 70 kDa heat shock protein family plays important cardiac protective roles against myocardial injuries. Reduced myocardial protection is a common feature of diabetic myocardium. This study was carried out to define the changes in the 70 kDa heat shock protein family in the myocardium in the of streptozotocin-diabetes rats, and to explore the mechanisms through which diabetes alters the abundance of Hsp70/Hsc70 in cardiac muscle. In the diabetic myocardium, the abundance of Hsc70 was significantly reduced. The abundance of Hsp70 was low in cardiac muscle and was not induced in the diabetic myocardium. Unlike Hsp60, Hsp70 and Hsc70 did not augment insulin-like growth factor-I receptor signaling in cardiac muscle cells. In cultured cardiomyocytes, insulin directly increased the abundance of Hsc70, whereas insulin could not modulate Hsp70. Treating diabetic rats with insulin restored myocardial Hsc70 level, but phlorizin treatment failed to restore myocardial Hsc70. These in vivo and in vitro studies showed that downregulation of Hsc70 in diabetic myocardium was secondary to insulin deficiency. Thus, insulin played a major role in maintaining adequate expression of Hsc70 in cardiac muscle.
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Cha, Jehyun, Joonghyun Ryu, Jin-Ho Choi, and Deok-Soo Kim. "Medial-ABC: an algorithm for the correspondence between myocardium and coronary artery mesh models based on the medial axis of coronary artery." Journal of Computational Design and Engineering 7, no. 6 (August 6, 2020): 736–60. http://dx.doi.org/10.1093/jcde/qwaa054.

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Abstract The role of coronary arteries is to supply sufficient blood to myocardium. Obstruction of coronary arteries limits blood supply and causes myocardial ischemia or acute myocardial infarction, a major cause of human death. Hence, the quantification of the regional amount of heart muscle subtended by obstructed coronary arteries is of critical value in clinical medicine. However, conventional methods are inaccurate and frequently disagree with clinical practice. This study proposes a novel medial-axis-based correspondence (Medial-ABC) algorithm to find the correspondence between myocardium and coronary artery in order to segment regional myocardium at risk subtended by any potentially obstructed coronary artery. Given the triangular mesh models of coronary artery and myocardium, the proposed algorithm (i) computes the medial axis of coronary artery, (ii) finds the correspondence using the medial axis of coronary artery, and (iii) segments the coronary artery and myocardium. The proposed algorithm provides a robust mathematical linkage between myocardium at risk and supplying coronary arteries so that ischemic myocardial regions can be accurately identified. Hence, both the extent and severity of myocardial ischemia can be quantified effectively, efficiently, and accurately. Furthermore, the constructed mesh model of segmented coronary artery and myocardium can be post-processed for applications such as building optimization models of cardiac systems. The CardiacVis program, which implements the Medial-ABC algorithm, is freely available at Voronoi Diagram Research Center (http://voronoi.hanyang.ac.kr/software/cardiacvis) and will be an invaluable tool for quantitative patient-specific risk stratification in clinical practice.
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Howard-Quijano, Kimberly, Tatsuo Takamiya, Erica A. Dale, Jasmine Kipke, Yukiko Kubo, Tristan Grogan, Andyshea Afyouni, Kalyanam Shivkumar, and Aman Mahajan. "Spinal cord stimulation reduces ventricular arrhythmias during acute ischemia by attenuation of regional myocardial excitability." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 2 (August 1, 2017): H421—H431. http://dx.doi.org/10.1152/ajpheart.00129.2017.

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Myocardial ischemia creates autonomic nervous system imbalance and can trigger cardiac arrhythmias. We hypothesized that neuromodulation by spinal cord stimulation (SCS) will attenuate local cardiac sympathoexcitation from ischemia-induced increases in afferent signaling, reduce ventricular arrhythmias, and improve myocardial function during acute ischemia. Yorkshire pigs ( n = 20) were randomized to SCS (50 Hz at 200-μs duration, current 90% motor threshold) or sham operation (sham) for 30 min before ischemia. A four-pole SCS lead was placed percutaneously in the epidural space (T1–T4), and a 56-electrode mesh was placed over the heart for high-resolution electrophysiological recordings, including activation recovery intervals (ARIs), activation time, repolarization time, and dispersion of repolarization. Electrophysiological and hemodynamic measures were recorded at baseline, after SCS/sham, during acute ischemia (300-s coronary artery ligation), and throughout reperfusion. SCS 1) reduced sympathoexcitation-induced ARI and repolarization time shortening in the ischemic myocardium; 2) attenuated increases in the dispersion of repolarization; 3) reduced ventricular tachyarrythmias [nonsustained ventricular tachycardias: 24 events (3 sham animals) vs. 1 event (1 SCS animal), P < 0.001]; and 4) improved myocardial function (dP/d t from baseline to ischemia: 1,814 ± 213 to 1,596 ± 282 mmHg/s in sham vs. 1,422 ± 299 to 1,380 ± 299 mmHg/s in SCS, P < 0.01). There was no change in ventricular electrophysiology during baseline conditions without myocardial stress or in the nonischemic myocardium. In conclusion, in a porcine model of acute ventricular ischemia, SCS reduced regional myocardial sympathoexcitation, decreased ventricular arrhythmias, and improved myocardial function. SCS decreased sympathetic nerve activation locally in the ischemic myocardium with no effect observed in the normal myocardium, thus providing mechanistic insights into the antiarrhythmic and myocardial protective effects of SCS. NEW & NOTEWORTHY In a porcine model of ventricular ischemia, spinal cord stimulation decreased sympathetic nerve activation regionally in ischemic myocardium with no effect on normal myocardium, demonstrating that the antiarrhythmic effects of spinal cord stimulation are likely due to attenuation of local sympathoexcitation in the ischemic myocardium and not changes in global myocardial electrophysiology.
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Zdebik, Natalia, Rafał Poręba, and Paweł Gać. "Importance of T1-Mapping Sequence in Patients with Hypertrophic Cardiomyopathy without Foci of Non-Ischemic Myocardial Injury in Late Gadolinium Enhancement Sequence." Biomedicines 12, no. 6 (June 14, 2024): 1330. http://dx.doi.org/10.3390/biomedicines12061330.

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Background: The aim of this study was to assess the importance of T1-mapping sequences in the diagnosis of hypertrophic cardiomyopathy (HCM) in patients without foci of non-ischemic myocardial injury in classic cardiac magnetic resonance (CMR) sequences. Methods: Two groups were compared: 28 patients with HCM, without any foci of myocardial injury in the late gadolinium enhancement (LGE) sequence (HCM group), and 28 patients without cardiomyopathy (CON group). Classic CMR sequences and T1-mapping sequences were performed. The following parameters were assessed: T1 time of the whole left ventricular myocardium, T1 time of myocardium in the basal, middle and apical layers of the left ventricle, and T1 time in individual segments of the left ventricular myocardium. Myocardial extracellular volume (ECV) was assessed similarly. Results: ECV was significantly higher in the HCM group than in the CON group, for the whole left ventricular myocardium, for the basal and apical layers of the left ventricle, and for segments 1–3, 8, and 13–16 of the left ventricle. Regression analysis showed that a higher left-ventricular mass index (LVMI), a higher body mass index and older age are factors independently associated with a higher ECV of the whole myocardium but only in the group with LVMI ≥ 131.84 g/m2. Conclusion: In patients with HCM without foci of non-ischemic myocardial injury, higher ECV values of the left ventricular myocardium are observed.
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Dissertations / Theses on the topic "Myocardium"

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Herrey, Annekatrin Synje. "Hibernating Myocardium." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.508720.

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Park, Jade. "Myocardial fibrosis and effect of AZT in myocardium of Y995CB mouse." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12581.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Pyrimidine nucleoside reverse transcriptase inhibitors (NRTIs), one of the primary classes of HIV/AIDS antiretroviral drugs, are known to cause mitochondrial toxicity by inhibiting polymerase gamma during extending mitochondrial DNA replication. Extensive, prolonged use of NRTIs, such as zidovudine (3'-azido-2',3'-deoxythymidine; AZT), is associated with cardiovascular complications, such as dilated cardiomyopathy, the most common form of heart failure in which cardiac fibrosis is seen. Moreover, cardiac fibrosis is part of the pathological response of the heart during the progression of heart failure. Thus, we hypothesized that AZT treatment will contribute to the progression of cardiac fibrosis indirectly. Our study specifically focused on the effects of AZT and the development of cardiac fibrosis in the myocardium of wildtype (WT) and Y955CB transgenic mice (TG). Y955CB TG expresses a dominant negative cardiac specific mutant mitochondrial DNA polymerase gamma and were used to enhance the mtDNA toxic effect of AZT. To estimate fibrosis, myocardial collagen levels in each treatment group were assessed using both the hydroxyproline assay and histological image analysis. WT mice treated with AZT 0.22 mg/day for 35 days revealed no change in the level of hydroxyproline. However, a significant increase in hydroxyproline abundance correlated with histologically detectable fibrosis in vehicle-treated Y955CB TG mice. Interestingly, there was no additional increase in the abundance of collagen in AZT-treated Y955CB mice. Taken together, these data demonstrate that Y955CB TG displays an increase in the collagen level of the heart, concomitant with its documented cardiomyopathy. However AZT treatment was insufficient to increase the abundance of collagen in the heart.
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White, Melanie Yvonne. "Proteomics of ischemia/reperfusion injury in rabbit myocardium." Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/27890.

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Myocardial stunning is best defined as the persistent, yet reversible, contractile dysfunction that occurs with brief myocardial ischemia / reperfusion (I/R) injury. In contrast, prolonged ischemia results in myocardial infarction that leads to cell death of necrosis of the tissue. The causes of stunning are not fully elucidated, however two major hypotheses currently exist; firstly changes to calcium handling resulting from lowered cellular pH by means of anaerobic respiration, and altered Nair/H)r antiporter kinetics, and secondly, the generation oxygen free radical (OFR) that may occur in a dramatic ‘surge’ at the onset of reperfusion. Treatment of ischemic myocardium with calcium channel blockers and / or OFR scavengers has been successfully shown to prevent stunning in various animal models. Whilst much is known about the physiological and biochemical changes that occur in stunned myocardium, very little is known about events at the molecular level. Since stunning occurs after only brief (15 minutes low-flow in the rabbit model) ischemia and subsequent reperfusion, we hypothesized that these molecular events are not predominated by large changes in protein expression and abundance, yet rather by subtle and / or transient changes to protein post-translational modifications (PTM). Such changes at the protein level are best analysed using the technologies encompassed under the term ‘proteomics’.
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Shenje, Lincoln Takura. "Studies assessing cardiac myocyte renewal and myocardial repair in the adult mammalian myocardium." Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/29896.

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The initial aims of this thesis were to investigate whether the myocardium contains resident progenitor cells that contribute to myocardial renewal and whether extra-cardiac bone marrow derived cells contribute to myocardial regeneration. I reveal that the myocardium has the capacity to produce humoral factors that enable extra-cardiac progenitors to survive in vitro though this was insufficient to induce cardiac differentiation. I have shown that the myocardium has the capacity to produce a heterogeneous population of cells in vitro, some of which express cardiac related markers but do not adopt a full cardiac phenotype. When these cells are transplanted into a normal or injured heart they integrate into the myocardium but fail to develop a full mature functional cardiac phenotype. I have set up the frame work for demonstrating and defining the qualitative histological structure of the myocardium using lineage tracing techniques and strengthening the criteria for defining various cell lineages in the heart and therefore demonstrated the deficiencies of seminal studies that claimed that adult stem cells had the capacity to differentiate into cardiomyocytes and secondly that cultured heart explants produce cardiac progenitors. From this work it is clear that more needs to be done to identify the various cell lineages and roles of endogenous cardiac cells. The identification of clusters of perivascular cells expressing cardiac markers using 3 dimensional confocal imaging by two photon molecular excitation provided a different approach for identifying putative cardiac progenitors. This in combination with lineage tracing techniques and cell isolation is now required to identify the role of these interesting perivascular cells in cardiac homeostasis.
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Sheehy, Sean Paul. "Design Considerations for Engineered Myocardium." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11607.

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The fabrication of biomimetic heart muscle suitable for pharmaceutical compound evaluation and disease modeling is hindered by limitations in our understanding of how to guide and assess the maturity of engineered myocardium in vitro. We hypothesized that tissue architecture serves as an important cue for directing the maturation of engineered heart tissues and that reliable assessment of maturity could be performed using a multi-parametric rubric utilizing cardiomyocytes of known developmental state as a basis for comparison. Physical micro-environmental cues are recognized to play a fundamental role in normal heart development, therefore we used micro-patterned extracellular matrix to direct isolated cardiac myocytes to self-assemble into anisotropic sheets reminiscent of the architecture observed in the laminar musculature of the heart. Comparison of global sarcomere alignment, gene expression, and contractile stress in engineered anisotropic myocardium to isotropic monolayers, as well as, adult ventricular tissue revealed that anisotropic engineered myocardium more closely matched the characteristics of adult ventricular tissue, than isotropic cultures of randomly organized cardiomyocytes. These findings support the notion that tissue architecture is an important cue for building mature engineered myocardium. Next, we sought to develop a quality assessment strategy that utilizes a core set of 64 experimental measurements representative of 4 major categories (i.e. gene expression, myofibril structure, electrical activity, and contractility) to provide a numeric score of how closely stem cell-derived cardiac myocytes match the physiological characteristics of mature, post-natal cardiomyocytes. The efficacy of this rubric was assessed by comparing anisotropic engineered tissues fabricated from commercially-available murine ES- (mES) and iPS- (miPS) derived myocytes against neonatal mouse ventricular myocytes. The quality index scores calculated for these cells revealed that the miPS-derived myocytes more closely resembled the neonate ventricular myocytes than the mES-derived myocytes. Taken together, the results of these studies provide valuable insight into the fabrication and validation of engineered myocardium that faithfully recapitulate the characteristics of mature ventricular myocardium found in vivo. These engineered tissue design and quality validation strategies may prove useful in developing heart muscle analogs from human stem cell-derived myocytes that more accurately predict patient response than currently used animal models.
Engineering and Applied Sciences
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Löwbeer, Christian. "Cardiac troponin T in clinical and experimental studies /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-426-6/.

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Shum-Tim, Dominique. "The protection of the newborn myocardium." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=26146.

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Definitive repair of complex congenital cardiac defects in early life has become the recent trend in pediatric cardiac surgery. This early aggressive surgical approach is to avoid the detrimental effects on the heart of chronic cyanosis, hypertrophy and volume overload which are the consequences of unrepaired congenital malformations. Adequate protection of the heart, not only during the period of corrective surgery, but also certain pre-ischemic events remain of paramount importance to the success of these operations. Profound systemic hypothermia followed by total circulatory arrest is widely used for the correction of congenital cardiac defects in the newborn. It involves a period of cold systemic perfusion on cardiopulmonary bypass before circulatory arrest is established. Using an isolated perfused piglet heart model, the first study demonstrated that prolonged cold perfusion of the immature heart could be detrimental in itself. When followed by a period of ischemic arrest, it further potentiated the myocardial injury and induced severe irreversible contracture. Further extension of this study showed that verapamil administered prior to prearrest cold perfusion could indeed minimize the functional and ultrastructural damage of prolonged myocardial cooling. This shed some light to the pathophysiology of prolonged prearrest cooling contracture of the newborn myocardium.
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Gray, Caroline Claudia. "Indogenous protection of the iscaemic myocardium." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252345.

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Ahmad, Maqsood. "Kinin peptides in the ischaemic myocardium." Thesis, University of Strathclyde, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248756.

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Al-Mohammad, Abdallah. "Hibernating myocardium : prevalence and surrogate markers." Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235453.

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The aims of this thesis are to determine: 1. The true prevalence of hibernating myocardium in patients with severely impaired left ventricular contraction. (Chapter 3) 2. The viability status of the left ventricular wall aneurysm as defined by positron emission tomography. (Chapter 4) 3. The relationship between the incidence of hibernating myocardium and the coronary artery flow grade determined angiographically. (Chapter 5) 4. The relationship between the presence of Q waves (with or without preserved R wave) on the surface electrocardiogram and the presence of scar in the myocardium as diagnosed by positron emission tomography. (Chapter 6) 5. The relationship between the incidence of hibernating myocardium and QT dispersion on the surface electrocardiogram. (Chapter 7) 6. Looking for other markers of hibernation by PET. (Chapters 8 and 9) I proposed to look at the relationship between continuing metabolic activity in 10 akinetic or severely hypokinetic segments as an alternative method and thus as a new definition of pre-operative determination of hibernating myocardium. This is the topic in Chapter 8. Following the completion of question number 3, and the observed role of collateral circulation, I proposed to look into the role of TIMI 0-1 and collaterals grade 2-3 in maintaining viability and their role as a marker of hibernating myocardium. This won support in the form of a research grant from the British Heart Foundation in 1998. This was the topic of my last project, which was added to the thesis after its initial completion on the 23rd of December 2000. This is the topic of Chapter 9. 7. Following the delayed submission of the Thesis in 2015, I was asked to add Chapter 11 which summarised both my contribution since the Thesis was concluded into the topic of Hibernating myocardium; and the knowledge progression into the detection of the phenomenon and its clinical usefulness to bring the Thesis up to date. Methods: The patients were those with coronary artery disease and impaired left ventricular contraction recruited into a series of studies of the presence of hibernating myocardium using positron emission tomography, as the method of choice to preoperatively detect this phenomenon. The patients were either recruited from the cardiac catheterization laboratory or from the cohort of patients presenting with myocardial infarction to the cardiology unit at Aberdeen Royal Infirmary. All the studies were approved by the Grampian Research Ethics Committee. In some of the studies, cardiac magnetic resonance imaging was used for simple assessment of the myocardial contraction and thickening in the study reported in Chapter 9. Results and Conclusions: 1.   Hiberanting myocardium affects over 50% of the patients with severe left ventricular systolic impairment with coronary artery disease. (Chapter 3).   2.   None of the aneurysmal segments are viable. (Chapter 4)   3.   Compared to the areas supplied by arteries with Thrpmbolysis In Myocardial Infarction (TIMI) flow grades 2-3, the areas supplied by almost occluded coronary arteries (TIMI 0-1 flow grades) are significantly more likely to have both evidence of scarred myocardium (highly significantly statistical difference p < 0.0001) and evidence of hibernating myocardium, just reaching statistical significance (p < 0.05). (Chapter 5)   4.   The specificity of Q waves on the electrocardiogram (ECG) as markers for 11 myocardial scarring is 79%, with a low sensitivity of 41%. (Chapter 6) 5.   Maintaining R waves following a pathological Q wave on the ECG is not helpful for predicting the presence of hibernating myocardium. (Chapter 6) 6.   The presence or absence of hibernating myocardium did not impact on native QT dispersion, rate corrected QTc dispersion or on the maximum adjacent QT dispersion on the ECG. (Chapter 7). 7.   A new definition of hibernating myocardium is proposed, helping to detect it preoperatively through the demonstration of metabolism – mechanical mismatch defect using a single radio-pharmaceutical. (Chapter 8) 8.   As a marker of the classical perfusion –metabolism mismatch defect, the new proposed metabolism-mechanical mismatch defect by PET is sensitive (92%) and specific (97%), with excellent positive and negative predictive accuracies (96% and 93%, respectively). (Chapter 8) 9.   While collaterals grade 2-3 supplying territories with blocked arteries and flow grades TIMI 0-1 may be sensitive markers (83%) of hibernating myocardium; they lack specificity (20%), and the differences between the two small groups completing the study did not reach statistical significance. (Chapter 9).
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Books on the topic "Myocardium"

1

Candell-Riera, Jaume, Joan Castell-Conesa, and Santiago Aguadé-Bruix, eds. Myocardium at Risk and Viable Myocardium. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5.

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2

1928-, Langer Glenn A., ed. The myocardium. 2nd ed. San Diego: Academic Press, 1997.

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3

J, Hearse David, ed. The developing myocardium. Mt. Kisco, NY: Futura Pub. Co., 1991.

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4

Jaume, Candell-Riera, Castell-Conesa Joan, and Aguadé-Bruix Santiago, eds. Myocardium at risk and viable myocardium: Evaluation by SPET. Dordrecht: Kluwer Academic Publishers, 2001.

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F, Goodwin John, ed. Heart muscle disease. Lancaster, England: MTP Press, 1985.

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Florence Meeting on Advances on Cardiomyopathies (2nd 1997). Advances in cardiomyopathies: Proceedings of the II Florence Meeting on Advances on Cardiomyopathies, April 24-26, 1997. Milano: Springer, 1998.

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7

G, Nayler Winifred, Parratt James R, and International Society for Heart Research. European Section. Meeting., eds. Myocardial response to acute injury. Houndmills, Basingstoke: Macmillan Academic and Professional, 1991.

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R, Parratt James, and Nayler W. G. 1930-, eds. Myocardial response to acute injury. Basingstoke: Macmillan Press, 1992.

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Vetter, Roland, and Ernst-Georg Krause, eds. Biochemical Regulation of Myocardium. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1289-5.

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Dr, Vetter Roland, and Krause Ernst-Georg, eds. Biochemical regulation of myocardium. Dordrecht: Kluwer, 1996.

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Book chapters on the topic "Myocardium"

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Garcia-Dorado, David, and Jordi Soler-Soler. "Stunned Myocardium and Hibernating Myocardium: Pathophysiology." In Myocardium at Risk and Viable Myocardium, 145–63. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5_7.

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Ortega-Alcalde, Domingo, and Santiago Aguadé-Bruix. "Radionuclides, Instrumentation and Procedures." In Myocardium at Risk and Viable Myocardium, 1–25. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5_1.

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Soler-Soler, Jordi, and Jaume Candell-Riera. "Clinical Value of Viable Myocardium Detection." In Myocardium at Risk and Viable Myocardium, 213–24. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5_10.

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Castell-Conesa, Joan, and Josefa Cortadellas-Angel. "Criteria for SPET Interpretation." In Myocardium at Risk and Viable Myocardium, 27–43. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5_2.

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Aguadé-Bruix, Santiago, and Joan Castell-Conesa. "Methods of Quantification." In Myocardium at Risk and Viable Myocardium, 45–67. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5_3.

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Santana-Boado, Cesar, and Jaume Candell-Riera. "Diagnostic Accuracy of SPET." In Myocardium at Risk and Viable Myocardium, 69–93. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5_4.

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Candell-Riera, Jaume, and Cesar Santana-Boado. "Myocardial Exercise SPET and with Pharmacologic Stimulation." In Myocardium at Risk and Viable Myocardium, 95–118. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5_5.

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Candell-Riera, Jaume, and Cesar Santana-Boado. "Myocardium in Jeopardy." In Myocardium at Risk and Viable Myocardium, 119–44. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5_6.

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Cinca-Cuscullola, Joan, and Amparo Garcia-Burillo. "Radionuclide Uptake in Experimental Ischaemia and Necrosis." In Myocardium at Risk and Viable Myocardium, 165–82. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5_8.

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Castell-Conesa, Joan, and Jose M. Gonzalez-Gonzalez. "Isotopic Diagnosis of Viable Myocardium." In Myocardium at Risk and Viable Myocardium, 183–211. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0906-5_9.

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Conference papers on the topic "Myocardium"

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Hu, Zhenhua, Dimitris Metaxas, and Leon Axel. "Heart Composite Material Model for Stress-Strain Analysis." In ASME 2003 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2003. http://dx.doi.org/10.1115/detc2003/vib-48334.

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Mechanical properties of the myocardium have been investigated intensively in the past four decades. Due to the non-linearity and history dependence of myocardial deformation, many complex strain energy functions have been used to describe the stress-strain relationship in the myocardium. These functions are good at fitting in-vitro experimental data from myocardial stretch testing into strain energy functions. However, it is difficult to model in-vivo myocardium by using strain energy functions. In a previous paper [1], we have implemented a transversely anisotropic material model to estimate in-vivo strain and stress in the myocardium. In this work, the fiber orientation is updated at each time step from the end of diastole to the end of systole; the stiffness matrix is recalculated using the current fiber orientation. We also extend our model to include residual ventricular stresses and time-dependent blood pressure in the ventricular cavities.
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Zuo, Heng, Chun Yang, Glenn Gaudette, Kristen L. Billiar, Tal Geva, Mehmet H. Kural, Pedro J. del Nido, and Dalin Tang. "3D Computational Fluid-Structure Interaction Model of Canine Heart With Different Patch Materials for Optimal Myocardium Regeneration." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14479.

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Myocardial tissue regeneration techniques are being developed for the potential that viable myocardium may be regenerated to replace scar tissues in the heart or used as patch material in heart surgery [1]. The material property of the patch on which myocardium cells are placed has important impact on cell adhesion and multiplication [2]. Fluid-structure interaction (FSI) models for canine heart with patch was introduced to quantify regional flow and mechanical conditions in the patch area and investigate the influence of the different patch materials on myocardium regeneration.
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Discher, Dennis, and Adam Engler. "Mesenchymal Stem Cell Injection After Myocardial Infarction Improves Myocardial Compliance." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176754.

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Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSC) into the acutely ischemic myocardium. Two weeks post-infarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were two-fold stiffer than myocardium from non-infarcted animals but softer than myocardium from vehicle-treated infarcted animals. After eight weeks, the following variables were evaluated: MSC engraftment and left ventricular geometry by histologic methods; cardiac function with a pressure-volume conductance catheter; myocardial fibrosis by Masson trichrome staining; vascularity by immunohistochemistry; and apoptosis by TUNEL assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated post-infarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.
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Valdez-Jasso, Daniela, Marc A. Simon, and Michael S. Sacks. "A Structural Constitutive Model for Right Ventricular Myocardium." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53956.

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Although right-ventricular (RV) function is an important determinant of cardio-pulmonary performance in health and disease, RV myocardium biomechanical function has received little attention. In particular, no multiaxial data of the full-thickness RV have been reported for the passive or active myocardial states, for either normal or pathological conditions. Since an understanding of tissue-level biomechanical behavior is integral to connecting cellular behavior to organ-level performance, investigations into the RV myocardial stress-strain relationship are central in providing this link. For example, ventricular wall stress is considered to be a major driver of ventricular remodeling, and thus a better understanding of how wall stress and deformation are linked would provide unique insight into the mechanisms of RV function and ultimately failure in disease. Such knowledge would have direct applicability to improving methods to detect RV dysfunction, predicting response to disease-specific therapies and improving the timing of therapy if or when needed. Here, we present the first report on the multiaxial biomechanical behavior of viable full-thickness right-ventricular free wall (RVFW) myocardium and our initial efforts in developing a structural constitutive model for this remarkable tissue.
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Veress, A. I., A. Giannakidis, and G. T. Gullberg. "Mechanical Effects of Myofibril Disarray on Cardiac Function." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14696.

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Myocardial disarray is a fiber distribution that deviates away from the tightly organized, parallel alignment of myocardial fibers that characterizes the normal myocardium. This coherently-organized distribution of the myofibers results in the twisting contraction of the normal left ventricle (LV). With myofiber disarray, the fibers have random directionality, either locally or globally, within the LV.
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Goktepe, Serdar, Joseph P. Ulerich, and Ellen Kuhl. "How to Treat the Loss of Beat: Modeling and Simulation of Ventricular Growth and Remodeling and Novel Post-Infarction Therapies." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193159.

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Heart disease is the primary cause of death in industrialized nations. In 2007 alone, an estimated 79 million adults in the U.S., one in three, had one or more types of cardiovascular disease, generating health care costs in excess of $430 billion. A leading cause of congestive heart failure is myocardial infarction. Within the first few hours after the infarct, a complex cascade of events is initiated in the myocardium manifesting itself clinically in disproportionate thinning and dilation of the infarct region accompanied by distortion in form and function of the entire heart, figure 1. As remodeling progresses, volume-overloaded hypertrophy and further deterioration of cardiac function are common natural consequences. Historically, therapies for myocardial infarction have been developed by trial and error methods, as opposed to therapy design and development through scientific understanding of the functional and structural changes in the infarcted tissue. Continuum theories, in combination with modern computer simulation technologies, offer the potential to provide greater insight into the complex pathways of myocardial infarction, and thereby guide the design of successful post-infarction therapies such as direct cell injection into the damaged myocardium1 and implantation of tissue engineered vascular grafts2 as sketched in figure 1.
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Coleman, Benjamin R., and Alexander I. Veress. "Deformable Image Registration Between Cardiac PET Images Encompassing a Range of Physical Heart Sizes." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53850.

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Cardiac mechanical performance depends upon myocardial tissue elongation and contraction. Deformation, stress and strain within the myofibers provide valuable information about potential tissue adaptation [1]. Specifically, the stress state of the tissue is believed to drive remodeling of the myocardium. Because it is not possible to measure in-vivo stress in the human heart, considerable research has gone into developing patient specific, mathematical models of the heart based on finite element (FE) analysis and cardiac imaging [2, 3]. Stress estimates from these models could yield valuable information about of the material behavior of the myocardium that would provide valuable information for research into cardiac pathologies.
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Vasilchenko, S. Yu, A. A. Stratonnikov, A. I. Volkova, V. B. Loschenov, E. A. Sheptak, and S. S. Kharnas. "Investigation of myocardial photodynamic revascularization method on ischemic rat myocardium model." In SPIE Proceedings, edited by Valery V. Tuchin. SPIE, 2006. http://dx.doi.org/10.1117/12.697420.

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Emery, Jeff L., Jeffrey H. Omens, and Andrew D. McCulloch. "Effects of Ventricular Overloading on Multiaxial Mechanics in Passive Myocardium." In ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1197.

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Abstract Passive overstretch of myocardium occurs in the ischemic and dilated heart, but the subsequent changes in local tissue mechanics and structure remain unclear. Therefore, we estimated changes in myocardial biaxial stiffness using by solving an inverse finite element problem. The differences between the strains measured on the epicardium of the isolated rat left ventricle (LV) during overstretch and those of a prolate-spheroidal finite element model were minimized by optimizing the material parameters of an exponential constitutive law. When passive LV pressure was increased from 10 to 120 mmHg, there were progressive decreases in wall stiffness up to 93% that were equal in fiber and cross-fiber directions. Thus, myocardium softens isotropically with progressive overstretch independently of muscle fiber direction. This local strain softening may, therefore, arise from damage to structures with uniform distribution of orientation rather than components aligned with myofibrils.
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Neubauer, Andre, and Rainer Wegenkittl. "Skeleton-based myocardium segmentation." In Electronic Imaging 2003, edited by Robert F. Erbacher, Philip C. Chen, Jonathan C. Roberts, Matti T. Groehn, and Katy Boerner. SPIE, 2003. http://dx.doi.org/10.1117/12.473945.

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Reports on the topic "Myocardium"

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Moridi, Mina, Parinaz Onikzeh, Aida Kazemi, and Hadi Zamanian. CABG versus myotomy in symptomatic myocardial bridge patients : A systematic Review and Meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0088.

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Review question / Objective: The aim of this study is to find which surgical intervention in myocardial bridge ( myotomy or CABG) is more effective in reducing adverse outcomes in symptomatic patients resistant to optimal medical therapy ? Condition being studied: Myocardial bridge : A myocardial bridge (MB) is a congenital heart defect in which a bridge of muscle fibers (myocardium) overlying a section of a coronary artery and the artery is squeezed and normal blood flow is disrupted. Most bridges don't seem to cause symptoms. However, some people can experience angina, or chest pain. In patients with symptoms, first line treatment is medication and if they have symptoms despite optimal medical treatment , invasive measures like CABG or myotomy should be taken.
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Nikitinа, N. V., A. V. Aleksandrov, N. V. Aleksandrova, I. А. Zborovskaya, and M. V. Levkina. COMBINED BASIC THERAPY WITH INCLUSION OF HYDROXYLOROHINE HAS A POSITIVE INFLUENCE ON CHANGES IN THE DIASTOLIC FUNCTION OF MYOCARDIUM IN PATIENTS WITH RHEUMATOID ARTHRITIS. "PLANET", 2019. http://dx.doi.org/10.18411/978-5-907192-54-6-2019-xxxvi-128-139.

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Brosius, III, F. C. Molecular mechanisms of enhanced [18F] fluorodeoxy glucose (FDG) uptake in isochemically injured myocardium: the role of glucose transporter and hexokinase expression. Final technical report for period August 1, 1993--November 30, 1997. Office of Scientific and Technical Information (OSTI), August 1999. http://dx.doi.org/10.2172/763949.

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Li, Xiao, Fayang Ling, Wenchuan Qi, Sanmei Xu, Bingzun Yin, Zihan Yin, Qianhua Zheng, Xiang Li, and Fanrong Liang. Preclinical Evidence of Acupuncture on infarction size of Myocardial ischemia: A Systematic Review and Meta-Analysis of Animal Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0044.

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Review question / Objective: Whether acupuncture is effective for infarction size on myocardial ischemia rat models. Condition being studied: Myocardial ischemia is a typical pathological condition of coronary heart disease (CHD), which has been a global issue with high incidence and mortality. Myocardial infarction caused by myocardial ischemia leads to cardiac dysfunction, and the size of myocardial infarction also determines the recovery and prognosis of cardiac function. Acupuncture, a long history of traditional Chinese medicine, is widely used to treat symptoms like thoracalgia and palpitation. Many researches based on rat experiments have shown that acupuncture affects infarction size, cardiac function, myocardial enzyme or arrhythmias severity on myocardial ischemia models; nevertheless, few literatures have systematically reviewed these studies, assessing the risk of bias, quality of evidence, validity of results, and summarizing potential mechanisms. A systematic review of animal studies can benefit future experimental designs, promote the conduct and report of basic researches and provide some guidance to translate the achievements of basic researches to clinical application in acupuncture for myocardial ischemia. Therefore, we will conduct this systematic review and meta analysis to evaluate effects of acupuncture on infarction size on myocardial ischemia rat models.
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Voynalovich-Khanova, Y. A. SYNDROME OF MYOCARDIAL REMODELING (CLINICAL OBSERVATION). "PLANET", 2019. http://dx.doi.org/10.18411/978-5-907192-54-6-2019-xxxvi-46-49.

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McDonough, Kathleen H., and Harvey I. Miller. Myocardial Dysfunction Contributes to Irreversible Hemorrhagic Shock. Fort Belvoir, VA: Defense Technical Information Center, February 2001. http://dx.doi.org/10.21236/ada389358.

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Pickard, Jeb S., and Joe E. Burton. Flying Waivers for History of Angioplasty and Myocardial Infraction. Fort Belvoir, VA: Defense Technical Information Center, November 1994. http://dx.doi.org/10.21236/ada292505.

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Hassanzadeh, Sara, Sina Neshat, Afshin Heidari, and Masoud Moslehi. Myocardial Perfusion Imaging in the Era of COVID-19. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0063.

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Review question / Objective: This review studies all aspects of myocardial perfusion imaging with single-photon emission computed tomography (MPI SPECT) after the COVID-19 pandemic. Condition being studied: Many imaging modalities have been reduced after the COVID-19 pandemic. Our focus in this review is to see if the number of MPIs is lowered or not and, if so, why. Furthermore, it is possible that a combination of CT attenuation correction and MPI could yield findings. In this study, we'll also look for these probable findings. Third, we know from previous studies that COVID might cause cardiac injuries in some people. Since MPI is a cardiovascular imaging technique, it might shows those injuries. So we'll review articles to find out in patients with active COVID infection, long COVID, or previous COVID cases what findings in MPI those cardiac injuries can cause.
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Li, Peng, Na jia, Bing Liu, and Qing He. Effect of cardiac shock wave therapy on adverse cardiovascular event for patients with coronary artery disease: an updated systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0103.

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Review question / Objective: We have previously demonstrated that cardiac shock wave therapy (CSWT) effectively improves myocardial perfusion in patients with coronary artery disease (CAD). In this study, we want to address whether CSWT could decrease the risk of adverse cardiovascular events in CAD patients unsuitable for revascularization. Eligibility criteria: Trials are considered eligible if they meet these criteria: (1) patients included are diagnosed as refractory angina or ischemic heart failure; (2) the study i a randomized controlled trial (RCT) or a prospective cohort study; (3) intervention consisted of CSWT; (4) patients in the control group are treated with optimal medical therapy, (5)the primary outcome of interest Is rate of MACE. Exclusion criteria were (1) patients with acute myocardial infarction, (2) repeated CSWT, (3) with coronary artery revascularization, (4) without primary outcome, (5) retrospective study, and (6)duplicated data.
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Dejong, Marla J., Kyungeh An, Candace C. Cherrington, and Debra K. Moser. Predictors of Symptom Appraisal for Patients with Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada427523.

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