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Myocardial Necrosis (myocardial + necrosis)
Selected AbstractsHYPERBARIC OXYGENATION APPLIED IMMEDIATELY AFTER CORONARY OCCLUSION REDUCES MYOCARDIAL NECROSIS AND ACUTE MORTALITY IN RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2009Leonardo Dos Santos SUMMARY 1Because in ischaemia there is a critical lack of O2, it has been reasoned that increasing O2 delivery to the ischaemic myocardium could serve as adjunctive therapy for acute myocardial infarction (MI). Accordingly, in the present study, the effect of early hyperbaric oxygenation (HBO) on mortality and MI size after coronary occlusion was examined in rats. 2After coronary occlusion, male Wistar rats were randomly assigned to receive either HBO for 1 h in a hyperbaric chamber (100% O2 at 253 kPa; n = 106) or ambient O2 as the control (n = 111). The extent of myocardial necrosis was assessed (triphenyltetrazolium) immediately after treatment in the HBO (n = 50) and control (n = 47) groups. The remaining rats were evaluated 24 h after occlusion to enable calculation of MI size and mortality. 3Immediately after therapy, the size of the MI was significantly greater in the control group compared with that in the HBO group (40 ± 3 vs 27 ± 2% of the left ventricle (LV), respectively; P < 0.001). The 24 h mortality of control rats was higher than that of HBO rats (34 vs 16%, respectively; P = 0.02). Control rats that survived 24 h had a larger MI than did HBO rats that survived 24 h (40 ± 4 vs 29 ± 3% of the LV, respectively; P = 0.005). Furthermore, large necrotic areas (> 40% of the LV) were more frequent in control than HBO rats (55 vs 27% of infarcted hearts, respectively; P = 0.01). There was less pulmonary congestion observed in HBO rats compared with control rats. 4In conclusion, early therapy with HBO during the onset of an acute ischaemic event decreases the necrotic area and reduces acute mortality. These data support further investigation of HBO as an adjuvant therapy for acute MI. [source] Cardioprotection of cariporide evaluated by plasma myoglobin and troponin I in myocardial infarction in pigsFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 2 2006Robert Létienne Abstract The cardioprotective effects of cariporide were investigated against myoglobin and troponin I elevation in a model of myocardial infarction in pig, and the possible relationship between these markers and myocardial infarct size. The left circumflex coronary artery was ligated for 60-min and then reperfused for 48-h. Plasma levels of myoglobin and troponin I were quantified during reperfusion. Vehicle or cariporide (2.5 mg/kg) were administered i.v. before ischaemia and infused throughout ischaemia and for the beginning of reperfusion. In vehicle-treated pigs, the infarct size represented 26% ± 3% of the area at risk. Cariporide significantly decreased the infarct size by 66% ± 9%, and significantly reduced plasma levels of myoglobin and troponin I. A strongly correlated linear relationship between myocardial necrosis and plasma levels of myoglobin (R = 0.966, P < 0.0001) or troponin I (R = 0.855, P < 0.0001) was clearly identified. In conclusion, in our porcine model of myocardial infarction, even with small infarcts (in the presence of cariporide), plasma levels of myoglobin and troponin I are predictive of the presence of necrosis and its extent. [source] Cardiotoxicity of doxorubicin/paclitaxel combination in rats: Effect of sequence and timing of administrationJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 2 2004Sherif Y. Saad Abstract The higher incidence of cardiotoxicity of doxorubicin (DOX)/paclitaxel (PTX) combination compared with DOX alone remains to be a major obstacle against effective chemotherapeutic treatment. We investigated the effect of sequence and time interval between administration of both drugs on the severity of cardiotoxicity of the combination. Male Wistar rats were divided into seven groups. DOX was administeded intraperitoneally (ip) at a single dose of 5 mg kg,1 every other 2 days, 2 doses per week for a total cumulative dose of 20 mg kg,1. PTX was administered by an ip route at a dose of 20 mg kg,1 every other 2 days. Both drugs were injected either alone or sequentially in combination. In one case, DOX preceded PTX by 30 min and 24 h and in the other case, PTX preceded DOX by 30 min and 24 h. Cardiotoxicity was evaluated by both biochemical and histopathological examination, 48 h after the last DOX dose. DOX-induced cardiotoxicity was manifested by abnormal biochemical changes including marked increases in serum creatine phosphokinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), glutathione peroxidase (GSH-Px), and aspartate aminotransferase (AST) activity levels. Myocardial tissue from DOX-treated rats showed significant increases in malondialdehyde (MDA) production and total nitrate/nitrite (NOx) levels, parallel with depletion of "endogenous antioxidant reserve," including GSH contents and GSH-Px activity level. PTX treatment produced significant changes in the biochemical parameters measured by a lower magnitude than those changes produced by DOX alone. Combination of both drugs resulted in aggravation of DOX-induced cardiotoxicity regardless the sequence and time interval between administration of either drug. Administration of PTX 30 min and 24 h after DOX treatment showed exaggeration of combination-induced cardiotoxicity compared with the reverse sequence. This exacerbation was manifested by much more pronounced changes in serum and cardiac tissue parameters measured. Histopathological examination of ventricles of rat's heart revealed that DOX treatment produced myo-cytolysis and myocardial necrosis. Administration of PTX following DOX treatment showed extensive myocardial necrosis compared with those rats treated with either DOX alone or the reverse sequence of administration. Moreover, rats treated with PTX 24 h after DOX treatment showed exaggeration of the combination-induced cardiotoxicity. In conclusion, PTX might synergistically aggravate DOX-induced cardiotoxicity. The effect might be much more pronounced with those rats treated with PTX 24 h after DOX treatment. © 2004 Wiley Periodicals, Inc. J Biochem Mol Toxicol 18:78,86, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20012 [source] Gold-Tip Electrodes,A New "Deep Lesion" Technology for Catheter Ablation?JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2005In Vitro Comparison of a Gold Alloy Versus Platinum, Iridium Tip Electrode Ablation Catheter Radiofrequency (RF) catheter ablation is widely used to induce focal myocardial necrosis using the effect of resistive heating through high-frequency current delivery. It is current standard to limit the target tissue,electrode interface temperature to a maximum of 60,70°C to avoid char formation. Gold (Au) exhibits a thermal conductivity of nearly four times greater than platinum (Pt,Ir) (3.17 W/cm Kelvin vs 0.716 W/cm Kelvin), it was therefore hypothesized that RF ablation using a gold electrode would create broader and deeper lesions as a result of a better heat conduction from the tissue,electrode interface and additional cooling of the gold electrode by "heat loss" to the intracardiac blood. Both mechanisms would allow applying more RF power to the tissue before the electrode,tissue interface temperature limit is reached. To test this hypothesis, we performed in vitro isolated liver and pig heart investigations comparing lesion depths of a new Au-alloy-tip electrode to standard Pt,Ir electrode material. Mean lesion depth in liver tissue for Pt,Ir was 4.33 ± 0.45 mm (n = 60) whereas Au electrode was able to achieve significantly deeper lesions (5.86 ± 0.37 mm [n = 60; P < 0.001]). The mean power delivered using Pt,Ir was 6.95 ± 2.41 W whereas Au tip electrode delivered 9.64 ± 3.78 W indicating a statistically significant difference (P < 0.05). In vitro pig heart tissue Au ablation (n = 20) increased significantly the lesion depth (Au: 4.85 ± 1.01 mm, Pt,Ir: 2.96 ± 0.81 mm, n = 20; P < 0.001). Au tip electrode again applied significantly more power (P < 0.001). Gold-tip electrode catheters were able to induce deeper lesions using RF ablation in vitro as compared to Pt,Ir tip electrode material. In liver and in pig heart tissue, the increase in lesion depth was associated with a significant increase in the average power applied with the gold electrode at the same level of electrode,tissue temperature as compared to platinum material. [source] Classically and alternatively activated macrophages contribute to tissue remodelling after myocardial infarctionJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 9b 2009C. Troidl Abstract An important goal in cardiology is to minimize myocardial necrosis and to support a discrete but resilient scar formation after myocardial infarction (MI). Macrophages are a type of cells that influence cardiac remodelling during MI. Therefore, the goal of the present study was to investigate their transcriptional profile and to identify the type of activation during scar tissue formation. Ligature of the left anterior descending coronary artery was performed in mice. Macrophages were isolated from infarcted tissue using magnetic cell sorting after 5 days. The total RNA of macrophages was subjected to microarray analysis and compared with RNA from MI and LV-control. mRNA abundance of relevant targets was validated by quantitative real-time PCR 2, 5 and 10 days after MI (qRT-PCR). Immunohistochemistry was performed to localize activation type-specific proteins. The genome scan revealed 68 targets predominantly expressed by macrophages after MI. Among these targets, an increased mRNA abundance of genes, involved in both the classically (tumour necrosis factor ,, interleukin 6, interleukin 1,) and the alternatively (arginase 1 and 2, mannose receptor C type 1, chitinase 3-like 3) activated phenotype of macrophages, was found 5 days after MI. This observation was confirmed by qRT-PCR. Using immunohistochemistry, we confirmed that tumour necrosis factor ,, representing the classical activation, is strongly transcribed early after ligature (2 days). It was decreased after 5 and 10 days. Five days after MI, we found a fundamental change towards alternative activation of macrophages with up-regulation of arginase 1. Our results demonstrate that macrophages are differentially activated during different phases of scar tissue formation after MI. During the early inflammatory phase, macrophages are predominantly classically activated, whereas their phenotype changes during the important transition from inflammation to scar tissue formation into an alternatively activated type. [source] Current Update on Glycoprotein IIb-IIIa and Direct Thrombin Inhibition in Percutaneous Coronary Intervention for Non-ST Elevation Acute Coronary Syndromes: Balancing Bleeding Risk and Antiplatelet EfficacyJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 2 2008ANDREW T. KWA M.D. Appropriate pharmacologic treatment for patients with acute coronary syndromes (ACS) remains a matter of controversy. Additionally, a substantial gap exists between recommended guidelines and current clinical practice. Questions remain regarding which antiplatelet/antithrombotic treatment strategies are appropriate for individual patients, based on their risk. We explore the role of glycoprotein IIb-IIIa inhibitors and the direct thrombin inhibitor bivalirudin in ACS patients, and consider the difficulties involved in reducing ischemic events while limiting bleeding risks. In patients with ACS who are undergoing percutaneous coronary intervention, high levels of microembolization and myocardial necrosis are potential risk factors for adverse long-term outcomes. Intensive antiplatelet/antithrombotic regimens may substantially affect these factors. Determination of risk levels, with the goal of targeting aggressive antithrombotic and interventional therapies to patients at higher risk, will help physicians choose appropriate pharmacologic therapy for patients with ACS. [source] Mechanism of protective action of mangiferin on suppression of inflammatory response and lysosomal instability in rat model of myocardial infarctionPHYTOTHERAPY RESEARCH, Issue 6 2009S. Prabhu Abstract Lysosomal instability has been suggested as a major factor in the development of cellular injury during myocardial necrosis through the formation of inflammatory mediators. The present study was designed to investigate the effect of mangiferin on lysosomal hydrolases and TNF- , production during isoproterenol (ISPH) induced myocardial necrosis in rats. The rats given ISPH (200 mg/kg body weight twice, subcutaneous) for 2 days showed a significant increase in plasma TNF- , production, serum and heart lysosomal hydrolases activity. ISPH administration to rats resulted in decreased stability of the membranes, which was reflected by the lowered activity of cathepsin-D and , -glucuronidase in mitochondrial, nuclear, lysosomal and microsomal fractions. Pretreatment with mangiferin (100 mg/kg body weight, intraperitoneally) for 28 days, significantly prevented the alterations and restored the enzyme activities to near-normal status. These findings demonstrate that mangiferin could preserve lysosomal integrity through decrease in the inflammatory process and hence establish the cardioprotective effect of mangiferin. Copyright © 2009 John Wiley & Sons, Ltd. [source] Prolonged strenuous exercise alters the cardiovascular response to dobutamine stimulation in male athletesTHE JOURNAL OF PHYSIOLOGY, Issue 1 2005Robert C. Welsh Prolonged strenuous exercise has been associated with transient impairment in left ventricular (LV) systolic and diastolic function that has been termed ,cardiac fatigue'. It has been postulated that cardiac ,-adrenoreceptor desensitization may play a central role; however, data are limited. Accordingly, we assessed the cardiovascular response to progressive dobutamine stimulation after prolonged strenuous exercise (2 km swim, 90 km bike, 21 km run). Nine experienced male athletes were studied: PRE (2,3 days before), POST (after) and REC (1,2 days later). The cardiovascular response to progressive continuous dobutamine stimulation (0, 5, 20, and 40 ,g kg,1 min,1) was assessed, including heart rate (HR), systolic blood pressure (SBP), LV cavity areas (two-dimensional echocardiography) and contractility (end-systolic elastance, SBP/end-systolic cavity area (ESCA)). POST there was limited evidence of myocardial necrosis (measured by troponin I), while catecholamines were elevated. HR was higher POST (mean ±s.d.; PRE, 58 ± 9; POST, 79 ± 9; REC, 57 ± 7 beats min,1; P < 0.05), while SBP was lower (PRE, 127 ± 15; POST, 116 ± 9; REC, 121 ± 12 mmHg; P < 0.05). A blunted HR, SBP and LV contractility (SBP/ESCA; PRE 29 ± 6 versus POST 20 ± 6 mmHg cm,2; P < 0.05) response to dobutamine was demonstrated POST, with values returning towards baseline in REC. Following prolonged strenuous exercise, the chronotropic and inotropic response to dobutamine stimulation is blunted. This study supports the hypothesis that beta-receptor downregulation and/or desensitization may play a major role in prolonged-strenuous-exercise-mediated cardiac fatigue. [source] Manganese alters mitochodrial integrity in the hearts of swine marginally deficient in magnesium,BIOFACTORS, Issue 2 2004Kevin B. Miller Abstract It was previously reported that pigs marginally deficient in magnesium (Mg) and fed diets high in manganese (Mn) died suddenly with signs of sudden cardiac death. Manganese, which has properties similar to Mg, may exacerbate Mg-deficiency and be accumulated by mitochondria resulting in ultrastructural damage. The objective of this study was to determine whether deaths of the type previously observed were mediated by adverse interactions of Mn and Mg resulting in ultrastructural damage to the myocardium, alterations in electrocardiographic recordings and tissue retention of Mn, Mg and calcium (Ca). Forty-eight pigs were fed one of six diets in a 2 × 3 factorial arrangement of Mg (100 or 1000 mg Mg/kg) and Mn (5, 50 or 500 mg Mn/kg) for 8 weeks. Left ventricle muscle samples were collected for examination by transmission electron microscopy. No differences in heart muscle ultrastructure were observed between pigs fed low and adequate dietary Mg. However, marked myocardial necrosis and mitochondrial swelling were observed in pigs fed high dietary Mn when combined with low Mg. Feeding low dietary Mg elevated minimum (P < 0.01), maximum (P < 0.05) and average (P < 0.001) heart rates. Low dietary Mg resulted in a 55% probability of a ventricular beat being recorded (P = 0.05) and lower Mg (P < 0.02) and Ca (P < 0.04) contents in heart atria and ventricles. These results suggest that high Mn, when fed in combination with low Mg, disrupts mitochondrial ultrastructure and is associated with the sudden deaths previously reported. [source] Anti-inflammatory actions of aprotinin provide dose-dependent cardioprotection from reperfusion injuryBRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2008J M Carter Background and purpose: Myocardial injury following ischaemia and reperfusion has been attributed to activation and transmigration of polymorphonuclear leukocytes (PMNs) with release of mediators including oxygen-derived radicals and proteases causing damage. Experimental approach: We studied the serine protease inhibitor aprotinin in an in vivo rabbit model of 1 h of myocardial ischaemia followed by 3 h of reperfusion (MI+R). Aprotinin (10 000 Ukg,1) or its vehicle were injected 5 min prior to the start of reperfusion. Key results: Myocardial injury was significantly reduced with aprotinin treatment as indicated by a reduced necrotic area (11±2.7% necrosis as percentage of area at risk after aprotinin; 24±3.1% after vehicle; P<0.05) and plasma creatine kinase activity (12.2±1.5 and 17.3±2.3 IU g,1 protein in aprotinin and vehicle groups, respectively, P<0.05). PMN infiltration (assessed by myeloperoxidase activity) was significantly decreased in aprotinin-treated animals compared to vehicle (P<0.01). Histological analysis also revealed a substantial increase in PMN infiltration following MI+R and this was significantly reduced by aprotinin therapy (44±15 vs 102±2 PMN mm2 in aprotinin vs vehicle-treated animals, P<0.05). In parallel in vitro experiments, aprotinin inhibited neutrophil-endothelium interaction by reducing PMN adhesion on isolated, activated aortic endothelium. Finally, immunohistochemical analysis illustrated aprotinin significantly reduced myocardial apoptosis following MI+R. Conclusions and implications: Inhibition of serine proteases by aprotinin inhibits an inflammatory cascade initiated by MI+R. The cardioprotective effect appears to be at least partly due to reduced PMN adhesion and infiltration with subsequently reduced myocardial necrosis and apoptosis. British Journal of Pharmacology (2008) 155, 93,102; doi:10.1038/bjp.2008.223; published online 9 June 2008 [source] Cardioprotection: spotlight on PKGBRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2007M V Cohen Classical ischaemic preconditioning, delayed or second window preconditioning and postconditioning are forms of cardioprotection that are dependent on cell surface receptors, intracellular signalling molecules and kinases that ultimately block formation of the mitochondrial permeability transition. The latter is presumed to cause myocardial necrosis as well as apoptosis, so prevention of its formation upon resumption of perfusion after a prolonged coronary occlusion should be cardioprotective. In all of these forms of cardioprotection, formation of cGMP and activation of protein kinase G (PKG) are recognized to be key steps in the signal transduction pathway. Burley et al. highlight the roles of cGMP and PKG in their comprehensive review. They describe the basic biology of PKG and emphasize its compartmentalization, which may be responsible for the frustration induced by assays for PKG in whole cell lysates and for the spurious conclusions about the role of PKG in cardioprotection. This review will be useful to both the novice and the seasoned investigator. British Journal of Pharmacology (2007) 152, 833,834; doi:10.1038/sj.bjp.0707453; published online 17 September 2007 [source] Anti-apoptotic effect of benidipine, a long-lasting vasodilating calcium antagonist, in ischaemic/reperfused myocardial cellsBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2001Feng Gao Ischaemia/reperfusion causes intracellular calcium overloading in cardiac cells. Administration of calcium antagonists reduces myocardial infarct size. Recent in vitro studies have demonstrated that calcium plays a critical role in the signal transduction pathway leading to apoptosis. However, whether or not calcium antagonists may reduce myocardial apoptosis induced by ischaemia-reperfusion, and thus decrease myocardial infarction, has not been directly investigated. The present study investigated the effects of benidipine, an L-type calcium channel blocker, on myocardial infarct size, apoptosis, necrosis and cardiac functional recovery in rabbits subjected to myocardial ischaemia/reperfusion (MI/R, 45 min/240 min). Ten minutes prior to coronary occlusion, rabbits were treated with vehicle or benidipine (10 ,g kg,1 or 3 ,g kg,1, i.v.). In the vehicle-treated group, MI/R caused cardiomyocyte apoptosis as evidenced by DNA ladder formation and TUNEL positive nuclear staining (12.2±1.1%). Treatment with 10 ,g kg,1 benidipine lowered blood pressure, decreased myocardial apoptosis (6.2±0.8%, P<0.01 vs vehicle) and necrosis, reduced infarct size (20±2.3% vs 49±2.6%, P<0.01), and improved cardiac functional recovery after reperfusion. Administering benidipine at 3 ,g kg,1, a dose at which no haemodynamic effect was observed, also exerted significant anti-apoptosis effects, which were not significantly different from those observed with higher dose benidipine treatment. However, treatment with this low dose benidipine failed to reduce myocardial necrosis. These results demonstrate that benidipine, a calcium antagonist, exerts significant anti-apoptosis effects, which are independent of haemodynamic changes. Administration of benidipine at a higher dose produced favourable haemodynamic effects and provided additional protection against myocardial necrotic injury and further improved cardiac functional recovery. British Journal of Pharmacology (2001) 132, 869,878; doi:10.1038/sj.bjp.0703881 [source] The impact of micro troponin leak on long-term outcomes following elective percutaneous coronary intervention,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 6 2009Richard V. Milani MD Abstract Objective: To evaluate the clinical impact of microleaks of troponin, which are below the reference standard defining troponin elevation, on cardiovascular outcomes in stable coronary patients undergoing elective percutaneous coronary intervention (PCI). Background: Troponin elevation, either pre- or post-PCI, has been shown to predict poor cardiovascular outcomes. However, troponin measurements that are above the limit of detection but below the 99th percentile limit defining elevation ("microleak") have uncertain clinical significance. Methods: We assessed subsequent myocardial infarction (MI) and death over a mean follow-up of 4.2 years in 2,272 patients undergoing elective PCI, where baseline troponins were normal and follow-up troponins were obtained 12,24 hr post-PCI. Patients were divided into three groups based on post-PCI troponin levels: Group 1 (n = 1,313) nondetectable; group 2 (n = 587) microleak, and group 3 (n = 372) elevated suggesting myocardial necrosis. Results: The combined endpoint of MI and death was similar in groups 2 and 3 (50.3 vs. 51.9%, respectively, P = NS), which was significantly more than group 1 patients (35.6%, P < 0.01) over the follow-up period. Multivariate analysis of patients in groups 1 and 2 demonstrated that troponin microleak was an independent predictor of MI and death (P = 0.01). Conclusions: Microleak of troponin following elective PCI suggests myocardial injury and predicts an increased risk of subsequent MI and death. Troponins should be routinely assessed following PCI, and preventive therapies are needed to reduce micro and macro troponin elevation in the PCI setting. © 2009 Wiley-Liss, Inc. [source] HYPERBARIC OXYGENATION APPLIED IMMEDIATELY AFTER CORONARY OCCLUSION REDUCES MYOCARDIAL NECROSIS AND ACUTE MORTALITY IN RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2009Leonardo Dos Santos SUMMARY 1Because in ischaemia there is a critical lack of O2, it has been reasoned that increasing O2 delivery to the ischaemic myocardium could serve as adjunctive therapy for acute myocardial infarction (MI). Accordingly, in the present study, the effect of early hyperbaric oxygenation (HBO) on mortality and MI size after coronary occlusion was examined in rats. 2After coronary occlusion, male Wistar rats were randomly assigned to receive either HBO for 1 h in a hyperbaric chamber (100% O2 at 253 kPa; n = 106) or ambient O2 as the control (n = 111). The extent of myocardial necrosis was assessed (triphenyltetrazolium) immediately after treatment in the HBO (n = 50) and control (n = 47) groups. The remaining rats were evaluated 24 h after occlusion to enable calculation of MI size and mortality. 3Immediately after therapy, the size of the MI was significantly greater in the control group compared with that in the HBO group (40 ± 3 vs 27 ± 2% of the left ventricle (LV), respectively; P < 0.001). The 24 h mortality of control rats was higher than that of HBO rats (34 vs 16%, respectively; P = 0.02). Control rats that survived 24 h had a larger MI than did HBO rats that survived 24 h (40 ± 4 vs 29 ± 3% of the LV, respectively; P = 0.005). Furthermore, large necrotic areas (> 40% of the LV) were more frequent in control than HBO rats (55 vs 27% of infarcted hearts, respectively; P = 0.01). There was less pulmonary congestion observed in HBO rats compared with control rats. 4In conclusion, early therapy with HBO during the onset of an acute ischaemic event decreases the necrotic area and reduces acute mortality. These data support further investigation of HBO as an adjuvant therapy for acute MI. [source] Two Brothers with Myocardial Infarction in the Absence of Atherosclerotic Coronary Artery Disease: Spontaneous Coronary Thrombosis: Case Reports of Two BrothersCLINICAL CARDIOLOGY, Issue 12 2009Jamal Hussain MD Myocardial infarction in the absence of significant atherosclerotic coronary artery disease is not uncommonly encountered in clinical practice. This has been more often seen with the current sensitive biomarker assays for myocardial necrosis. Acute illnesses, spontaneous coronary dissection, sepsis, pulmonary embolism and coagulation disorders are some of the common clinical situation where elevated cardiac markers are noted. We describe two brothers presenting with acute myocardial infarction due to thrombus without any obvious cause. Copyright © 2009 Wiley Periodicals, Inc. [source] | |||||||||||||||||||||||||