1.Idiopathic arterial calcification of infancy:report of a case.
Feng-lan GAO ; Chun-ling LIU ; Yin-po ZHANG ; Yan-xin ZHANG
Chinese Journal of Pathology 2013;42(11):771-772
Autopsy
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Female
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Heart Failure
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etiology
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pathology
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Humans
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Infant
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Myocardial Infarction
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etiology
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pathology
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Vascular Calcification
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complications
;
pathology
2.Acute myocardial infarction due to myocardial bridge.
Zhao-Feng LI ; Shu-Guang YANG ; Jun-Bo GE
Chinese Medical Journal 2012;125(19):3589-3590
3.The changes of potassium currents in rabbit ventricle with healed myocardial infarction.
Nian, LIU ; Huiyan, NIU ; Yang, LI ; Cuntai, ZHANG ; Qiang, ZHOU ; Yanfei, RUAN ; Jun, PU ; Zaiying, LU
Journal of Huazhong University of Science and Technology (Medical Sciences) 2004;24(2):128-31
To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), the changes of action potential duration (APD), transient outward potassium current (Ito), delayed rectifier potassium current (IK) and inward rectifier potassium current (IK1) of left ventricular myocytes in non-infarcted zone of HMI were investigated. Rabbits were randomly assigned into two groups: HMI group, in which animals were subjected to thoracotomy and ligation of the circumflex coronary and sham-operated group, in which rabbits underwent thoracotomy but no conorary ligation. 3 months after the operation, the whole myocyte patch clamp technique was used to record APD, Ito, IK, and IK1 of ventricular myocytes in non-infarcted zone. Our results showed that the membrane capacitance was larger in HMI group than in sham-operated group. Action potential duration was significantly lengthened in HMI group and early afterdepolarization (EAD) appeared in HMI group. The densities of Ito, I(K, tail), and IK1 were reduced significantly in HMI group, from 6.72 +/- 0.42 pA/pF, 1.54 +/- 0.13 pA/pF and 25.6 +/- 2.6 pA/pF in sham-operated group to 4.03 +/- 0.33 pA/pF, 1.14 +/- 0.11 pA/pF and 17.6 +/- 2.3 pA/pF, respectively. It is concluded that the reduced densities of Ito, I(K, tail) and IK1 in ventricular myocytes of non-infarcted zone in HMI were responsible for the prolongation of APD and the presentation of EAD which played important roles in the development of malignant arrhythmia in HMI.
Action Potentials
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Arrhythmia/*etiology
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Heart Ventricles/metabolism
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Myocardial Infarction/complications
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Myocardial Infarction/metabolism
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Myocardial Infarction/*pathology
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Myocytes, Cardiac/*cytology
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Patch-Clamp Techniques
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Potassium Channels/*metabolism
5.One case of neonatal myocardial infarction.
Chinese Journal of Pediatrics 2004;42(5):394-394
6.Bupivacaine Induced Cardiac Toxicity Mimicking an Acute Non-ST Segment Elevation Myocardial Infarction.
Ho Yoel RYU ; Jang Young KIM ; Hyun Kyo LIM ; Junghan YOON ; Byung Su YOO ; Kyung Hoon CHOE ; Seung Hwan LEE
Yonsei Medical Journal 2007;48(2):331-336
Bupivacaine is widely used as a local anesthetic. Central nervous system (CNS) and cardiovascular toxicity are well known side effects. However, there has been no report of bupivacaine-induced myocardial injury. We present a case of bupivacaine cardiac toxicity mimicking an acute non-ST segment elevation myocardial infarction, which was eventually diagnosed as bupivacaine-induced cardiac toxicity without CNS toxicity. As soon as a healthy young woman at a private clinic was given a spinal anesthesia of 6mg bupivacaine for hemorrhoidectomy, she developed arrhythmia and hypotension. She was transferred to our emergency room. There was an accelerated idioventricular rhythm with ST segment depression on electrocardiogram, coarse breathing sounds with rales on whole lung field and a butterfly sign on the chest radiograph. 2D transthoracic echocardiography (TTE) revealed reduced left ventricle systolic ejection fraction (approximately 27%). There was regional wall motion abnormality of the left ventricle on 2D TTE and the cardiac marker was increased. We diagnosed the patient as having acute non-ST segment elevation myocardial infarction but her impaired cardiac function improved gradually. On the seventh day from admission, there was a complete spontaneous recovery of cardiac function, and coronary angiography revealed a normal coronary artery. Therefore, we firmly believe that bupivacaine directly injures the cardiac cell.
Myocardium/*pathology
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Myocardial Infarction/chemically induced/*diagnosis/etiology
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Humans
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Heart/*drug effects
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Female
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Electrocardiography
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Diagnosis, Differential
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Bupivacaine/*adverse effects
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Adult
7.Myocardial Contrast Defect Associated with Thrombotic Coronary Occlusion: Pre-Autopsy Diagnosis of a Cardiac Death with Post-Mortem CT Angiography.
Heon LEE ; Hyejin PARK ; Jang Gyu CHA ; Sookyoung LEE ; Kyungmoo YANG
Korean Journal of Radiology 2015;16(5):1024-1028
We report the case of a female who died of suspected acute myocardial infarction. Post-mortem CT angiography (PMCTA) was performed with intravascular contrast infusion before the standard autopsy, and it successfully demonstrated the complete thrombotic occlusion of a coronary artery and also a corresponding perfusion defect on myocardium. We herein describe the PMCTA findings of a cardiac death with special emphasis on the potential benefits of this novel CT technique in forensic practice.
*Autopsy
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Coronary Occlusion/*diagnosis/etiology/radiography
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Coronary Vessels/pathology/radiography
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Female
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Humans
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Middle Aged
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Myocardial Infarction/etiology/pathology
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Myocardium
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Thrombosis/complications/*diagnosis
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Tomography, X-Ray Computed
8.ST-elevated acute myocardial infarction happening 1 month post stent implantation: late thrombosis in-stents or new lesions?
Guang-yuan SONG ; Yue-jin YANG ; Bo XU ; Jian-jun LI ; Run-lin GAO ; Shu-bin QIAO ; Jin-qing YUAN ; Yi-da TANG ; Shi-jie YOU ; Han-jun PEI ; Zhen-yan ZHAO ; Xi-mei WANG ; Yong-jian WU
Chinese Medical Journal 2009;122(14):1610-1614
BACKGROUNDST-elevated acute myocardial infarction (STEAMI) happening in the first month post percutaneous coronary intervention (PCI) is almost related to acute thrombosis or subacute thrombosis in-stents. This study aimed to investigate the possible causes of myocardial infarction one month later.
METHODSPatients who had a history of successful PCI, and received coronary angiography or re-PCI due to STEAMI were included in this study. The AMI-related lesions and previous angiographic findings such as the number of lesions, the degree of the stenosis, the type of stents and acute results of last PCI were recorded. If the AMI-related lesion was localized in-stents or at the edge of stents (distance apart from the edge < or = 5 mm), it was defined to be late thrombosis; otherwise as a new-lesion induced AMI.
RESULTSOne hundred and ninety-two patients aged 40 - 79 years were included in this study. New lesions, as the cause of STEAMI, were found in 144 patients (Group A, 75%), and late thrombosis in 48 patients (Group B, 25%). Almost all newly built thromboses were found at the sites of previous insignificant lesions (diameter stenosis < 50%). There was a significant difference in the average time from previous PCI to AMI ((30.1 +/- 12.4) vs (20.3 +/- 11.9) months) between the two groups. Diabetes mellitus (DM) and drug-eluting stent (DES) utilization were associated with markedly higher morbidity of late thrombosis in adjusted Logistic regression (hazard ratio (HR) 3.4, 95% confidence interval (CI) 1.1 - 10.9 and 5.3, 95% CI 1.1 - 26.5).
CONCLUSIONSSTEAMIs happening 1 month after PCI are more likely to develop from previous insignificant lesion rupture than from late thrombosis in-stents. Moreover, DM and DES are associated with the high incidence of late thrombosis, which may indicate that intensive antiplatelet therapy should be considered in patients with diabetes.
Adult ; Aged ; Angioplasty, Balloon, Coronary ; adverse effects ; Coronary Angiography ; Coronary Thrombosis ; etiology ; pathology ; Drug-Eluting Stents ; adverse effects ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; etiology ; pathology
9.Morphological analysis of cardiac rupture due to blunt injury, cardiopulmonary resuscitation and myocardial infarction in forensic pathology.
Dianshen WANG ; Fu ZHANG ; Yunle MENG ; Yangeng YU ; Kai ZHOU ; Leping SUN ; Qi MIAO ; Dongri LI
Journal of Southern Medical University 2018;38(12):1514-1520
OBJECTIVE:
To analyze the morphological features and forensic pathological characteristics of cardiac ruptures of different causes for their differential diagnosis.
METHODS:
We analyzed the data of 44 autopsy cases of cardiac rupture from 2014 to 2017 in our institute, including 11 cases caused by blunt violence with intact pericardium, 4 caused by cardiopulmonary resuscitation (CPR), 9 by myocardial infarction, and 20 by aorta dissection rupture.The gross features and histopathological characteristics of cardiac rupture and pericardial effusion were analyzed and compared.
RESULTS:
Cardiac ruptures caused by blunt violence varied in both morphology and locations, and multiple ruptures could be found, often accompanied with rib or sternum fractures; the volume of pericardial effusion was variable in a wide range; microscopically, hemorrhage and contraction band necrosis could be observed in the cardiac tissue surrounding the rupture.Cardiac ruptures caused by CPR occurred typically near the apex of the right ventricular anterior wall, and the laceration was often parallel to the interventricular septum with frequent rib and sternum fractures; the volume of pericardial blood was small without blood clots; microscopic examination only revealed a few hemorrhages around the ruptured cardiac muscular fibers.Cardiac ruptures due to myocardial infarction caused massive pericardial blood with blood clots, and the blood volume was significantly greater than that found in cases of CPR-induced cardiac rupture ( < 0.05);lacerations were confined in the left ventricular anterior wall, and the microscopic findings included myocardial necrosis, inflammatory cell infiltration, and mural thrombus.Cardiac tamponade resulting from aorta dissection rupture was featured by massive pericardial blood with blood clots, and the blood volume was much greater than that in cases of cardiac ruptures caused by blunt violence, myocardial infarction and CPR ( < 0.05).
CONCLUSIONS
Hemorrhage, inflammatory cell infiltration, and lateral thrombi around the cardiac rupture, along with pericardial blood clots, are all evidences of antemortem injuries.
Aneurysm, Dissecting
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complications
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Aortic Aneurysm
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complications
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Cardiopulmonary Resuscitation
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adverse effects
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Forensic Pathology
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Heart Rupture
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etiology
;
pathology
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Heart Rupture, Post-Infarction
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pathology
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Humans
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Myocardial Contusions
;
complications
10.Protective effect of right coronary artery ischemic preconditioning on myocardial ischemia reperfusion injury in rabbit heart.
Jun LI ; Guoqiang LIN ; Rimao HUANG ; Huihui LU ; Zhong YANG ; Wanjun LUO
Journal of Central South University(Medical Sciences) 2016;41(10):1047-1051
To explore the protective effects of right coronary artery ischemic preconditioning and post-conditioning on myocardial ischemia reperfusion injury in rabbit heart.
Methods: A total of 30 rabbits were randomly divided into 4 groups: a control group (n=7), an ischemia reperfusion group (IR group, n=8), an ischemic preconditioning group (IPC group, n=8) and an ischemic post-conditioning group (IPO group, n=7). Venous blood samples were taken at pre-operation, 1 and 6 h post-operation, and the concentration of serum creatine kinase isoenzyme (CK-MB) and cardiac troponin-T (cTn-T) were measured. The infarct area of cardiac muscle was calculated.
Results: Compared with the IR group, the levels of CK-MB and cTn-T at 1 and 6 h post-operation in the IPC group and the IPO group were reduced (all P<0.05). Compared with the IR group, the infarct size in the IPC group and the IPO group was significantly decreased, with significant difference (both P<0.05) .
Conclusion: Right coronary artery ischemic preconditioning and post-conditioning exert significant protective effects on the myocardial ischemia reperfusion injury in New Zealand rabbits.
Animals
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Coronary Vessels
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Creatine Kinase, MB Form
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blood
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Heart
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Ischemia
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Ischemic Postconditioning
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Ischemic Preconditioning
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Ischemic Preconditioning, Myocardial
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Myocardial Infarction
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etiology
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pathology
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physiopathology
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prevention & control
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Myocardial Ischemia
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complications
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therapy
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Myocardial Reperfusion Injury
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prevention & control
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Myocardium
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Rabbits
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Troponin T
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blood