Journal of Yeungnam Medical Science

Original article

Complete or incomplete revascularization in patients with left main culprit lesion acute myocardial infarction with multivessel disease: a retrospective observational study: Sun Oh Kim, Hong-Ju Kim, Jong-Il Park, Kang-Un Choi, Jong-Ho Nam, Chan-Hee Lee, Jang-Won Son, Jong-Seon Park, Sung-Ho Her, Ki-Yuk Chang, Tae-Hoon Ahn, Myung-Ho Jeong, Seung-Woon Rha, Hyo-Soo Kim, Hyeon-Cheol Gwon, In-Whan Seong, Kyung-Kuk Hwang, Seung-Ho Hur, Kwang-Soo Cha, Seok-Kyu Oh, Jei-Keon Chae, Ung Kim; J Yeungnam Med Sci. 2025;42:18. Published online December 19, 2024; DOI: https://doi.org/10.12701/jyms.2025.42.18 [Epub ahead of print]

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Abstract PDF: Background
Complete revascularization has demonstrated better outcomes in patients with acute myocardial infarction (AMI) and multivessel disease. However, in the case of left main (LM) culprit lesion AMI with multivessel disease, there is limited evidence to suggest that complete revascularization is better.
Methods
We reviewed 16,831 patients in the Korea Acute Myocardial Infarction Registry who were treated from July 2016 to June 2020, and 399 patients were enrolled with LM culprit lesion AMI treated with percutaneous coronary intervention. We categorized the patients as those treated with complete revascularization (n=295) or incomplete revascularization (n=104). The study endpoint was major adverse cardiac and cerebrovascular events (MACCE), a composite of all-cause death, myocardial infarction, ischemia-driven revascularization, stent thrombosis, and stroke. We performed propensity score matching (PSM) and analyzed the incidence of MACCE at 1 year.
Results
After PSM, the two groups were well balanced. There was no significant difference between the two groups in MACCE at 1 year (12.1% vs. 15.2%; hazard ratio, 1.28; 95% confidence interval, 0.60–2.74; p=0.524) after PSM. The components of MACCE and major bleeding were also not significantly different.
Conclusion
There was no significant difference in clinical outcomes between the groups treated with complete or incomplete revascularization for LM culprit lesion AMI with multivessel disease.

Review

Tests for Acute Coronary Syndrome.: Kyung Dong Kim; Yeungnam Univ J Med. 2001;18(1):13-29. Published online June 30, 2001; DOI: https://doi.org/10.12701/yujm.2001.18.1.13

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1 Crossref

The enzyme activities of creatine kinase(CK), its isoenzyme MB(CK-MB) and of lactate dehydrogenase isoenzyme 1(LD-1) have been used for years in diagnosing patients with chest pain in order to differentiate patients with acute myocardial infarction(AMI) from non-AMI patients. These methods are easy to perform as automated analyses, but they are not specific for cardiac muscle damage. During the early 90's the situation changed. First, creatine kinase MB mass(CK-MB mass) replaced the measurement of CK-MB activity. Subsequently cardiac-specific proteins, troponin T(cTnT) and troponin I(cTnI) appeared and displacing LS-1 analysis. However troponin concentration in blood increase only from four to six hours after onset of chest pain. Therefore a rapid marker such as myoglobin, fatty acid binding protein or glycogen phosphorylase BB could be used in early diagnosis of AMI. On the other hand, CK-MB isoforms alone may also be useful in rapid diagnosis of cardiac muscle damage. Myoglobin, CK-MB mass, cTnT and cTnI are nowadays wisely used in diagnosing patients with acute chest pain. Myoglobin is not cardiac-specific and therefore requires supplementation with some other analysis such as troponins to support the myoglobin value. Troponins are very highly cardiac-specific. Only the sera of some patients with severe renal failure, which requires hemodialysis, have elevated cTnT and/or cTnI without there being any evidence of cardiac damage. The latest studies have shown that elevated troponin levels in sera of hemodialysis patients point to an increased risk of future cardiac events in a similar manner to the elevated troponin values in sera of patiets with unstable angina pectoris. In addition, the bedside tests for cTnT and cTnI alone or together with myoglobin and CK-MB mass can be used instead of quantitative analyses in the diagnosis of patients with chest pain. These rapid tests are easy to perform and they do not require expensive instrumentation. For the diagnosis patients with chest pain, routinely myoglobin and CK-MB mass measurements should be performed whenever they are requested (24 h/day) and cTnT and cTnI on admission to the hospital and then 4-6 and 12 hours later and maintained less than 10% imprecision.

Citations

Citations to this article as recorded by

The Usefulness of Rapid Triple Test for Cardiac Marker in Forensic Paragnosis of Sudden Cardiac Death
Chae-Won Lim, Jin-Gak Kim
The Korean Journal of Clinical Laboratory Science.2017; 49(2): 108. CrossRef

Original Article

Diagnostic Efficiency of Lactate Dehydrogenase, Crreatine Kinase and Troponin T in Acute Myocardial Infarction.: Chae Hoon Lee, Kyung Dong Kim, Chung Sook Kim; Yeungnam Univ J Med. 1995;12(1):48-55. Published online June 30, 1995; DOI: https://doi.org/10.12701/yujm.1995.12.1.48

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Abstract PDF: The present study was designed to evaluate the efficiency of total lactate dehydrogenase, total creatine kinase, LD1/LD2 ratio, CK-MB and newly developed troponin T in acute myocardial infarction. The level of troponin T was 0.010.02 pg/L in 34 healthy person, but the peak vaule of acute myocardial infarction ranged in 4.7-24.2 pg/L. Total lactate dehydrogenase was peaked in 1 to 3 days after chest pain and then progressively decreased, but LD1/LD2 ratio was persistently higher than 1.0 for 10 days in most patients. Total creatine kinase and CK-MB were peaked in 1-2 days, and normalized in 3-4 days, so they, were useful in early diagnosis of acute myocardial infarction, but not for the late stages of acute myocardiz l infarction. Troponin T is early elevated and persistently high level for more than 10 days. Comparing with total lactate dehydrogenase, total creatine kinase, LD1/LD2 ratio and CK-MB, troponin-T test improves the efficiency of serodiagnostic method for the detection of ischemic myocardial damage.

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