ACUTE CORONARY SYNDROME: Assessment of the Extent of Myocardial Damage

Author(s):  
Vinayak Agrawal
2009 ◽  
Vol 55 (5) ◽  
pp. 938-945 ◽  
Author(s):  
Kim Pettersson ◽  
Susann Eriksson ◽  
Saara Wittfooth ◽  
Emilia Engström ◽  
Markku Nieminen ◽  
...  

Abstract Background: Cardiac troponin (cTn) is an established marker of myocardial infarction. Pronounced heterogeneity and the minute amounts released into the circulation constitute significant challenges for cTn detection. Recently, autoantibody formation to cTn was shown to be common and to interfere with immunoassay performance. In this study, we investigated cTn autoantibodies and cardiac troponin I (cTnI) in acute coronary syndrome (ACS) patients over a 1-year period after the index event. Methods: We used a second-generation cTnI assay designed to reduce the interference of cTn autoantibodies. The assay for cTn autoantibodies used 2 anti-cTnI antibodies to capture the ternary cTnI-complex, enabling unrestricted binding of the autoantibodies, which were detected with a labeled antihuman IgG antibody. We analyzed serum samples from 81 non–ST-elevation ACS patients taken at admission and after 1 week and 3 and 12 months. Results: We found 14 cTn autoantibody–positive patients (21%) among the 67 cTnI-positive and none among the 14 cTnI-negative patients. Nine were autoantibody-positive at admission, and 5 became positive at 1 week. Autoantibody signals significantly increased in the 1-week and 3-month samples. At all time points, cTnI was significantly increased in the autoantibody-positive group relative to the negative group. Persistent cTnI elevations at 3 and 12 months were seen in the patients already autoantibody positive at admission. Conclusions: During ACS, patients with cTn autoantibodies have higher cTnI release and therefore larger myocardial damage than patients without autoantibodies. Their cTnI release also lasts longer, at least months. The possible prognostic impact of these observations must be evaluated in larger clinical cohorts.


2009 ◽  
Vol 55 (12) ◽  
pp. 2098-2112 ◽  
Author(s):  
Walter E Kelley ◽  
James L Januzzi ◽  
Robert H Christenson

AbstractBackground: Although cardiac troponin (cTn) is a cornerstone marker in the assessment and management of patients with acute coronary syndrome (ACS) and heart failure (HF), cTn is not diagnostically specific for any single myocardial disease process. This narrative review discusses increases in cTn that result from acute and chronic diseases, iatrogenic causes, and myocardial injury other than ACS and HF.Content: Increased cTn concentrations have been reported in cardiac, vascular, and respiratory disease and in association with infectious processes. In cases involving acute aortic dissection, cerebrovascular accident, treatment in an intensive care unit, and upper gastrointestinal bleeding, increased cTn predicts a longer time to diagnosis and treatment, increased length of hospital stay, and increased mortality. cTn increases are diagnostically and prognostically useful in patients with cardiac inflammatory diseases and in patients with respiratory disease; in respiratory disease cTn can help identify patients who would benefit from aggressive management. In chronic renal failure patients the diagnostic sensitivity of cTn for ACS is decreased, but cTn is prognostic for the development of cardiovascular disease. cTn also provides useful information when increases are attributable to various iatrogenic causes and blunt chest trauma.Summary: Information on the diagnostic and prognostic uses of cTn in conditions other than ACS and heart failure is accumulating. Although increased cTn in settings other than ACS or heart failure is frequently considered a clinical confounder, the astute physician must be able to interpret cTn as a dynamic marker of myocardial damage, using clinical acumen to determine the source and significance of any reported cTn increase.


Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Takashi Unoki ◽  
Motoko Kametani ◽  
Takaaki Toyofuku ◽  
Yutaka Konami ◽  
Hiroto Suzuyama ◽  
...  

Background: Short-term mortality of lethal cardiogenic shock (CS) patients due to acute coronary syndrome (ACS) remains to be improved. The veno-arterial extracorporeal membrane oxygenation (VA-ECMO) has been applied as the effective lifesaving modality for CS patients. While VA-ECMO maintains end-organ perfusion, it increases the damaged left ventricular (LV) afterload. Combined treatment of VA-ECMO and a micro-axial Impella pump, ECPELLA, simultaneously provides the systemic circulatory support and LV unloading. However, it remains unknown whether LV unloading effect by ECPELLA can reduce the myocardial damage and the mortality. Purpose: This study was to assess whether ECPELLA reduces myocardial damage and improves the mortality of CS patients due to ACS. Methods: From January 2012 to May 2021, 66 consecutive patients with lethal CS (SCAI stage-E) due to ACS were enrolled. All patients received VA-ECMO support prior to or after the percutaneous coronary intervention. Among them, 34 patients received ECPELLA and 32 patients received VA-ECMO + IABP. We assessed serum CK-MB levels and the cumulative 30-day mortality. Results: There were no significant difference in age, rate of male sex, coronary risk factors, ST elevated ACS, left main trunk (LMT) lesion, and the time from onset to reperfusion between two treatment groups. The ECPELLA group had significantly lower peak CK-MB and lower 30-day all-cause mortality compared to the VA-ECMO + IABP group [Peak CPK level: median (IQR); 295 (92-507) vs.580 (219-1090): p=0.002, the 30-day mortality rate: 50% vs. 76%: p=0.02, respectively]. Multivariate Cox proportional hazard analysis including age, the time form onset to reperfusion, LMT lesion, E-CPR, and ECPELLA revealed that the ECPELLA (HR: 0.30 95% confidence interval:0.13-0.64; p=0.002) was independently associated with the 30-day all-cause mortality. Conclusion: Results suggest that the ECPELLA reduces the myocardial damage shown by peak CK-MB and improves the 30-day mortality.


2012 ◽  
Vol 3 ◽  
pp. 449-454 ◽  
Author(s):  
Magdalena Babińska ◽  
Michał Holecki ◽  
Fryderyk Prochaczek ◽  
Aleksander Owczarek ◽  
Danuta Kokocińska ◽  
...  

2018 ◽  
Vol 03 (04) ◽  
pp. 240-244 ◽  
Author(s):  
Rachel Jacob ◽  
Mahmood Khan

AbstractCardiac biomarkers are of great importance in the timely, accurate diagnosis and management of acute coronary syndrome as well as the prognosis. Diagnosis in the golden period is of utmost importance to institute therapy at the earliest and possibly reverse the myocardial damage. Cardiac biomarkers are also a powerful tool for triaging. Among the many biomarkers, the earliest examined were the myocardial enzymes, several myocardial proteins, peptides, and many other molecules. The latest addition to the repertoire is the microRNAs, which are stable molecules detectable in circulation. About four groups are found to be involved in regulation of circulatory system, and some show promise as specific and early markers of acute coronary syndrome and cardiac dysfunction. As in other fields of medicine, personalized precise treatment may be possible with the use of microRNAs. However, as of now, a multipronged approach, involving different markers of which troponins are necessary, seems to be the best way forward.


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