Biomarkers of Myocardial Injury and Inflammation after Permanent Pacemaker Implantation: The Lead Fixation Type Effect

Varvarousis, Dimitrios; Goulas, Nikolaos; Polytarchou, Kali; Psychari, Stavroula N.; Paravolidakis, Konstantinos; Konstantinidou, Agapi; Tsoukalas, Dionysios; Vlad, Delia; Bouki, Konstantina P.; Kotsakis, Athanasios

doi:10.4022/jafib.1798

Cited by 6 publications

(5 citation statements)

References 14 publications

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“…Cardiac injury markers and systemic inflammatory markers have been reported to rise transiently after mechanical myocardial injury following cardiac device implantation. 15 We had performed AICD implantation once the cytokine levels had normalized and the patient was free of active COVID infection. However, the inflammatory markers and VPC burden showed a significant resurge following the procedure.…”

Section: Discussionmentioning

confidence: 99%

COVID-19 induced ventricular tachycardia storm unmasking a clinically silent cardiomyopathy: a case report

Mukhopadhyay

Uppal

Yusuf

et al. 2021

European Heart Journal - Case Reports

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Background Coronavirus disease (COVID-19) is a systemic illness characterized by raging impact of cytokine storm on multiple organs. This may trigger malignant ventricular arrhythmias and unmask a clinically silent cardiomyopathy. Case summary A 57-year-old gentleman, known case of hyperthyroidism and diabetes, was referred to our emergency department with history of two ventricular tachycardia (VT) episodes requiring direct current cardioversion in last 3 h followed by another episode in our emergency department that was cardioverted. There was no past history of cardiac illness. His 12-lead electrocardiogram (during sinus rhythm) along with screening echocardiography suggested Arrhythmogenic right ventricular cardiomyopathy (ARVC). He was coincidentally found to be COVID-19 positive by reverse transcription-polymerase chain reaction (RT-PCR) as part of our routine screening. However, he had no fever or respiratory complaints. We noted raised systemic inflammatory markers and cardiac troponin T which progressively increased over the next 4 weeks paralleled by an increase in ventricular premature contraction burden and thereafter started decreasing and returned to baseline by 6th week when the patient became COVID-19 negative by RT-PCR. Subsequently, a single-chamber automated implantable cardioverter-defibrillator implantation was done following which there was a transient increase in these biomarkers that subsided spontaneously. The patient is asymptomatic during 6 weeks of follow-up. Discussion COVID-19-associated cytokine surge triggering VT storm and unmasking a clinically silent ARVC has not yet been reported. The case highlights a life-threatening presentation of COVID-19 and indicates a probable link between inflammation and arrhythmogenicity.

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Section: Discussionmentioning

confidence: 99%

COVID-19 induced ventricular tachycardia storm unmasking a clinically silent cardiomyopathy: a case report

Mukhopadhyay

Uppal

Yusuf

et al. 2021

European Heart Journal - Case Reports

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“…A number of studies have demonstrated that the mechanical effect of lead fixation on the myocardium may cause local injury, as evidenced by raised levels of plasma troponin and inflammatory biomarkers 1,2 . It is reported that transvenous insertion of the leads is followed by a sequence of cardiac histopathological changes, leading eventually to the formation of a fibrous connective tissue scar 3 . In the traditional way of pacing, most patients have a very slight troponin elevation after pacemaker implantation, leading to consider that it is not harmful to cardiac function and structure 4 .…”

Section: Introductionmentioning

confidence: 99%

Quantification of Acute Myocardial Damage Secondary to Implantation of Electrodes for the Left Bundle Branch Area Pacing

Chen

et al. 2021

RIC

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Background: Different from the traditional right ventricular pacing, the left bundle branch area pacing (LBBAP) is accomplished with deeper lead implantation and more attempts. However, myocardial damage is unclear in LBBAP. Objective: The objective of the study was to observe the change of troponin T and explore possible factors associated with greater myocardial damage in LBBAP. Methods: Patients with an indication for pacemaker implantation underwent attempts for LBBAP by transventricular septal method. Levels of troponin T were determined before operation, 12 h and 1 week after the operation. Parameters of intraoperation and follow-up were recorded and analyzed. Results: In total, successful LBBAP was achieved in 126 patients. The levels of troponin T increased significantly at 12 h after the operation compared with those before operation (96.45 ± 11.07 [69.06] vs. 16.59 ± 1.84 [11.92] ng/L, p < 0.001), while there were no significant differences between pre-and post-operative levels at 1 week. Correlation and regression analysis showed that only the number of attempts was an independent factor related to the change of troponin T. During 1 year of follow-up, LBBAP was safe and feasible with few complications. Conclusions: Myocardial damage of LBBAP was clinically significant. The number of attempts was an independent factor related to the myocardial damage. (REV INVEST CLIN. [AHEAD OF PRINT]

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“…Ulinastatin has been proposed to serve as a myocardial protective agent, and it has been reported that ulinastatin improved the myocardial contractility, reduced the myocardial infarct size and decreased the levels of creatine kinase and cTnI in myocardial IR injury ( 16 ). cTnI is a highly sensitive and specific marker of myocardial injury ( 27 ). Mitochondria are important organelles for cardiomyocytes that not only provide the energy for cells, but can also trigger cell apoptosis ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Ulinastatin attenuates lipopolysaccharide‑induced cardiac dysfunction by inhibiting inflammation and regulating autophagy

et al. 2020

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Ulinastatin exerts protective effects against lipopolysaccharide (LPS)-induced cardiac dysfunction. Autophagy has been demonstrated to serve an important role in sepsis-induced cardiomyopathy; however, whether ulinastatin has an anti-autophagic effect in sepsis requires further investigation. The present study aimed to determine the protective effects of ulinastatin on cardiac dysfunction and its role in autophagy during sepsis. C57BL/6J mice were randomly divided into a control, LPS and LPS + ulinastatin group, the survival status of the mice was observed every 6 h and the survival rate at each time point was calculated for 7 days. Furthermore, JC-1 dye and ELISAs were used to analyze the mitochondrial membrane potential (MMP) and serum cardiac troponin I (cTnI) levels, respectively. Western blotting and ELISAs were used to measure the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6. In addition, the cardiac ultrastructure and the number of autophagosomes formed were visualized using transmission electron microscopy, and the pathological changes in the myocardial tissues were analyzed using hematoxylin & eosin staining. Finally, the expression levels of autophagy-related proteins were analyzed using western blotting and immunofluorescence staining. The current study indicated that ulinastatin significantly improved the survival rate of septic mice. It was suggested that ulinastatin may protect against LPS-induced myocardium injury through its anti-inflammatory activity, as decreased cTnI levels, increased MMP and decreased expression levels of TNF-α and IL-6 were all observed following ulinastatin treatment. Furthermore, the number of autophagosomes formed, and the expression levels of microtubule-associated protein light chain 3 and Beclin 1 were significantly decreased following ulinastatin treatment. It was further observed that ulinastatin suppressed LPS-induced autophagosome formation, as indicated by the accumulation of sequestosome 1/p62, and the elimination of lysosome-associated membrane glycoprotein 1. In conclusion, the results of the present study suggested that ulinastatin treatment may improve survival and exert a protective effect over LPS-induced cardiac dysfunction. Furthermore, this protective effect may be associated with its anti-inflammatory and anti-autophagic activity.

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Biomarkers of Myocardial Injury and Inflammation after Permanent Pacemaker Implantation: The Lead Fixation Type Effect

Abstract: cTnI and CRP can increase early after permanent pacemaker implantation, indicating mechanical myocardial injury and inflammation. The extent of these biomarkers elevation depends on the lead fixation type, and is not related to worse short-term prognosis.

Cited by 6 publications

References 14 publications

COVID-19 induced ventricular tachycardia storm unmasking a clinically silent cardiomyopathy: a case report

COVID-19 induced ventricular tachycardia storm unmasking a clinically silent cardiomyopathy: a case report

Quantification of Acute Myocardial Damage Secondary to Implantation of Electrodes for the Left Bundle Branch Area Pacing

Ulinastatin attenuates lipopolysaccharide‑induced cardiac dysfunction by inhibiting inflammation and regulating autophagy

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