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Table of Contents
ORIGINAL ARTICLE
Year : 2018  |  Volume : 1  |  Issue : 1  |  Page : 31-34

Prevalence and determinants of myocardial damage after occluder implantation in patients with atrial septal defect


1 Department of Cardiology, King George’s Medical University, Lucknow, Uttar Pradesh, India
2 Department of Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, Kerala, India

Date of Web Publication24-Aug-2018

Correspondence Address:
Dr. Mahim Saran
B10/18, Sector-K, Aliganj, Lucknow - 226 024, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IHJI.IHJI_5_17

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  Abstract 


Objective: The objective was to study the prevalence and extent of myocardial damage in patients undergoing atrial septal defect device closure (ASDDC) and to examine its determinants. Background: Little is known about myocardial lesions after occluder implantation in children. The influence of defect size and anatomy, device size, and other baseline patient characteristics on the occurrence and extent of myocardial damage remains unclear. We evaluated the occurrence and extent of myocardial damage and its relationship to the various patient characteristics using cardiac troponin T (cTnT) as the marker of myocardial damage. Methods: In a retrospective analysis, case records of patients undergoing ASDDC from May 2015 to June 2016 were analyzed. Anthropometric data, atrial septal defect (ASD) characteristics, and device characteristics were compared between troponin-positive (Group 1; cTnT ≥0.05 µg/L) and troponin-negative (Group 2; cTnT <0.05 µg/L) groups. Results: Troponin T was significantly increased following occluder implantation in 32 out of 200 patients who underwent the procedure. Complex ASDs (particularly multiple defects [odds ratio [OR] = 13.23] and deficient posterior rim [OR = 13.23]) contributed significantly to myocardial damage following occluder implantation as evidenced by significant troponin T release of ≥0.05 µg/L (P = 0.004). Considering quantitative troponin T estimation as a measure of extent of myocardial damage, there was a weak correlation between device size and the extent of myocardial damage (r2 = 0.125; P = 0.047). Conclusions: Complex ASDs, particularly those with multiple defects or deficient posterior rim, contribute significantly to myocardial damage following ASDDC. Larger device size is associated with greater myocardial damage.

Keywords: Atrial septal defect device closure, myocardial damage, troponin T


How to cite this article:
Saran M, Sivasubramonian S, Ganapathi S, Sasikumar D, Krishnamoorthy K M, Kumar VA. Prevalence and determinants of myocardial damage after occluder implantation in patients with atrial septal defect. Indian Heart J Interv 2018;1:31-4

How to cite this URL:
Saran M, Sivasubramonian S, Ganapathi S, Sasikumar D, Krishnamoorthy K M, Kumar VA. Prevalence and determinants of myocardial damage after occluder implantation in patients with atrial septal defect. Indian Heart J Interv [serial online] 2018 [cited 2018 Sep 21];1:31-4. Available from: http://www.ihji.org/text.asp?2018/1/1/31/239781




  Introduction Top


Manipulation of the heart to treat various congenital malformations could result in myocardial damage which could be minimized by less invasive interventional procedures precluding the need for cardiotomy and cardiopulmonary bypass.[1],[2]Although percutaneous atrial septal defect (ASD) occlusion produces much less myocardial damage[1] than surgical closure of the defect,[2] there is limited literature on myocardial damage following percutaneous ASD closure. Troponin T is a useful cardiac biomarker for myocardial injury in adults; however, its use in pediatric population is not uncommon. Cardiac troponin T (cTnT) has been found to be elevated in cases of myocardial damage following neonatal asphyxia, cardiac or noncardiac surgery, and doxorubicin chemotherapy.[3],[4]These elevations have been found to be related to the degree of myocardial damage.[4] We evaluated the occurrence and extent of myocardial damage and its relationship to the various patient characteristics using cTnT as the marker of myocardial damage.


  Methods Top


Study population

Case records of all patients who underwent ASD device closure (ASDDC) from May 2015 to June 2016 were retrospectively analyzed.

Exclusion criteria

All patients with prior elevation of cTnT or troponin T elevation due to other causes (e.g., acute coronary syndrome, preprocedural renal failure [acute or chronic], pericarditis/myocarditis, acute or chronic heart failure, cardiotoxic chemotherapy, and current cardioversion defibrillation) were excluded from the study.

Methodology

ASD device size was assessed using transesophageal echocardiography. Standard procedure was adopted to close the defect in cardiac catheterization laboratory by experienced operators under general anesthesia and transesophageal echocardiography guidance assisted by fluoroscopy. All patients were kept on dual antiplatelets for 6 months postprocedure.

For all patients, cTnT was measured 1 day before the procedure or at the time of sheath insertion (T1) and 4–6h after the procedure (T2). Patients with negative T1 and elevated T2 (cTnT ≥0.05 µg/L) were assigned to Group 1 and those with no significant elevation in T2 (cTnT <0.05 µg/L) were assigned to Group 2.

Sampling and assays

Radiometer AQT90 FLEX (RADIOMETER, Copenhagen, Denmark) bench-top immunoassay analyzer (which has a cutoff value of 0.017 µg/L) was used to measure cTnT in all cases.

Statistical analysis

Case sheets of all patients who did not meet the exclusion criteria were studied using a prespecified pro forma for the study. Baseline characteristics of the two groups were compared using multivariate logistic regression analysis.

Data were expressed as mean ± standard deviation as appropriate. Relationship of various measurable and binominal variables to the presence or absence of troponin T elevation was determined using multivariate logistic regression analysis. Odds ratio using a two-by-two frequency table was calculated to determine the significance of various anatomical defects separately. Linear regression was used to determine the relationship between baseline parameters and troponin T values (extent of myocardial damage). Association was considered statistically significant if P < 0.05.

Appropriate informed written consent was obtained for the procedure as per the institutional protocol. The study was reviewed and approved by the ethical committee of our institute.


  Results Top


Two hundred patients underwent ASD device closure during the study period with a median age of 12 years. Females constituted 129/200 (64.5%) of the patients. Baseline characteristics of the patients are mentioned in [Table 1].
Table 1: Baseline characteristics of the patients undergoing atrial septal defect device closure from May 2015 to June 2016 (n = 200)

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In 32/200 (16%) of the patients, postprocedural cTnT values were elevated to ≥0.05 µg/L, suggesting significant myocardial damage.[5] The troponin T elevations ranged from 0.052 µg/L to 0.276 µg/L with a mean of 0.088±0.47 µg/L. Baseline characteristics of the two groups are presented in [Table 2].
Table 2: Baseline characteristics of the two groups

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After multivariate logistic regression analysis, it was found that complex ASDs, particularly those with deficient posterior rim and multiple ASDs, were independent predictors of postprocedural cardiac troponin elevations [Table 2] and [Table 3]. None of the other parameters including age, sex, height, weight, ASD size, device size, ratio of ASD size to body surface area (BSA), and ratio of device size to BSA contributed to myocardial injury.
Table 3: Subsets of complex atrial septal defects with odds ratio

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Three different ASD devices were used, namely  Heart R (Lifetech Scientific, China), Cocoon (Vascular Concepts Limited, Bangalore, India), and Amplatzer (St. Jude Medical, Minnesota, USA). The most commonly used device was Amplatzer (107/200, 53.5%) followed by Cocoon and Heart R. There was no correlation between the type of device and troponin T elevation. (Amplatzer – 15.8%, Cocoon – 15.6%, and Heart R – 17.2%).

A weak linear relationship was observed between device size and cTnT values (r2 = 0.125; P = 0.047) [Figure 1]. A significant correlation could not be observed between any other parameters and the extent of myocardial damage.
Figure 1: Correlation of myocardial damage with device size. Cardiac troponin T release (values in ng/L) after myocardial damage by occluder implantation for atrial septal defect closure is plotted against device size. Linear regression: r2 = 0.125, P = 0.047. Each point represents data of an individual patient

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  Discussion Top


The incidence of ASD device-related myocardial injury has varied over a wide range in older studies owing to incomplete reporting and failure of these studies to use cardiac biomarkers as a determinant of myocardial injury.[6],[7]

Device-related erosion is a relatively rare complication associated with percutaneous closure of ASD. The risk tends to increase during the first 96h and decreases thereafter.[8] Whether postprocedural evidence of myocardial injury is a predictor of device erosion in the future is currently unknown. Cardiac troponins are widely used as markers of myocardial injury and cTnT values ≥0.05 µg/L are considered to be indicative of significant myocardial injury.[5] Indeed, cTnT is also found in skeletal muscles to a small extent, but the current troponin T assays do not identify skeletal troponin T.[9] Hence, although raised cTnT is a marker of myocardial damage, it may not necessarily mean myocardial infarction. In fact, 30% of the patients with elevated troponin T do not fit into the conventional acute coronary syndrome (ACS).[10] Troponin T is also found to be elevated in secondary myocardial ischemia due to various reasons (large pulmonary embolism, dilated cardiomyopathy, hypertrophic cardiomyopathy, coronary intervention, and spasm)[11],[12],[13],[14] and nonischemic myocardial injury (myopericarditis, trauma, sepsis, and chemotherapy).[15],[16],[17],[18] Whether this troponin elevation in conditions other than ACS represents reversible or irreversible damage is also unclear.[19] Few studies have attempted to identify the risk factors associated with myocardial injury secondary to percutaneous device closure using cardiac troponins as markers of myocardial injury. Chung et al.[7] found postprocedural cTnT release to correlate with device size/BSA, while Tárnok et al.[20] in their study showed a significant increase in myocardial damage with device size. Tárnok et al.[20] also showed that cardiac catheterization alone was not associated with significant troponin T elevation. These studies had not analyzed the ASD anatomy. While analyzing all parameters along with ASD anatomy, we found a complex anatomy of the defect, especially deficient posterior rim and multiple ASDs to be the only predictor of myocardial damage. Among the patients with myocardial damage, greater injury occurred in patients with larger device size as evidenced by greater cTnT release (r2 = 0.125, P = 0.47). There was no association of myocardial damage with the type of device used.

Embolization or hemodynamic instability during the procedure can be another reason for troponin release. However, none of our patients had any episodes of hypotension or ST-T changes during the procedure as an evidence for the same. Type of anesthesia and drugs used were standard in all patients and hence we do not consider that any of these factors could have contributed to inadvertent myocardial damage and troponin release. None of the patients had any evidence for adverse drug reaction and hence it is also not likely to have caused the troponin release.

Our retrospective study failed to capture the finer procedural details such as duration of the procedure, number of attempts, total cTnT release, and whether right pulmonary vein deployment was associated with higher troponin release.

Obtaining pre- and post-procedural cTnT can help in identifying the high-risk patients prompting the need for a closer follow-up. Whether this clinically silent myocardial damage translates into future risk of erosions or embolization is yet to be determined.


  Conclusions Top


Complex ASDs, particularly those with multiple defects or deficient posterior rim, contribute significantly to myocardial damage following ASDDC. Larger device size is associated with greater myocardial damage.

Implications of the study

Point-of-care cTnT is a simple and easily available tool which can be used as a marker of myocardial damage postprocedure. Proper selection of patients can minimize myocardial damage. Close follow-up of patients with evidence of postprocedural myocardial damage may help in the early detection of erosion or embolization.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Pees C, Haas NA, von der Beek J, Ewert P, Berger F, Lange PE, et al. Cardiac troponin I is increased after interventional closure of atrial septal defects. Catheter Cardiovasc Interv 2003;1:124–9.  Back to cited text no. 1
    
2.
Hirsch R, Dent CL, Wood MK, Huddleston CB, Mendeloff EN, Balzer DT, et al. Patterns and potential value of cardiac troponin I elevations after pediatric cardiac operations. Ann Thorac Surg 1998;1:1394–9.  Back to cited text no. 2
    
3.
Costa S, Zecca E, De Rosa G, De Luca D, Barbato G, Pardeo M, et al. Is serum troponin T a useful marker of myocardial damage in newborn infants with perinatal asphyxia? Acta Paediatr 2007;1:181–4.  Back to cited text no. 3
    
4.
Lipshultz SE, Rifai N, Sallan SE, Lipsitz SR, Dalton V, Sacks DB, et al. Predictive value of cardiac troponin T in pediatric patients at risk for myocardial injury. Circulation 1997;1:2641–8.  Back to cited text no. 4
    
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Collinson PO, Stubbs PJ, Kessler AC; Multicentre Evaluation of Routine Immunoassay of Troponin T Study. Multicentre evaluation of the diagnostic value of cardiac troponin T, CK-MB mass, and myoglobin for assessing patients with suspected acute coronary syndromes in routine clinical practice. Heart 2003;1:280–6.  Back to cited text no. 5
    
6.
Amin Z, Hijazi ZM, Bass JL, Cheatham JP, Hellenbrand WE, Kleinman CS, et al. Erosion of Amplatzer septal occluder device after closure of secundum atrial septal defects: Review of registry of complications and recommendations to minimize future risk. Catheter Cardiovasc Interv 2004;1:496–502.  Back to cited text no. 6
    
7.
Chung HT, Su WJ, Ho AC, Chang YS, Tsay PK, Jaing TH, et al. Cardiac troponin I release after transcatheter atrial septal defect closure correlated with the ratio of the occluder size to body surface area. Pediatr Neonatol 2011;1:267–71.  Back to cited text no. 7
    
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Amin Z. Echocardiographic predictors of cardiac erosion after Amplatzer septal occluder placement. Catheter Cardiovasc Interv 2014;1:84–92.  Back to cited text no. 8
    
9.
Ricchiuti V, Voss EM, Ney A, Odland M, Anderson PA, Apple FS, et al. Cardiac troponin T isoforms expressed in renal diseased skeletal muscle will not cause false-positive results by the second generation cardiac troponin T assay by Boehringer Mannheim. Clin Chem 1998;1:1919–24.  Back to cited text no. 9
    
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Collinson PO, Stubbs PJ. Are troponins confusing? Heart 2003;1:1285–7.  Back to cited text no. 10
    
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Goldhaber SZ. Pulmonary embolism. Lancet 2004;1:1295–305.  Back to cited text no. 11
    
12.
Sato Y, Yamada T, Taniguchi R, Nagai K, Makiyama T, Okada H, et al. Persistently increased serum concentrations of cardiac troponin t in patients with idiopathic dilated cardiomyopathy are predictive of adverse outcomes. Circulation 2001;1:369–74.  Back to cited text no. 12
    
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Setsuta K, Seino Y, Ogawa T, Arao M, Miyatake Y, Takano T, et al. Use of cytosolic and myofibril markers in the detection of ongoing myocardial damage in patients with chronic heart failure. Am J Med 2002;1:717–22.  Back to cited text no. 13
    
14.
Sato Y, Taniguchi R, Nagai K, Makiyama T, Okada H, Yamada T, et al. Measurements of cardiac troponin T in patients with hypertrophic cardiomyopathy. Heart 2003;1:659–60.  Back to cited text no. 14
    
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Lauer B, Niederau C, Kühl U, Schannwell M, Pauschinger M, Strauer BE, et al. Cardiac troponin T in patients with clinically suspected myocarditis. J Am Coll Cardiol 1997;1:1354–9.  Back to cited text no. 15
    
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Imazio M, Demichelis B, Cecchi E, Belli R, Ghisio A, Bobbio M, et al. Cardiac troponin I in acute pericarditis. J Am Coll Cardiol 2003;1:2144–8.  Back to cited text no. 16
    
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Ammann P, Fehr T, Minder EI, Günter C, Bertel O. Elevation of troponin I in sepsis and septic shock. Intensive Care Med 2001;1:965–9.  Back to cited text no. 17
    
18.
Cardinale D, Sandri MT, Martinoni A, Tricca A, Civelli M, Lamantia G, et al. Left ventricular dysfunction predicted by early troponin I release after high-dose chemotherapy. J Am Coll Cardiol 2000;1:517–22.  Back to cited text no. 18
    
19.
Sharma S, Jackson PG, Makan J. Cardiac troponins. J Clin Pathol 2004;1:1025–6.  Back to cited text no. 19
    
20.
Tárnok A, Bocsi J, Osmancik P, Häusler HJ, Schneider P, Dähnert I, et al. Cardiac troponin I release after transcatheter atrial septal defect closure depends on occluder size but not on patient’s age. Heart 2005;1:219–22.  Back to cited text no. 20
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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