Troponin I and colonoscopy

We report on a greater than 50% increase in troponin I (TnI) concentration following elective colonoscopy (Table 1).

Table 1

	Preprocedure TnI concentration (μg/L)	Postprocedure TnI concentration (μg/L)	Electrocardiogram changes	Known heart disease
Patient 1	0.03	0.05	Yes	Yes
Patient 2	<0.01	0.05	No	No
Patient 3	0.03	0.06	Yes	Yes
Patient 4	0.04	0.06	Yes	Yes

This was observed in four of 197 patients recruited to a prospective assessment of the cardiac risks of colonoscopy using continuous 12-lead electrocardiogram (ECG) Holter monitoring before, during and after the procedure. TnI was measured before and 20–28 h after colonoscopy. Both the pre- and postprocedure concentrations remained below the laboratory-derived reference range of ≤0.08 μg/L. ¹

Three of the four patients had a history of stable heart disease. The ECG recordings were analysed and concurred by two independent cardiologists and demonstrated evidence of cardiac strain during the procedure in the patients known to have heart disease, as evidenced by ST segment depression (>1 mm) on the chest leads, which developed during the procedure but settled in the postprocedure phase. None of the four patients had tachycardia during the procedure. No patient had any underlying renal dysfunction.

TnI concentrations were measured on an Abbott Architect analyser using the STAT TnI assay. The coefficient of variation (CV) of the assay at 0.023, 0.055 and 0.09 μg/L has been reported as 20%, 10% and 6%, respectively. ^1,2 The critical difference (result ±2 SD) between the two sets of results, calculated from these CV data, showed that in patients 2 and 3, the increase in TnI could not be explained by analytical imprecision. The difference in pre- and post-TnI concentrations for patients 1 and 4 were within the predicted analytical imprecision of the measurement at these concentrations and so could not be confirmed as being statistically significant, but did show the same overall trend.

Although the significance of this TnI increase is unknown, the presence of the synchronous ECG change could point to the presence of a troponin leak from the myocardium. Further work needs to be done to confirm this possibility but we wish to draw attention to a hitherto unrecognized potential cause of a significant increase in cTnI concentration.

DECLARATIONS

Competing interests: None.

Funding: This research was funded by the Bran Calcraft Fund and the Research Small Grants fund of Gwent Trust.

Ethical approval: The ethics committee of the South East Wales approved this study (08/WSE04/7).

Guarantor: ATG.

Contributorship: ATG carried out the study. AB was involved in analysing the samples. JT helped in calculating the reference values and writing of the letter.