G. Armstrong

Causes of elevated troponin I with a normal coronary angiogram

Abstract

Contrast-enhanced cardiac magnetic resonance in a patient with familial isolated ventricular non-compaction.

Isolated ventricular non-compaction (IVNC) is an idiopathic form of cardiomyopathy. Recent clinical reports have suggested that this form of cardiomyopathy is more frequently associated with complications of congestive heart failure, thromboembolism and malignant ventricular arrhythmias. Contrast enhanced cardiac magnetic resonance imaging with its excellent spatial resolution, its large field of view and its ability to demonstrate thrombus and myocardial scar is an excellent modality to non-invasively assess patients with this form of cardiomyopathy. This paper presents a case of familial isolated ventricular non-compaction. We describe the echocardiographic, X-ray angiographic and cardiac MRI findings. Cine imaging using a steady-state free precession sequence (BFFE) was performed in axial and short axis planes. Left ventricular (LV) mass was estimated both with and without the incorporation of trabeculations from a contiguous stack of short axis images. Trabecular mass was expressed as a percentage of total left ventricular mass. We compared trabecular mass: total LV mass in 10 patients with dilated cardiomyopathy. The mean percentage trabecular mass: LV mass in dilated cardiomyopathy was 11.3% (range 1.5%-19%), and this differed significantly from the trabecular mass of the noncompaction patient (two-tailed Mann-Whitney test, p = 0.028). Trabecular mass of greater than 20% of total myocardial mass may be a useful index to suggest the diagnosis of IVNC. Gadolinium was administered (0.1 mmol/kg). Qualitative analysis of first pass perfusion suggested reduced trabecular perfusion. Early imaging with an inversion recovery sequence and a fixed long inversion time did not demonstrate LV thrombus. Late imaging with the same sequence (TI = 280-300 msec) did not demonstrate myocardial fibrosis.

All troponins are not created equal.

Troponin measurement is central to the management and risk stratification of acute coronary syndromes. Decisions are made by categorizing troponin as positive or negative. We sought to evaluate categorical agreement between four troponin assays. Sixty blood samples were analysed by three troponin I assays (Centaur, Architect and point‐of‐care i‐STAT) and one troponin T (TnT) assay (Roche Elecys). The upper reference limit was taken as the lowest value with a coefficient of variation of 10% or less. Continuous agreement between assays was good (Pearson’s correlation coefficient 0.871–0.995). Categorical agreement assessed by Cohen’s kappa varied from poor (between Architect and Centaur κ = 0.37, and between TnT and Centaur κ = 0.48) to good (between Architect and i‐STAT κ = 0.68, and between TnT and i‐STAT κ = 0.68). Percentage of positive results varied almost twofold, from 37% for the Centaur to 72% for the Architect. Comparison of four troponin assays showed up to twofold variations in the proportion of positive results. This implies that either a large proportion of troponin‐positive diagnoses are missed by some assays or the assays with higher positivity are generating large numbers of false positives. Clinicians should evaluate troponin results in the clinical context and not base decisions solely on the ‘normal range’ of their local troponin assay.