LAUSR

also underwent cardiac troponin I (cTnI) measurement. Known causes of cTnT elevation were excluded by means of 12-lead ECG (performed at the same time of cTnT sampling), clinical history, clinical evaluation (hemodynamic stability), laboratory findings, clinical follow-up, and further investigations (if required in each single case). The exclusion criteria included acute or chronic heart failure, coronary artery disease, arrhythmias, renal failure. Twenty-two consecutive patients (16 males, 6 females, mean age ± s.d. 68.6 ± 8.5 years) have been enrolled in this study. The reference values for males were: CK = 30–240 U/L, CK-MB = 0.00–6.73 μg/L, hs-cTnT = 15 ng/L (99° percentile). Reference values for females: CK = 30–170 U/L, CK-MB = 0.00–3.77 μg/L, hs-cTnT = 10 ng/L (99° percentile). The clinical phenotypes of ALS were: classic (n = 12), bulbar (n = 5), flail arm (n = 2), flail leg (n = 1), and pure upper motor neuron (n = 2); one patient with the bulbar variant also had frontotemporal dementia. All cases, except for one, were sporadic ALS. Genetic testing was available in four patients (positive for C9ORF72 in the familial case). The mean (± s.d.) disease duration (defined as the time interval, in months, from diagnosis to last observation) was 37.9 ± 24.0 months. Some patients underwent more than one determination (each performed at scheduled controls, usually at 2–3 months intervals, unless differently required by the clinical conditions). Altogether, a total of 64 assays were performed; more specifically, the number of measurements per single patient was as follows: one (n = 11), two (n = 2), three (n = 1), four (n = 1), five (n = 2), six (n = 3), and seven (n = 2). The mean (± s.d.) hs-cTnT follow-up was 14.6 ± 5.0 months (males 12.3 ± 4.5, females 18.8 ± 2.9). To the Editor,