Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 26

Whereas troponin I and T are also present in skeletal muscles, the muscular configuration is different and is not detected by the cardiac troponin assays. Cardiac troponin I and T are highly specific for a myocardial injury. However, this myocardial injury may not be secondary to a coronary event but to other insults (e.g., critical illness, HF, hypoxemia, hypotension), without additional clinical, ECG, or echocardiographic features of MI.

High-sensitivity troponin (hs-troponin) assays have a much lower detection cutoff than the conventional, sensitive troponin assays (eg, detection cutoff = 0.005 ng/ml vs. 0.04 ng/ml); they detect troponin in ≥50% of healthy individuals, and in fact, some very-high-sensitivity assays can measure troponin in almost all individuals. This detection cutoff is not to be confused with MI cutoff of hs-troponin, which is close to that of conventional, sensitive troponin (~0.04 ng/ml). Yet, even MI cutoff is lower and more precise with hs-troponin, with precision at the 3^rd decimal; also, this fine precision allows MI cutoff to be lower in women than men, as women normally have smaller myocardial mass and troponin values.⁴⁵ Thus, hs-troponin slightly increases the diagnosis of MI in comparison to sensitive troponin (by ~20%). ⁴ More importantly, it rises earlier and allows delineation of a very low level within the non-MI range, allowing stratification of troponin values within this non-MI range (e.g., undetectable=very low risk). Note: to avoid the confusion of decimals, hs-troponin is reported as a whole number in ng/L (e.g., detection cutoff 5 ng/L); this may be divided by 1000 to provide a conventional ng/ml value.

Troponin rises above MI cutoff within 3 hours of an episode of ischemia lasting > 20-30 min. Hs-troponin rises above detection cutoff rapidly, usually within 1 hour of ischemia.⁴

Kidney disease may be associated, per se, with a chronic mild elevation of troponin I. This is not related to reduced renal clearance of troponin, a marginal effect at best. It is rather due to the underlying myocardial hypertrophy, chronic CAD, and BP swings. This leads to a chronic ischemic imbalance, and, as a result, a chronic myocardial damage.

Kinetics of troponin rise and decline- In MI, troponin peaks at 18-24 hours and remains elevated for 7-14 days. However, in small MI, troponin usually normalizes within 2–3 days. Note that the troponin peak and downslope are much slower than the upslope; thus, patients presenting late after an infarct may have a plateau pattern of stable troponin (Figure 1.2).^1,2 In acutely reperfused infarcts (STEMI or NSTEMI), those markers peak earlier (e.g., 12–18 hours) and sometimes peak to higher values than if not reperfused, but decline faster. Hence, the total amount of biomarkers released, meaning the area under the curve, is much smaller, and the troponin elevation resolves more quickly (e.g., 4–5 days). The area under the curve, rather than the actual biomarker peak, correlates with the infarct size.

Note on CK-MB- Troponin I or T is much more sensitive and specific than CK-MB. Frequently, NSTEMI is characterized by an elevated troponin and a normal CK-MB; CK-MB only rises with large MI, when troponin exceeds 0.5 ng/ml. CK-MB rises at 3-6 hours, peaks at 12-24 hours, and normalizes at 2-3 days. Overall, CK-MB testing is not recommended on a routine basis but has one potential application: in patients with marked troponin elevation and subacute symptom onset, CK-MB helps diagnose the age of the infarct (a normal CK-MB implies that MI is several days old).