Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 59

While troponin release above MI cutoff reflects myocardial cell necrosis, low but detectable hs-troponin typically represent physiological levels of troponin release, or ischemia without necrosis. This may be due to expulsion of the cytosolic pool of troponin without cell death (most of the troponin is in the myofibrils and degrades over 12-24 hours after cell death, but ~8% is cytosolic and may be released physiologically or pathologically without cell death). For example, myocardial stretching, ischemia, or fast heart rate may increase cell membrane permeability without necrosis.¹⁸⁴ This may explain why, following rapid atrial pacing for a few minutes, hs-troponin levels rise, and sometimes double or triple (without exceeding MI cutoff) even in patients without CAD and sometimes even without ischemia (as evidenced by a lack of lactate release in the coronary sinus).¹⁸⁴ This also explains why, after a positive stress test, hs-troponin slightly rises, even while remaining well below MI cutoff, and is associated, in this case, with the presence and severity of perfusion defects.¹⁸⁵ As such, physiological demands or transient provoked ischemia can release troponin in the absence of necrosis. The change is so small that it cannot be detected with conventional troponin, and troponin level does not usually rise above MI cutoff even if stress-induced ischemia is severe. Ischemia or injury must be sustained to raise troponin above MI cutoff.

Hs-troponin is more likely to be chronically detectable in patients with underlying CAD and in patients with comorbidities such as hypertension or diabetes.^184,186 In fact, even in the outpatient setting, an undetectable hs-troponin, or a detectable troponin that is in the lower tertile of detection, is associated with a very low risk of long-term events (even lower than that of a normal stress test), and a low probability of obstructive CAD.^187,188 In another study that screened asymptomatic outpatients with a mean age of 62, an undetectable troponin (<0.003 ng/ml) predicated a very low risk of cardiac events, 0.5% per year, similar to the risk of patients with a calcium score of 0.¹⁸⁹

The only circumstance wherein troponin may exceed MI cutoff physiologically, without necrosis, is marathon exercise among non-highly trained individuals. After marathon, ~50% of nonelite participants have a rise in troponin above MI cutoff (>0.03, up to 0.8 ng/ml), along with transient LV diastolic dysfunction and RV dilatation.¹⁹⁰ Yet troponin rise is brief and normalizes within a few hours, and there is no evidence of late gadolinium enhancement on MRI (troponin leak from myocardial stretch rather than cell necrosis?).¹⁹¹