Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 194

A totally silent severe myocardial ischemia is uncommon (10- 15% of CAD). The more common form of silent myocardial ischemia consists of silent ischemia interspersed with symptomatic ischemia, such as angina or prior MI. Even if asymptomatic, ischemia is a strong predictor of cardiac events and mortality and may have the same prognostic significance as symptomatic ischemia.²⁹

However, revascularization does not modify this prognosis, and screening asymptomatic patients based solely on risk factors is not indicated, nor is screening of post-PCI patients indicated. In the DIAD study, asymptomatic diabetic patients, who constitute a relatively

high-risk population, were screened for CAD with nuclear stress imaging. These asymptomatic patients actually had a low risk of cardiac events (0.6% per year), and while this risk was higher in the small subgroup of patients with moderate or severe ischemia (2.5% per year), 70% of events eventually occurred in patients with normal testing. In fact, a 0.6% event rate in 90% of the population leads to more total events than a 2.5% event rate in 10% of the population. Even if revascularization reduces the risk of late MI in this small subgroup, the benefit is nullified by the periprocedural risk of MI and by the risk of unnecessary diagnostic angiograms in patients with false positive stress tests. This explains why the event rate was similar in the screened and non-screened diabetic populations. Thus, stress testing is not generally useful in asymptomatic patients, even those at seemingly high risk, particularly if risk factors and hemoglobin A1c are well controlled (as in the DIAD study).³⁰ These findings were corroborated by another study, wherein asymptomatic diabetic patients were randomized to coronary CTA screening vs. routine care. Coronary CTA found significant CAD (>70% stenosis) in 11% of patients and resulted in a 6% revascularization rate, which did not translate into any reduction of death, MI, or unstable angina (FACTOR-64 study).³¹ Moreover, the following 3 ideas argue against testing and stenting asymptomatic patients:

 ~75% of MIs arise from a plaque that was not obstructive (<50%) on a recent CT or coronary angiography (within the last couple of years).³² This is particularly true if the patient is asymptomatic, even more so if asymptomatic despite being active.

 Atherosclerotic burden, as assessed by CT calcium scoring, is at least as good a predictor of coronary events as the presence of obstructive CAD. Stenting does not modify this major driver of outcomes, i.e., plaque burden.³³

 Occlusion of a stenosis>70% is far less likely to cause a large MI than occlusion of mild disease (30% vs. 75% likelihood), and far more likely to be preceded by angina as first presentation (70%). This is because chronic collaterals reduce infarct size in the former. Thus, seeking stenoses >70% is seeking the less deadly disease.³⁴

The only valuable test in asymptomatic patients is CT calcium scoring, a powerful risk stratifier that dictates more aggressive risk factor modification, not revascularization. If stress testing is done in asymptomatic patients, the detection of severe ischemia would lead to revascularization only in extensive CAD, mainly left main disease.

Silent ischemia 6 months after PCI, even if severe, is not clearly associated with increased death or MI. In-stent restenosis is asymptomatic ~50% of the time, in which case the prognosis is very good; routine angiographic follow-up and PCI of asymptomatic in-stent restenosis does not improve outcomes compared to angina-driven PCI.³⁵