Contralateral Angiography in Acute Myocardial Infarction Patients: Is Less Really More?

Myonecrosis results from the absence of myocardial perfusion in the setting of acute coronary occlusion and no collateral flow. Therefore, myocardial salvage depends not only on the early restoration of epicardial flow but also on the presence of adequate microcirculatory flow after the acute occlusion. In patients with ST-elevation myocardial infarction (STEMI), early and adequate restoration of myocardial perfusion requires an integration of efforts in 3 fundamental phases of care: 1) pre emergency-medical-service (EMS) activation, 2) pre catheterization laboratory care, and 3) catheterization laboratory care. Myocardial salvage is most likely to occur with early reperfusion, and the mortality rate increases proportionally with the duration of ischemia. Accordingly, with regard to the pre EMS-activation phase, the American Heart Association has focused its educational campaign on increasing the early recognition of the symptoms of myocardial infarction, thus shortening the time from the onset of symptoms to the seeking of medical attention. Phases 1 and 2 (above) involve expediting either transfer to the hospital for primary percutaneous coronary intervention (PCI) or rapid on-site initiation of thrombolytic therapy. Recently, Pinto and co-authors1 reviewed the National Registry of Myocardial Infarction (NRMI) and showed that the survival benefit in patients transferred for PCI versus those who undergo on-site thrombolysis decreases progressively with door-to-balloon (DTB) times of more than 90 minutes; when the DTB time approaches 120 minutes, there is no longer a difference in mortality rate between these 2 groups. These data reflect the efforts of many hospitals to “streamline” their STEMI care protocol by creating recommended processes, policies, and procedures. Rapid reperfusion is associated with in-hospital processes (EMS activation and door-to-page, page-to-laboratory, and laboratory-to-intervention intervals), rather than with pre-hospital processes.2 Once the patient arrives in the catheterization laboratory, the main goal is rapid restoration of normal epicardial flow (Thrombolysis in Myocardial Infarction [TIMI]-3 flow). Without complete normalization of flow, myocardial perfusion is impaired, and myocardial salvage is compromised.3 In this issue of the Texas Heart Institute Journal, Dib and associates4 evaluate an approach that is designed to minimize the DTB time in primary PCI. The authors found that they decreased the mean DTB time by 12 minutes when they first performed electrocardiography (ECG)-guided PCI of the culprit coronary vessel and then obtained a contralateral angiogram, rather than pursue the more conventional approach of obtaining a full diagnostic angiogram before performing PCI of the culprit vessel. Because their study is retrospective, the conclusions drawn from it are limited. Interestingly, the outcomes were similar regardless of whether full or focused (culprit-artery-only) coronary angiograms were obtained. In 10% of Dib's patients who underwent ECG-guided PCI of the culprit coronary artery first, the contralateral coronary artery was later shown by complete angiography to be the culprit vessel. Misdiagnosis of the culprit artery occurred especially in patients with inferior infarcts. In misdiagnosed cases, a significant delay in recanalizing the culprit coronary can occur, owing to the decision to intervene in a nonculprit coronary artery; in STEMI patients, such intervention is contraindicated according to the current American College of Cardiology/American Heart Association guidelines.5 In the patients of Dib and colleagues who presented with anterior STEMI, however, ECG proved quite reliable in indicating the culprit artery. It is important to consider that diagnostic angiography before PCI might provide valuable information that would change the interventional approach (for example, use of a more aggressive guiding catheter to improve backup support for guidewire manipulation and stent delivery in the presence of tortuous coronary arteries). Moreover, in patients with a high thrombus burden, adjuvant pharmacotherapy before instrumentation of the lesion might decrease the rate of procedural complications by reducing distal embolization and the incidence of no reflow. In conclusion, because “time is muscle” in treating STEMI patients, every effort should be made to expedite the transfer of these patients to the catheterization laboratory. Dib and colleagues have provided evidence that obtaining a “culprit-artery angiogram only” can save time and reduce the DTB time. However, a few minutes devoted to obtaining additional diagnostic information that might make the coronary intervention safer or more effective would probably be time wisely spent. On the basis of the present study, it would seem logical to perform a full coronary angiogram in patients with inferior STEMI and an angiogram of only the culprit artery in patients with anterior STEMI. Ultimately, practitioners will have to decide what is best for their patients on a case-by-case basis. A prospective randomized study of focused versus complete coronary angiography in STEMI patients might resolve this issue.