Dynamic modulation of coronary arterio-venous communications

A 62 year-old man with multiple coronary risk factors – including uncontrolled hypertension, smoking habit, abdominal obesity and family history of ischemic heart disease – was admitted to our Emergency Department for a prolonged episode of chest pain occurring at rest. He had no relevant past medical history except recently diagnosed chronic obstructive pulmonary disease; however, in the last year he suffered from sporadic episodes of effort angina (Canadian Class II–III) with spontaneous regression after few minutes of rest. During the last week he experienced worsening angina, with daily episodes of chest pain, mainly occurring during mild exertion but with some episodes occurring even at rest in the last two days. On admission the patient was symptomatic for angina. Physical examination was unremarkable, except for rhonchi and wheezing sounds in the chest, the blood pressure was 200/95 mmHg and the ECG revealed sinus tachycardia with ST segment elevation and QS waves in V1–V4 leads. Pharmacological treatment was immediately started with loading doses of Aspirin and Clopidogrel, iv. morphine, i.v. nitroglycerin and i.v. beta-blockers, with partial pain resolution. Cath lab team was promptly alerted for urgent coronary angiography. In the meantime, a trans-thoracic echocardiogram was performed, showing a hypertrophic and mildly dilated left ventricle with regional wall motion abnormalities in the left anterior descending (LAD) coronary artery territory: apical and mid septal akinesia, anterior wall hypokinesia. The estimated left ventricular ejection fraction was 35–40%. No other relevant findings. Fifteen minutes after the admission the patient was still mildly symptomatic for angina and ST segment elevation was still present on the ECG, although reduced, thus the patient was transferred directly to the cath lab to undergo coronary angiography. The selective right coronary angiography revealed significant stenosis of the posterolateral branch of the right coronary artery (RCA) and, more importantly, the presence of collaterals to the LAD and three artero-venous fistulae, which allowed the RCA to communicate with the pulmonary artery, the coronary sinus and a posterolateral branch of the cardiac venous system (Fig. 1A ). Prior to the selective angiography of the left coronary artery, the patient's chest pain resolved together with the concomitant resolution of the ST segment elevation. The left coronary angiography (Fig. 2C ) was performed and showed the presence of significant proximal LAD stenosis, likely representing the culprit lesion, which appeared spontaneously reperfused. Angiography also revealed sub-occlusion of the first diagonal and significant stenosis of the first obtuse marginal (OM) branch. Due to these findings, a new right coronary angiography was performed, which documented the disappearance of both arterial and venous communications (Fig. 1 B). Because of the spontaneous reperfusion of the culprit lesion, together with the total regression of symptoms and ST segment elevation, urgent revascularization was not deemed necessary. Furthermore, considering the presence of multivessel disease, a joint clinical case meeting with cardiac surgeons and invasive cardiologists was arranged and a staged PCI was felt to be the best treatment option and thus was scheduled the following day. A successful revascularization procedure was performed with the implantation of two everolimus eluting stents (EES), 2.75×23 mm on LAD and 2.75×32 mm on OM, and a POBA of the first diagonal branch with a 2.5×25 mm balloon. The patient was discharged with the indication to complete the percutaneous revascularization later. The pre-discharge echocardiogram confirmed global left ventricular dysfunction (LVEF 35–40%) with the above described regional wall motion abnormalities. One month later the revascularization was completed with an elective PCI of the posterolateral branch of the RCA with the implantation of another EES 2.75×16 mm and the angiography confirmed the complete disappearance of collateral circulation and arterio-venous fistulae (Fig. 2 D,E).