Acute myocardial infarction in a young athlete: Optical coherence tomographic features of the culprit lesion.

OBJECTIVES: We report on a young male athlete who suffered from acute myocardial infarction immediately after a vigorous training.
METHODS: A comprehensive optical coherence tomographic investigation of the culprit coronary artery was performed after the combined mechanical and pharmacological thrombus removal. RESULTS AND
CONCLUSION: The imaging discovered a tear at the junction of the non-obstructive, largely fibrotic plaque with the normal arterial wall. This exertion-related vessel damage resulted in a dynamic thrombosis that almost completely occluded the culprit artery. As the vessel obstruction was not considered flow-limiting, the stent implantation was not required and the patient was discharged on the double antiplatelet therapy and statin.

Introduction

Despite the recognized benefits of regular training on cardiovascular health, vigorous exercise may provoke acute coronary events in patients with latent coronary artery disease (CAD). For example, among 3617 asymptomatic men selected for the Lipid Research Clinics Primary Prevention Trial, 62 (1.7%) participants sustained an acute myocardial infarction (MI) or sudden death clearly related to exertion during a mean follow-up of 7 years.[1] Pathomorphological studies have demonstrated that the acute events usually result from the abrupt vessel narrowing caused by thrombosis based on plaque rupture, erosion, or superficial calcified nodule.[2] Rupture of a thin-capped fibroatheroma (TCFA) is by far the leading cause of ST-segment elevation MI (STEMI).[3,4] Interestingly, rather distinctive features of plaques that rupture on exertion have been described compared with those that are found at rest-onset events.[5,6] To further clarify this subject, we report the optical coherence tomography (OCT) features of the culprit lesion in a young athlete who suffered from STEMI after a strenuous training.

Case report

A 31-year-old recreational male athlete used to run 10 km daily; however, he intensified his training for the past few days. As a result, right-sided chest discomfort began to appear while running. Eventually, severe substernal pain accompanied by sweats and nausea awakened him early in the morning. His past medical history was unremarkable, he did not take any medications, and smoked 10 cigarettes per day. On admission, the pain was still present, his heart rate was 74/min, blood pressure was 135/75 mm Hg, and his lungs were clear. There were marked ST-segment elevations in the anterior electrocardiographic leads (Figure 1). The emergent coronary angiography showed a tight thrombotic lesion in the proximal left anterior descending artery (LAD) with a Thrombolysis in Myocardial Infarction (TIMI) grade 2 epicardial flow (Figure 2(a)). Percutaneous coronary intervention (PCI) was attempted under protection of unfractionated heparin, double antiplatelet therapy (DAPT), and venous eptifibatide. Manual thrombectomy with the Export 6F catheter (Medtronic Vascular, Santa Rosa, CA, USA) managed to achieve the TIMI 3 flow, but failed to remove all thrombotic masses. Therefore, it was decided to provisionally stop the PCI without any balloon dilatation or stent implantation. At the Coronary Care Unit, the patient was daily given aspirin 100 mg, ticagrelor 180 mg, rosuvastatin 20 mg, and eptifibatide 2 µg/kg/min for 24 h. He remained asymptomatic, troponin T increased to 1.84 µg/L (upper limit of normal ⩽0.1 µg/L), Q waves did not develop in the anterior leads, and transthoracic ultrasound did not discover any major contractility impairment.

Figure 1.

A 12-lead electrocardiogram at admission shows acute anterior ischemia with marked ST-segment elevations in leads I, aVL, and V2–6.

Figure 2.

(a) Left coronary angiogram in the right anterior oblique view at admission. Note a tight, thrombotic lesion (black arrow) of the proximal left anterior descending artery. (b) At repeat angiography, the previous lesion has completely disappeared.

The angiography was repeated 12 days later; the TIMI 3 flow was confirmed without any significant obstruction of the LAD (Figure 2(b)). At that point, OCT imaging was performed using the Dragonfly™ Duo imaging catheter and the Ilumien™ Optis™ System (LightLab Imaging, Inc., Westford, MA, USA; St Jude Medical, St Paul, MN, USA). The culprit lesion was recognized as a long, eccentric plaque extending from the distal left main artery to the proximal LAD (Figure 3(a)). The plaque was largely fibrotic and the fibrous cap, if lipids were visible, always exceeded 130 µm. Minimal lumen area (MLA) was 6.1 mm2, thus only moderately (55%) obstructing the LAD. Distal to the MLA, a 3-mm-long intimal tear appeared penetrating the medial layer (Figure 3(b)–(d)). The tear was confined to the junction of the fibrous plaque with the normal arterial wall creating a thick flap. There were no thrombotic residues left. The vessel obstruction was not considered flow-limiting, and therefore, the stent implantation did not seem required. Further hospital course was uneventful and the patient was discharged on DAPT and statin.

Figure 3.

(a) Optical coherence tomographic pullback throughout the left coronary artery is shown in the longitudinal view. All the numbers are indicating a millimeter scale. Note the tip of the guiding catheter (55) and the left main (LM) bifurcation (43); left circumflex artery is hidden in this lateral view. A largely fibrotic plaque is extending from the distal LM (46) to the proximal left anterior descending artery (16). The arterial tear (green insert) appears distal to the minimal obstruction area (yellow arrow). (b) The eccentric, crescent-shaped fibrous plaque is spreading from four to nine o’clock. The junction with the three-layered normal arterial wall (white arrow) seems to be intact. (c) The same plaque with a small intimal tear at the junction. (d) The same plaque with a large tear penetrating the medial layer resulting in a ~0.5-mm-thick flap (white arrow).

Discussion

We report on the young athlete who suffered from STEMI immediately after a vigorous training. A comprehensive OCT investigation, performed after the thrombus removal, revealed the intimal tear at the junction of the fibrotic plaque with the normal arterial wall. As the remaining vessel obstruction was not flow-limiting, the medical therapy was continued without stent implantation.

An extensive analysis of the available OCT-based literature showed a convincing prevalence of plaque rupture and TCFA in STEMI patients (70.4% and 76.6%, respectively).[4] However, morphologies of rest-onset and exertion-triggered rupture seem to differ considerably. Tanaka et al.[6] detected more ruptures to occur at the junction between the culprit plaque and normal arterial wall in the exertion-triggered group (93% vs 57% in the rest-onset group, p = 0.014). Indeed, we observed the intimal tear at the junction region, although we were not able to see any vulnerable features (i.e. large necrotic core, thin fibrous cap) or related consequences (i.e. cavity formation). Alternatively, about one-quarter of thrombotic occlusions are caused by plaque erosion in which thrombus overlies the atherosclerotic plaque without cap rupture.[3] Such lesions are described to contain lesser lipid amounts, thicker fibrous caps, and less severe vessel obstructions.[7] Since the manual thrombectomy preceded the OCT imaging, intimal tear may have been caused by the aspiration catheter and the lesion may have had an intact fibrous cap initially. Finally, our culprit lesion certainly looked like a coronary dissection (Figure 3(d)). Spontaneous coronary dissection (SCD) is a rare cause of MI, with an incidence of 3%–4% according to the OCT studies.[8,9] SCD is defined as a non-traumatic and non-iatrogenic separation of the arterial wall, creating a false lumen. One of the proposed mechanisms involves also an intimal tear resulting in blood from the vessel lumen entering the intimal space. SCD has been related with various clinical situations including pregnancy, peripartum and perimenopausal periods, use of oral contraceptives, collagen disease, and heavy exercise.[8] The high prevalence of men presenting with SCD in population with higher cardiovascular risk suggests that at least in some cases, SCD might be related to the presence of latent CAD.[10] Clinical diagnosis relies on the visualization of a radiolucent intimal flap on the coronary angiography. However, OCT also discovers the double-lumen morphology and identifies the entry tear, the circumferential and longitudinal extent of the disease.[9] In our case, we were able to demonstrate the corresponding intimal tear with distinct flap and medial involvement, while the double lumen remained elusive.

The risk of plaque rupture is related to both vulnerable plaque features and extrinsic stresses. Proposed triggering mechanisms applicable to heavy exercise include increased wall stress from elevated heart rate and blood pressure, spasms in diseased vessel segments, and vigorous flexing of epicardial arteries.[11] It has been proven that circumferential stress is greatest at the junction between the fibrous cap and the normal wall.[5] Indeed, our culprit tear was located at the junction site distal to the MLA and away from the direction of the blood flow. Despite the “favorable” position and low lipid content, the vessel injury resulted in excessive thrombosis that nearly completely occluded the culprit vessel. There are three major determinants for the thrombotic response to the vessel injury: (a) character and extent of exposed thrombogenic plaque materials, (b) degree of stenosis and surface irregularities, and (c) thrombotic–thrombolytic equilibrium at the time of injury. Vigorous exercising is known not only to enhance plaque rupture but also to increase platelet reactivity and blood coagulation.[12] Furthermore, abundant thrombus formation has been frequently experienced in the acute setting of the SCD and has been located within the true as well as false lumen.[9]

According to the current guidelines, for patients with the clinical presentation of STEMI within 12 h of symptom onset, mechanical or pharmacological reperfusion should be performed as early as possible.[13] Manual thrombectomy can improve the results by dramatically reducing thrombus load, but a complete disappearance is rarely obtained, and real benefits of the technique have recently been challenged.[14] Stenting is recommended over balloon angioplasty alone.[13] Stent deployment in a thrombotic lesion may dislodge thrombus, leading to microcirculatory embolization with a no-reflow effect; furthermore, stent outcomes may be suboptimal due to malapposition.[14] A few studies have reported that stent implantation may be deferred in selected patients until adjunctive anticoagulation and antiplatelet therapy have allowed for thrombus burden meltdown. The repeat angiography was usually left to the operator’s discretion and was performed after up to 30 days.[14-16] The LAD in our case was cleared of thrombus after 12 uneventful days and we were able to fully appreciate the culprit lesion. Treatment of the SCD is mainly based on the presence of ongoing ischemia, extent of dissection, and hemodynamic status. Medical treatment does not differ from the general treatment for acute coronary syndrome. In patients with an evolving MI, any attempt to improve coronary flow is justified if technically feasible. PCI should be considered in the case of relatively localized proximal dissections with ongoing ischemia or TIMI 0–1 flow; a residual distal dissection may be left untreated provided there is no significant residual stenosis and the coronary flow is normal.[10] Finally, OCT has a fairly moderate diagnostic efficiency in identifying significant coronary stenosis. The optimal geometrical cutoff value of 1.95 mm2 has been calculated for the fractional flow reserve of 0.80.[17] As the MLA in our patient was considerably larger, we reasonably decided on optimal medical therapy without stent implantation.