Persistent Iron Within the Infarct Core After ST-Segment Elevation Myocardial Infarction

Abstract

ObjectivesThis study sought to determine the incidence and prognostic significance of persistent iron in patients post–ST-segment elevation myocardial infarction (STEMI).BackgroundThe clinical significance of persistent iron within the infarct core after STEMI complicated by acute myocardial hemorrhage is poorly understood.MethodsPatients who sustained an acute STEMI were enrolled in a cohort study (BHF MR-MI [Detection and Significance of Heart Injury in ST Elevation Myocardial Infarction]). Cardiac magnetic resonance imaging including T2* (observed time constant for the decay of transverse magnetization seen with gradient-echo sequences) mapping was performed at 2 days and 6 months post-STEMI. Myocardial hemorrhage or iron was defined as a hypointense infarct core with T2* signal <20 ms.ResultsA total of 203 patients (age 57 ± 11 years, n = 158 [78%] male) had evaluable T2* maps at 2 days and 6 months post-STEMI; 74 (36%) patients had myocardial hemorrhage at baseline, and 44 (59%) of these patients had persistent iron at 6 months. Clinical associates of persistent iron included heart rate (p = 0.009), the absence of a history of hypertension (p = 0.017), and infarct size (p = 0.028). The presence of persistent iron was associated with worsening left ventricular (LV) end-diastolic volume (regression coefficient: 21.10; 95% confidence interval [CI]: 10.92 to 31.27; p < 0.001) and worsening LV ejection fraction (regression coefficient: −6.47; 95% CI: −9.22 to −3.72; p < 0.001). Persistent iron was associated with the subsequent occurrence of all-cause death or heart failure (hazard ratio: 3.91; 95% CI: 1.37 to 11.14; p = 0.011) and major adverse cardiac events (hazard ratio: 3.24; 95% CI: 1.09 to 9.64; p = 0.035) (median follow-up duration 1,457 days [range 233 to 1,734 days]).ConclusionsPersistent iron at 6 months post-STEMI is associated with worse LV and longer-term health outcomes. (Detection and Significance of Heart Injury in ST Elevation Myocardial Infarction [BHF MR-MI]; NCT02072850)

Keeping heart homeostasis in check through the balance of iron metabolism

“…This might occur because of the fact that more severe MI and more severe ischaemia might lead to more cardiac dysfunction because of higher iron load and cellular oxidative stress. This is in line with studies which have revealed that persistent iron deposition in infarcted hearts is detrimental to cardiac function and is related to adverse outcomes …”

“…Preserving fine iron protein balance seems to protect the heart during MI. In addition, higher myocardial iron content is associated with lower EF and larger area of infarctions, while persistence of high iron content predicts the occurrence of HF . All these data have created the rationale for using chelation therapy in MI to prevent cardiac damage.…”

Cardiovascular Magnetic Resonance in Acute ST-Segment–Elevation Myocardial Infarction

“…15 Carberry and colleagues 57 have recently confirmed these findings in a cohort of 203 STEMI patients. They showed that 36% of their cohort had intramyocardial hemorrhage by T2*-mapping and 59% of those had residual myocardial iron at 6 months.…”

“…Residual myocardial iron was associated with adverse LV remodeling at 6 months and worse clinical outcomes after a median follow-up of 4 years. 57 Figure 4a shows an example of a patient with an acute inferior STEMI treated by PPCI, and with late microvascular obstruction and intramyocardial hemorrhage despite restoring normal flow in the epicardial coronary artery during PPCI. At follow-up, there was residual myocardial iron and persistently elevated T2 values in the areas surrounding the residual iron, which may represent persistent myocardial inflammation.…”

“…Their approach would be ideal to identify high-risk patients but the CMR indices and cut-off values included in each study differed and further validation work is required to build on their findings. Furthermore, CMR could identify those with intramyocardial hemorrhage, and they could be targeted with anti-inflammatory agents or chelation therapy 15, 98 , to minimize the cardiotoxic effects of the residual iron (which has been shown to occur in two-third of patients with intramyocardial hemorrhage from a pooled analysis of 4 studies) 57 during the convalescent phase of an acute STEMI and this warrants further investigation.…”