Association Between Haptoglobin Phenotype and Microvascular Obstruction in Patients With STEMI: A Cardiac Magnetic Resonance Study
G Pontone, D Andreini, AI Guaricci et al.

KEYWORDS
cardiac magnetic resonance; haptoglobin; microvascular obstruction; myocardial infarction

OBJECTIVES - This study aimed to evaluate the correlation between different haptoglobin (Hp) phenotypes and myocardial infarction characteristics as detected by cardiac magnetic resonance (CMR) in consecutive patients after ST-segment elevation myocardial infarction (STEMI).

BACKGROUND - Hp is a plasma protein that prevents iron-mediated oxidative tissue damage. CMR has emerged as the gold standard technique to detect left ventricular ejection fraction (LVEF), extent of scar with late gadolinium enhancement (LGE) technique, microvascular obstruction (MVO), and myocardial hemorrhage (MH) in patients with STEMI treated by primary percutaneous coronary intervention (pPCI).

METHODS - A total of 145 consecutive STEMI patients (mean age 62.2 ± 10.3 years; 78% men) were prospectively enrolled and underwent Hp phenotyping and CMR assessment within 1 week after STEMI.

RESULTS - CMR showed an area at risk (AAR) involving 26.6 ± 19.1% of left ventricular (LV) mass with a late LGE extent of 15.2 ± 13.1% of LV mass. MVO and MH occurred in 38 (26%) and 12 (8%) patients, respectively. Hp phenotypes 1-1, 2-1, 2-2 were observed in 15 (10%), 62 (43%), and 68 (47%), respectively. Multivariable analysis demonstrated that body mass index, Hp2-2, diabetes, and peak troponin I were independent predictors of MVO with Hp2-2 associated with the highest odds ratio (OR) (OR: 5.5 [95% confidence interval [CI]: 2.1 to 14.3; p < 0.001]). Hp2-2 significantly predicted both the presence (area under the curve [AUC]: 0.63 [95% CI: 0.53 to 0.72; p = 0.008]) and extent of MVO (AUC: 0.63 [95% CI: 0.54 to 0.72; p = 0.007]).

CONCLUSIONS - Hp phenotype is an independent predictor of MVO. Therefore, Hp phenotyping could be used for risk stratification and may be useful in assessing new therapies to reduce myocardial reperfusion injury in patients with STEMI.