CC-BY 4.0 · TH Open 2018; 02(02): e167-e172
DOI: 10.1055/s-0038-1645875
Original Article
Georg Thieme Verlag KG Stuttgart · New York

Risk of Thrombosis in Patients Presenting with Myocardial Infarction with Nonobstructive Coronary Arteries (MINOCA)

Sivabaskari Pasupathy
1  Discipline of Medicine, University of Adelaide, Adelaide, South Australia, Australia
2  Central Adelaide Local Health Network, Adelaide, South Australia, Australia
,
Susan Rodgers
3  Division of Hematology, SA Pathology, Adelaide, South Australia, Australia
4  School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia
,
Rosanna Tavella
1  Discipline of Medicine, University of Adelaide, Adelaide, South Australia, Australia
2  Central Adelaide Local Health Network, Adelaide, South Australia, Australia
,
Simon McRae
2  Central Adelaide Local Health Network, Adelaide, South Australia, Australia
3  Division of Hematology, SA Pathology, Adelaide, South Australia, Australia
4  School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia
,
John F. Beltrame
1  Discipline of Medicine, University of Adelaide, Adelaide, South Australia, Australia
2  Central Adelaide Local Health Network, Adelaide, South Australia, Australia
› Author Affiliations
Further Information

Publication History

02 January 2018

19 March 2018

Publication Date:
03 May 2018 (online)

Abstract

Patients presenting with myocardial infarction (MI) in the absence of obstructive coronary artery disease (CAD) is termed MI with nonobstructive coronary arteries (MINOCA). The underlying pathophysiology of MINOCA is multifactorial and in situ formation and subsequent spontaneous lysis of a coronary thrombus is often hypothesized as one of the mechanisms. The objective of this study is to determine whether MINOCA patients had a greater prothrombotic tendency in comparison to MI patients with obstructive CAD (MICAD). Prospectively, blood samples of 25 consecutive MINOCA patients (58 (interquartile range [IQR]: 48, 75) years, 48% women) and 25 age-/gender-matched MICAD patients (58 (IQR: 50, 66) years, 48% women) were obtained at 1 month after the initial presentation and overall thrombin generation potential and congenital/acquired thrombophilia states were assessed. As regard to results, overall thrombin generation parameters were similar (p > 0.05) between the MINOCA and MICAD groups, highlighting similar endogenous thrombin potential (1,590 nM/min; IQR: 1,380, 2,000 vs. 1,750 nM/min; IQR: 1,500, 2,040, respectively). There were no significant differences between MINOCA and MICAD, respectively, in respect to the numbers of patients with congenital thrombophilia states including factor V Leiden (0 vs. 4%) and prothrombin gene mutation (8 vs. 4%), decreased antithrombin (8 vs. 0%), protein C (0 vs. 0%), and protein S (4 vs. 0%). None of the patients demonstrated presence of lupus anticoagulant and anticardiolipin antibodies. Although MINOCA patients revealed thrombotic characteristics that are similar to those with MICAD, the results from this study are inconclusive and a larger study with healthy control subjects is required to assess the risk of thrombosis in MINOCA.