The Comorbidity of Peripheral Arterial Disease Attenuates Complications During Primary Percutaneous Coronary Intervention in ST-Elevation Myocardial Infarction
- Volume 10 - Issue 8 - August 2013
- Posted on: 7/31/13
- 0 Comments
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Alaa Mabrouk Salem Omar, MD, PhD1, Toshiro Shinke, MD, PhD1, Hiromasa Otake, MD, PhD1, Osama Rifaie, MD, FSCAI2, Mohammed Abdel-Rahman, MD2, Hazem Khorshid, MD2, Masayuki Nakagawa, MD1, Takumi Inoue, MD1, Hirotoshi Hariki, MD1, Junya Shite, MD, PhD1, Ken-ichi Hirata, MD, PhD1
ABSTRACT: Background: In animal studies, chronic skeletal muscle ischemia induces myocardial remote ischemic preconditioning (RIPC). We hypothesized that a history of peripheral arterial disease (PAD) might attenuate complications during primary percutaneous coronary intervention (PCI) in patents with acute ST-elevation myocardial infarction (STEMI). Methods: Seventy-five STEMI patients (40 with PAD and 35 without PAD) were retrospectively studied. PAD was defined as ankle brachial index <0.9, or brachial ankle pulse wave velocity >1,800 cm/s. MI size and acute complications during PCI were compared. For patients without post-stenting coronary flow worsening, the difference between post-stenting and pre-stenting fluoroscopic frame count (∆FFC) was also compared. Results: Mean age was 68±12 years and 60 patients were males. Apart from greater age and more cases with hypertension in the PAD group, basic clinical and PCI data were similar. PAD patients had lower complications during PCI (20 vs 8, P=.001), lower peak CK-total (3,590±2,657 vs 2,035±1,353 IU/L, P=.003), and lower peak CK-MB (298±192 vs 185±129 IU/L, P=.021). For the 53 patients without coronary flow worsening, PAD patients had lower ∆FFC (-2.26±8.5, SE=1.94 vs -4.28±1.19, SE=2.20 frames, P=.035). Conclusion: Our observation study suggests that PAD attenuates complications during PCI and infarct size in patients with STEMI, probably by PAD-induced RIPC.
VASCULAR DISEASE MANAGEMENT 2013:10(8):E142-E151
Key words: myocardial infarction, peripheral vascular disease, percutaneous coronary intervention, reperfusion injury
One of the concerns in the acute setting of ST-elevation myocardial infarction (STEMI) is cardiac ischemia/reperfusion injury (IRI).1 Recently, ischemic preconditioning (IPC) was shown to attenuate IRI if brief ischemic insult followed by reperfusion was introduced before the development of index myocardial ischemia.2,3 It is also found that myocardial infarction (MI) size can be reduced if a brief period of ischemia was applied to a distant organ before myocardial ischemia, an extension of IPC that was called remote ischemic preconditioning (RIPC).4 Myocardial RIPC was found to occur after ischemia in a variety of remote tissues4,5 of which skeletal muscles attracted most interest, being accessible and manipulated without great clinical risk, and myocardial RIPC was shown to decrease MI size in animal studies.6,7
Chronic skeletal muscle ischemia represents an exaggerated model of RIPC, which induces the formation of local collateral circulation.8,9 Animal studies have shown that chronic limb ischemia also induces coronary collateral circulation that was associated with smaller MI10,11 less inducible ventricular arrhythmia,12 and better coronary flow after MI.11
Peripheral arterial disease (PAD) is found in approximately 60% of patients with coronary artery disease (CAD).13 PAD increases the long-term risk among patients with CAD and predicts worse outcomes of acute coronary syndrome.14
Recent studies found that the presence of PAD, indicated by low ABI15-17 or high brachial ankle pulse wave velocity (baPWV) values,18-20 might lead to the elevation of the circulating levels of some anti-inflammatory, vasodilator, or angiogenesis-inducing substances, raising questions about whether PAD-induced chronic skeletal muscle ischemia could be a source of RIPC.
Accordingly, the purpose of our study was to test the hypothesis that patients presenting with STEMI associated with the comorbidity of PAD, suggested by abnormal ABI or baPWV values, have less complications during primary PCI.
We retrospectively reviewed our hospital database for patients who underwent primary PCI because of acute STEMI between April 2005 and December 2011. The study protocol was approved by the Institutional Review Board on Biochemichal Research at Kobe University Hospital, Kobe, Japan. Clinical, demographic, laboratory, and echocardiographic data, in addition to PCI reports and fluoroscopic runs, were reviewed from our local network server.
STEMI diagnosis was made if patients had ST elevation of 1 mm or more in 2 or more contagious leads associated with reciprocal ST-segment depression together with abnormally increasing cardiac enzymes.21 Patients were included if they had been tested for the presence of PAD by ABI and baPWV prior to STEMI-related admission or during their hospital stay.
Defining peripheral arterial disease
ABI and baPWV were measured using an automatic oscillometric device (Form PWV/ABI, BP-203RPE II, Omron Colin Co., Ltd.) as previously described.22,23 In our study, PAD was defined as ABI <0.924 or baPWV>1,800 cm/s25 on either or both limbs.
STEMI-related complications on presentation
Patients were classified to have complications on presentation if they presented with cardiopulmonary arrest (CPA), cardiogenic shock, or their occurrence before restoration of the culprit vessel flow (door-to-balloon window).