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Peripheral artery disease (PAD) is estimated to affect approximately 8.5 million individuals in the US above the age of 40, and is associated with significant morbidity, mortality, and impairment. Despite the significant adverse limb and cardiovascular (CV) outcomes seen in patients with PAD, there is typically less attention paid to risk factor modification relative to other atherosclerotic diseases such as coronary artery disease (CAD) or stroke. In the current literature, statins have been shown to reduce mortality, major adverse CV events, major adverse limb events, and improve symptomatic outcomes in patients with PAD. In addition, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are emerging as an additional lipid-lowering therapy for patients with PAD. However, despite current guideline recommendations based on growing evidence, PAD patients are consistently undertreated with lipid-lowering therapies. We provide an extensive literature review and evidence-based recommendations for the use of statins and PCSK9 inhibitors in patients with PAD.

Aims  Spontaneous coronary artery dissection (SCAD) diagnosis is challenging as angiographic findings are often subtle and differ from coronary atherosclerosis. Herein, we describe characteristics of patients with acute myocardial infarction (MI) caused by first septal perforator (S1) SCAD. Methods and results  Patients were gathered from SCAD registries at Minneapolis Heart Institute and Vancouver General Hospital. First septal perforator SCAD prevalence was 11 of 1490 (0.7%). Among 11 patients, age range was 38–64 years, 9 (82%) were female. Each presented with acute chest pain, troponin elevation, and non-ST-elevation MI diagnosis. Initial electrocardiogram demonstrated ischaemia in 5 (45%); septal wall motion abnormality was present in 4 (36%). Angiographic type 2 SCAD was present in 7 (64%) patients with S1 TIMI 3 flow in 7 (64%) and TIMI 0 flow in 2 (18%). Initial angiographic interpretation failed to recognize S1-SCAD in 6 (55%) patients (no culprit, n = 5, septal embolism, n = 1). First septal perforator SCAD diagnosis was established by review of initial coronary angiogram consequent to cardiovascular magnetic resonance (CMR) demonstrating focal septal late gadolinium enhancement with corresponding oedema (n = 3), occurrence of subsequent SCAD event (n = 2), or second angiogram showing healed S1-SCAD (n = 1). Patients were treated conservatively, each with ejection fraction >50%. Conclusion  First septal perforator SCAD events may be overlooked at initial angiography and mis-diagnosed as ‘no culprit’ MI. First septal perforator SCAD prevalence is likely greater than reported herein and dependent on local expertise and availability of CMR imaging. Spontaneous coronary artery dissection events may occur in intra-myocardial coronary arteries, approaching the resolution limits of invasive coronary angiography.

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