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BACKGROUND Coronary vasomotor dysfunction can be diagnosed in a large proportion of patients with angina in the presence of non-obstructive coronary artery disease (ANOCA) using comprehensive protocols for coronary vasomotor function testing. Although consensus on diagnostic criteria for endotypes of coronary vasomotor dysfunction have been published, consensus on a standardised study testing protocol is lacking. AIMS In this review we provide an overview of the variations in coronary vasomotor function testing used and discuss the practical principles and pitfalls of coronary vasomotor function testing. METHODS For the purpose of this review we assessed study protocols that evaluate coronary vasomotor response as reported in the literature. We compared these protocols regarding a number of procedural aspects and chose six examples to highlight the differences and uniqueness. RESULTS Currently, numerous protocols co-exist and vary in vascular domains tested, the manner to test these domains (e.g. pre-procedural discontinuation of medication, provocative agent, solution, infusion time, and target artery) and techniques used for measurements (e.g. doppler vs thermodilution technique). CONCLUSIONS This lack of consensus on a uniform functional testing protocol hampers both a broader clinical acceptance of the concepts of coronary vasomotor dysfunction, and the widespread adoption of such testing protocols in current clinical practice. Furthermore, the endotype of coronary vasomotor dysfunction might differ between the few specialised centres that perform coronary vasomotor function testing as a result of the use of different protocols. In this review we provide an overview of the variations in coronary vasomotor function testing used and discuss the practical principles and pitfalls of coronary vasomotor function testing.

Objectives In this study the concordance between the Routine Assessment of Patient Index Data 3 (RAPID3) and the Disease Activity Score 28-joint count (DAS28) was investigated in a clinical routine outpatient setting. Patients and methods A sample of 150 adult patients with stable RA treated with biological DMARDs (bDMARDs) was asked to complete the RAPID3 (digital or on paper) just before their outpatient routine visit during which DAS28 assessment took place. The RAPID3 correlation with and the agreement in four DAS28 categories was studied using Spearman’s rank order and Cohen’s observed kappa statistics respectively. The positive (PPV) and negative (NPV) predictive values were calculated to test whether RAPID3 could make distinction in active disease (DAS28 >3.2) or not. Results A moderate correlation (ρ 0.576) and a poor kappa value of 0.13 were found in the whole study population. Patients reported a higher disease severity than was measured by DAS28. The PPV of RAPID3 for active disease by DAS28 was 0.59 (95 % CI 0.50–0.68) and the NPV was 0.91 (95 % CI 0.75–0.98) with a sensitivity and specificity of 96 and 40 % respectively. Discussion While RAPID3 correlates to some extent with DAS28 at the group level, agreement between RAPID3 and DAS28 at the individual patient level is to poor to rely on RAPID3 results in monitoring patients with RA. RAPID3 tends to over-report disease activity as assessed by DAS28.