Carotid artery atherosclerosis, low and high volumes of high-intensity interval training in patients after myocardial infarction: the precision of measurement embarks on a precise measurement protocol

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Aispuru-Lanche et al. published in a recent issue a study titled, “Vascular-endothelial adaptations following low and high volumes of high-intensity interval training in patients after myocardial infarction.”^ 1 ^ The authors wrote that endothelial dysfunction and oxidative stress could be attenuated by high-intensity aerobic interval exercise training (HIIT).^ 1 ^ The study aimed to evaluate “the impact of two volumes of HIIT, low (LV-HIIT, <10 min at a high intensity) and high (HV-HIIT, >10 min at a high intensity), on vascular-endothelial function in individuals after an acute myocardial infarction (AMI).”^ 1 ^ Included were 80 patients with AMI (58.4 ± 8.3 years, 82.5% men) “with three study groups: LV-HIIT (n = 28) and HV-HIIT (n = 28) with two sessions per week for 16 weeks and control group (CG, n = 24) with unsupervised physical activity recommendations.”^ 1 ^ As a surrogate marker for preclinical atherosclerosis, the carotid intima-media thickness (cIMT) was determined before and after the intervention period.^ 1 ^ The authors stated, “The assessment of cIMT enabled us to gauge the extent of atherosclerosis among the study participants. The average cIMT within the sample stood at 0.675 ± 0.183 mm, and there were no discernible differences at baseline among groups. Following a 16-week HIIT intervention, there were noteworthy yet slight alterations in carotid atherosclerosis means compared to the attention control (AC) group (ANOVA p = 0.019). Participants in the LV-HIIT program experienced a mean reduction of −3.0 ± 1.1% (p = 0.0389), while those in the HV-HIIT program exhibited a mean reduction of −3.2 ± 1.2% (p = 0.0305).”^ 1 ^ Two comments (within the predefined brevity of a letter) are fundamentally needed to evaluate the cIMT results of this study.^ 1 ^ The authors wrote, “To maintain consistency, parameters such as depth of field, gain, input power, dynamic range, monitor intensity, and other instrumentation settings were documented for replication in subsequent visits.”^ 1 ^ However, the most important documentation for the follow-up ultrasound cIMT measurements was missed by the authors, namely marking the segment where precisely the baseline cIMT measurement occurred. “The measurements were conducted on the posterior wall of both common carotid arteries, positioned between 1 and 2 cm from the carotid bifurcation, . . .,” this, by authors^ 1 ^ described method, is a highly imprecise and unreliable “marker” to delineate the measurement areal and unavoidably will lead to selecting a different areal (also within the 2 cm margin!) for the follow-up that may present with other wall characteristics. Important in the evaluation of atherosclerosis is that atherosclerosis while a systemic disease presents in an asymmetric fashion.^ 2 ^ It is important to recall, when we are using cIMT as a surrogate marker for preclinical atherosclerosis that cIMT values are expressed at the sub-millimetric range (the cut-off provided by the authors was 0.8 mm),^ 1 ^ consequently, smallest differences in cIMT values are equally sufficient to categorize subjects into different cIMT categories, from which important clinical, therapeutic or pathophysiological conclusions are deduced. The by the authors^ 1 ^ observed cIMT differences between follow-up and baseline examination can be the result of having selected a slightly different carotid artery areal for the follow-up measurement with other wall characteristics (which potentially were already present at baseline!): consequently the observed cIMT values in the follow-up examination can be totally independent of the performed intervention (here, HIIT). As the authors^ 1 ^ apparently also did not synchronize with the cardiac cycle (i.e., end-diastolic phase),^ 3 ^ they introduced a further major measurement bias, as cIMT measures unavoidably were made randomly in both cardiac phases, rendering the measures cross-sectionally and longitudinally for the same subject and between the subjects, incomparable. Mean cIMT differences between systole (vessel diameter expansion) and diastole (vessel diameter reduction) of 0.037–0.041 mm were reported.^4,5^ Considering these multiple and critical flaws in cIMT evaluation, the cIMT data and related conclusions of the Airspuru-Lanche et al. study^ 1 ^ should be considered with caution.