Conclusion:To potentially assess response to antiatherosclerotic therapy, measurement of total plaque volume is superior to both measurement of intima-media thickness (IMT) and total plaque area (TPA).Summary: Progression of IMT, TPA, and total plaque volume (TPV) have all been advocated as methods for risk prediction of cardiovascular events. In this study, the authors report a comparison of progression/ regression of carotid IMT, TPA, and TPV in patients attending vascular prevention clinics. The goal of the study was to determine which variable could be best used to assess response to antiatherosclerotic therapy. IMT, TPA, and TPV were measured at baseline in 349 patients attending vascular prevention clinics. To qualify for enrollment, a TPA of 40 to 600 mm 2 was required. Follow-up was for #5 years (median, 3.17 years). End points were vascular death, myocardial infarction, stroke, and transient ischemic attacks. Follow-up measurements at 1 year were available in 323 patients for IMT and TPA, and in 306 for TPV. Progression of TPV predicted stroke, death, or transient ischemic attack (TIA) (Kaplan-Meier log-rank P ¼ .001), stroke/death/myocardial infarction (MI) (P ¼ .008), and stroke/death/ TIA/MI (any cardiovascular event) (P ¼ .001). Progression of TPA weakly predicted stroke/death/TIA (P ¼ .097) but not stroke/death/MI (P ¼ .59) or any cardiovascular event (P ¼ .143). IMT also did not predict stroke/death/MI (P ¼ .13) or any cardiovascular event (P ¼ .455). With adjustment for coronary risk factors, TPV progression remained a significant predictor (P ¼ .001), but a change in TPA did not. Regression of IMT predicted events (P ¼ .004).Comment: The data suggest that TPV at the carotid bifurcation should be considered as the variable of choice to measure response to antiatherosclerotic therapy. Interestingly in this study, regression of IMT rather than progression predicted events. This may be consistent with the growing thought that IMT is more representative of hypertensive medial hypertrophy and is not truly representative of atherosclerosis (Finn AV et al, Arterioscler Thromb Vasc Biol 2010;30:177-81).

This study tested the hypothesis that normotensive black males differ from white males in their autonomic and cardiovascular responses to severe orthostatic stress. College age men (9 blacks, 9 whites) underwent graded lower body negative pressure (LBNP; 10 mmHg steps of 6 min each) to either -100 mmHg or presyncope. LBNP tolerance between the two groups did not differ (LBNP tolerance index: 378 +/- 34 vs 404 +/- 1 9mmHg.min, blacks vs whites). Responses to LBNP common to all subjects (< or = -40 mmHg), including spontaneous baroreflex sensitivity (sequence technique), did not differ between groups except whites experienced an earlier and more pronounced decline in total peripheral conductance than blacks (P < 0.01). At test termination, the heart rate variability measure of low frequency/high frequency ratio increased more in blacks than whites (5.2 +/- 1.1 vs 2.7 +/- 0.7 units; P < 0.05) while cardiac output and total peripheral conductance were lower in whites (both P < 0.05). These data suggest that blacks and whites have similar LBNP tolerances. They maintain blood pressure equally well when exposed to graded LBNP to presyncope, yet they differ in their mechanisms for doing so.

The reproducibility of heart rate variability (HRV) measures during graded lower body negative pressure (LBNP) have not been studied in sufficient detail. Active college age men (n=14) underwent an orientation exposure and two trials of graded LBNP to presyncope or -100 mmHg, separated by 1 week. Heart rate, stroke volume (impedance cardiography), blood pressure (Finapres), and forearm blood flow were assessed, as was HRV in both time and frequency domains. The trial-to-trial responses to LBNP common to all subjects (LBNP< or =-60 mmHg and at test termination) showed parallel changes, suggesting similar responses between both trials. Good reproducibility estimates were found for the resting HRV data (lowest: R=0.62 for low frequency/high frequency ratio; highest: R=0.94 for standard deviation of normal R-R intervals). During LBNP, reproducibility estimates varied but were generally similar to that seen at rest. At test termination, they were unacceptably low (R<0.41) for the HRV data assessed in the frequency domain and expressed in absolute units. LBNP tolerance was lower in the first trial [LBNP tolerance index: 404 (21) versus 437 (15) mmHg min(-1); P<0.05] but the intraclass correlation coefficient was high (R=0.87). These data suggest that (1) HRV responses to submaximal LBNP up to -60 mmHg are consistent across trials, (2) the considerable variability seen in the HRV parameters at maximal LBNP can be reduced by expressing these data in either the time domain or using normalized units in the frequency domain, and (3) cardiovascular responses to sub- and maximal LBNP are reproducible. Data are presented as mean (SEM) unless otherwise stated.

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