Globally, recent hypertension management guidelines have pointed out the importance of out-of-office blood pressure (BP), measured by home BP and 24-h ambulatory BP, for hypertension management [1]. These validated approaches are able to identify hypertension phenotypes such as white coat hypertension and masked hypertension. The prognostic value of home BP measurement (HBPM) is superior to that of office BP measurement and appears to be better than that of daytime systolic BP (SBP) and daytime diastolic BP (DBP) obtained from 24-h ambulatory BP measurement (ABPM) [2]. In addition, HBPM is more practical in clinical practice than ABPM, particularly among those who are on antihypertensive medication. Home BP monitoring consists of performing morning and evening BP measurements twice on each occasion, with a minimum of 3 days and a preferred period of 7 days [3]. Previous studies revealed that higher levels of HBPM were associated with an increased risk of cardiovascular disease (CVD), both in general and hypertensive populations [1]. Morning minus evening home BP (MEdif), calculated as the difference in the home morning BP and the evening BP, was significantly associated with a greater risk of CVD [4].

The present study by Hoshide et al. demonstrates that lower oxygen saturation (SpO2) during the nighttime was associated with higher MEdif (≥20 mm Hg), independent of cardiovascular risk factors, among the outpatient population with at least one cardiovascular risk [5]. Nocturnal hypoxia, characterized by severe oxygen desaturation, which is commonly observed in patients with obstructive sleep apnea, was associated with a hypoxia-peak SBP and nocturnal SBP surge [6] and consequently may lead to increased morning BP [7]. Sympathetic excitation may explain the association of nocturnal hypoxia with increased MEdif. Nocturnal hypoxia causes the activation of sympathetic activity through chemoreflex stimulation during apneic episodes [8]. Sympathetic activation could cause an acute transient BP elevation, and this repeated brief surge of sympathetic activity during sleep and increase in nocturnal BP may eventually occur during the daytime, leading to the elevation of morning BP. Additionally, the magnitude of BP elevation during sleep is dependent on oxygen desaturation and specific sleep stages [6]. This chemoreflex-mediated hypoxic stimulation of sympathetic activity declines progressively during the deeper stage of nonrapid eye movement [6]. Moreover, a association of nocturnal BP with morning hypertension has been observed among hypertensive patients [7]. Figure 1 shows a schematic diagram of the possible relationship between nocturnal hypoxia and MEdif.

Fig. 1
figure 1

Schematic diagram of the proposed relationship between nocturnal hypoxia and morning evening home BP difference (MEdif)

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Hoshide et al. also found that only the lowest SpO2, but not the mean SpO2 and oxygen desaturation index, was significantly associated with MEdif ≥20 mm Hg [5]. A prior study also found that the lowest SpO2 was inversely associated with the hypoxia-peak SBP, nocturnal BP surge and maximum value of BP surge [6]. Generally, morning BP is likely to be higher than evening BP in Japanese individuals. The morning hours are crucial period due to the major changes in physiological mechanisms that occur during arousal. Many of the mechanisms have a direct impact on the cardiovascular system and BP. Morning home SBP was significantly associated with the risk of stroke and coronary artery disease [9]. Hoshide et al. also previously reported that morning home SBP ≥ 135 mm Hg was associated with a higher risk of stroke than morning home SBP < 135 mm Hg [10]. From the morning and evening BP measurements, Kario et al. defined abnormal MEdif based on a cutoff value of highest quartile of morning and evening SBP differences. The group with an MEdif of ≥20 mm Hg had higher stroke incidence and CVD events compared to the group with an MEdif <20 mm Hg [4, 11]. Similar to nocturnal hypoxia, MEdif was also significantly associated with markers of subclinical CVD and cardiac damage parameters such as total cholesterol levels [12], night glucose variability [13], left ventricular hypertrophy, relative wall thickness and left ventricular diastolic dysfunction [14, 15] among hypertensive patients. Available evidence has shown that the cutoff value of 20 mm Hg is a potential threshold for clinical MEdif. However, the hypertension status and control could affect the variability of MEdif [16].

Hoshide et al. also found that the association between the lowest SpO2 during the nighttime and MEdif was unchanged even after the exclusion of those who were taking antihypertensive medication [5]. The findings further emphasized the independent association of nocturnal hypoxia and MEdif regardless of antihypertensive medication status. The Japan Morning Surge-Home Blood Pressure (J-HOP) study provides an excellent opportunity to understand the prognostic value of home BP from a nationwide population that involves a large number of participants with CVD risk factors. Moreover, the application of the validated devices and standardized HBPM schedules in this study provide strong scientific evidence for hypertension research. Identifying patients with high MEdif in the clinic and community and then planning appropriate treatment strategies might be beneficial to reduce the risk of nocturnal hypoxia. On the other hand, treating patients with sleep disorders might also improve BP prognosis. The causal relationship between nocturnal hypoxia and MEdif is still unknown. Even so, the present study demonstrated a significant association between nocturnal hypoxia and MEdif. Hence, a longitudinal study examining the association between nocturnal hypoxia and MEdif is needed to identify the cause-and-effect relationship.