Blood pressure (BP) and heart rate (HR) undergo physiological circadian variations with daytime peaks and night-time troughs. Nondipping, the phenomenon of insufficient day-to-night decline in BP and HR, reflects sympathetic predominance persisting overnight associated with elevated cardiovascular risk. Indeed, nondipping systolic BP is considered a cardiovascular risk factor and is generally determined during ambulatory blood pressure monitoring (ABPM). Nondipping HR has also been shown to predict adverse cardiovascular disease (CVD) prognosis in the general population as well as in hypertension, type 2 diabetes and chronic kidney disease patients, and yet unfortunately it remains overlooked during ABPM.1

An impressive study by Hermida et al.2 on improving CVD risk stratification by using BP-derived parameters from 48-hour ABPM was recently published in Revista Española de Cardiología. In the study, 19 949 participants (10 478 men and 9471 women, aged 58.5±14.2 years, without prior CVD events) in the Hygia Project were assessed by 48-hour ABPM and followed up for up to 12.7 years. During the follow-up, 1854 participants experienced a primary CVD event that was defined as per the Framingham study as CVD death, myocardial infarction, coronary revascularization, heart failure, stroke, angina pectoris, or peripheral artery disease. According to the results, substituting BP-derived parameters (asleep systolic BP mean and sleep-time relative systolic BP decline) from 48-hour ABPM for office BP measurement in the Framingham risk score significantly improved calibration, diagnostic accuracy, discrimination, and performance of CVD risk stratification. This highly important study in CVD risk assessment was predominantly based on the Hygia Project, a primary care-based research network established to incorporate ABPM as a routine procedure for cardiovascular risk assessment and diagnosis and management of hypertension.

The authors indicated that they chose asleep systolic BP mean and sleep-time relative systolic BP decline, ie, systolic BP dipping, based on their previous study published in the European Heart Journal, in which these were the only BP-derived parameters from 48-hour ABPM that were jointly significant in predicting CVD risk.3 In fact, in that study, the authors also showed HR-derived parameters (asleep HR mean and sleep-time relative HR decline) from 48-hour ABPM to be associated with adverse CVD outcome. Nonetheless, the significance of HR-derived parameters from ABPM in CVD risk assessment remained unrecognized. Importantly, however, a study by Ben-Dov et al.,4 including 3957 patients (58% treated for hypertension) assessed by 24-hour ABPM with a mean 7-year follow-up, showed a 34% increase in all-cause mortality per 10% less HR decline at night. In addition, the study compared the effect of nondipping systolic BP and nondipping HR on all-cause mortality prediction. The risk of all-cause mortality was lower among patients with nondipping systolic BP alone, higher in patients with nondipping HR alone, and highest in patients with both nondipping systolic BP and nondipping HR.

Given these results, an opinion is emerging that taking HR-derived parameters (particularly sleep-time relative HR decline, ie, HR dipping), albeit not included in the original Framingham risk score, into account with BP-derived parameters from ABPM and other traditional risk factors would improve CVD risk assessment even further. Moreover, as HR is commonly determined during ABPM, no supplementary measurements are needed. Thus, HR dipping appears to be a readily accessible parameter potentially enabling fine-tuning of CVD risk management, including hypertension pharmacotherapy, at no additional financial burden.