Targeting BP non-dippers


MEDICINE IS NOT AN EXACT SCIENCE

RAMON F. ABARQUEZ, JR., MD, EFACC, FASCC, FPCP, FPCC, CSPSH

Dr. Ramon F. Abarquez, Jr. has been one of the most prolific consultant writers of H&L and its sister publication, Vital Signs. Highly esteemed in the medical community, he is an emeritus professor of the University of the Philippines College of Medicine, and an academician of the National Academy of Science and Technology.

For comments, ramonfabarquezjr@yahoo.com.ph


Blunted sleep time, orthostatic hypotension, obstructed sleep apnea, ‘lazy legs’ during sleep, restlessness in AM upon waking up, antagonistic and impulsive related traits, positive Micral test and obesity among diabetics can suggest a non-dipper BP characteristics.

Any other non-dipper clues or consequences?

Targeting BP non-dippers 2Non-dippers linked with insulin resistance, aortic stiffness

Insulin resistance has been related to elevated blood pressure (BP) in obese children and may adversely affect the vasculature by aortic-arterial stiffening, as the initial resistance (diastolic BP) confronting cardiac output (systolic BP). The objective was to investigate whether daytime and nighttime BP were elevated and related to insulin resistance and arterial stiffness in obese children and adolescents.

Mean ± SD daytime systolic BP (SBP) (obese: 125±8.3mm Hg; control: 121±10.1mm Hg; P = 0.03) and nighttime SBP (obese: 108±10.7mm Hg; control: 102±8.2mm Hg; P = 0.0001) were higher in the obese group when compared with the control group, although BP standard variation overlapping is obvious.

No difference was found in daytime DBP, whereas nighttime DBP (obese: 60±6.6mm Hg; control: 57±4.8mm Hg; P = 0.001) and night-to-day BP ratios were higher in the obese group. Nighttime SBP was related to BMI z score (ß = 6.0; 95% confidence interval (CI) = 2.9-9.1; P = 0.0002) and waist/height ratio (ß = 36.7; 95% CI = 5.6-67.9; P = 0.02) in the obese group. HOMA index (obese: median = 3.7, interquartile range (IQR) = 2.3-6.0; control: median = 2.6, IQR = 1.8-3.4; P = 0.002) was higher, whereas cfPWV (obese: 4.8±0.8 m/s; control:5.1±0.6 m/s; P = 0.03) was lower in the obese group. CfPWV was not related to logHOMA index.

In multiple regression analyses, the higher nighttime BP in the obese group was independent of logHOMA and cfPWV. Obese children had a higher nighttime BP when compared with the control group independently of insulin resistance and arterial stiffness. No relationship was found between insulin resistance and arterial stiffness. (Hvidt, Am J Hypertens. 2014 Nov;27(11):1408-15.) Due to standard deviations from the mean were obviously overlapping, as well as mean differences < 5mmHg, clinical relevance is questionable to my appreciation.

Targeting BP non-dippers 3Non-dipper predicts ESRD?

Seventy-nine patients [mean age 57+11], 47 men, BMI 28 (4), office BP 151+25/92+14 mmHg, estimated glomerular filtration rate 28+14 ml/min per 1.73 m3] were included. The causes of renal disease were nephrosclerosis (n = 33), glomerulonephritis (n = 19), interstitial (n = 12) and others (n = 15). The average follow-up was 44 months (range 9-72 months). The primary outcome was a composite of death, from any cause, or the development of end-stage renal disease (ESRD) that require initiation of renal replacement therapy. During the follow-up period, 41 (52 percent) patients progressed to ESRD.

In addition, nine (11 percent) patients died, four before reaching ESRD. Then the combined endpoint rate, 45 patients, was 6.3/100 patients per year. In a multivariate Cox proportional hazard model, which includes age, sex, angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker status and the estimated glomerular filtration rate, office BP still provided no further prognostic information on risk of the primary outcome.

Furthermore, daytime ambulatory BP and the no-dipper status did not further discriminate in terms of predicting endpoint. Nocturnal SBP more than 130 mmHg was associated with a doubling of risk [heart rate 2.07 (95 percent confidence interval 1.01-4.25)] on top of the other significant factors. Glomerular filtration rate and nocturnal SBP values, but not nondipper pattern, were associated with risk to develop ESRD. (Redon, J Hypertens. 2010 Mar;28(3):602-7.) Nocturnal SBP > 130 mmHg with office SBP 151+25 mmHg (range 126 – 176 mmHg) can still be a non-dipper, such that the conclusion given is still questionable.

Targeting BP non-dippers 4Converting non-dipper to dipper reduces CV risk

It is known that the non dipping (ND) pattern of SBP circadian rhythm determined by ambulatory blood pressure monitoring (ABPM) is a predictor of cardiovascular (CV) events. However it is not known if changing to a dipper pattern changes the CV prognosis. Retrospective observational analysis of hypertensive outpatients who repeated ABPM during the period of 1994 until 2013. Follow-up was defined from first appointment to 31st of December 2014 or cardiovascular event (CV) (acute coronary syndrome, stroke, heart failure or arrhythmia and sudden death). 226 patients were included, 181 female (48,9 percent), mean age 56,4+/- 16,4 years.

Each patient had at least 2 ABPM in a total of 634 ABPM. During a mean follow-up of 4,7 +/-1.37 years, 28 patients (7,6 percent) had CV event and there were 16 deaths (37,5 percent CV). When comparing patients with vs. without events, patients with events were older (69,0+/-13,4 vs. 55,4 +/- 16,2 years p < 0,01), had higher 24 h SBP (136,8+/- 15,6 vs. 129,8+/- 12,4 mmHg; p 0,005) [SBP range 121.2 to 152.4mmHg] and casual DBP (82,6+/- 17,2 vs. 89,0+/-13,6 mmHg: p 0,02) but lower 24 h DBP (71,3+/- 11,0 vs. 75,5+/- 9,8 mmHg; p 0,03). Nocturnal fall of SBP was less pronounced in patients with events (5,9+/- 9,4 vs. 10,5+/- 7,5 mmHg; p 0,03) [SBP fall range -3.5 to 5.3 mmHg vs control fall range 3.0 to 18.0 mmHg]. Analyzing the SBP pattern of nocturnal fall, in 52,7 percent of ABPM the pattern remained the same.

When we selected only patients with a ND pattern in the initial ABMP, the Kaplan Meier free of events survival curves showed that, comparing those who stayed ND with those who changed to dipper (D) and to reverted dipper (RD), those who changed to D had significantly less CV events then those who remained ND and those who changed to RD (log rank 6,2 p < 0,05).

In the study, the modification from ND to D vs the persistence of ND is associated with less CV events.

These results suggest that SBP nocturnal dipping is not only a static marker of CV risk but can undergo therapeutic intervention to improve prognosis (Sousa, J Hypertens. 2015 Jun;33 Suppl 1:e6.) BP is never a constant numerical value and 47.3 percent ND can change to D status due to intervention on, not merely BP, but including co-morbidity management.