Nocturnal BP control reduces CVD risk

Optimal control of nocturnal and early morning hypertension can prevent cardiovascular diseases (CVD), says a Japanese expert.

The importance of nocturnal hypertension should not be taken for granted, said Professor Yutaka Imai, of the Tohoku University Graduate School of Pharmaceutical Sciences and Medicine in Sendai.

A study on the risk of differential CVD in different time zones showed elevated morning/daytime blood pressure (BP) conferred the lowest risk of hemorrhage, whilst nocturnal hypertension increased the risk of cerebral infarction and ischemic heart disease. [Lancet 2007;370:1219-29; Hypertension 2005; 23:1653-60] Another 24-hour study showed that an increase of only 1 mmHg after awakening led to an 8 percent decrease in CV mortality. [JAMA 1999;282:539-46]

BP can have infantile and random or periodic variations. The Ohasama study showed that patients with non-dipper or riser BP patterns had an increased risk of CV mortality compared with those with extreme dipper BP patterns. [Jpn J Clin Med 2004;62 Suppl 3:18-21] The study suggests that the cause of masked hypertension may be attributed to insufficient duration of antihypertensive medications, especially in the early morning, or abnormal circadian BP variation with non-dipper or riser patterns. [J Am Coll Cardiol 2004;34:255-63; Am J Hypertens 1997;10:409-18]

Dr. Genjiro Kimura, of Nagoya City University, Japan, went on to say that sodium-sensitive hypertensive patients on low- or high-sodium diets had non-dipper BP patterns from day to night. However, when sodium retention was reduced through natriuresis and intake was restricted at night, BP patterns normalized to dipper BP patterns. The study suggests that restriction of sodium intake can normalize the circadian BP rhythm. [Circulation 1997;96:1859-62]

Non-dipper BP pattern, microalbuminuria, glomerular hypertension, nocturnal hypertension and sodium sensitivity are all major risk factors for CV events. Sodium sensitivity and non-dipper patterns appear to cause stroke, but not coronary heart disease (CHD), said Kimura at the recent 7th Asian Pacific Congress of Hypertension.

A study showed that patients with chronic kidney disease (CKD) had decreased glomerular filtration rate (GFR), and higher CV events and total mortality. [N Engl J Med 2004;351:1296-1305] Other studies have shown an inverse relationship between GFR and night/day BP ratio. [Kidney Int 2004;65:621-25; Hypertens Res 2005;28:301-06]

Most patients with sodium-sensitive hypertension have non-dipper BP patterns and impaired renal capacity to excrete sodium, said Kimura. Hence, nocturnal hypertension promotes natriuresis to increase sodium excretion.

According to Professor Trefor Morgan, of Melbourne University, Australia, high BP during the day, a rapid fall when sleeping and a sudden rise when awakening is probably caused by an interaction between the CV sympathetic nervous system and renin-angiotensin system.

Daytime BP is controlled by the sympathetic nervous system and sleep BP is predominantly controlled by the renin-angiotensin system. The intake of sodium at night is thought to interact with the renin-angiotensin system that converts dippers to non-dipper BP patterns. In the early morning, the remaining activity of the renin-angiotensin system, combined with an active CV sympathetic nervous system, causes a sudden surge of BP.

More attention should be paid to sleep BP since it can cause target-organ damage and is more predictive of ischemic events than day BP even in normotensive patients. Although there is a close correlation between day, night and sleep BP, it is important to control absolute BP with medications that can reduce sleep and 24-hour BP effectively. Sleep BP can be better reduced by ACE inhibitors and angiotensin-receptor blockers (ARBs) than with other classes of antihypertensive drugs, concluded Morgan.

[JAMA 1999;282:539-46]