Atrioventricular conduction in the hypertensive patient: influence of aging, pulse pressure, and arterial stiffness.

Atrioventricular (AV) conduction time (PR interval) lengthens with age. Hypertension is often presented as an accelerated aging of the heart and arteries. The principal marker of arterial aging is an increase in arterial stiffness and pulse pressure. We were interested to find out whether parameters of blood pressure and arterial stiffness were related to the PR interval and whether they influenced its long-term progression. We examined factors linked to the PR interval at baseline in a cohort of untreated hypertensive patients including office and 24-hr blood pressure and arterial stiffness (QKD(100-60)). Long-term evolution of the PR interval and related factors were obtained during follow-up of this population. Baseline data were obtained in 1,034 untreated hypertensive patients. At baseline, four variables emerged as significantly and independently correlated with PR interval: Gender, age, weight, and heart rate. During follow-up (137 ± 78 months), 328 of these patients were re-examined. In this group, PR increased from 159 ± 20 to 167 ± 25 msec (p<0.001), a mean alteration of 8 ± 19 msec. This change was correlated with the baseline 24 hr PP (r=0.17, p=0.004) and with the duration of follow-up (r=0.13, p=0.02). In the group with baseline evaluation of arterial stiffness (n=141), QKD(100-60) was correlated with the change in PR interval (r= -0.33, p<0.0001) along with the duration of follow-up (r=0.22, p=0.005). This study shows a link between baseline increased pulse pressure or arterial stiffness with the prolongation of the PR interval with aging. Because this link was observed during follow-up, it is possible that increased arterial stiffness favors the increase in the PR interval with age.

Impact of malignant arterial hypertension on the heart.

OBJECTIVES: To assess the consequences of malignant hypertension and its evolution with antihypertensive treatment. BACKGROUND: Malignant hypertension can be considered as a model of the effects of very high blood pressure and renin-angiotensin levels on target organs. However, the consequences on the heart have been little studied. METHODS: The consequences of malignant hypertension on left-ventricular function and its evolution with treatment were assessed with echocardiography in a prospective study between January 2004 and June 2009. RESULTS: During the study period, 46 patients were referred to our unit for malignant hypertension of whom 25 could be included in the echocardiographic study. These patients showed at baseline important left-ventricular hypertrophy and alteration in systolic function. Global longitudinal strain was the most sensitive tool to assess impaired systolic function and was significantly reduced in 13 patients (<12.8, 52%). Short-term follow-up (1-3 months) showed a rapid improvement in systolic function together with significant hypertrophy regression. With a follow-up of 11 months on average all patients had recovered a normal global longitudinal strain with further but incomplete regression of hypertrophy. CONCLUSIONS: Our study highlights the significant impact of malignant hypertension on systolic function of the left ventricle, and the ability of this ventricle to quickly recover normal systolic function under antihypertensive treatment.

Long-term decline in renal function is linked to initial pulse pressure in the essential hypertensive.

OBJECTIVES: In the absence of malignant hypertension, the mechanisms for the decline in renal function in hypertensive patients are not well known. Several recent studies, essentially cross-sectional, point to a role for an increase in arterial stiffness and its corollary, the increased pulse pressure (PP), in barotrauma of the renal glomerulus. METHODS: We examined relations between the PP measured on consultation or by 24-h ambulatory blood pressure monitoring and the long-term decline in renal function in a population of essential hypertensive patients initially untreated, with normal renal function and without proteinuria. We evaluated the renal outcome of 375 patients of mean age 49 years in a baseline state over a mean follow-up period of 14 years. RESULTS: At follow up, the glomerular filtration rate estimated from the modification of diet in renal disease formula was below 60 ml/min per 1.73 m2 in 51 of these patients, two of whom required dialysis. The blood pressure parameter best correlated with subsequent renal failure, independently of other factors of risk such as age or type 2 diabetes, was the PP measured either in consultation or by ambulatory blood pressure monitoring before starting treatment. CONCLUSION: The PP either measured on consultation or by ambulatory monitoring emerged as an independent determinant of the decline in renal functions in this population, pointing to the possibility of barotrauma of the glomeruli from increased arterial stiffness.

Long-term influence of antihypertensive treatment on arterial stiffness assessed by ambulatory measurement of the QKD interval.

An increase in arterial stiffness is an important risk factor for cardiovascular events. However, there are few data on the long-term evolution of arterial stiffness in treated hypertensives. We evaluated the progression of arterial stiffness in 120 initially untreated hypertensive patients whose arterial stiffness was assessed by the ambulatory monitoring of the QKD interval measured at baseline and then more than 1 year later. The ambulatory method produced an isobaric index of arterial stiffness, the QKD(100-60). Out of these patients, 30 with white coat hypertension did not receive any treatment, and over a mean follow-up period of 5 years their QKD(100-60) was unchanged. The 90 other patients received antihypertensive treatment (average of 2.5 classes of drug) over a mean period of 6 years. In this population, the mean 24 h blood pressure (BP) was significantly reduced (-9 mm Hg for systolic BP, -6 mm Hg for diastolic BP) and the QKD(100-60) was prolonged (+3.5 ms, P<0.05). The presence of type 2 diabetes in 17 of these patients was the sole factor negatively correlated with the improvement in QKD(100-60). An initial reduction in QKD(100-60) appeared to be a factor of resistance to the BP-lowering action of the medication. Antihypertensive treatment has a long-term action on arterial stiffness. The existence of diabetes appeared to have a negative influence on this improvement. Furthermore, an increase in arterial stiffness may be a factor of resistance to the action of antihypertensive medication.

Can ambulatory blood-pressure monitoring provide reliable indices of arterial stiffness?

BACKGROUND: The use of ambulatory recordings of blood pressure (BP) was proposed to estimate arterial stiffness (AS). We compared the relative value of the ambulatory AS index (AASI), and of the slope of pulse pressure (PP) according to mean BP (MBP) obtained from 24-h ambulatory BP monitoring, to the monitoring of the arrival time of Korotkoff sounds (QKD interval) in the prediction of cardiovascular (CV) events. METHODS: Twenty-four-hour ambulatory BP and QKD monitoring were recorded at baseline, before antihypertensive treatment of hypertensive patients in our Bordeaux cohort. From these recordings, the AASI, the PP/MBP slope, and the theoretical value of the QKD for a systolic pressure of 100 mm Hg and a heart rate of 60 beats/min (QKD100-60) were calculated. The patients were then given antihypertensive treatment and followed by their family physicians, who were unaware of the QKD, AASI, and PP/MBP slope results. Regular updates on patients were obtained. The reproducibility of measurements was studied in 38 normal subjects evaluated on two occasions. RESULTS: The reproducibility of the AASI and the PP/MBP slope was less than that of BP over 24 h and of QKD100-60. The cohort comprised 469 patients. With an average follow-up of 70+/-39 months, 62 CV complications, including 13 deaths, were recorded. In the monovariate analysis, age, PP over 24 h, QKD100-60, AASI, and the PP/MBP slope were significantly related to the occurrence of complications. In the multivariate analysis, when age and PP over 24 were included in the model, only QKD100-60 remained significantly linked to CV events. CONCLUSIONS: Our data support the value of the AASI as an indirect estimate of AS and as an element in the evaluation of CV risk in hypertensive patients. However, the reproducibility of this index is less, and its predictive value for complications is poorer, than that of QKD100-60, a parameter that we believe is more closely linked to AS.

Arterial stiffness evaluated by measurement of the QKD interval is an independent predictor of cardiovascular events.

BACKGROUND: The QKD interval is the time between the QRS wave on the electrocardiogram (ECG) and the detection of the last Korotkoff sound during BP measurement. Measurement of the QKD interval during ambulatory blood pressure (BP) monitoring provides an automatic evaluation of arterial stiffness. The objective of this longitudinal study was to examine the relationship between arterial stiffness assessed by this method and the occurrence of cardiovascular complications in a cohort of initially untreated hypertensive patients. METHODS: The initially untreated hypertensive patients were included in the cohort of hypertensives recruited to our center between January 1992 and December 1999. All benefited from ambulatory measurement of the QKD interval and BP over 24 h. Most of these patients were given antihypertensive treatment and were followed up by their family physicians, who were unaware of the QKD results. Their outcome was evaluated in 2003 by inquiring of the patients themselves or of their family physicians. RESULTS: The initial population comprised 412 patients. At the end point, 33 had been lost to follow-up. We recorded 49 cardiovascular events in this population with an average follow up of 65 +/- 36 months. In a Cox model, the arterial stiffness assessed by the QKD(100-60) as a percentage of the height-predicted normal value was significantly associated with the occurrence of cardiovascular complications, independent of age and mean 24-h BP. CONCLUSIONS: This study using ambulatory measurement of the QKD interval showed that an increase in arterial stiffness was a marker of cardiovascular risk. We show for the first time that its value persists after taking account of the mean systolic pressure over 24 h.

Blood pressure surge on rising.

OBJECTIVES: Since cardiovascular complications tend to occur more often in the morning, it is tempting to link this to the surge in blood pressure (BP) on rising. Our objective was to measure BP and heart rate (HR) on rising and compare values with those recorded immediately beforehand and seek variables related to marked changes in the two parameters in a cohort of initially untreated hypertensives. METHODS: The 24-h ambulatory BP measurement along with an accurate measurement of the BP on rising (either manually or automatically from the device coupled with a position sensor) was obtained in untreated hypertensives. Left ventricular mass was measured with echocardiography at baseline. Patients were then treated and followed by their general physician and news was obtained at regular intervals. RESULTS: A total of 507 patients with adequate recordings were included. Rising led to a mean increase of 14 mmHg in systolic blood pressure (SBP) and a 13 beats per minute (bpm) increase in HR. This elevation in BP on rising in the morning differed from the alteration in BP on normal changes in position. It was associated with left ventricular hypertrophy at baseline and an increased risk of future cardiovascular complications. CONCLUSIONS: Our study confirms the surge in BP on rising in the morning. This elevation in BP is accompanied by an acceleration in cardiac rhythm with no significant correlation between the two parameters. The increase in BP on rising was linked with the overall variability in BP, but was independent of the mean BP over 24 h. It was associated with an increased risk of cardiovascular complications independently of age and average 24-h SBP.