Georgios Papaioannou

ECG detection of left ventricular hypertrophy: the simpler, the better?

Objective: ECG is commonly employed to identify left ventricular hypertrophy (LVH) and a high risk of cardiovascular events (CVE) in hypertensive patients. However, the multiplicity of the existing criteria does not simplify interpretation of the data. We compared a number of common criteria in hypertensive patients by taking as references left ventricular mass (LVM) measured by echocardiography and prediction of incident CVE. Methods: The population was a cohort of 958 hypertensive patients (mean age 48 years) recruited before any treatment and having benefited from an ECG and an echocardiography. We evaluated their outcomes at regular intervals. We examined the relationships between several ECG criteria of LVH and LVM as well the occurrence of CVE. Results: Among the various parameters tested (Sokoloff, Cornell, Cornell product) the simple measurement of the RaVL wave offered the best correlations to LVM and the best prediction of the existence of an echocardiographic LVH (receiver-operating characteristic curves). Its alterations were best correlated with the changes in LVM during the follow-up period. Moreover, this simple measurement offered the best performance for the prediction of the occurrence of CVE (123 events after a mean lapse of 12 years). Conclusion: In the interpretation of an ECG in the hypertensive patient, the single measurement of the R wave in aVL gives results at least as good as those of more complicated indices, which do not appear to contribute further to the diagnosis of LVH and the prediction of cardiovascular risk.

Prognostic value of the extent of left ventricular hypertrophy and its evolution in the hypertensive patient.

Objective: Left ventricular hypertrophy (LVH) is a marker of cardiovascular risk. However, the progression of the risk as a function of the course of the LVH has only been the subject of few studies. Methods: We report the consequences of the evolution of the left ventricular mass (LVM) in a cohort of hypertensive patients whose LVM was measured before any antihypertensive treatment. Results: We followed up for an average of 12 years, 763 hypertensives with LVM measurement by echocardiography on inclusion. In this population, 117 cardiovascular complications occurred and the initial LVM appeared to be the most powerful marker of risk. A cutoff of 51 g/m2.7 for the LVM index (LVMI) offered the best compromise of sensitivity and specificity in the prediction of complications. A second determination of LVM was carried out in 436 patients on average 5 years after inclusion. In this sub-group, 82 complications were recorded after an average interval of 13 years. The 51 g/m2.7 value of LVMI over the follow-up offered the same sensitivity (74%) and specificity (52%) in the prediction of complications. The progression of the LVM was related to the occurrence of complications independently of the basal value and other risk factors. Conclusions: We confirm LVMI as a powerful risk factor in hypertension with a cutoff of 51 g/m2.7, which offers the same sensitivity and specificity whether the LVM was determined before or during treatment. The progression of LVM, on average 5 years after the initial measurement had a prognostic value independent of the initial determination.

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.

Arterial Stiffness From Monitoring of Timing of Korotkoff Sounds Predicts the Occurrence of Cardiovascular Events Independently of Left Ventricular Mass in Hypertensive Patients

Several studies have established that the increase in arterial stiffness (AS) is a cardiovascular risk factor but to date no studies have evaluated in hypertensive patients its prognostic value in comparison with another powerful risk factor, left ventricular mass (LVM) as measured by echocardiography. We prospectively evaluated the prognostic value of AS and LVM in patients with essential hypertension. The population studied comprised 793 patients (56% men) aged 54±14 years. For 519 patients, baseline measurements were made before any antihypertensive treatment, for 274 patients, the measurement were obtained during the follow-up period under antihypertensive treatment. AS was assessed from ambulatory monitoring of blood pressure and timing of Korottkoff sounds. Left ventricular mass was measured in 523 patients. After a mean follow-up of 97 months, 122 cardiovascular events were recorded in the whole population and 74 in the group with LVM determination. AS as continuous or discontinuous variable was independently related to cardiovascular events. The existence or not of antihypertensive treatment at the time of its measurement did not affect its prognostic value. When LVM was forced in the model, AS remained significantly related to cardiovascular events. Thus, AS has an independent prognostic value in the hypertensive, whether measured before or after the administration of antihypertensive treatment. This prognostic value persists after taking LVM into account.

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.

Increased arterial stiffness is an independent predictor of atrial fibrillation in hypertensive patients.

Objective: Atrial fibrillation is the most common arrhythmia, and confers a high risk of stroke and heart failure. Hypertension and ageing are two important risk factors of incident atrial fibrillation and are both associated with increased arterial stiffness. The possible relationship between arterial stiffness and atrial fibrillation is insufficiently documented and is probably complex. We tested these relations in a cohort of hypertensive patients. Methods: The population belongs to a registry which includes patients referred before administration of antihypertensive treatment and fulfilling the following criteria: office blood pressure (BP) above 140/90 mmHg, essential hypertension, no history of cardiovascular events, type 1 diabetes or atrial fibrillation, 24-h ambulatory measurement of BP coupled with the measurement of timing of Korotkoff sounds to assess arterial stiffness [indexed theoretical value of QKD interval for a SBP of 100 mmHg, at heart rate (HR) of 60 b.p.m., indexed for height and QRS duration (QKDh)]. An echocardiographic examination was carried out at baseline in the majority of patients. Atrial fibrillation-free survival was analysed with a Cox model including sex, diabetes, smoking, hypercholesterolaemia, QKDh, average 24-h pulse pressure and mean BP, mean 24-h HR, BMI and left atrial diameter (LAD), when available. Results: We included 853 patients and recorded 67 new onsets of atrial fibrillation (mean follow-up = 102 ± 62 months). Analysis found three variables significantly and independently linked to the occurrence of atrial fibrillation: age, QKDh and 24-h average HR. When LAD was introduced (n = 480, 35 incident atrial fibrillation), three variables were linked to incident atrial fibrillation: age, QKDh and LAD. Conclusion: Arterial stiffness is a strong predictor of future atrial fibrillation in hypertensive patients, independently of age, 24-h pulse pressure and LAD.

Comments on the reproducibility of Ambulatory Arterial Stiffness Index and QKD.

Fourth, the use of different formulations of doxazosin (short-acting vs. extended-release) may explain, at least in part, the differences of the occurrence of heart failure between our study [1], ALLHAT [4], ASCOT-BPLA [2] and Barrios’ study [3]. Although the short acting form of doxazosin reduces blood pressure with a sympathetic stimulation, the extended-release form of doxazosin does not produce any significant sympathetic stimulation [6]. These differential effects on the cardiovascular autonomic system may contribute to the differential cardiac outcome among the four studies [1–4].

Determination of central blood pressure by a noninvasive method (brachial blood pressure and QKD interval): a noninvasive validation.

Objective: We validated against invasive measurements a measure of central SBP based on the QKD interval. The present objective is a comparison to the SphygmoCor device. Materials and methods: A first cohort was used to redefine an algorithm for estimating ascending aorta SBP (cSBP) with respect to SphygmoCor. This algorithm was then tested in a second cohort under static conditions and in a third cohort during a head-up tilt to study blood pressure variations. Results: The first cohort (36 patients, mean age: 46 ± 20 years, SBP: 114 ± 19 mmHg) defined the estimation algorithm as cSBP = 62.687 + 1.35 × meanBP-0.207 × heart rate−0.251 × height−0.1 × QKD (mean difference with SphygmoCor = 0 ± 7 mmHg). In the second cohort (105 patients, mean age: 51 ± 19 years, SBP: 132 ± 22 mmHg), the average difference between the two techniques was 2 ± 6 mmHg (R2 = 0.93). The dynamic cohort included 31 patients (mean age: 49 ± 23 years, SBP: 110 ± 19 mmHg) with 224 pairs of measurement. We studied the changes in central blood pressures compared with the basal state of each of the two techniques during head-up tilt. With QKD, the average cSBP was 104 ± 19 mmHg, the average variation was −13.00 mmHg ± 15 (range 7–74 mmHg). With SphygmoCor, average cSBP was 101 mmHg ± 18, the average variation was −14 mmHg ± 16 (range 2–81 mmHg). The variations in blood pressure with the two techniques were well correlated (R2 = 0.93). Conclusion: cSBP estimation based on the QKD interval is comparable in precision to the SphygmoCor. Its ability to measure cSBP variations suggests that it could be employed for ambulatory measurements over 24 h.

Investigating the association of vitamin D with blood pressure and the renin–angiotensin–aldosterone system in hypertensive subjects: a cross-sectional prospective study

The hypothesis that vitamin D (25(OH)D) insufficiency plays a role in occurring of various disease has led to a rise in requests of dosages and to an increase of health-care costs. 25(OH)D insufficiency is associated with increased risk of cardiovascular disease and hypertension in many studies. Animal studies demonstrated that 25(OH)D insufficiency activates renin angiotensin system but corresponding humans data are limited. The aim of the study was to document relationship between 25(OH)D, blood pressure, and renin angiotensin system in hypertensive subjects. In all, 248 hypertensive individuals, 46.8 years (±14), were hospitalized for an etiological assessment of hypertension in this cross-sectional study over two calendar years. 25(OH)D, plasma renin activity, and aldosterone were determined in stringent conditions and blood pressure was measure. Statistical analyses were carried out to analyze the association between 25(OH)D, blood pressure, and renin angiotensin system using linear and logistic regressions with adjustments on relevant variables. In all, 80% of the studied population had a 25(OH)D insufficiency. There were no significant association between 25(OH)D and levels of systolic or diastolic blood pressure, plasma renin activity, and aldosterone whatever the statiscal method used after adjustment. 25(OH)D is not associated with blood pressure and renin angiontensin component in hypertensive subjects. These results corroborate the interventional studies which are for a large majority negatives. A new definition of the 25(OH)D insufficiency in general population is necessary.