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Left ventricular hypertrophy is a common finding during echocardiography. A precise evaluation of the left ventricular wall thickness, ventricular mass and distribution of hypertrophy is crucial both for diagnostic workup, follow-up and for prognostic evaluation. The differential diagnosis of left ventricular hypertrophy includes hypertrophic cardiomyopathies, hypertrophy secondary to abnormal left ventricular filling conditions, hypertrophy linked to intense physical training and the isolated basal septal hypertrophy of the elderly. Amongst the tools at the disposition of the cardiologist, regional analysis of longitudinal strain appears promising in helping distinguish cardiac amyloidosis form other forms of hypertrophy., Competing Interests: Les auteurs n’ont déclaré aucun conflit d’intérêts en relation avec cet article.

A 54-year-old woman was hospitalized for an acute pulmonary oedema revealing a severe aortic stenosis (AS) associated with an aortic aneurysm and a left ventricular hypertrophy (LVH). The coronary angiography found an equivocal left main lesion. Fractional flow reserve (FFR) showed hemodynamic significance (FFR=0.78) and optical coherence tomography confirmed this result with a minimal lumen area of 4.9mm 2 . FFR-guided percutaneous intervention is reported to improve outcome in patients with stable coronary disease. However, only few data are available in cases of AS. In this condition, secondary LVH is associated with microcirculatory dysfunction, which interferes with optimal hyperemia. An elevated right atrial pressure could also modify FFR measurement. This risk of underestimation of a coronary lesion in patients with severe AS has to be taken into consideration in clinical practice., (Copyright © 2016 Elsevier Masson SAS. All rights reserved.)

Heart failure with preserved ejection fraction (HF-PEF) represents half of all heart failure. Morbi-mortality for HF-PEF is similar to that of reduced ejection fraction HF (HF-REF). Diagnosis of HF-REF is difficult because of the lack of highly specific criteria. It is based on the presence of signs and symptoms of heart failure, associated with a preserved or moderately decreased left ventricular function, the absence of left ventricular dilatation, and the presence of relevant structural disease such as left ventricular hypertrophy. Despite the use of prognosis modifying drugs commonly used for HF-REF, no therapeutic strategy has been shown to reduce morbi-mortality of HF-PEF. Evidence based guidelines are limited. Management of HF-PEF therefore resides in treatment of high blood pressure and cardiac rate, that of comorbidities, and the use of diuretics in case of congestion.

The coronary microcirculatory impairment is a key feature of the pathophysiology of aortic stenosis (AS), the most operated valvular disease over the world. Several studies showed this coronary microcirculatory impairment in AS, using different tools and protocols, in various patient population of AS. This article will review the impairment of the coronary microcirculation in AS underlining its multifactorial origin, its functional part related to the hemodynamic consequences of AS, its complex relationship with left ventricular hypertrophy, and its potential diagnostic and prognostic value., (Copyright © 2014 Elsevier Masson SAS. All rights reserved.)

The association between left ventricular hypertrophy and microalbuminuria is actually admitted. Recent studies shown that patients with microalbuminuria have higher left ventricular mass index, worst systolic function and often concentric geometric kind of left ventricular hypertrophy. The efficiency of an adapted and early therapeutic on a potential relationship between reduction of microalbuminuria and improvement of target organ injury, principally heart and kidney, is still to evaluate. The aim of our study is to review geometric and hemodynamic aspect of left ventricular hypertrophy in hypertensive micro-albuminuria patients.

Specific treatment of age-related aortic wall arteriosclerosis and stiffening is lacking. As anti-inflammatory ligands for peroxisome proliferator-activated receptor-gamma have beneficial effects on the arterial wall in atherosclerosis, we investigated whether chronic pioglitazone treatment protects against another form of vascular wall disease, arteriosclerosis. In a rat model of elastocalcinotic arteriosclerosis (hypervitaminosis D and nicotine, VDN), we evaluated whether pioglitazone attenuated arteriosclerosis and its consequences, aortic wall rigidity, increased aortic pulse pressure and left ventricular hypertrophy. In VDN rats, medial calcification was associated with monocyte/macrophage infiltration and induction of TNF-alpha and IL-1B. Pioglitazone decreased TNF-alpha and IL-1B mRNA expression, blunted aortic wall calcification and prevented fragmentation of elastic fibers. Pioglitazone reduced aortic wall stiffness, aortic pulse pressure and left ventricular hypertrophy. Our results may be clinically relevant in elderly patients suffering from aortic wall stiffening and isolated systolic hypertension.

We report the case of a patient presenting with unrelenting isolated or repetitive monomorphic ventricular extra-systoles, with left block and right axis deviation, which appeared to arise from the right ventricular chamber, but for which ablation was finally performed in the left Valsalva sinus. The ECG and endocavity electro-physiological features which led us to suspect this atypical, although not exceptional, situation are reported, as well as the techniques for ablation available in this case.

Unlabelled: Left ventricular hypertrophy (LVH) is an independent risk factor in hypertensive patient., The Aim: Of our study is to evaluate prospectively the relationship between left ventricular mass and clinical, echocardiographical and ambulatory blood pressure data in hypertensive subjects., Methods: We studied 88 hypertensive patient who underwent clinical and laboratory investigation, echocardiography and 24 hours ambulatory blood pressure monitoring. Correlations were made between these data and left ventricular mass., Results: Clinical data, which correlated well with left ventricular mass, were duration of hypertension, systolic arterial pressure and pulse arterial pressure. In echocardiography left atrial area and left ventricular dysfunction correlated significatively with left ventricular mass. Data from 24 hours blood pressure monitoring as daytime systolic pressure, nighttimes diastolic pressure, ambulatory systolic pressure and ambulatory pulse pressure., Conclusion: In hypertensive patient, left ventricular mass correlated well with left atrial dilation and diastolic left ventricular dysfunction. It also correlated with 24 hours ambulatory blood pressure monitoring data.

Serum response factor (SRF) is a widely expressed transcription factor involved in the transcription of various genes linked to muscle differentiation and cellular growth. Recent studies show the pivotal role of SRF in orchestrating genetic programs essential for cardiac development and function. Dominant negative isoforms of SRF resulting from caspase cleavage or alternative splicing have been identified in different forms of cardiomyopathies. This review summarizes the role of SRF, its structure, function and its role in human cardiopathies. Finally, we discuss the results of recently developed murine models which address the role of SRF in the adult heart in vivo. The existing biological data suggest that SRF could be a target of neurohumoral activation which is involved in myocardial hypertrophy. Conversely, inhibition of SRF activity in different murine models leads to dilated cardiomyopathy.

Variations in the expression of cytokines from the interleukin-6 (IL-6) family: ciliary neurotrophic factor (CNTF), leukaemia inhibitory factor (LIF), and cardiotrophin 1 (CT-1) were studied during cardiac remodelling leading to left ventricular hypertrophy (LVH) in TGR(mRen2)27 rats at the age of 8 and 20 weeks. The cytokines mRNA levels within the free wall of the left ventricle were measured by semi-quantitative RT-PCR standardised with 18S. They were compared between heterozygous rats for the mRen2 transgene (TG+/-) and control rats (TG-/-). No significant difference was observed between results obtained at 8 and 20 weeks of age. At 20 weeks of age, TGR(mRen2)27 rats showed higher levels of mRNA LIF and IL-6 respectively by 52 and 55% compared to the control rats [LIF TG+/-: 3.17 +/- 0.21, TG-/-: 2.09 +/- 0.03; p < 0.001; n = 5; and IL-6 TG+/-: 1.53 +/- 0.13; TG-/-: 0.99 +/- 0.17; p < 0.05; n = 5]. By contrast, no variation of mRNAs levels of CT-1 and gp 130 genes was observed between control and transgenic rats. Concerning the cytokine receptors, the levels of mRNA for IL-6R did not vary while those of receptor subunits LIFR and CNTFR were decreased respectively by 48 and 42% in transgenic rats vs controls [LIFR TG+/-: 0.48 +/- 0.01; TG-/-: 0.92 +/- 0.08 p < 0.001; n = 5; and CNTFR TG+/-: 1.07 +/- 0.08; TG-/-: 1.85 +/- 0.18; p < 0.01; n = 5]. Therefore, these results show a specific pattern of activation of the cytokines pathway in the LVH of the TGR(mRen2)27 rat.

Background: The present study was designed to assess whether the angiotensin-converting enzyme (ACE) gene I/D polymorphism influence the ACE inhibitors effect on the regression of left ventricular hypertrophy., Methods: Sixty hypertensive subjects never treated by antihypertensive drugs, aged 46 +/- 11 years, were included in the study. Follow-up with ACE inhibitor treatment was 60 +/- 26 months. Genotypes for ACE I/D polymorphism (DD, ID or II) were determined by PCR. The left ventricular mass index (LVMI) was assessed by two-dimensional directed M-mode echocardiography., Results: ACE genotype distribution was in agreement with the Hardy-Weinberg equilibrium: 21 patients had the DD genotype, 29 were ID, and 10 were II. At baseline, age, systolic arterial pressure and LVMI didn't differ on the basis of genotype. Body mass index was significantly higher in II than in ID and DD groups. Regression of LVMI with ACE inhibitor treatment was similar in the 3 genotypes (-8.9%, -0.6%, -12.1% in DD, ID and II groups respectively). In addition, decrease of systolic arterial pressure was identical in 3 groups., Conclusion: ACE gene I/D polymorphism seems not to influence regression of left ventricular hypertrophy by ACE inhibitors in essential hypertension.

During chronic mechanical overload induced by hypertension, left ventricular hypertrophy predisposes to atrial and ventricular arrhythmias. Atrial arrhythmias, mainly atrial fibrillation, decrease cardiac output and increase the risk of embolism whereas ventricular arrhythmias remain the major cause of sudden death. In hypertensive patients, Holter EKG recordings frequently detect atrial or ventricular premature beats and more rarely atrial or ventricular tachycardia. In these patients, the presence of non-sustained ventricular tachycardia is considered as an independent predictor of mortality. Moreover, this non invasive method through the assessment of heart rate variability allows the study of the autonomic control of the heart, known to modulate occurrence of arrhythmias.

Left ventricular hypertrophy (LVH) entails numerous functional and molecular changes that ultimately lead to cardiac insufficiency. The renin-angiotensin system and adrenergic receptor signalling pathway have both been implicated in LVH progression and interactions between these factors may precipitate contractile dysfunction. We therefore investigated cardiac function in hypertensive rats transgenic for the human renin and angiotensinogen genes (TGR) having a genetic activation of the renin-angiotensin system, stroke-prone spontaneously hypertensive rats (SHR) and normotensive controls (CTR) aged 6 weeks. The isolated perfused heart model was used and the effect of isoproterenol (0.1-1000 nmol/L on cardiac function was studied. Cardiac protein and gene expression was studied by Western blot and RNase protection assay. TGR had 75 mmHg higher blood pressure and a 24% higher cardiac/body weight ratio than CTR; blood pressure in SHR was 17 mmHg higher without heart weight difference (p < 0.05). Basal Pmax, +dP/dt and -dP/dt were higher in TGR and SHR compared with CTR hearts. Isoproterenol stimulated these parameters by a maximum factor 6-8 in CTR and SHR but had almost no effect in TGR (p < 0.05). Basal CF per g heart weight was similar in all experimental groups. Isoproterenol produced a significantly smaller vasodilation in TGR compared with CTR or SHR. beta 1 and beta 2 receptor and Gs alpha proteins were similar in TGR, SHR and CTR. Gi alpha was increased in TGR hearts (p < 0.05). Converting enzyme and atrial natriuretic factor mRNA expression was increased (p < 0.01) while beta 1 receptor, adenylyl-cyclase V, SERCA2a and phospholamban mRNA expression was unchanged in TGR compared with CTR. Thus, LVH in TGR is characterised by early adrenergic dysfunction and beta 1 receptor signalling abnormalities indicating progressive functional deterioration. The data may serve as support for an early preventive intervention in angiotensin-II dependent cardiac hypertrophy and may have also implications for patients with genetic alterations of the renin-angiotensin system.

PRINCIPAL CARDIOVASCULAR COMPLICATIONS IN END STAGE RENAL DISEASE: Cardiovascular diseases are the leading causes of morbidity and mortality in end stage renal disease patients. Very often, complications observed are left ventricular hypertrophy and various forms of arterial degenerative lesions involving coronary arteries, less frequently pericarditis and calcifying valvulopathy are diagnosed. THE REASONS ARE COMPLEX: Risk factors can be either specific of uremia per se such as anemia, overhydration, fistula or the same as in the general population. Hemodynamic alterations including tensile stress or blood flow play a major role associated to various locally or generally generated substances whose role remains currently to be determined. THEIR TREATMENTS: Treatments of cardiovascular complications are not specific in this end stage renal disease population but are more often the treatment of the etiology: reduction of fistula blood flow, increase of hemoglobin, best control of weight gain between two hemodialysis sessions or blood pressure control.

Left ventricular hypertrophy (LVH) is a physiological process of adaptation of the heart to mechanical load increase. Despite depression of left ventricular (LV) contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in hypertensive patients with LVH. To assess the differences between patients with and without LVH, LV contractile performance, the ventriculoarterial coupling and mechanical efficiency were compared in 2 groups of hypertensive patients with similar body surface area and arterial pressures, 23 without LVH (group 1) and 30 with LVH (group 2) and compared to data of 20 normotensive subjects. Left ventricular angiography coupled with simultaneous recording of pressures with micromanometer were used to determine end-systolic stress-to-volume ratio (ESSVR), end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW) and pressure-volume area (PVA). Left ventricular contractile performance assessed by Ees/100 g myocardial mass and EESVR were lower in group 2 than in group 1 (1.23 +/- 0.28 vs 1.89 +/- 0.48 mmHg/mL/100 g and 6.22 +/- 1.07 vs 9.56 +/- 0.97 g/cm2/mL/m2, respectively, both p < 0.0001, control subjects: 1.47 +/- 0.41 and 6.97 +/- 1.22, respectively). Ventriculoarterial coupling evaluated through Ea/Ees ratio (0.51 +/- 0.05 in group 1 vs 0.53 +/- 0.08 in group 2, 0.49 +/- 0.09 in control subjects), and work efficiency evaluated through EW/PVA ratio (0.80 +/- 0.02 in group 1 vs 0.78 +/- 0.03 in group 2, 0.80 +/- 0.03 in control subjects), were similar in the 2 groups and were comparable to control subject values. In conclusion, this study shows that ventriculoarterial coupling and work efficiency are comparable in hypertensive patients with and without LVH. These results suggest that in patients without LVH the matching between left ventricle and arterial receptor is preserved through an enhancement of myocardial contractility which is energetically costly. Conversely, LVH seems to be a useful adaptation which minimizes the energetical cost of high pressure generation.

Impaired coronary reserve (CR) with angiographic coronary arteries has been demonstrated in patients with left ventricular hypertrophy (LVH) in response to valvular heart disease or hypertension. To determine if adaptive LVH induced by intensive training may alter myocardial blood flow (MBF) and CR, 8 highly trained endurance tri- athletes (29.6 +/- 4.0 yrs, with echographic LVH) were compared with 6 control subjects (33.0 +/- 7.9 yrs, with a normal echographic examination). Triathletes entered the study if they had a left ventricular mass >120 g/m2 at 2-D echocardiographic measurements (mean = 148.6 +/- 19.8 g/m2). MBF was assessed using positron emission tomography (PET) with H2O15. Subjects underwent an intravenous bolus of 17- 25 mCi of H2)15 at baseline and after intravenous infusion of 0.80 mg/kg of dipyridimole; H2O15 examination was followed by an F18-fluorodeoxyglucose (FDG) myocardial imaging. CR was determined as the ration of maximal to basal myocardial blood flow. In comparison with controls, triathletes with LVH showed normal MBF values (0.74 +/- 0.1 vs 0.8 +/- 0.2 ml/ml/min, p = 0.2), but an increased CR (3.8 +/- 0.7 vs 6.1 +/-1.9, p < 0.05). In contrast with other forms of LVH, CR is not altered in LVH due intense physical training. These results suggest that LVH due to intensive physical training is associated with an increase in coronary blood flow capacity.

Objective: This study was aimed at determining factors acting on the regression of left ventricular hypertrophy due to essential hypertension., Methods: It was a non-randomized, echocardiographic study of 60 previously untreated hypertensive subjects (20 to 75 years of age)., Results: Following a 5-year therapy, the decrease in the left ventricular mass was 14%. Normalization of blood pressure and reversal of left ventricular hypertrophy were obtained in 50% and 58% of patients, respectively. Patients of the non-responder group (non-response being defined as a less than 10% decrease in the left ventricular mass) were older and had a longer history of high blood pressure. A positive correlation was observed between age and decrease in the left ventricular mass, the latter being less marked in older patients. Antihypertensive drugs classes had no influence on reversal of left ventricular hypertrophy., Conclusion: Ageing may be a factor of resistance to the decrease in left ventricular mass with therapy. These results suggest that early screening and management of hypertension are essential.

In previous studies, we demonstrated that in ANG II-treated rats, prevention of cardiac hypertrophy (CH) by enalapril was blunted by bradykinin (BK) blockade by Hoe140. The putative role of BK was assessed by chronic exogenous BK infusion and in 46 male Sprague-Dawley rats infused with ANG II. ANG II (200 ng/kg/min) alone and associated with BK at low (BKlow, 15 ng/kg/day), mid (BKmid, 100 ng/kg/day) and high doses (BKhigh, 100 ng/kg/min) were delivered by Alzet osmotic pumps for 10 days and compared to control animals (Veh). Values of systolic arterial pressure (SAP, mmHg) in conscious rats and heart weight (HW, mg/g bw) at the end of the study are reported below. Results were submitted to ANOVA and are expressed as mean +/- SEM.

Left ventricular remodelling occurring after myocardial infarction is a complicated issue. This review aims to propose that the clinical background of cardiac remodelling, namely systolic and diastolic dysfunctions and arrhythmias is arranged around three, perhaps four, simple biological paradigms: (i) the deleterious aspects of the adaptational process to mechanical overload, (ii) fibrosis which does not belong to the adaptational process and is multifactorial, with two major etiologies, namely senescence and ischemia, (iii) cell death due to necrosis or apoptosis, the later is also multifactorial. (iv) A fourth additional parameter may be of importance, namely the phenotypic specific modifications of the cardiocytes which are directly provoked by either ischemia or certain hormones and which may modify, or even reverse the changes due to the adaptational process.

Unlabelled: Obesity and hypertension are frequently associated. The aim of our study was to assess the effects of high fat diet on weight, blood pressure and left ventricule in dogs. We studied 6 male Beagle dogs before and after 7 weeks of hypercaloric hyperlipidic diet. Echocardiography was used to measure left ventricular wall thickness, volumes, ejection fraction and mass. Results are expressed as % of variation of initial values. After 20 weeks, dogs presented abdominal obesity with increased body weight (11.9 +/- 2.3 to 15.2 +/- 2 kg; p < 0.03) associated with an increasing of systolic (196.5 +/- 14.6 to 260.1 +/- 17.5 mmHg; p < 0.03), diastolic (76.6 +/- 9 to 110.6 +/- 10.2; p < 0.004) and mean blood pressure (128.8 +/- 7 to 152.7 +/- 7.6 mmHg; p < 0.004). There were non significant changes concerning diastolic thickness of septum and posterior wall. Left ventricular volumes increased in diastole (41.1 +/- 4.5 to 48.9 +/- 10.3 cm3; p < 0.03) and systole (12.2 +/- 1.7 to 14.9 +/- 3.2 cm3; p < 0.03). So, despite any changes in wall thickness, we observed an increased of ventricular mass (67 +/- 15 to 80 +/- 24.3 g; p < 0.03). Ejection fraction remained unchanged., Conclusion: it appears that hight fat diet induces obesity and hypertension in dogs; changes in left ventricule suggest a volodependent hypertension.

Systolic blood pressure and body mass index (BMI) are the main determinants of the left ventricular mass (LVM). The mechanism of this cardiac hypertrophy in the obese individual is multifactorial and involves hemodynamic as well as metabolic factors. The association of LVM with the morphologic features of the individual are well known. The aim of this study was to assess the influence of the morphologic and metabolic features of obese women on LVM. 2D echocardiography evaluation of LVM was done in 24 normotensive, normoglycemic obese women (BMI [27.5-52.2 Kg/m2). Lean and fat body mass were determined by bio-impedancemetry, insulin sensitivity (Si) by the minimal model (Bergman), and basal metabolism by using indirect calorimetry. There was a positive correlation between LVM and BMI (r = 0.61; p = 0.001), waist to hip ratio (r = 0.45; p = 0.03), basal metabolism (r = 0.61, p = 0.001), lean (r = 0.74, p = 0.0002) and fat (r = 0.49; p = 0.01) body mass. Fasting glycemia was positively correlated with LVM (r = 0.62; p = 0.001), but not Si. LVM was also positively correlated to the triglyceride level. No relations were found with systolic or diastolic blood pressure. Multivariate regression analysis was performed to determine the relative contribution of lean body mass (the morphologic variable with the best association to LVM in univariate analysis), blood glucose, waist to hip ratio, age and triglycerides. The multiple r for the model was 0.87 (p < 0.001). Lean body mass and blood glucose were found to be the only significant and independent predictors of LVM (p = 0.001 and p = 0.03 respectively). We conclude that: 1) lean body mass is an important determinant of LVM in obese normotensive individuals. Hence, in obese women, correcting LVM for lean body mass might be more accurate than correcting it for body surface area or height. 2) There is no relationship between LVM and insulin sensitivity. The link between blood glucose and LVM needs to be studied further.

Unlabelled: It has been shown that 1) contractile performance of hypertrophied left ventricle (LV) of hypertensive patients (HP) is depressed, and 2) ventriculoarterial (VA) coupling is altered when myocardial contractile performance is reduced and when afterload is increased. To assess the relationship between contractile performance of hypertrophied LV and the VA coupling in hypertensive patients. LV angiography coupled with simultaneous recording of pressures with micromanometer were used to determine end-systolic stress/volume index ratio (ESS/ESVi), the slope of end-systolic pressure-volume relationship, i.e. end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW) and pressure-volume area (PVA). Comparison of results in 30 HP and 20 control subjects (CS) showed that LV contractile performance assessed by Ees/100 g left ventricular myocardial mass (LVM, echocardiographic determination) was depressed (HT: 4.35 +/- 1.13; CS: 5.21 +/- 1.89 mmHg/ml/100 g; p < 0.02) and was negatively correlated to the LVM (Ees = -0.026 LVM + 3.363; r = 0.581; p < 0.001), when ESS/ESVi, another estimate of LV contractile performance, was comparable in the 2 groups (6.66 +/- 1.55 g/cm2/ml/m2 in HT vs 6.72 +/- 1.36 in CS; NS) and negatively correlated with the LVM (ESS/ESVi = -0.019 LVM + 8.947; r = 0.369; p < 0.01). Ventriculoarterial coupling evaluated through Ea/Ees ratio (Ea and Ees in mmHg/ml/m2) was slightly higher in HT (0.53 +/- 0.08 vs 0.48 +/- 0.09 in CS; p < 0.05), work efficiency (EW/PVA) was similar in the 2 groups (0.78 +/- 0.04 in HP vs 0.80 +/- 0.03 in CS) and PVA, which is representative of the myocardial oxygen demand per beat, is negatively related to LVM (PVA = -0.003 MVG + 1.44; r = 0.434; p < 0.01)., Conclusions: this study shows that despite a slight depression of LV contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in HP with LV hypertrophy. Thus, it appears that LV hypertrophy might be a useful means of preservation of matching LV and arterial receptor with minimal energetical cost.

Objective: Hypertensive left ventricular hypertrophy (LVH) is associated with increased risk of arrhythmias and mortality. However, no clinical study demonstrated a significant relation between ventricular arrhythmias and mortality in systemic hypertension., Design and Methods: To evaluate the prognostic value of arrhythmogenic markers in systemic hypertension, we included between 1987 and 1993. 214 hypertensive patients, 59.1 +/- 12.8 years old, without symptomatic coronary disease, myocardial infarction, systolic dysfunction, electrolyte disturbances or antiarrhythmic therapy. At inclusion, an ECG, a 24 h Holter ECG (204 patients) with Lown classification of ventricular arrhythmias, an echocardiography (reliable in 187 patients) with left ventricular mass index and ejection fraction calculation, a SAECG (125 patients, enrolled after 1988) with ventricular late potentials (LP) were recorded. QT interval dispersion (QTd) was calculated on 12 leads standard ECG and LVH was appreciated., Results: At baseline echocardiographic LVH was recorded in 63 patients (33.7%) with normal ejection fraction (75 +/- 7.4%). Non-sustained ventricular tachycardia (Lown IVb) was found in 33 pts (16.2%) and LP in 27 patients (21.6%). After a mean follow up of 42.4 +/- 26.8 months, all-cause mortality was 11.2% (24 patients); 17 patients died of cardiac causes (7.9%); of these 9 patients (4.2%) died suddenly. In univariate analysis, age, strain pattern of LVH, advanced Lown classes and abnormal QT dispersion (> 80 ms) were significantly related to global, cardiac and sudden death (p < or = 0.01). Left ventricular mass index was closely related to cardiac mortality (p = 0.002). LP failed to predict mortality. In multivariate analysis, only Lown class IVb was an independent predictor of global and cardiac mortality, increasing the risk of global death 2.6 fold [1.2-6.0] (CI 95%) and the risk of cardiac death 3.5 fold [1.2-9.7] (CI 95%)., Conclusions: In hypertensive patients the presence of non-sustained ventricular tachycardia on 24 h Holter has a prognostic value.

The role of left ventricular hypertrophy as an independent risk factor for subsequent cardio-vascular events is well established, therefore the authors, in this brief review, describe the endocrine function of the heart and the role played by various factors, including hormones, in the development of cardiac remodeling during the course of hypertension. They then outline the present state of our knowledge concerning transmembrane signaling in the cardiomyocyte in response to an activation of specific receptors for vasoactive hormones of the renin-angiotensin II-aldosterone system.

Left ventricular hypertrophy in patients with hypertensive heart disease is associated with impaired relaxation and myocardial interstitial fibrosis leading to enhanced filling pressure, referred to as left ventricular diastolic dysfunction. Impairment of systolic function, characterized by reduced ejection fraction occurs at a later stage. Activation of the renin-angiotensin-aldosterone system contributes to progression to heart failure by at least two mechanisms: (1) increased left ventricular loading conditions due to vasoconstriction and retention of sodium; (2) direct effects on the myocardium resulting in myocyte hypertrophy and interstitial fibrosis.

Left-ventricular hypertrophy is the main cardiac consequence of systemic hypertension. Since it is an established, independent cardiovascular risk factor, its recognition is important. As the sensitivity of electrocardiography in this field is considered insufficient, echocardiography is the most widely used method for the determination of left-ventricular mass. In spite of its well-known limitations, we recommend applying the Penn convention using M-mode echo. In current practice we suggest including echocardiography in the diagnostic work-up of a hypertensive patient, provided that at least one additional cardiological argument is present-such as the suspicion of a structural or functional anomaly-since it generates not only left-ventricular mass but also a wealth of other information, particularly about the valvular as well as the systolic and diastolic left-ventricular function.

Arterial hypertension is a major risk factor for myocardial infarction and cardiovascular disease. The presence of left-ventricular hypertrophy in hypertensive patients is associated with a risk of mortality from cardiovascular disease three times greater than the risk with hypertension alone. Hypertension is also associated with an increased mortality and morbidity following myocardial revascularization. This risk is further augmented when left ventricular hypertrophy is present. Calculation of the ventricular mass by echocardiographic methods seems important, particularly in patients with hypertension and poor preoperative left-ventricular function (LVEF < or = 40%), in order to estimate operative risks. In this high-risk group the outcome of surgical revascularization can be improved by utilizing a preoperative intra-aortic balloon support.

Myocardial hypertrophy due to volume and pressure overload is common in hemodialysis patients because renal failure is usually responsible for arterial hypertension. The left ventricular filling pattern often exhibits abnormalities denoting a relaxation disorder. These abnormalities increase after hemodialysis sessions, which are sometimes followed by severe hypotension. This sequence of left ventricular hypertrophy, altered relaxation, and severe postdialysis hypotension sometimes associated with severe ventricular rhythm disorders deserves to be studied in detail. The data gathered would help to determine the prognosis in this situation, which often depends on cardiac function.

Similar to endothelial modulation of vascular tone, nitric oxide (NO) released from the coronary and endocardial endothelium may modulated LV performance with an improvement of LV diastolic distensibility. The aim of the present study was to assess a potential relationship between endothelial function and LV performance in essential hypertension. Thirty-nine normotensive subjects (NT) and 46 never treated hypertensive patients (HT) were grouped according to the renal vasodilatatory response to infusion of L-arginine (30 g within 60 min). HT patients responders to L-arginine (n = 19) were defined by an increased > or = 5% of renal plasma flow (RPF) estimated by the clearance of I-Hippuran. LV mass index and afterload-corrected fractional shortening were determined by echocardiography. Mitral peak early (E) and late (A) diastolic flow velocity were assessed by Doppler. Results of ANOVA were (means +/- SD): [table: see text] In HT patients E/A was positively correlated with %RPF (r = 0.27; p < 0.01) and negatively correlated with age (r = -0.52 p < 0.01) and systolic BP (r = -0.36 p < 0.01). In multiple regression analysis the relation between E/A and %RPF was dependent of age. This results confirm that aging and hypertension are the main determinants of the alteration of LV diastolic function. The link between these factors may be the endothelium which abnormal regulatory function secondary to aging and HT may be associated to an impairment of NO dependent LV relaxation.

Unlabelled: The purpose of this study was the assessment of the left systolic atrial function (LSAF) in 45 hypertensive subjects (HS) with left ventricular hypertrophy (LVH). (LV mass index) (LVMI) (> 134 g/m2 for men, > 110 g/m2 for women) and in 32 normal subjects (NS). The both groups were matched for age, body surface, heart rate and LV fractional shortening. Left atrial volume (LAV) was calculated by the formula: LAV = 8 A1 x A2/3 pi l in which A1 is the area of the four-chamber view, A2 is the area of the two-chamber view and L is common length in the two views. The atrial function contractility was evaluated by the following parameters: 1. LA stroke volume (LASV) = LAV - LAMV where LAV is the volume before atrial systole and LAMV is the LA minimal volume. 2. LA ejection fraction (LAEF) = LASV/LAV. 3. Atrial ejection force (AEF) = peak A/MOA in which peak A wave is the maximal late diastolic velocity and MOA is the mitral orifice area. 4. Atrial transport (AT) = A/M in which M area is under the mitral velocity curve and A-area under the late diastolic velocity curved assessed by Doppler echo. [table: see text] Thus all above parameters are significantly increased in HS. In HS, LASV is correlated to LAV (r = 0.84; p < 0.001) and to LVMI (r = 0.32; p < 0.05). LAEF is correlated to peak A (r = 0.90; p < 0.001) and LVMI (r = 0.34; p < 0.05)., Conclusions: In HS with LVH in comparison with N, the increase of the LA contractility is considered to be urged by the increase of LAV (Frank-Starling's law). These data could be explained by the less distensibility of LV chamber in relation to LVH.

Aim of the Study: To compare heart rate (HR) and blood pressure (BP) variability in hypertensives with or without left ventricular hypertrophy (LVH)., Methods: Thirty-three mild to moderate hypertensive patients, mean age 45 +/- 15 years, underwent an echocardiogram, a 24 hr ambulatory BP monitoring (ABPM), a 24 hr ECG monitoring and a continuous BP recording over 15 minutes both in supine and standing positions, by using digital plethysmography (Finapres device)., Statistical Analysis: non parametric tests., Results: [table: see text], Conclusion: LVH is associated with a reduction in the markers of sympathetic activity and a decreased baroreflex sensitivity.

Objective: To evaluate the correlation between QT interval dispersion (QTd) and ventricular arrhythmias in hypertensive patients (pts) with or without left ventricular hypertrophy (LVH). A secondary aim was to investigate correlations of QTd with other markers of arrythmogenic propensity: ventricular late potentials (LP) and heart rate variability (HRV)., Methods: We retrospectively measured the QTd on the 12 standard surface ECG leads in 230 hypertensive pts (94F, 136M; 59.6 +/- 12.7 years old). A 24 hours ECG Holter recording was performed in 218 pts and ventricular arrhythmias were appreciated using the Lown classification. Left ventricular mass was determined by echocardiography (LVM-Devereux formula) and left ventricular mass index (LVMI) were determined in 202 subjects. LP (122 pts) and HRV (55 pts) were investigated., Results: The QTd varied between 20 and 160 msec (57.8 +/- 32.7 msec). The distribution of pts classified using Lown criteria was: 29 pts (13.3%) class O; 106 pts (48.6%) class I; 8 pts (3.6%) class II; 13 pts (6%) class III; 29 pts (13.3%) class IVa; 33 pts (15.1%) class IVb; 116 pts (69.5%) had LVH determined by echocardiography. The QTd was strongly correlated with the Lown classes (p < 0.0001). The QTd was significantly broader in Lown classes III, IVa and IVb compared to classes O, I and II cumulated (p < 0.002); there was no difference concerning QTd between Lown classes III, IVa and IVb. The QTd was also correlated with the absolute number of premature ventricular depolarizations/24 hours (p = 0.02; r = 0.16). The 75 pts with an increased LVMI had significantly elevated QTd compared to pts without it (p < 0.0001). Qtd was correlated with LVMI (r = 0.37; p < 0.0001). There was no correlation between QTd and the existence of LP (which were correlated with the Lown classes; p < 0.03) and HRV parameters., Conclusion: Elevated QT interval dispersion is associated with more severe ventricular arrhythmias in hypertensive subjects with LVH. The mechanism of an increased inhomogeneity of repolarisation is probably related to the anatomic modifications induced by LVH. No significant correlation between QTd, LP and HRV was observed.

Experimental studies and molecular biological techniques have demonstrated the importance of angiotensin II in ventricular and vascular remodelling and in atherogenesis. Large scale clinical trials analysing the effects of converting enzyme inhibitors on the mortality and morbidity in post-infarction left ventricular dysfunction, have shown beneficial effects of these agents on major events of coronary artery disease. Experimental studies have shown reduction of intimal thickening and of the multiplication and migration of smooth muscle cells and of vascular fibrosis. Converting enzyme inhibitors seem to restore endothelial function by acting as donors of NO and could play a role in the stabilisation of atheromatous plaque, the prevention of platelet aggregation and on the activation of intravascular fibrinolytic systems. Large scale clinical trials (SOLVD and the prevention and treatment arms of SAVE) have also shown a 23% reduction in the risk of reinfarction and a 15% reduction in the risk of unstable angina. The results of ongoing trials in patients with coronary artery disease without cardiac failure are awaited with great impatience.

Hypertension has two major consequences on the heart: left ventricular hypertrophy and morphological and functional alterations of the coronary macro- and microvessels. These two cardiac modifications are responsible for three types of complications: myocardial ischaemia, left ventricular dysfunction and electrical instability which are involved in the pathogenesis of ventricular arrhythmias in hypertensive patients. The mechanisms of ventricular arrhythmias in hypertension, their incidence and severity, and their therapeutic and clinical implications will be discussed in this review article.

Sudden cardiac death is defined as natural death due to cardiac causes, heralded by abrupt loss of consciousness within one hour after the onset of symptoms. The mechanisms are the following: 1. ventricular fibrillation, 2. ventricular tachycardia and flutter with subsequent ventricular fibrillation, 3. torsade de pointe, 4. bradyarrhythmias and asystolic arrest. White the main risk factor is the presence of coronary artery disease, any organic or functional disease of the heart can predispose for sudden cardiac death. To evaluate the risk of sudden cardiac death noninvasive (Holter, echocardiography, exercise test and signal averaged (ECG) and often invasive (electrophysiological study) tests are necessary. The therapy is based on drugs (mainly beta blockers and amiodarone), coronary revascularization, catheter ablation techniques and the implantation of a cardioverter defibrillator; the latter appears to be the most promising approach.

The selection of a group of patients based on a high value of a clinical or biological parameter leads to the finding of a tendency to a reduction of this value when remeasured, known as "regression towards the mean". The amplitude of this phenomenon is greater when the selected subjects are far from normal values and the intra-individual variability of the parameter under consideration is very high. Measurement of left ventricular mass is very affected by this statistical phenomenon. The authors undertook a prospective study to analyse the components of variability of repeated echocardiographic measurements of left ventricular mass and to quantify the expected effect of regression towards the mean in the follow-up of patients with left ventricular hypertrophy. Twenty-five randomly chosen subjects underwent 2 echocardiographic examinations at 2 week intervals: at each visit, the patient had two recordings and each recording was measured twice by the same "blinded" operator. Variance analysis showed intra-individual variability represented 30% of total variability, comprising only 2% for the measurements and 28% for the recordings and the visits. The importance of regression towards the mean was calculated with respect to the initial value of the left ventricular mass index: for example, when the left ventricular mass index was 150 g/m2, a spontaneous regression of 18 g/m2 can be expected at the next measurement. This phenomenon should be taken into consideration in the interpretation of longitudinal echocardiographic studies.

Unlabelled: The objective is to study the relation between left ventricular (LV) effect (index of LV mass (LVMI) and index of inotropic state) and arterial compliance determined but the proximal aortic pressure waveform and by the carotid femoral pulse wave velocity., Material: 72 untreated hypertensives; systolic blood pressure (SBP) 170 +/- 18 mmHg/diastolic blood pressure (DBP); heart rate: 69 +/- 9 batt/min; age: 48 +/- 13 years; duration of hypertension 4.6 +/- 4.8 years; sex ratio 49 M/23 F., Objective: Proximal aortic pressure waveform (carotid artery) was studied by applanation tonometry. We derived the index of amplification (AI = Pmax-Pinflex)/PP, %), pulse pressure (PP), the maximum rate of rise of pressure (dpdt, mmHg.s-1). Echocardiography was used to define the index of LV mass (VLMI), end systolic volume (ESV), end systolic stress (ESS), myocardial contractile force (ESS/ESV), inotropic state (SBP/ESV). Carotid-femoral pulse wave velocity was determined by mechanogram (PWW m/s)., Results: 1. Relationship of physiological changes of AI and SDA to age, height, PP, DBP, PWV, and LVMI were observed in table I (r-Pearson cor. coefficient, * < p 0.05; **: p < 0.001). [table: see text] In stepwise regression analysis, even allowing for BP, age, and height, there was no relationship between LVMI and the index of aortic amplification (AI). 2. In the subjects with LVH (LVMI > 110 g/m2) we found a bimodal distribution of the AI which defines two groups in agreement with the Murgo Classification. [table: see text] In type B, where AI is weaker, the indices of aortic rigidity are reduced, there is an increased ESS and a paradoxal fall in LV performances., Conclusion: Analysis of proximal aortic pressure waveform don't allow to predict index of LV mass. These results suggest that in the sphere of LV aortic compiling the reduction of LV function contributes to modification of the BP waveform with diminution of dpdt and the index of amplification.

The level of arterial pressure is not the sole determinant of cardiac and vascular adaptation to hypertension. In order to identify other factors (such as preload) we categorized by echocardiography, 55 never treated hypertensive patients and 39 age and gender-matched normal subjects, according to values of relative wall thickness and left ventricular mass index. Normal left ventricular anatomy was found in 63% hypertensives, whereas among hypertensives 7% had "concentric left ventricular remodeling", 16% concentric left ventricular hypertrophy and 14% had eccentric left ventricular hypertrophy. Systolic left atrial area (LA) was obtained from the four-chamber views. Mitral peak early diastolic (E) and late diastolic (A) flow velocity was assessed by Doppler. Because clinical characteristics such age and sex differed among the 5 groups only results of ANCOVA were reported (means +/- SD). [table: see text] We conclude that eccentric left ventricular hypertrophy may be associated with a parallel increase of left atrial area. Thus the association of an increase of cardiac volume in hypertensive patients with normal diastolic function suggest that volume overload may modulate the effect of arterial pressure on cardiac morphology.

Unlabelled: Hypertensive patients complaining of chest pain often have a normal coronary angiogram despite a pathological exercise tolerance test. The aim of the present study was to establish whether the prevalence of these "false-positive" tests could be lowered by adjusting ST segment depression for exercise-induced increase in heart rate., Methods: 60 hypertensive patients, mean age 59 years, with typical or atypical chest pain, underwent both a symptom-limited exercise test and a coronary angiogram within a median period of 1 day. The ST segment depression was measured every 20 ms from the J point. A stepwise discriminant analysis was performed: a canonical variable took into account the Detrano index, the quantified rate-recovery loop index (QRL index) as well as the presence of a LV hypertrophy (Romhilt Estes Score)., Results: [table: see text], Conclusion: in hypertensive patients with chest pain, the specificity and the positive predictive value of exercise test are significantly improved by adjusting ST segment depression for heart rate both during effort and recovery and by taking into account the score of Romhilt Estes on the baseline ECG recording.

Unlabelled: The atrial emptying index (AEI) was used to access the rapid phase of diastolic filling of the left ventricle (LV) in 27 hypertensive (HTA) untreated patients and in 27 normotensive (N) subjects, matched for age, body, surface and heart rate. All the patients had left ventricular hypertrophy (LVH): LV mass index (LVmi) > 134 g/m2 for men, 110 g/m2 for women. All subjects had normal systolic function by echocardiography. We derived: LV wall thickness (h); antero-posterior radius (r); h/r ratio; LVmi; LAmi (before atrial contraction); AEI; A/E ratio., Results: [table: see text] The AEI demonstrated a negative correlation with LAvi in N (r = -0.49; p = 0.005) and in HTA (r = -0.53; p = 0.002). This index was correlated significantly to A/E (r = 0.74; p < 0.001) and to LV mi (r = -0.32; p < 0.05 only in HTA. CONCLUSION. In HTA with LVH in comparison with N, there are conjointly an increase of the A/E ratio and a reduction of the AEI which is considered to be compensated by the increase of LAvi. These data could be explained by the less distensibility of LV chamber in relation to LVH.

In almost 200 case of left ventricular hypertrophy (LVH) secondary to hypertension (HT), including 75 cases with conduction disorders, 100 cases of normal adults and 20 cases of normal children, segmental (initial horizontal vector, maximal anterior and posterior vector of the QRS) and spatial vectorial parameters were correlated to segmental echocardiographic parameters (septum, anterior and posterior wall of the left ventricle) and mass parameters (left ventricular mass index). The only significant quantitative variables in hypertensive LVH are: on electrocardiography: the AQRS and Sokolow's index: on vectocardiography: the spatial vector: its magnitude, azimuth and elevation, the maximal posterior vector: its amplitude, the maximal anterior vector: its amplitude, the maximal width of the QRS azimuth of the efferent limb of the QRS, the ventricular gradient in the horizontal, frontal and sagittal planes; on echocardiography: the left ventricular mass index, the diastolic thickness of the septum and the VMNES, the diastolic thickness of the posterior wall of the left ventricle and its percentage thickening. The only significant correlations were observed between: the maximal posterior vector of QRS and the diastolic thickness of the posterior wall of the left ventricle: 0.01 < alpha < 0.02; the spatial vector and the left ventricular mass index: 0.01 < alpha < 0.001. The presence of a conduction disorder does not modify these last two qualitative variables but alters their correlation.

The raised mean arterial pressure observed in hypertension increases the stress on the walls of large arteries by increasing the mechanical forces to which they are submitted. Cardiac and arterial wall hypertrophy seem to be adaptive mechanisms tending to reduce the stress in each musculo-elastic unit of the cardiovascular system. However, this adaptation only partially explains the development of cardiovascular hypertrophy. Cardiovascular changes are sometimes observed before the increase in blood pressure, as in normotensive children of hypertensive parents. Moreover, a dissociation has been shown between the antihypertensive effects of different antihypertensive agents. For the same reduction in mean arterial pressure, some drugs are associated with a greater regression in these changes than others. At present, it is acknowledged that other factors than mean arterial pressure may cause these changes. For example, the pulse pressure is a major factor, independent of mean arterial pressure, in developing cardiovascular hypertrophy. The activation of hormonal systems, especially the angiotensin converting enzyme system, influences cardiovascular structure. Therefore, hyperactivity of the renin-angiotensin system may stimulate the growth factor responsible for cardiac and arterial hypertrophy.

Left ventricular hypertrophy is frequent in hypertension although there is no close correlation between the level of blood pressure and the cardiac mass. The HYCAR study has shown a dissociation in the reversibility of left ventricular hypertrophy: ramipril at doses of 1.25 or 5 mg per day reduces left ventricular mass independently of its effects on the blood pressure. Nevertheless, it remains to be shown by a prospective study that the reduction of the blood pressure and the cardiac mass have additional benefits in the prevention of coronary artery disease in hypertensive subjects. In the meantime, two points resume the objectives of treatment of hypertension with respect to left ventricular hypertrophy and coronary risk. Firstly, prevention of left ventricular hypertrophy is better than its cure. Early prevention is based on accurate measurement and interpretation of the blood pressure according to international recommendations. Prevention necessitates good control of the blood pressure and it would appear to be particularly effective in patients who respond well to angiotensin converting enzyme inhibitors. Secondly, when left ventricular hypertrophy is present, it is possible to reduce the left ventricular mass: however, it remains to be seen whether this is accompanied by a normalisation of structure and function. This requires control of the blood pressure using either an angiotensin converting enzyme inhibitor in good responders to this family of drugs or another type of antihypertensive agent. In the latter case, the association of a low dose of ramipril may be envisaged when left ventricular hypertrophy persists despite good control of the blood pressure. This hypothesis requires testing with an appropriate prospective therapeutic trial.

Left ventricular hypertrophy (LVH) is an early complication of hypertension. To a certain degree, this process counteracts the parietal stress induced by high blood pressure. Genetic factors, obesity, high salt diet and different growth factors, notably angiotensin II and noradrenaline, can also predispose to hypertrophic cardiomyopathy. Left ventricular mass is increased on echocardiography in about 20% of hypertensive subjects. LVH is initially associated with a change in myocardial diastolic function and later with abnormal systolic function. It is a major risk factor, a cause of cardiac failure, reduction in coronary reserve and of ventricular arrhythmias. Treatment of hypertension is associated with regression of LVH and preservation or improvement in myocardial diastolic and systolic functions. The decrease in left ventricular mass could reduce the incidence of cardiovascular complications in hypertension.

Dietary sodium is an environmental factor capable of amplifying or limiting the consequences of hypertension on the heart. In a given population of hypertensive subjects, recent clinical trials have shown a positive relationship between sodium intake and the degree of left ventricular hypertrophy, independently of the value of blood pressure and body weight. In addition, dietary sodium could play a role in modulating the myocardial response to a decrease in blood pressure by antihypertensive therapy. The logical consequence of these observations is to try and prove the possible advantages of restricting dietary sodium in reducing the blood pressure and reversing left ventricular hypertrophy. With this in mind, the evaluation of dietary sodium excretion is certainly an element to take into account in the initial evaluation and also the follow-up of hypertensive subjects and of the effects of antihypertensive therapy.

Left ventricular hypertrophy is now recognized to be a major and independent risk factor of mortality and morbidity. Although all classes of antihypertensives are able to reduce left ventricular mass, two recent metaanalyses have shown that ACE inhibitors are the most effective. The antihypertensive efficacy of perindopril in man is accompanied with a significant improvement in the functional properties of large arteries and with a reduction of LVH. This study was designed to assess the course of left ventricular mass by echocardiography in a population of 893 hypertensive patients with moderate left ventricular hypertrophy, treated with perindopril for 3 months. A significant fall in blood pressure was observed by the 6th week. The morphological and functional echocardiographic parameters on a large population provided more valid statistical results than in a small series. The left ventricular cavity was found to undergo symmetrical remodelling, adapted to the new haemodynamic status. The reduction of the thickness of the wall was in line with the reduction of the size of the ventricular chamber, and left ventricular mass was reduced by 8% (p < 0.001). Systolic function was preserved and diastolic function was improved. In particular, the E/A ratio was increased by 8% (p < 0.001) and the duration of isometric relaxation was decreased by 11 ms (p < 0.02). This improvement of filling was confirmed by the reduction of the diameter of the left atrium by 0.2 mm (p < 0.001). This open study in 893 patients therefore confirmed that perindopril corrects LVH in hypertensive patients.