Initial Left Ventricular Mass Research Articles

Prevalence of Left Ventricular Hypertrophy Caused by Systemic Hypertension Preceding the Development of Severe Aortic Stenosis

It is generally assumed that left ventricular (LV) hypertrophy in aortic stenosis (AS) is a compensatory adaptation to chronic outflow obstruction. The advent of transcutaneous aortic valve replacement has stimulated more focus on AS in older patients, most of whom have antecedent hypertension. Accordingly, our aim was to investigate the interaction between hypertension and AS on LV remodeling in contemporary practice. We studied consecutive patients referred for echocardiograms with initial aortic valve (AV) peak velocity <3.0 m/s and a peak velocity of >3.5 m/s on a subsequent study performed at least 5 years later. LV size and geometry were measured echocardiographically. Midwall fractional shortening (FSmw) and peak systolic stress were calculated from 2-dimensional echocardiographic and Doppler data. Of 80 patients with progressive AS, 59% were women with mean age 82 ± 9 years. The average interval between the 2 echocardiograms was 5.9 ± 1.8 years. During the study period, peak velocity increased from 2.5 ± 0.4 to 4.2 ± 0.6 m/s (p < 0.01) and LV mass indexed to body surface area increased from 80 ± 28 to 122 ± 51 g/m2 (p < 0.01) with a corresponding shift from normal or concentric LV remodeling geometry to concentric hypertrophy. There was no correlation between change in LV mass index and AV mean gradient or valvulo-arterial impedance. However, change in LV mass index did correlate positively with initial peak velocity and inversely with initial LV mass. Plots of FSmw against circumferential stress at baseline and follow-up suggest that systolic function more than compensates for increasing load in many patients. In conclusion, most patients seen in our practice with severe AS have antecedent hypertension and LV remodeling at a time when outflow obstruction is mild. LV remodeling worsens in parallel with worsening severity of AS. Remodeling in these patients features increasing concentric remodeling of the LV, rather than LV dilation. Systolic function, as assessed by FSmw, remains compensated, or even improves relative to afterload, during progression of AS. Given these findings, we speculate that regression of LV hypertrophy to normal will not be affected by transcutaneous aortic valve replacement because LV hypertrophy preceded hemodynamically severe AS.

Impact of visit-to-visit blood pressure variability on hypertensive-mediated target organ damage and future cardiovascular events: the Campania salute network.

Exaggerated variability of blood pressure (BP) poses additional stress on cardiovascular system independent of BP average value, increasing risk of target organ damage (HMOD) and cardiovascular events. We assessed the impact of visit-to-visit variability (VVV) of BP on development of cardiovascular events and HMOD. Standard deviation (SD) and coefficient of variability of mean SBP and DBP were calculated in 3555 patients from the Campania Salute Network registry, with available echocardiogram and more than six visits during follow-up. Values from the first visit were excluded. The impact of VVV of BP on cardiovascular events, and mediation of HMOD were assessed at final visit. Mean number of visits was 11 ± 6 with mean interval between visits of 9.1 ± 3.7 months. Mean visit-to-visit SD during follow-up was 13 ± 5 for systolic and 8 ± 3 mmHg for DBP; coefficients of variability were 9.7 ± 3.5 and of 9.6 ± 3.2, respectively. In multivariable analysis, left ventricular mass at follow-up was correlated with systolic VVV of BP independently of significant effect of age, BMI, mean SBP during follow-up and initial left ventricular mass. Follow-up GFR was inversely associated with systolic and diastolic VVV, independently of significant effect of age, mean glucose and SBP during follow-up, and initial GFR. In Cox regression, high VVV of BP was also associated with increased risk of cardiovascular events (hazard ratio 1.49, 95% confidence interval 1.08-2.06, P = 0.015), independently of significant effect of HMOD. VVV is associated with prevalent HMOD and development of cardiovascular events, independently of mean BP value during follow-up and HMOD.

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

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. 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. 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/m(2.7) 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/m(2.7) 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. We confirm LVMI as a powerful risk factor in hypertension with a cutoff of 51 g/m(2.7), 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.

Echocardiographic Serial Changes of Hypertensive Cardiomyopathy With Severely Reduced Ejection Fraction: Comparison With Idiopathic Dilated Cardiomyopathy

Hypertensive cardiomyopathy with reduced ejection fraction (HTCMREF) is known as an important cause of reversible cardiomyopathy, but its serial changes on echocardiography is yet to be elucidated. HTCMREF on serial echocardiography has distinctive points as compared to idiopathic dilated cardiomyopathy (idDCM). We retrospectively studied 18 hypertensive patients (mean age, 63 ± 13 years, 56% women) admitted with severe left ventricular (LV) systolic dysfunction and heart failure. We compared clinical characteristics and echocardiographic parameters at admission and follow-up between the patients with HTCMREF and 18 age-matched patients with idDCM. Left ventricular mass (LVM) and left atrial volume (LAV) were calculated by a formula using echocardiographic measurement. In HTCMREF, left ventricular ejection fraction improved to 52.3 ± 8.8% during a mean follow-up of 574 days. In HTCMREF, initial left atrial diameter was greater than in idDCM (43.6 ± 5.8 mm vs 38.9 ± 6.3, p = 0.027). At follow-up, LAV index decreased in HTCMREF (from 31.9 ± 8.3 mL/m(2) to 21.0 ± 8.9, P < 0.001), as opposed to a significant increase in idDCM (from 28.5 ± 10.9 mL/m(2) to 31.9 ± 8.3, P < 0.001). There was no significant difference in initial LVM index between the 2 groups, but only in HTCMREF did LVM index decrease significantly (151.4 ± 42.1 g/m(2) from 192.2 ± 43.7, P < 0.01) at follow-up. In HTCMREF, LV wall on M-mode was thicker than in idDCM. Hypertensive cardiomyopathy with severe LV systolic dysfunction might be characterized by eccentric left ventricular hypertrophy and enlarged left atrium in comparison with idDCM.

Initial left-ventricular mass predicts probability of uncontrolled blood pressure in arterial hypertension

Left-ventricular hypertrophy (LVH) is a marker of organ damage in hypertension and helps stratifying cardiovascular risk. Initial left-ventricular mass (LVM) is also a predictor of progression to hypertension, independently of initial blood pressure (BP) and other confounders. To evaluate whether baseline LVM can influence BP control in treated hypertension. We evaluated risk of uncontrolled BP (>140 or 90 mmHg under at least two medications), in relation to initial LVM in 4693 hypertensive outpatients (mean age 53±11 years, 43% women, 5% diabetic), without prevalent cardiovascular disease, from the Campania Salute Network. Uncontrolled BP was found in 2240 patients (48%). Participants with initial LVH were more often men, older, diabetic, had higher initial BP, fasting glucose, uric acid and triglycerides, and lower heart rate (HR), high-density lipoprotein-cholesterol and glomerular filtration rate than those without LVH (all P<0.05). Of 1440 patients with initial LVH, 803 (56%) were uncontrolled at follow-up compared to 44% without LVH (P<0.0001). In multivariate analyses, odds of uncontrolled BP increased with higher baseline systolic BP [odds ratio (OR)=1.13×5 mmHg, 95% confidence interval (CI) 1.10-1.15], HR (OR=1.04×5 beats/min, 95% CI 1.01-1.07), BMI (OR=1.03×kg/m, 95% CI 1.01-1.04), LVM index (OR=1.05×5 g/m, 95% CI 1.01-1.10) and prevalence of diabetes (OR=5.22, 95% CI 3.52-7.76; all P<0.05) independently of age, sex, metabolic parameters and number of antihypertensive meds (P>0.1). Among medication classes, only angiotensin-converting enzyme inhibitors or angiotensin receptor blockers were associated with lower risk of uncontrolled BP (OR=0.83, 95% CI 0.71-0.96; P=0.01), independently of covariates. In a population of treated hypertensive patients, initial LVM is a significant predictor of uncontrolled BP, independently of major risk factors and antihypertensive therapy.

LEFT VENTRICULAR MASS IS A PREDICTOR OF FOLLOW-UP UNCONTROLLED BLOOD PRESSURE IN HYPERTENSIVE PATIENTS: 4B.04

Background: Left ventricular (LV) hypertrophy (LVH) is considered as a target organ response to chronic arterial hypertension and is used to stratify cardiovascular (CV) risk. LV mass (LVM) is also increased in subjects developing subsequent hypertension. Whether initial LVM also influences effective therapeutic control of blood pressure (BP) is unknown. Methods: We estimated risk of suboptimal BP control in relation to baseline LVM index (LVMi) in 4693 hypertensive outpatients from the Campaniasalute Network, with at least 1 yr follow-up (mean 4 ± 3yrs) and without prevalent CV disease (age 53 ± 11 yrs, 43% women, 5% diabetic). BP was defined uncontrolled when systolic BP> = 140mmHg or/and diastolic BP>=90mmHg (or BP>=130 or/and 80 mmHg in diabetic patients) at the last available outpatient visit. Results: Poor BP control was detected in 2240 patients (48%), despite treatment with 2 or more antihypertensive drugs. Patients with uncontrolled BP were older, more often obese (28% versus 21%) and diabetic (9% versus 1.6%), with a longer duration of hypertension and higher baseline BP, heart rate, LVMi, and prevalence of LVH (36% versus 26%, all p < 0.0001), with no difference in sex distribution. Of 1440 patients with baseline LVH, 803 (or 56%) had uncontrolled BP at follow-up, compared to 44% of those without LVH (p < 0.0001). In multivariate analyses, odds of uncontrolled BP increased significantly with higher baseline systolic BP, heart rate, BMI, duration of hypertension, diabetes (all p < 0.0001) and greater baseline LVMi (OR = 1.10/10 g/m2.7, 1.04–1.20, p = 0.002) independent of age, gender and number of medications. When specific classes of medications were added to the previous model, only use of anti-Renin-Angiotensin System reduced the risk of uncontrolled BP (OR = 0.83, 0.71–0.95, p = 0.01), with no impact for other classes of drugs (diuretics, β-blockers, Ca++-channel blockers and α-blockers). Conclusions: We conclude that in a large population of treated hypertensive patients, higher baseline left ventricular mass is significantly associated with risk of uncontrolled BP independently of age, gender, body max index, diabetes and antihypertensive therapy.

A New Therapeutic Strategy for Hypertrophic Nonobstructive Cardiomyopathy in Humans A Randomized and Prospective Study With an Angiotensin II Receptor Blocker

A randomized and prospective study was designed to prove the efficacy of angiotensin II receptor blockers (ARB) in the amelioration of myocardial impairment in hypertrophic nonobstructive cardiomyopathy (HNCM). Nineteen consecutive patients with HNCM were randomly assigned to two groups and then underwent cine magnetic resonance evaluation of left ventricular mass (LVM) twice just before and after one year of observation. In the ARB group, 50 mg of losartan potassium was administered once daily during the observation period. The ratio of LVM after the observation period over that before the period was blindly compared between the two groups to estimate morphologically the ameliorative effect of ARB. In the ARB group, LVM was 203 +/- 47 cm(3) before the treatment period and 190 +/- 55 cm(3) after the period and the ratio of the final LVM over the initial LVM was 0.93 +/- 0.10. In the non-ARB group the initial and final LVM values were 177 +/- 48 cm(3) and 179 +/- 45 cm(3), and the ratio of the final LVM over the initial LVM was 1.02 +/- 0.07. The ratio of the final LVM over the initial LVM in the ARB group was significantly smaller (P = 0.03) than that in the non-ARB group. The smaller ratio in the ARB group strongly indicates that ARB ameliorated the natural course of HNCM during the one year observation period. Thus, this is the first demonstration of the therapeutic efficacy of ARB in human HNCM.

Reduced left ventricular mass after treatment of obese patients with sibutramine: an echocardiographic multicentre study

In obesity, left ventricular hypertrophy is frequently observed, especially in the presence of hypertension. Following body weight reduction, the left ventricular mass (LVM) is reduced. It is not known to which extent this occurs after treatment with sibutramine. In this multicentre trial, 195 male and female patients (18-65 years of age, body mass index 30-40 kg/m2) were treated for 12 weeks with either 15 mg/day sibutramine or placebo. They were advised to follow mildly hypocaloric reducing diets. Exclusion criteria were blood pressure values >180/110 mmHg and tachycardia (heart rate > or =100 beats/min). Echocardiography in M-mode was performed to determine LVM as well as systolic function. Body weight was reduced by 6.9 +/- 0.3 kg under sibutramine and by 2.1 +/- 0.6 kg under placebo; body fat was reduced by 5.2 +/- 0.4 kg and 1.6 +/- 0.7 kg respectively. In the sibutramine group, LVM was reduced by 10.9 +/- 24.2 g; LVM indexed for body surface area was reduced by 2.3 +/- 11.8 g/m2 and LVM indexed for body height was reduced by 2.5 +/- 6.0 g/m(2.7). In the placebo group, LVM and LVM indices were not significantly changed. Changes in LVM correlated with reductions in body weight and initial LVM but not with changes in blood pressure or heart rate. After 3 months of treatment with sibutramine, obese patients lost about three times as much of body weight and LVM than patients treated with placebo. Therefore, sibutramine may be recommended not only to reduce body weight but also to obtain a regression of the LVM in obese patients with and without hypertension.

Prediction of left ventricular mass in youth with family histories of essential hypertension.

To determine predictors of left ventricular mass (LVM) and hypertrophy (LVH), 56 black and 30 white normotensive healthy youths (mean age 12.6 +/- 2.3 years at initial visit) were studied twice, 2.5 years apart. During the initial visit, anthropometric variables and hemodynamics were measured at rest and before, during, and after 4 physical and behavioral stressors. 2-D directed M-mode echocardiography was performed to derive LVM. Hierarchical multiple regression analyses indicated that follow-up LVM was predicted by initial LVM, weight, height (ht), and gender (males > females; total model R2 = 0.77, P < 0.0001). Predictors of LVM/ht2.7 were initial LVM/ht2.7, weight, ethnicity (blacks > whites), and the aggregate index of blood pressure reactivity (total model R2 = 0.66, P < 0.0001). Youth with LVH at follow-up were taller, heavier, and exhibited greater blood pressure reactivity at initial evaluation. These findings are important since interventional strategies can be developed that target obesity and exaggerated reactivity to stress.

Effect of donor-recipient size mismatch on left ventricular remodeling after pediatric orthotopic heart transplantation

Left ventricular (LV) hypertrophy has been reported after orthotopic heart transplantation. This study was designed to determine the pattern of LV remodeling in the first year after pediatric orthotopic heart transplantation and to elucidate the mechanism responsible for changes in LV dimensions. Serial echocardiograms of 20 children who underwent cardiac transplantation were analyzed off-line, and the following LV parameters were measured and indexed to body surface area (BSA): short-axis diameters, posterior wall thickness, length, mass, and volume in systole and diastole. Mass/ volume and short-axis diameter/length ratios and ejection fraction were calculated. In 5 patients, the donor's echocardiogram was also available for analysis. The patient's systemic blood pressure at the time of the echocardiogram, ischemic time of the donor heart, number of rejection episodes, biopsy scores, and body size of the donor and patient were recorded. Patients were assigned to 2 groups based on their donor-recipient weight ratio: group 1, ≤1.2 (n = 9); and group 2, >1.2 (n = 11). In group 1, LV mass index remained within normal limits throughout the study period. In group 2, mass index was significantly increased 2 weeks after transplantation (72 ± 24 vs 133 ± 37 g/BSA 1.5, p = 0.0008). LV volume, geometry, ejection fraction, systemic blood pressure, and number of rejection episodes did not differ significantly between groups. The excess LV mass index in group 2 regressed significantly during the first year after transplantation from 133 ± 37 to 93 ± 17 g/BSA 1.5 (p < 0.005). Similarly, LV mass/volume ratio decreased from 2.4 ± 0.9 to 1.5 ± 0.4 (p < 0.02). The degree of initial LV hypertrophy in group 2 correlated with the degree of donor-recipient size mismatch (r = 0.86, p < 0.0001). This correlation persisted at 6 months after transplantation (r = 0.72, p = 0.0015), but was not present at 12 months. The initial LV mass in group 2 was significantly smaller when indexed to the donor's BSA (Z score = 2.0 ± 1.8 SD) than when indexed to the recipient's BSA (Z score = 6.9 ± 3.3 SD, p = 0.0008). There was no significant difference between LV mass measured in the donor before transplantation and the mass measured in the recipient 2 weeks after transplantation. These results indicate that increased LV mass found immediately after transplantation can largely be accounted for by donor-recipient size mismatch. In patients with LV hypertrophy, the left ventricle remodels during the first year after transplantation, with regression of excess mass and a decrease in mass/volume ratio toward the normal range.

Predictors of blood pressure and left ventricular mass in the young: the Hypertension in Pregnancy Offspring Study.

The present study evaluates potential predictors for the future blood pressure and left ventricular mass in children. Fifty-two children were studied at mean age 12.6 +/- 1.5 years and reexamined after 5.6 years. Thirty-six children were born to mothers who had hypertension during pregnancy and 16 children were born after normotensive pregnancies by mothers who remained normotensive at follow-up. Blood pressure was measured at rest and during physical exercise. Left ventricular mass was calculated from M-mode echocardiography, and erythrocyte sodium and potassium concentrations were determined. A stepwise multiple linear regression analysis was used to predict subsequent blood pressure and left ventricular mass. Final systolic blood pressure was best explained by initial systolic blood pressure, erythrocyte potassium concentration, gender, and erythrocyte sodium concentration. Final diastolic blood pressure was best explained by erythrocyte potassium concentration. Gender and initial left ventricular mass were predictors of left ventricular mass at follow-up. This prospective study corroborates previous findings that blood pressure measured in children predicts their future blood pressure. Furthermore, an independent inverse relationship between childhood erythrocyte potassium concentration and adolescent blood pressure is demonstrated. Male gender and an early increased left ventricular mass are independent predictors of an increased left ventricular mass in adolescents.

Left ventricular mass and exercise responses predict future blood pressure. The Muscatine Study.

Increased blood pressure and left ventricular mass are associated with increased morbidity and mortality in adults with coronary heart disease. To define the predictors of subsequent childhood blood pressure and left ventricular mass, serial echocardiograms and blood pressure responses during exercise were studied in 274 children aged 6 to 15 years, whose systolic blood pressures were in the high, middle, or low range. Persistence of rank order for left ventricular mass and blood pressure, at rest and during exercise, was maintained over a mean follow-up period of 3.4 years, with correlations ranging from 0.33 to 0.44. Subsequent systolic blood pressure was best predicted from initial resting and maximal exercise systolic blood pressures and left ventricular mass. Subsequent left ventricular mass was best predicted from initial left ventricular mass and maximal exercise diastolic blood pressure, but resting systolic blood pressure did not add to this latter prediction. Since left ventricular mass relates best to exercise blood pressure and not to resting blood pressure, left ventricular mass may provide an integrated view of the effects of blood pressure both at rest and during stress. We speculate that increased left ventricular mass in childhood may be an important predictor of subsequent hypertension and its consequences.