Increased Left Ventricular Wall Thickness Research Articles

Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: Part II: the aging heart in health: links to heart disease.

The preceding article in this series1 reviewed evidence as to why age-associated changes in the central arterial system are risky with respect to vascular disease. In a similar vane, the focus of this article is on the potential link between age-associated changes in the heart and clinical cardiac disease outcomes. Left ventricular hypertrophy, heart failure, and atrial fibrillation increase dramatically with age (Figure 1). The prevalence of left ventricular hypertrophy (LVH) also increases with rising blood pressure and body mass index, a measure of obesity.2–4 Whether identified by electrocardiography or echocardiography, left ventricular hypertrophy has been shown to be associated with increased risk for coronary heart disease, sudden death, stroke, and overall cardiovascular disease.4,5 Figure 1. A, Prevalence of echocardiographic left ventricular hypertrophy (LVH) in women according to baseline age and systolic blood pressure. B, Prevalence of echocardiographic LVH in men according to baseline age and systolic blood pressure. Both A and B are reprinted from Levy D, Anderson KM, Savage DD, et al. Echocardiographically detected left ventricular hypertrophy: prevalence and risk factors: the Framingham Heart Study. Ann Intern Med . 1988;108:7–13. C, Prevalence of heart failure by age in Framingham Heart Study men (light bars) and women (dark bars). Reprinted from Ho KK, Pinsky JL, Kannel WB, et al. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol 1993;22:6A–13A. D, Prevalence of AF by age in subjects from the Framingham Heart Study. Reprinted from Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke . 1991;22:983–988. It has been increasingly appreciated that the development of heart failure with apparently preserved systolic function, as evidenced by a “normal” ejection fraction, occurs in about one-third to one-half of older patients with heart failure.6–9 In a …

Left ventricular remodeling with age in normal men versus women: Novel insights using three-dimensional magnetic resonance imaging

Echocardiographic left ventricular (LV) wall thickness increases with age, suggesting LV hypertrophy. However, autopsy studies have shown no change, or even a decrease, in LV mass with age. With many pathologies, LV remodeling results in changes in ventricular shape. Age-associated LV shape change might explain this discrepancy, although this has not been studied. Magnetic resonance imaging (MRI) was used in 336 healthy, normotensive adults (mean age 56 ± 18 years; 200 women, 136 men) to measure LV mass, end-diastolic LV wall thickness, length, diameter, and shape. Echocardiographic LV mass was measured in a subset of 86 subjects by a standard algorithm. In women, LV wall thickness increased by 14% (r = 0.19, p <0.02), whereas LV length decreased by 9% (r = −0.26, p = 0.0006); LV diameter was unchanged. Thus, LV mass did not vary with age (r −0.04, p = 0.06) and the sphericity index decreased (r = −0.165, p <0.05). In men, LV wall thickness and diameter were unrelated to age, but there was an 11% decrease in LV length (r = −0.29, p = 0.003); therefore, there was an 11% decrease in LV mass (r = −0.20, p = 0.019) and a decrease in the sphericity index (r = −0.218, p <0.04). No change occurred in echocardiographic LV mass with age in either gender, although echocardiographic LV wall thickness increased in both. The left ventricle becomes more spherical with age in normal adults due to reduced LV length. In women, increased LV wall thickness offsets the decreasing LV length, whereas in men, LV wall thickness fails to compensate, resulting in decreased LV mass with age.

Relationship of impaired glucose tolerance to left ventricular structure and function: The Strong Heart Study

Background We have identified increased left ventricular (LV) mass, wall thickness, relative wall thickness, and reduced systolic function in diabetic individuals after adjusting for blood pressure and body mass index. However, the cardiovascular correlates of impaired glucose tolerance (IGT), a precursor of diabetes, are unknown. Methods We compared LV measurements between 457 American Indian participants in the Strong Heart Study with IGT (34% men) by World Health Organization criteria and 888 participants (49% men) with normal glucose tolerance. Results Participants with IGT were older (60 vs 59 years, P < .01), more overweight (body mass index, 32 ± 6 vs 29 ± 5 g/m2), and had higher systolic blood pressure (129 ± 20 vs 124 ± 18 mm Hg, P < .001) and heart rate (67 ± 10 vs 66 ± 11 beats/min, P = .011). In univariate analyses, women but not men with IGT had higher LV mass (mean, 150 vs 138 g, P < .001) and cardiac index (2.6 vs 2.5 L/min/m2, P < .05). LV wall thicknesses and relative wall thickness were greater in women and men with IGT. Regression analysis, adjusting for multiple covariates in the entire study population, identified independent associations of IGT with higher LV relative wall thicknesses, LV mass/height2.7, and cardiac output/height1.83. Conclusions IGT is associated with increased LV wall thickness, mass, and cardiac output independent of effects of relevant covariates. (Am Heart J 2001;141:992-8.)

Differences in Echocardiographic Findings and Systemic Hemodynamics among Non-Diabetic American Indians in Different Regions: The Strong Heart Study

PURPOSE: This study was undertaken to determine whether differences in left ventricular (LV) and systemic hemodynamic findings exist between American Indians in different regions that might contribute to known differences in cardiovascular morbidity rates among American Indians. METHODS: We compared echocardiography results in 290 non-diabetic Strong Heart Study (SHS) participants in Arizona, 595 in Oklahoma and 572 in North/South Dakota (ND/SD). RESULTS: Participants in the 3 regions were similar in age and gender but those in Arizona had the highest body mass indices and lowest heart rates while those in ND/SD had the lowest diastolic blood pressures (BP). In analyses that adjusted for significant covariates, ND/SD participants had larger aortic (Ao) anular, Ao root, and LV chamber size as well as higher cardiac output and lower peripheral resistance, whereas Arizona participants had increased LV wall thickness and mass and reduced LV myocardial contractility. These findings may contribute to the known high rates of cardiovascular events in ND/SD Indians and to the proportionately higher rate of cardiovascular death than of non-fatal cardiovascular events that has been recently documented in Arizona Indians. CONCLUSIONS: Application of echocardiography to non-diabetic SHS participants reveals that LV chamber and arterial size are larger in ND/SD Indians and that LV wall thicknesses and mass are higher and LV myocardial contractility lower in Arizona Indians, possibly contributing to the higher than expected rates of cardiovascular morbidity and mortality among Indians in Arizona.

Progressive cardiac dysfunction and fibrosis in the cardiomyopathic hamster and effects of growth hormone and angiotensin-converting enzyme inhibition.

Growth hormone (GH) improves cardiac function in the rat with myocardial infarction, but its effects in a model of primary dilated cardiomyopathy have not been reported. GH effects were examined at early (4 months) and late (10 months) phases of disease in the cardiomyopathic (CM) hamster, and the combination of GH with chronic ACE inhibition was assessed in late-phase heart failure. CM hamsters (CHF 147 line) at 4 months showed severe systolic left ventricular (LV) dysfunction with normal LV filling pressure, and at 10 months there was more severe systolic as well as diastolic dysfunction with increasing myocardial fibrosis. Recombinant human GH alone for 3 weeks at age 4 months increased LV wall thickness and reduced systolic wall stress without altering diastolic wall stress, whereas at 10 months, wall stress and fractional shortening did not improve. The LV dP/dt(max) was enhanced at both ages by GH, which at 4 months reflected increased contractility, but at 10 months was most likely caused by elevation of the LV filling pressure. The increasing degree of fibrosis correlated inversely with LV function but was unaffected by GH. In other CM hamsters, high-dose ACE inhibition alone (quinapril), started at 8 months and continued for 11 weeks, improved LV function and inhibited unfavorable remodeling, but the addition of GH for 3 weeks at age 10 months produced increased wall thickness with little additional functional benefit and increased the LV filling pressure and diastolic wall stress. GH treatment alone improved LV dysfunction at 4 months of age in CM hamsters by increasing contractility and reducing wall stress but had few beneficial effects at 10 months in severe LV failure. After chronic ACE inhibition, addition of GH at 10 months had no additional beneficial effects and further increased LV diastolic pressure. These differing effects of GH may relate to the progressive increase of LV fibrosis in the CM hamster.

Alterations in cardiac morphology and function in elite multi-disciplinary athletes.

Early echocardiographic studies of left ventricular (LV) morphology and function focused on single discipline athletes, primarily endurance and strength trained. To date there are few studies examining multi-disciplinary trained athletes. The present echocardiographic study examined LV morphology and function in 18 elite triathletes (swimming, cycling, and running) and 11 elite modern pentathletes (running, swimming, shooting, fencing, and show-jumping) compared with age- and sex-matched controls. Elite triathletes demonstrated significantly (p < 0.05) increased LV wall thickness and cavity dimensions together with LV mass, both in absolute terms and scaled for body surface area, compared with controls. Elite modern pentathletes demonstrated significantly (p < 0.05) increased LV wall thickness with a non-significant increase in LV internal diameter. Despite significant LV enlargement, the distribution of hypertrophy and diastolic filling indices were normal in both triathletes and modern pentathletes and significantly increased in the triathletes. It is concluded that multi-disciplinary training results in variations in LV morphology. The inciting stimulus resulting in LV enlargement in triathletes is associated with prolonged endurance activity, together with an isometric component accompanying cycling. In contrast, elite modern pentathletes experience a reduced endurance component combined with a high isometric component associated with fencing.

Familial predisposition of left ventricular hypertrophy

OBJECTIVESThe study evaluated the contribution of familial predisposition to the risk of left ventricular hypertrophy (LVH).BACKGROUNDLeft ventricular hypertrophy is a multifactorial condition that serves as an important predictor of cardiovascular mortality. At present it is unclear whether familial predisposition contributes to the manifestation of LVH. Thus, we determined whether siblings of subjects with LVH are at increased risk to present with an elevation of LV mass or an abnormal LV geometry.METHODSEchocardiographic and anthropometric measurements were performed in 2,293 individuals who participated in the echocardiographic substudies of population-based MONICA Augsburg surveys. In addition, a total of 319 siblings of survey participants with echocardiographic evidence of LVH were evaluated. The risk of these siblings to present with LVH or abnormal LV geometry was estimated by comparison with 636 subjects matched for gender and age that were selected from the entire echocardiography study base.RESULTSBlood pressure, body mass index, age, and gender (i.e., known determinants of LV mass) were comparable in LVH-siblings and the matched comparison group. However, septal and posterior wall thicknesses, relative wall thickness as well as LV mass index were significantly elevated in LVH-siblings (p < 0.001, each) whereas LV dimensions did not differ. Likewise, the prevalence of LVH was raised in LVH-siblings, as was the relative risk of LVH after adjustment for confounders (p < 0.05). More specifically, LVH-siblings displayed increased prevalences of concentric remodeling and concentric LVH (p < 0.05) but not of eccentric LVH.CONCLUSIONSFamilial predisposition appears to contribute to increased LV wall thickness, to the development of LV hypertrophy and abnormal LV geometry.

Left ventricular cavity obliteration during dobutamine stress echocardiography is associated with female sex and left ventricular size and function

We investigated 568 consecutive patients undergoing dobutamine stress echocardiography to elucidate the mechanism of left ventricular (LV) obliteration. Baseline clinical and echocardiographic variables were related to dobutamine-induced LV cavity obliteration defined as approximation of LV endocardium associated with an intracavitary flow acceleration of at least 2 m/s in the absence of a distal residual cavity. The LV cavity obliteration was observed in 89 (16%) of the 568 patients and was more frequent in women and those with smaller LV dimensions, increased LV wall thickness, and higher resting ejection fractions. Despite similar peak stress levels, the cavity obliterators were less likely to have chest pain and detectable stress-induced wall motion abnormalities. We conclude that LV cavity obliteration during dobutamine stress is common and is associated with female sex, smaller LV size, presence of LV hypertrophy, and higher LV ejection fraction. Despite similar stress levels, chest pain and reversible wall motion abnormalities are observed less frequently in patients with cavity obliteration, raising the possibility of lower prevalence of coronary artery disease or masking of ischemia in this patient population. (J Am Soc Echocardiogr 1998;11:957-60.)

Remodeling of the left ventricle in primary aldosteronism due to Conn's adenoma.

Since hyperaldosteronism has been experimentally related to myocardial interstitial fibrosis, we investigated the effects of hypertension and excess aldosterone due to aldosterone-producing adenomas (APAs) on the heart. In 52 hypertensive individuals, we performed Doppler echocardiography for estimation of left ventricular (LV) wall thickness and dimensions, transmitral LV filling flow velocity indexes, and 24-hour ambulatory blood pressure monitoring. Consecutive patients with APAs (n = 26) and essential hypertension (EH, n = 26) were individually matched for age, sex, race, body mass index, casual blood pressure, and known duration of hypertension. The matched groups were similar for demography, casual and 24-hour blood pressure values and variability, and duration of hypertension but differed for serum potassium, plasma renin activity, and aldosterone levels (all P < .001). A thicker interventricular septum (P = .015) and posterior wall (P = .009) and a higher LV mass index (118 +/- 5 versus 100 +/- 4 g/m2, P = .009) were observed in APA compared with EH patients. Both septum and posterior wall thicknesses had a significant direct relationship with age, plasma aldosterone, and mean blood pressure. The integral of the early diastolic filling wave (Ei) (P = .011) and the ratio Ei/Ai (A wave integral) (P = .038) were lower and the atrial contribution to LV filling was higher (52 +/- 2% versus 46 +/- 2%, P = .038) in APA than in EH patients. The ratio Ei/Ai was significantly (P = .008) inversely related only to age and plasma aldosterone. In APA patients, the excess aldosterone is associated with both increased LV wall thickness and mass and decreased early diastolic LV filling indexes compared with demographically similar EH with superimposable blood pressure values, profile, and variability.

Serial echocardiographic-Doppler assessment of left ventricular geometry and function in rats with pressure-overload hypertrophy. Chronic angiotensin-converting enzyme inhibition attenuates the transition to heart failure.

Although chronic pressure overload may progress to left ventricular (LV) failure, the pathophysiology of this transition is not well understood. In addition, the effects of chronic angiotensin-converting enzyme (ACE) inhibition on this transition are largely undefined. To examine changes in LV structure and function during the transition to heart failure, rats with LV hypertrophy due to banding of the ascending aorta (LVH, n = 22) and age-matched sham-operated rats (n = 6) were studied 6, 12, and 18 weeks after aortic banding. Two-dimensionally guided transthoracic M-mode echocardiograms and transmitral Doppler spectra were recorded for assessment of LV geometry and systolic and diastolic functions. LVH rats were randomized to no treatment (n = 10) or treatment with the ACE inhibitor fosinopril (50 mg/kg per day, n = 12) after the baseline echocardiogram. Six weeks after banding, LVH rats had increased LV wall thickness with normal cavity dimensions and supranormal endocardial systolic shortening. However, midwall shortening was mildly depressed, and a restrictive diastolic filling pattern was present. After 18 weeks of untreated pressure overload, LV wall thickness was unchanged, but cavity dilation, a fall in endocardial shortening, and further deterioration of diastolic filling were evident. In contrast to untreated LVH rats, the fosinopril-treated rats showed no change in LV diastolic cavity dimension, and systolic and diastolic functions did not deteriorate or improved. Closed chest LV systolic pressures at 18 weeks were not different in LVH or LVH-fosinopril rats (197 versus 198 mm Hg), although end-diastolic pressure was higher in the untreated rats (18 versus 11 mm Hg). Calculated LV systolic wall stress was lower in fosinopril-treated than untreated LVH rats. The severity of LV diastolic filling abnormalities correlated strongly with operating LV chamber stiffness (r = .88, P < .0001). This model of pressure overload is characterized initially by concentric LV hypertrophy with compensated LV chamber performance; however, markedly abnormal diastolic filling is present. The transition from compensated hypertrophy to early failure is heralded by LV dilation, impairment of systolic function, and progression of the abnormalities in LV filling. Chronic ACE inhibition in rats with supravalvular aortic banding (1) does not change in vivo LV systolic pressure but prevents increased LV cavity size and increased LV wall stress and (2) attenuates impairment of (or improves) both systolic and diastolic functions. The effects of fosinopril could be explained in part by inhibition of an intracardiac renin-angiotensin system.

Exercise-induced cardiac hypertrophy is associated with an increased myocardial compliance.

Left ventricular (LV) chamber and myocardial wall compliance were investigated in rats with exercise-induced cardiac hypertrophy. Voluntary exercise training was performed on running wheels. After 16 wk of exercise training, cardiac performance was measured in anesthetized open-chest ventilated rats. LV end-diastolic performance was calculated from both short-axis external diameter and long-axis segmental length measurements. Exercise-trained rats developed significant LV hypertrophy (1.03 +/- 0.02 g) compared with control rats (0.91 +/- 0.03 g; P < 0.01). The physiological hypertrophy was associated with an increased LV wall thickness-to-internal radius ratio consistent with a concentric geometry. LV end-diastolic stiffness (slope of the linearized LV end-diastolic pressure-strain relationship) was decreased in both the short (P < 0.02) and long (P < 0.02) axis of LV as a result of exercise training. The LV end-diastolic chamber stiffness (slope of the linearized LV end-diastolic pressure-volume relationship) was also decreased in the exercised group (P < 0.05). The decreased chamber stiffness occurred as a consequence of a decrease in the regional myocardial wall elastic stiffness (slope of the linearized LV end-diastolic stress-strain relationship; P < 0.05). Thus an increased LV wall thickness as a result of exercise-induced LV hypertrophy is associated with an enhanced ventricular chamber compliance, which in turn is attributed to a decrease in the diastolic stiffness of the myocardial wall.

Myocardial adaptation and weight fluctuation in college wrestlers.

Myocardial adaptation and weight fluctuation of seven college wrestlers was examined during a competitive season. Standard M-mode measurements were used to determine left ventricular (LV) end diastolic and end systolic dimensions, fractional shortening, LV diastolic posterior wall thickness (DPW), diastolic interventricular septal thickness (DIVS), and LV mass (LVM) during preseason (test 1) and four months later at the season's end (test 2). The wrestlers' qualifying weights ranged from 53.6 to 80.5 kg and each competed in an average of 17 meets. Systolic and diastolic blood pressure, heart rate, and body weight (BW) were measured at both tests. Daily weight records and qualifying weights were used to calculate seasonal weight fluctuation as a percentage of the highest weight attained between each meet and the wrestler's subsequent qualifying weight. Paired t-tests were used to determine differences between tests 1 and 2. DPW, DIVS and LVM increased from 8.8 +/- 1.0 to 10.3 +/- 1.0 mm, 7.9 +/- 1.5 to 9.9 +/- 0.6 mm, and 171.2 +/- 24.3 to 209.7 +/- 12.9 mm3 respectively while BW declined from 70.3 +/- 9.2 to 67.1 +/- 9.4 (X +/- SD, p < .01) from test 1 to 2. The other variables remained constant across tests. The wrestlers' mean % weight fluctuation throughout the season was 7.5 +/- 1.5 ranging from 4.4 to 9.1%. These findings suggest that significant increases in myocardial mass occur over the course of a competitive wrestling season resulting from increased LV wall thickness. The magnitude and cyclic method of weight loss used by wrestlers does not appear to prevent myocardial hypertrophy.

Echocardiographic assessment of left ventricular structure and diastolic filling in elderly subjects with borderline isolated systolic hypertension (the Framingham Heart Study)

Abnormalities in left ventricular (LV) structure and function have been shown in patients with diastolic hypertension and recently in subjects with isolated systolic hypertension. The purpose of this study was to determine whether abnormalities of cardiac structure or function are present in elderly subjects with borderline isolated systolic hypertension (defined as systolic blood pressure [BP] between 140 and 159 mm Hg, and diastolic BP < 90 mm Hg). Ninety-one subjects (mean age 77 years) from the original Framingham Heart Study with untreated borderline isolated systolic hypertension, who were free of cardiovascular disease, were compared with 139 normotensive (BP < 140/ 90 mm Hg) subjects (mean age 76 years). Measurements included M-mode values for LV structure, and 6 Doppler indexes of LV diastolic filling. Subjects with borderline isolated systolic hypertension and the control group differed in mean systolic (147 vs 125 mm Hg) and diastolic (76 vs 70 mm Hg) BP. Borderline systolic hypertension was the most frequent form of untreated hypertension in this elderly group. The sum of LV wall thicknesses (septum + posterior wall) was significantly higher in borderline hypertensive subjects than in normotensive ones (20.5 vs 19.7 mm; p = 0.002). No difference was detected in LV internal dimension or systolic function. After adjustment for age and other clinical variables, comparisons between the groups revealed significant differences in indexes of Doppler diastolic filling. Peak velocity of early filling, and the ratio of early to late peak velocities were lower in the hypertensive group (40 vs 44 cm/s [p = 0.03] and 0.69 vs 0.76 [p = 0.01], respectively). Healthy elderly subjects with borderline isolated systolic hypertension have similar LV systolic function, mildly increased LV wall thickness and evidence of impaired Doppler diastolic filling compared with normotensive subjects.

Sex differences in cardiac adaptation to isolated systolic hypertension

This study examines the association of isolated systolic hypertension with left ventricular (LV) mass and geometry in men and women. The subjects of this study were surviving members of the Framingham Heart Study and the Framingham Offspring Study who attended the index examination (between 1979 and 1983) and were aged ≥50 years, free of clinically apparent cardiovascular disease, not taking antihypertensive medication and without diastolic hypertension (diastolic blood pressure <90 mm Hg), and in whom LV mass could be determined by echocardiography. Examinations routinely included 12-lead resting electrocardiography, measurements of resting blood pressure, anthropometry, blood glucose levels, and M-mode echocardiography. M-mode echocardiograms adequate to assess LV hypertrophy were obtained for 1,282 normotensive subjects (538 men and 744 women) and 79 subjects with isolated systolic hypertension (26 men and 53 women). Adjusting for age, body mass index and diastolic Mood pressure, the relative odds of LV hypertrophy associated with isolated systolic hypertension were 2.58 (95% confidence interval 0.97 to 6.86) in men and 5.94 (95% confidence interval 3.06 to 11.53) in women. Women with isolated systolic hypertension had increased LV wall thickness and mass without LV chamber enlargement, but men had LV dilation and increased LV mass without increased wall thickness. In conclusion, although isolated systolic hypertension was associated with increased LV mass in men and women, the geometric pattern of increased LV mass differed by sex; although women demonstrated a pattern of concentric hypertrophy, an eccentric pattern was observed in men.

Significant Left Ventricular Hypertrophy in Subjects with Normal Resting Pressures but Exaggerated Pressure Response During Light Exertion

Concentric left ventricular hypertrophy (LVH) frequently occurs in subjects with normal resting systolic and diastolic pressures (SP and DP, respectively). LVH in this normotensive-hypertrophic group (NH) may be due to an abnormally exaggerated pressure response to exercise. The SP and DP responses to exercise were studied in 130 subjects free from coronary artery disease or cardiomyopathy. The NH subjects (n = 35) had normal resting pressure (SP < or = 140 and DP < or = 85 mmHg) and increased LV wall thickness (T) by echocardiography (T > 1.1 cm). A normal control group (NN) (n = 57) and a hypertensive control group (HH) (n = 23) were simultaneously evaluated. The original groups, subgroups censored for age and weight, and matched-pair subgroups demonstrated greater exercise SP for NH than for NN (p < 0.005). Moreover, the rate of SP increase with exercise was greater for NH than for NN or HH (p < 0.05). Hence, an exaggerated exercise SP response may have been the stimulus for LVH in these NH subjects.

Clinical and haemodynamic features in relation to severity of aortic stenosis in adults

The main symptoms of aortic stenosis (AS), angina pectoris, dyspnoea, and syncope/effort dizziness, are thought to reflect the severity of AS. This assumption is based on studies in relatively young patients, and may not apply to older age groups. Thus, in 100 consecutive adults (age 41-79 years) referred to cardiac catheterization with suspected AS, clinical and haemodynamic variables were assessed in relation to significant (less than or equal to 0.50 cm2 m-2) (n = 70) and nonsignificant AS (n = 30), and to symptoms. Prevalence of symptoms, functional class, and systolic murmur grade greater than or equal to 3, was similar in the groups. However, patients with significant AS more often had an abnormal second heart sound, electrocardiographic left ventricular (LV) hypertrophy with strain, severe echocardiographic aortic valve calcification, and increased LV wall thickness. Multivariate analysis identified an abnormal second heart sound, and aortic calcification grade, as independent predictors of significant AS. When the Doppler mean gradient was added to the analysis, it became the best predictor. Angina pectoris (n = 74) was related to coronary artery disease, but not to severity of AS. However, 31% of patients without angina also had coronary artery disease. Dyspnoea (n = 69) was only related to age, and syncope/effort dizziness (n = 26) was more frequent in women. Functional class grade was not related to severity of AS. Thus, in adults with assumed symptomatic AS, clinical symptoms do not predict severity of AS. Therefore, the decision for valve replacement should rely on Doppler assessment of the severity of AS. Furthermore, in adults with AS, coronary artery disease cannot be excluded without selective coronary angiography.

Non‐invasive assessment of left ventricular diastolic function in patients with systemic sclerosis

To evaluate the extent of left ventricular (LV) diastolic impairment in systemic sclerosis, we examined 30 consecutive patients (15 men and 15 women) with this condition, and compared the findings with the data for 48 age- and sex-matched randomly sampled controls. All patients were investigated by phonocardiography, pulse curve recording, and M-mode echocardiography. Twenty-three of 30 (77%) patients had LV hypertrophy and/or diastolic impairment. Interventricular septum (P = 0.0001), LV posterior wall (P less than 0.05), and the wall thickness to cavity dimension ratio (P less than 0.001) were increased in patients compared to controls, as was LV mass index (P less than 0.002). Five patients had asymmetric septal hypertrophy. LV end-diastolic dimension did not differ between groups. LV distensibility was impaired, as judged from apexcardiographic a/H ratio (P less than 0.05) and from an increased left atrial index (P less than 0.005). LV early filling was impaired, with a reduced left atrial emptying index (P = 0.0001), and a reduced rate of dimension increase in digitized M-mode (P less than 0.02). We found no evidence of impaired LV relaxation. Blood pressure did not differ between patients and controls. With longer duration of the disease, left atrial dimension appeared to increase (r = 0.42, P less than 0.05), while other variables were not related to disease duration. The impaired LV filling was not secondary to systolic dysfunction. We conclude that systemic sclerosis patients have an increased LV wall thickness, with impaired early filling properties and LV distensibility.

One- and two-dimensional echocardiography in bodybuilders using anabolic steroids

The object of this study was to investigate the possible concentric increase in the left ventricular (LV) wall thickness by intensive strength training and to differentiate between the specific effect of the strength training itself and the influence of anabolic drugs. In this study 21 top-level bodybuilders [users of anabolic steroids (A): n = 14; non-users (N): n = 7] underwent one-dimensional and two-dimensional echocardiography as well as a cycle ergometer test. In both groups blood pressure at rest and during ergometric exercise was within the normal range. In spite of the same amount of time being spent on training, A showed significantly better power results than N. Total heart volume (A = 11.3 +/- 0.9 ml.kg-1; N = 11.9 +/- 0.9 ml.kg-1) and LV muscle mass were almost identical in A and N and correlated significantly with body weight and lean body mass respectively. The body dimension-related diastolic LV diameter was significantly lower in A (0.567 +/- 0.062 mm.kg-1) than in N (0.639 +/- 0.040 mm.kg-1). An increase in the LV posterior wall (p less than 0.01) and septum thickness (ns) resulted in increased LV wall thickness:diameter (p less than 0.01) and LV muscle mass:volume (p less than 0.05) ratios in A (0.458 +/- 0.590; 1.38 +/- 0.25 g.ml-1) in comparison to N (0.356 +/- 0.077; 1.16 +/- 0.17 g.ml-1). The septal:posterior wall thickness ratio was similar for both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Increasing Intraabdominal Pressure and Volume on Left Ventricular Function in Continuous Ambulatory Peritoneal Dialysis (CAPD)

To determine the effect of increasing intraabdominal pressure on left ventricular (LV) systolic function in patients undergoing continuous ambulatory peritoneal dialysis (CAPD), we studied 15 patients who had been on CAPD for at least 2 months. The study protocol included measurement of echocardiographic LV internal dimensions in diastole and systole, LV wall thickness and mass, LV ejection time, the mean velocity of circumferential fiber shortening (mean Vcf), heart rate, BP, and intraabdominal pressure. Measurements were obtained at baseline (OL) and following intraperitoneal infusion of 1-L increments of dialysate solution (up to 4 L) in both the recumbent and standing positions. Significant differences in LV systolic function resulting from intraperitoneal infusion of dialysate were confined to the subgroup with increased LV wall thickness (n = 8). In this subgroup, mean Vcf decreased progressively from 0.99 +/- 0.18 circumferences/second at baseline to 0.88 +/- 0.16 circumferences/second at 1 L (P = NS), to 0.86 +/- 0.16 circumferences/second at 2 L (P = NS), to 0.66 +/- 0.18 circumferences/second at 3 L (P less than 0.005), and to 0.60 +/- 0.14 circumferences/second at 4 L (P less than 0.005) in recumbent position. Measurements obtained in the standing position paralleled those observed during recumbency. These changes were accompanied by a significant decrease in the mean LV internal dimension in diastole and a significant increase in intraabdominal pressure, but no significant change in the mean LV internal dimensions in systole, mean heart rate, or mean systolic or diastolic BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Sensitivity and specificity of electrocardiographic criteria for left and right ventricular hypertrophy in morbid obesity

To determine the sensitivity and specificity of standard electrocardiographic criteria for left ventricular (LV) and right ventricular (RV) hypertrophy in morbid obesity, resting electrocardiograms and M-mode echocardiograms were obtained in 65 patients whose actual body weight was more than twice their ideal body weight and who were free from hypertension and organic heart disease not directly attributable to obesity. Electrocardiographic criteria for LV hypertrophy were tested using increased LV wall thickness, LV enlargement and increased LV mass (all determined echocardiographically) as diagnostic standards. Electrocardiographic criteria for RV hypertrophy were tested using echocardiographic RV enlargement or RV hypertrophy as a diagnostic standard. Sensitivity values for the electrocardiographic criteria for LV hypertrophy ranged from 0 to 13%, 0 to 20% and 0 to 12% using echocardiographic increased LV wall thickness, LV enlargement and increased LV mass, respectively, as diagnostic standards. Specificity values ranged from 73 to 100%, 87 to 100% and 83 to 100%, respectively, using these diagnostic standards. Sensitivity values for the electrocardiographic criteria for RV hypertrophy ranged from 0 to 16% and specificity values ranged from 95 to 100%. Combining electrocardiographic criteria within groups did not appreciably increase sensitivity and often decreased specificity to unacceptably low levels. The electrocardiogram is very limited in its ability to detect ventricular hypertrophy and chamber enlargement in morbidiv obese patients.