Parallel increase in carotid, brachial and left ventricular cross-sectional areas in arterial hypertension

Few data have been published about the relation between the vessels geometry and development of left ventricular (LV) hypertrophy in patients with arterial hypertension. The aim of this study is to describe arterial and LV geometry changes due to mild-to-moderate arterial hypertension in an untreated hypertensive population. In 95 untreated patients with mild-to-moderate hypertension and 23 age- and sex-matched healthy normotensives, we measured the end-diastolic diameter and wall thickness of the left ventricle and the internal diameter and intimal-medial thickness (IMT) of carotid and brachial arteries. From these data, the cross-sectional areas (CSAs) of arterial and myocardial walls were calculated. Hypertensive patients were further subdivided on the basis of the presence of LV hypertrophy defined according to Devereux et al as anatomical LV mass >125 g/m. In hypertensive patients with hypertrophy, carotid and brachial CSAs increased, without significant changes in thickness/diameter ratio (arterial 'enlargement'), while the left ventricle developed 'concentric' hypertrophy. Arterial and LV CSAs showed a significant direct correlation with systolic blood pressure (BP). However, when data were corrected for BP, the correlation between the increase in arterial and LV CSAs became much improved than for the raw data. In conclusion patients with untreated mild-to-moderate hypertension, both carotid and brachial arterial walls showed an enlargement that was proportional to the development of LV hypertrophy. These results suggest that the effects of arterial hypertension on carotid, brachial and LV wall geometry have a common modulation.     

Left ventricular geometric patterns and QT dispersion in untreated essential hypertension

The spectrum of left ventricular adaptation to hypertension, different types of hypertrophy patterns, and QT dispersion in different types of hypertrophy was investigated in 107 patients with untreated essential hypertension and 30 age- and gender-matched normal adults studied by 12-derivation electrocardiogram (ECG), two-dimensional, and M-mode echocardiography. Left ventricular mass (LVM), body mass index, total peripheral resistance (TPR), relative wall thickness (RWT), and QT dispersion were found to be statistically significantly higher in the hypertension group (P < .001 for all). Among hypertensive patients, 41.1% had both normal LVM and RWT, here called normal left ventricle in hypertension; 10.3% had concentric hypertrophy with increased LVM and RWT; 14.95% had eccentric hypertrophy with increased LVM and normal RWT; and 32.7% had concentric remodeling with normal LVM and increased RWT. Echocardiographically derived cardiac index was higher in the concentric hypertrophy and eccentric hypertrophy patterns (P = .002 and P < .0001, respectively), whereas TPR was higher in the concentric hypertrophy and concentric remodeling patterns (P = .017 and .02, respectively). QT dispersion values were found to be increased in the hypertensive group (P = .001), whereas similar values were calculated for different types of hypertrophy patterns. We conclude that the more common types of ventricular adaptation to essential hypertension are eccentric hypertrophy and concentric remodeling. Concentric hypertrophy is found to be associated with both volume and pressure overload, whereas eccentric hypertrophy is associated with volume overload only and concentric remodeling is associated with pressure overload. But different left ventricular geometric patterns seem to have similar effects on QT dispersion.     

Elderly patients in chronic hemodialysis: risk factors for left ventricular hypertrophy

In the past few years in Western countries, there has been an increasing proportion of elderly patients beginning renal replacement therapy. Left ventricular hypertrophy (LVH) is associated with an increased mortality rate due to cardiovascular disease, the main cause of death in patients on chronic hemodialysis. In this study, we evaluated 67 chronic hemodialysis patients older than 65 years (33 women and 34 men; mean age, 72.6 years; mean time on chronic hemodialysis, 51.3 months). Several biological and laboratory data were analyzed. The left ventricular mass was calculated using the Penn convention criteria. LVH was observed in 49 patients (73%). These 49 patients were divided into two groups (group 1, concentric hypertrophy, n = 22; and group 2, eccentric hypertrophy, n = 27) and compared with a control group (patients without LVH, n = 18). Group 1 (P = 0.06) and group 2 (P = 0.055) showed higher systolic blood pressures and group 2 showed a lower hematocrit (P = 0.024). The echocardiographic parameters were expectedly different: group 1 had higher posterior left ventricular wall thickness (P = 0.0001), interventricular septum thickness (P = 0.0001), and left ventricular wall relative thickness (P = 0.002), and group 2 had higher left ventricular end-diastolic diameter (P = 0.0001), interventricular septum thickness (P = 0.01), and posterior left ventricular wall thickness (P = 0.023). Using the left ventricular mass index as the dependent variable and the evaluated biological and laboratory data as the independent variables, we found in a stepwise multiple regression model that only systolic blood pressure (t = 3.430; P = 0.0011), age (t = 2.059; P = 0.044), interdialytic weight gain (t = 2.236; P = 0.029), and hematocrit (t = -1.961; P = 0.054) independently influenced the left ventricular mass index (R2 = 0.313; P = 0.0001). Further studies are needed to determine whether reduction of the left ventricular mass index, through control of blood pressure and correction of anemia, will decrease the cardiovascular events in this particular population.     

Clinical significance of magnetic resonance and echocardiographic correlations in the evaluation of hypertrophic cardiomyopathy

Relatively few clinical studies have investigated the role of MRI in the patients with hypertrophic cardiomyopathy. To assess MR capabilities in defining the presence, distribution and severity of left ventricular hypertrophy, the prevalence and clinical correlations of right ventricular hypertrophy and the prevalence and clinical implications of structural myocardial abnormalities, MRI and echocardiography were performed on 37 unselected patients with hypertrophic cardiomyopathy. The two methods were in agreement in 100% of cases in diagnosing the disease and classifying left ventricular hypertrophy as asymmetric, concentric or apical, and in 92% of cases in assessing the topographic distribution of hypertrophy of ventricular segments. A statistically significant linear correlation was found between echocardiographic and MR measurements of interventricular septum (r = 0.69, p < 0.0001, SEE = 4) and left posterior wall of the left ventricle (r = 0.67, p < 0.0001, SEE = 2.4). Right ventricular hypertrophy (right anterior wall diastolic thickness > 5 mm) was demonstrated by MRI in 23 of 33 patients (70%). In this group, left posterior wall thickness and left atrial diameter were higher (15 +/- 4 vs 11 +/- 2, p < 0.01 and 45 +/- 9 vs 38 +/- 5 mm, p < 0.05, respectively). On T2-weighted sequences, areas of reduced signal intensity, probably due to myocardial fibrosis, were detected in 16 cases (43%). This group was characterized by higher max. septal thickness (25 +/- 7 vs 21 +/- 6 mm, p < 0.05) and max. left posterior wall thickness (15 +/- 9 vs 7 +/- 8 mm, p < 0.05). All the three cases with dilated and hypokinetic left ventricle showed this kind of tissue abnormality. In conclusion, MRI provided clear, accurate and exhaustive data on the presence and distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy. Right ventricular hypertrophy and structural abnormalities of ventricular myocardium can also be detected and quantified. Right ventricular involvement is associated with more severe hypertrophy of left ventricular posterior wall. Structural myocardial abnormalities, probably due to fibrosis, are related to the extent of left ventricular hypertrophy.     

Effect of 3 hypertensive++ agents on ventricular geometry and function

BACKGROUND: To assess the prevalence of left ventricular hypertrophy in hypertensive patients referred to an outpatient cardiology unit, and to assess its evolution under antihypertensive treatment. METHODS: One hundred and seven mild to moderate hypertensive patients were randomized to receive either xipamide, verapamil or atenolol. Cross-sectional echocardiography was performed in order to assess left ventricular mass and function. RESULTS: Mean age was 56 years, with a 4:1 female/male ratio. Mean follow-up was 120 days. Left ventricular hypertrophy was very common (65%) and decreased to 54% under antihypertensive treatment. Left ventricular mass decreased from 134.3 g/m2 to 118.1 g/m2 (p < 0.001). Concentric hypertrophy was the most common geometric pattern (42%), decreasing to 30% with treatment. Xipamide decreased ventricular mass by decreasing left ventricular diameters, while verapamil and atenolol decreased left ventricular thickness, mainly in septal wall. Systolic function was not modified during the treatment period. Diastolic function was not modified by xipamide and verapamil, and improved with atenolol. CONCLUSIONS: Left ventricular hypertrophy is very frequent when determined by echocardiography and all three drugs produced regression of left ventricular hypertrophy in a different way with respect to left ventricle geometry, an effect which could have potential therapeutic implications.     

Vascular and cardiac remodeling in world class professional cyclists

BACKGROUND: Numerous studies have demonstrated that left ventricular (LV) hypertrophy is often associated with conditioning. METHODS AND RESULTS: The aim of the study was to evaluate cardiac and carotid artery changes induced by professional cycling. We collected M-mode left ventricle and B-mode right common carotid artery data from 149 male professional cyclists before the 1995 "Tour de France" race and 52 male control subjects. LV mass indexed to body surface area in cyclists was double that in control subjects, with no overlap of 95% confidence intervals (cyclists 100.9 to 187 g/m2 and control subjects 51.8 to 96.3 g/m2). Both mean arterial diameter and mean arterial diastolic intima-media thickness (IMT) were 13% higher in cyclists than in control subjects, with overlap of 95% confidence intervals (for arterial IMT 0.45 to 0.65 mm in cyclists and 0.38 to 0.60 mm in control subjects). CONCLUSIONS: Our results suggest that intense cycling has an effect on the cardiovascular system, more pronounced on the left ventricle and less pronounced on large arteries. Nevertheless, athletic training should be considered as a potential determinant of carotid modification.     

Left ventricular geometry as an independent predictor for extracardiac target organ damage in essential hypertension

Left ventricular hypertrophy (LVH) is an independent cardiovascular risk factor. It has not been established, however, whether left ventricular geometry is an independent predictor of extracardiac target organ damage in essential hypertension. Study groups were classified according to relative wall thickness: 27 patients with concentric LVH and 50 patients with eccentric LVH. Age and left ventricular mass indexes of two groups were matched. As indexes of extracardiac target organ damage, retinal funduscopic grade, and serum creatinine level were measured. The severity of hypertensive retinopathy and the renal involvement were more severe in patients with concentric LVH than in patients with eccentric LVH. Extracardiac target organ damage was consistently higher in patients with concentric LVH than in those with eccentric LVH. Systemic hemodynamics paralleled ventricular geometric patterns, with higher peripheral resistance and lower aortic compliance in patients with concentric LVH, whereas end-diastolic volumes and stroke volumes were higher in patients with eccentric LVH than in patients with concentric LVH. In addition, total peripheral resistance was related to retinal fundoscopic grade (r = 0.41, P < .01), and serum creatinine level (r = 0.28, P < .05). Even in the presence of an identical degree of LVH, echocardiographically determined left ventricular geometry may provide a further independent stratification of extracardiac target organ damage in essential hypertension.     

Magnesium transport across the basolateral plasma membrane of the fish enterocyte

The aim of the study was to assess the influence of aortic valve replacement on left ventricular size and muscle hypertrophy according to the type of preexisting valve disease (aortic stenosis, insufficiency or combined disease). The study group consisted of 143 consecutive patients (pts) after aortic valve replacement (109 men, 34 women, mean age 48.1 +/- 10.9 years). Reason for the operation was aortic stenosis in 35 pts, aortic insufficiency in 64 pts and combined disease in 44 pts. Echocardiography was performed before surgery, 1 month and 1 year after operation, and yearly during 5-year follow-up. Transvalvular aortic pressure gradients decreased significantly after valve replacement in all subsets without further changes during follow-up (Pmax (mmHg): from 54.2 +/- 20.7 to 17.9 +/- 9.6 in combined disease pts, from 72.3 +/- 19.9 to 21.6 +/- 14.6 in aortic stenosis and from 34.5 +/- 24.2 to 15.6 +/- 11.3 in aortic insufficiency pts, respectively, P < 0.0005). One year after surgery the diastolic dimension of the left ventricle decreased significantly in all subjects, whereas the systolic dimension only in aortic insufficiency and combined disease pts (from 44 +/- 11.8 to 31.6 +/- 5.4 mm, P < 0.001 and from 41.9 +/- 11.5 to 33 +/- 6.7 mm, P < 0.05, respectively). Further decrease of both diastolic and systolic dimensions was observed only in the aortic insufficiency group. Ejection fraction of left ventricle increased only in combined disease pts (from 51.6 +/- 10% to 56.8 +/- 8.2%, P < 0.05). Wall thickness of the left ventricle decreased 1 year after valve replacement only in the aortic stenosis group and in further follow-up in the aortic stenosis and combined disease group. Normalization of left ventricular size is observed in more than 90% of patients during 5-year follow-up as opposed to left ventricular muscle hypertrophy, regressed only in less than a half of the study population. In patients with aortic valve disease the greatest hemodynamic improvement is observed 1 year after valve replacement. This is expressed by marked reduction of the left ventricular dimensions and wall thickness, without significant improvement of the ejection fraction. Further regression of left ventricle dimensions occurs in patients operated on due to predominant valve insufficiency, whereas regression of left ventricular hypertrophy is observed in patients with preexisting valvular stenosis.     

Various ways of calculating echocardiographic left ventricular mass and their relative prognostic values

OBJECTIVE: To compare the calculations of left ventricular mass according to thick-wall [American Society of Echocardiography (ASE) and Penn convention] and thin-wall (Wikstrand formula) models. METHODS: We have reexamined the data from the cross-sectional study on the general population sample of Vobarno and from a prospective longitudinal study of hypertensive patients assessing the prognostic significance of changes in left ventricular mass during a follow-up period of 10 years on average (Brescia population). RESULTS: For the Vobarno and Brescia populations, we found a close relationship between values of left ventricular mass calculated by using a thin-wall ellipsoidal model (Wikstrand formula) and those calculated using a thick-wall model with Penn convention or ASE left ventricle measurements (r = 0.99, for both the Vobarno and Brescia populations). Highest values of Penn left ventricle mass were slightly underestimated by use of the thin-wall formula. The numbers of nonfatal cardiovascular events and the relative risks, evaluated by Cox proportional hazard models for 151 patients seen at follow-up did not differ for patients with persistence of left ventricular hypertrophy (LVH), those with regression of LVH, and those with normal left ventricle mass, both at baseline and at follow-up, when these different ways of measuring left ventricle mass and partition values for LVH were used. CONCLUSIONS: The calculation of left ventricle mass according to the ASE recommendations or to the Penn convention, both of which are based on the assumption that the left ventricle can be represented by a prolate ellipsoid with both the internal and external long axes twice the short axis, produces results similar to those obtained using an alternate formula for the calculation of left ventricle mass, considering wall thickness constant around the ellipsoidal cavity. The cardiovascular risk stratification, in relation both to baseline left ventricular mass and to its change during long-term antihypertensive treatment, does not differ significantly among the results of these three different calculations.     

Mitochondrial dysfunction in neurodegenerative disorders

Left ventricular hypertrophy with adequate wall thickness, preserved adult phenotype and extracellular matrix may be useful in the prevention of heart failure. Because activation of subtype 1 of angiotensin II (AT1) receptors is thought to be involved in the hypertrophic response of cardiomyocytes, we tested the potential of systemic AT1 blockade to modify the development of left ventricular hypertrophy due to pressure overload. Sham-operated rats and rats with ascending aorta constriction were treated with losartan (30 mg/kg/day) for 8 weeks. Left ventricular geometry, dynamics of isovolumic contractions, hydroxyproline concentration as well as myosin isozymes (marker of fetal phenotype) were assessed. Rats with aortic constriction exhibited a marked increase in left ventricular weight and the diastolic pressure-volume relationship was shifted to smaller volumes. An enlarged ventricular pressure-volume area and increased (p < 0.05) peak values of +dP/dtmax and- dP/dtmax demonstrated an enhanced overall ventricular performance. Signs of congestive heart failure were not apparent. In contrast, parameters of myocardial function (normalized length-stress area, +d delta /dtmax and -d delta /dtmax) were depressed (p < 0.05), indicating an impaired myocardial contractility. The hydroxyproline concentration remained unaltered. However, the proportion of beta-myosin heavy chains (MHC) was increased (p < 0.05). Administration of losartan decreased (p < 0.05) blood pressure and body weight in sham operated and pressure overloaded rats. By contrast, neither the concentric left ventricular hypertrophy or depressed myocardial function nor the increased beta-MHC expression were significantly altered. Thus, activation of AT1 receptors appears not to be involved in the initial expression of the fetal phenotype of pressure overloaded heart which may be responsible for the progressive functional deterioration of the hypertrophied ventricle.     

Regression of increased left ventricular masses in elderly hypertensive patients on lisinopril as assessed by magnetic resonance imaging

RATIONALE AND OBJECTIVES: We investigated, using magnetic resonance imaging, whether the addition of lisinopril could reduce increased left ventricular (LV) masses in hypertensive patients whose blood pressure was well controlled with nifedipine. METHODS: Fourteen hypertensive patients being treated with nifedipine and having an interventricular septum thickness of more than 12 mm were studied. Half of them were given 5 mg lisinopril, and the others were not. Short-axis images of the left ventricle from the base to the apex were obtained by a standard spin-echo pulse sequence. The entire LV mass was calculated from the area of short-axis slices of the left ventricle multiplied by slice thickness. RESULTS: Blood pressure fell slightly and almost equally in both groups. The LV mass and LV mass index showed a significant decrease in the lisinopril-treated group but not in the control group. CONCLUSION: Results demonstrate the effectiveness of lisinopril in reducing increased LV masses, at least in combination with nifedipine.     

Familial hypertrophic cardiomyopathy. Cardiac ultrasonic abnormalities in genetically affected subjects without echocardiographic evidence of left ventricular hypertrophy

AIMS: It is not known whether the apparent normality of echocardiographic examination results, in subjects bearing a mutation for hypertrophic cardiomyopathy but without ultrasonic left ventricular hypertrophy, is due to incomplete phenotypic expression, or inaccurate echocardiographic criteria. The aim of this study was to search for echocardiographic abnormalities in these patients. METHODS AND RESULTS: Echocardiography was performed in 100 subjects from two families with a mutation in the beta-MHC (720) or My-BPC (714) genes. We compared genetically affected subjects with an apparently normal left ventricle (thickness < 13 mm) (20 patients), and nonaffected first-degree relatives (61 normal subjects). (1) Patients had a thicker left ventricular wall (9.7 +/- 1.4 vs 8.9 +/- 1.4 mm, P = 0.03), a greater indexed mass (107 +/- 18 vs 97 +/- 17 g. m-2, P = 0.03), a larger left atrium (27 +/- 9 vs 23 +/- 10 mm3, P = 0.09) and lower wall stress (78 +/- 11 vs 89 +/- 15 10(3) dynes. cm-2, P = 0.002); these differences were highly significant after adjustment for height, age and systolic blood pressure either for wall thickness (P = 0.000003), mass (P = 0.005) or atrial volume (P = 0.001), and the ventricular systolic dimension appeared smaller (P = 0.01); (2) results remained significant (P < 0.01) when a lower cut-off value (< or = 11 mm) or only adults (> or = 18 years) were considered; (3) a subanalysis of Family 714 (13 patients, 25 normals matched for sex, age and height) showed the same trends. CONCLUSION: In familial hypertrophic cardiomyopathy, genetically affected subjects with an apparently normal heart by echocardiography show slight ultrasonic structural and functional left ventricular modifications, suggesting that the phenotype of the disease is a continuous spectrum from normal structure to typical hypertrophy.     

Echocardiography in the evaluation of ventricular function

The ultrasonic beam used for quantitative assessment of left ventricular (LV) function traverses the heart in a projection similar to the familiar angiographic left anterior oblique projection. It crosses the anterior wall of the right ventricle, the right ventricular cavity, the interventricular septum, the LV cavity and the posterior wall of the left ventricle. Whereas the cyclic changes of the right ventricular diameter are rarely clearly determined by echocardiography, the easily assessed cyclic changes of the LV endocardial transverse diameter are useful measure of LV FUNCTION. Of practical importance are the percentage of systolic shortening of the LV diameter (%Sh) and the mean velocity of circumferential fiber shortening (VCF). There are several factors, such as placing of the ultrasonic transducer, the shape and size of the LV cavity and rotational movements of the heart as a whole, that influence echocardiographic determination of the transverse LV diameter. In patients with asynergic contraction, %Sh and VCF cannot be used as measures of overall LV performance, but localized contraction disturbances of the septum and the posterior wall may be detected from the reduced extent of wall motion in a given LV segment during a full sweep from the base to the apex. The most important indications for echocardiographic assessment of LV function are valvar diseases with chronic LV pressure or volume overload, and congestive cardiomyopathy. Echocardiography has proved useful in serial evaluation of LV function in patients undergoing valvar heart surgery. Assessment of LV volume by standard echocardiography using the cubic formula is not satisfactory. More accurate determination of volumes is provided by formulas that include the actual ratio of the LV long axis to the minor axis.     

Latent impairment of left ventricular filling in hypertension without left ventricular hypertrophy and improvement by dipyridamole treatment: pulsed Doppler echocardiography study

Left ventricular (LV) filling impairment in patients with hypertension (HT) not necessarily associated with LV hypertrophy has not been sufficiently investigated. Therefore, we examined the response of LV filling to isometric exercise in patients with HT without LV hypertrophy and LV filling abnormality at rest. We studied 25 patients (aged 40 to 66 years, mean 51 +/- 7 years) and 13 age-matched normal subjects. The HT patients were selected by the following criteria: 1) systolic blood pressure (sBP) over 160 mmHg and/or diastolic BP over 90 mmHg was observed at least three times during the last 6 months, 2) LV wall thickness was under 11 mm, and 3) the ratio of peak atrial LV inflow velocity (A) to peak early diastolic LV inflow velocity (E) was within the mean +/- SD of normal subjects. LV inflow was measured by pulsed Doppler flowmetry before and during handgrip exercise (50% maximal effort for one minute and a half) in the patients before [HT-D (-)] and after [HT-D (+)] dipyridamole (D) administration (0.28 mg/kg/4 min) and in the normal subjects (N). Doppler-derived indices were A, E, A/E, DR (the deceleration rate from peak to half of the early diastolic inflow velocity), % delta A/E (% change in A/E from baseline), and % delta DR (% change in DR from baseline). There was no significant difference in LV wall thickness between the HT and N groups. There was also no significant difference in A/E at rest between the three groups. Increase of sBP and heart rate were similar in all groups during handgrip exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of age and exercise training on size and composition of the rat left main coronary artery

This study evaluated the effects of age and exercise training on the left main coronary artery (LMCA) in young (Y-5 months) and old (O-27.5 months) female Fischer 344 rats. Both age groups were divided into trained (T) and weight-matched sedentary (S) control groups. Training consisted of 10 weeks of treadmill running progressing to a maximum workload of 15% grade, 1 hr/day, 5 d/wk at speeds of 36 and 15 m/min for the Y and O rats, respectively. Aging resulted in a 40% increase in left ventricle (LV) weight which was proportional to the increased body weight of the old animals. Exercise training produced a mild (approximately 10%) but significant left ventricular hypertrophy (LVH) in both trained groups. Cross-sectional area of the LMCA lumen and wall, wall thickness, and areas of collagen (C), elastin (E), and collagen-to-elastin ratio (C/E) of the LMCA wall were determined morphometrically in all four groups. A method for pinpointing the coronary ostium for use as a reference point was also developed. LMCA lumen area almost doubled (p < .001) across the measured age difference, but was unaffected by training. With aging, the increase in LMCA wall area bordered on significance (p < .053), while wall thickness, C area, and the C/E ratio were unchanged. Our results indicate that there is a disproportionate increase in the cross-sectional area of the rat LMCA with respect to LV mass changes with aging. This finding presumably reflects adaptation of this vessel to elevated resistances further downstream in the coronary circulation so that tissue perfusion can be maintained.(ABSTRACT TRUNCATED AT 250 WORDS)     

Angiographic and morphologic features of the left ventricle in Ebstein's malformation

Quantitative and qualitative cineangiographic analysis of the left ventricle (LV) was performed in 26 patients with isolated Ebstein's malformation, having a mean age of 23 +/- 17 years. Nine autopsied hearts with isolated Ebstein's malformation were submitted to morphologic and morphometric analysis. In 4 of the cases, it was possible to make a direct correlation between the angiographic data obtained during life and the autopsy findings. On the basis of the LV end-diastolic volume we identified 3 groups of patients: 7 with volume <60 ml/m2, another 7 with volume between 60 and 80 ml/m2, and 12 with volume >80 ml/m2. The LV ejection fraction was reduced in 2 patients with normal LV end-diastolic volume and in 6 with increased LV end-diastolic volume. The ratio of ventricular mass to LV end-diastolic volume was always adequate, but a reduction of the ventricular contractive performance (end-systolic pressure to end-systolic volume ratio <3 mm Hg/ml/m2) was found only in patients with a dilated left ventricle. No correlation was demonstrated between the extent of the atrialized component of the right ventricle (mean value 67 +/- 31 cm2, range 13 to 133) and the LV dimensions. All but 2 patients showed a leftward diastolic displacement of the ventricular septum, but in only 1 did this produce an elongated shape of the left ventricle. Sixteen had anomalies of LV dynamics: 10 with hypokinesia (3 of the posterior wall, 4 of the apex, 1 of the inferior wall, 1 of the septum, and 1 global), 6 with dyskinesia (1 of the posterior wall, 2 of the apex, 1 of the posterior wall and apex, 1 of the superior part of the septum, and 1 of the anterior wall), and 8 with premature diastolic distension of the anterobasal wall. Morphometric analysis produced mean values for myocytes of 59 +/- 10%, for the interstitium of 21 +/- 4%, and for fibrous tissue of 20 +/- 9% (normal 4 +/- 1%). Five autopsied hearts had a prolapsing and/or dysplastic mitral valve.     

Quantitative two-dimensional echocardiographic assessment of regional wall motion during transient ischemia and reperfusion in the rat

Nonlethal myocardial ischemia produces profound and long-lasting effects on regional ventricular function and metabolism (myocardial stunning) and protects against myocardial infarction from subsequent prolonged ischemia (ischemic preconditioning). Two-dimensional echocardiography (2DE) is an essential tool for quantitative analysis of regional and global left ventricular (LV) function during myocardial ischemia and reperfusion and the study of these phenomena. However, the inability to perform 2DE in the open-chest rat heart has seriously limited the use of this model. To investigate the effect of transient coronary occlusion on segmental wall motion and LV geometry, we employed a 20 MHz intravascular ultrasound catheter placed on the epicardial surface of the rat heart (n = 15) to yield 2DE images suitable for quantitative analysis. Three 2-minute left coronary occlusions were made, separated by 5 minutes of reperfusion, with imaging during occlusion and at 5 and 60 minutes of reperfusion. Ischemic and nonischemic wall thicknesses, LV cross-sectional area, estimated LV volume, and the fractional changes of these parameters were measured. In eight animals these values were also compared with necropsy measurements of wall thickness, LV cross-sectional area, and volume. LV and right ventricular structures were well visualized in short-axis cross-sectional images in all animals, and images suitable for quantitative analysis were obtained in 92% of the periods. Coronary occlusion caused immediate, marked LV cavitary expansion, which rapidly returned to normal by 5 minutes of reperfusion. Active systolic thickening of the anterior wall at baseline (47% +/- 3%) became passive thinning during occlusion (-6% +/- 2%) and recovered partially, to 30% +/- 3% at 5 minutes of reperfusion and 42% +/- 4% at 60 minutes (p < 0.0005 at 5 minutes of reperfusion vs baseline; p not significant at 60 minutes). Recovery of thickening after 5 minutes of reperfusion was not different after the first versus third occlusion (23% +/- 4% vs 30% +/- 3%; p = 0.19). Measurements made by 2DE correlated well with those made by necropsy, although wall thickness was slightly thicker by 2DE. We conclude that epicardial echocardiography with an intravascular ultrasound catheter provides quantifiable 2DE images in this model and yields accurate information on segmental wall thickening and ventricular geometry not available by other techniques. Left coronary occlusion in the rat is associated with marked global and segmental LV expansion, which rapidly reverses with reperfusion. Postischemic regional wall motion abnormalities are present after coronary occlusion as brief as 2 minutes and can be measured accurately. The effect of multiple brief occlusions is not cumulative.(ABSTRACT TRUNCATED AT 400 WORDS)     

Dynamic stiffness and implications for assisting the operation of the left ventricle

The distribution of bending strain and stiffness in the wall of the left ventricle (LV) is relevant to the augmentation of its function by a modified skeletal-muscle wrap in the new surgical procedure of cardiomyoplasty. A novel approach to ventricular mechanics is presented which blends some finite-element results in engineering with new data available on ventricular geometry. Two simplified axisymmetric strip-element models of the LV are used to illustrate aspects of myocardial stiffness in the bending-strain-energy distribution and the effect on wrap synchronization of a change in cross-fibre stiffness when the heart has nonuniform or ectopic beats. The nonlinear and time-dependent nature of both camping and wall stiffness is derived from differential equations governing the dynamic paths from systole to diastole of finite wall elements around the periphery of an oblique LV slice using magnetic resonance imaging (MRI) data. This leads to a geometric method for determining these parameters. Results for time-dependent stiffnesses of elements in their trajectories are presented for a normal heart.     

Effect of endurance training on cardiac morphology in Alaskan sled dogs

The cardiac morphology of 77 conscious Alaskan sled dogs before and after 5 mo of endurance training (20 km/day team pulling a sled and musher) was studied using two-dimensional and M-mode echocardiography. Subgroups included dogs with at least one season of previous training ("veterans") and dogs undergoing their first season of training ("rookies"). Training resulted in a significant (P < 0.05) decrease in resting heart rate (-15%) and significant increases in interventricular septal thickness (systole, 15%; diastole, 13%), left ventricular (LV) internal dimension in diastole (LVIDd, 4%), LV free wall thickness in systole (9%) and diastole (LVWd, 9%), and left atrial diameter (5%) in all dogs, but the increase in LVWd was greater in rookies (16%) than in veterans (7%). Training increased end-diastolic volume index (8%), LV mass index (24%), and heart weight index (24%) and decreased the LVIDd-to-LVWd ratio (-6%) but did not alter cardiac index. We conclude that increased LV mass attributable to LV dilation and hypertrophy is associated with endurance training in Alaskan sled dogs. Disproportionate LV wall thickening accompanying LV dilation suggests that cardiac morphological changes are due to volume and pressure loading. These training-induced changes are similar to those documented in human athletes undergoing combined isometric and isotonic training and differ from studies of dogs trained on treadmills.     

Differential responsiveness of murine T lymphomas to local growth and invasion factors may determine metastasis formation in the ovaries

Iodine-123-metaiodobenzylguanidine [123I-MIBG] has been used to evaluate the cardiac sympathetic nervous system. We evaluated the effect of pulmonary hypertension on the sympathetic neuronal function of the left ventricle in patients with pulmonary hypertension. We studied 20 patients with either chronic lung disease or pulmonary vascular disease. The patients were divided into a pulmonary hypertensive group and a control group. Single photon emission tomography was performed in the resting state 15 min and 4 h after administration of 123I-MIBG. Regions of interest (ROI) were set in the left ventricular (LV) free wall, the interventricular septum (IVS) and outside the LV free wall on short-axis images. The washout rate and the ROI/LV uptake ratio were calculated in each ROI. The IVS:LV uptake ratio was significantly lower in the pulmonary hypertensive group than in the control group. Our results suggest that left heart sympathetic neuronal dysfunction initially occurs in the IVS before it involves the LV free wall subsequently.