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Biomedical subjects

G de Simone

Publications and source records attributed to G de Simone.

At least 91 records · Page 5Linked to original sources
PubMed1994

Assessment of left ventricular function by the midwall fractional shortening/end-systolic stress relation in human hypertension.

OBJECTIVES: This study examined left ventricular performance in relatively unselected hypertensive patients by use of physiologically appropriate midwall shortening/end-systolic stress relations. BACKGROUND: Supranormal left ventricular function has been reported in hypertensive patients, possibly due to an artifact of mismatching endocardial rather than midwall fractional shortening to mean left ventricular end-systolic stress. METHODS: Samples of 474 hypertensive patients (150 women, 324 men) and 140 normal subjects (68 women, 72 men) were drawn from a large urban employed population. The inverse relations (p < 0.0001) of both echocardiographic endocardial and midwall fractional shortening to end-systolic stress in normal subjects were used to calculate the ratios of observed to predicted endocardial and midwall fractional shortening in hypertensive patients. Midwall shortening was calculated from an elliptic model, taking into account the epicardial migration of the midwall during systole. RESULTS: Use of midwall fractional shortening in hypertensive patients reduced the proportion of patients with function above the 95th percentile of normal from 22% to 4% (p < 0.0001) and fractional shortening as a percent of predicted from 107% (p < 0.001 vs. 100% in normotensive control subjects) to 95% (p < 0.0001; p < 0.001 vs. 101% in normotensive control subjects). Midwall shortening was below the 5th percentile of normal in 16% of hypertensive patients instead of 2% with endocardial shortening (p < 0.0001): They tended to be older than other hypertensive patients and had concentric left ventricular hypertrophy. Among hypertensive patients, those with concentric left ventricular hypertrophy or remodeling had reduced midwall shortening as a percent of predicted from end-systolic stress (p < 0.0001). CONCLUSIONS: Use of the physiologically more appropriate midwall shortening/end-systolic stress relation 1) markedly reduces the proportion of hypertensive subjects identified as having high endocardial left ventricular function; and 2) identifies a substantial subgroup of patients with reduced left ventricular function who have concentric geometry of the left ventricle, a pattern associated with high cardiovascular risk.

Adult↗
PubMed1994

Echocardiographic assessment of left ventricular hypertrophy in rats using a simplified approach.

To determine whether left ventricular (LV) mass could be determined relatively simply in rats, without loss of accuracy, we reanalyzed previously reported echocardiographic measurements of 41 normotensive and 17 hypertensive male Wistar rats. Rats were divided into separate learning and test series. We assumed LV weight (g) = 1.04 x 4 x tau x [(D+h)2(L+h)-D2L]/3 x 10(3), where D was the LV short axis, h was the mean thickness of posterior wall and septum, measured in mm by M-mode echocardiography, and L was the long axis. Because L was not measurable by two-dimensional echocardiography, due to the high heart rate, it was estimated to be 12.28 mm by nonlinear regression analysis in the learning series of 29 rats. Correlation between necropsy LV weight and echocardiographic LV mass was 0.91 in the learning series and 0.89 in the test series (standard error of estimate [SEE] = 0.09 and 0.11 g). Mean values in the test series were 0.77 +/- 0.28 g and 0.78 +/- 0.25 g for LV weight and LV mass, respectively. LV mass was systematically underestimated by the cube-function formula (0.59 +/- 0.23 g, P < .0001 v necropsy LV weight). Echocardiographic LV mass using the ellipsoidal model with the above constant to estimate LV long axis had 78% sensitivity and 100% specificity for anatomic LV hypertrophy, suggesting that this method may be useful for research on rat models of hypertension.

Animals↗
PubMed1994

Cardiac abnormalities in young women with anorexia nervosa.

OBJECTIVE: To identify the characteristics of cardiac involvement in the self-induced starvation phase of anorexia nervosa. METHODS: Doppler echocardiographic indices of left ventricular geometry, function, and filling were examined in 21 white women (mean (SD) 22 (5) years) with anorexia nervosa according to the DSMIII (Diagnostic and Statistical Manual of Mental Disorders) criteria, 19 women (23 (2) years) of normal weight, and 22 constitutionally thin women (21 (4) years) with body mass index < 20. RESULTS: 13 patients (62%) had abnormalities of mitral valve motion compared with one normal weight woman and two thin women (p < 0.001) v both control groups). Left ventricular chamber dimension and mass were significantly less in women with anorexia nervosa than in either the women of normal weight or the thin women, even after standardisation for body size or after controlling for blood pressure. There were no substantial changes in left ventricular shape. Midwall shortening as a percentage of the values predicted from end systolic stress was significantly lower in the starving patients than in women of normal weight: when endocardial shortening was used as the index this difference was overestimated. The cardiac index was also significantly reduced in anorexia nervosa because of a low stroke index and heart rate. The total peripheral resistance was significantly higher in starving patients than in both control groups. The left atrial dimension was significantly smaller in anorexia than in the women of normal weight and the thin women, independently of body size. The transmitral flow velocity E/A ratio was significantly higher in anorexia than in both the control groups because of the reduction of peak velocity A. When data from all three groups were pooled the flow velocity E/A ratio was inversely related to left atrial dimension (r = -0.43, p < 0.0001) and cardiac output (r = -0.64, p < 0.0001) independently of body size. CONCLUSIONS: Anorexia nervosa caused demonstrable abnormalities of mitral valve motion and reduced left ventricular mass and filling associated with systolic dysfunction.

Adult↗
PubMed1994

Relation of obesity and gender to left ventricular hypertrophy in normotensive and hypertensive adults.

Although it is recognized that both hypertension and obesity are associated with increased left ventricular mass, the relative impacts of obesity, arterial hypertension, and gender on the prevalence of ventricular hypertrophy remain uncertain. Accordingly, echocardiographic left ventricular mass normalized for height to the power of the allometric or growth relation between ventricular mass and height was compared in 164 normotensive subjects (85 men [24 obese] and 79 women [28 obese], aged 45 +/- 12 years) and 475 hypertensive patients (325 men [126 obese] and 150 women [85 obese], aged 54 +/- 10 years) from an adult employed population. Gender-specific upper normal limits were used to identify ventricular hypertrophy. Left ventricular mass/height 2.7 was higher in obese than normal-weight normotensive subjects (P < .004) independently of the level of blood pressure and identified a higher prevalence of hypertrophy (mainly eccentric) in obese than in normal-weight normotensive subjects (14% versus 5%, P < .04), a difference that was not detected by left ventricular mass/body surface area. Left ventricular mass/height identified hypertrophy in 52% of obese and 30% of normal-weight hypertensive patients (P < .0001) because of higher prevalences in obese than normal-weight patients of both eccentric (34% versus 20%) and concentric ventricular hypertrophy (18% versus 10%). The increase in left ventricular mass was independent of blood pressure values in obese normotensive women (but not men), and the prevalence of supranormal left ventricular mass/height 2.7 was even higher in hypertensive obese women (58%) than men (49%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Cardiac and arterial hypertrophy and atherosclerosis in hypertension.

Clinical evaluation of the hypertensive patient has traditionally relied on physician measurement of blood pressure and assessment of target-organ involvement by simple laboratory tests. However, this approach is limited in its ability to identify individual patients at high or low risk of complications. In recent years, noninvasive methods have been developed to identify pathological transformations of the heart and arteries that collectively comprise "preclinical hypertensive disease." Measurements by echocardiogram or other methods of left ventricular mass and relative wall thickness identify a spectrum of cardiac adaptations to hypertension, including concentric and eccentric hypertrophy, the recently described pattern of "concentric left ventricular remodeling" (normal mass but increased relative wall thickness), and normal ventricular geometry. In clinical studies, each anatomic pattern is associated with a distinct profile of resting hemodynamics, ambulatory blood pressure, myocardial contractility, and risk of adverse outcomes. Ultrasonic imaging of the carotid or other arteries makes it possible to detect increased arterial wall thickness and discrete atheromas noninvasively. Carotid wall thickness and lumen diameter parallel similar ventricular dimensions in normotensive and hypertensive humans, indicating the presence of integrated patterns of cardiac and vascular adaptation to hypertension. Furthermore, peripheral atherosclerosis is associated with higher ventricular mass and a more adverse 24-hour blood pressure profile. In summary, noninvasive visualization of the heart and blood vessels reveals a spectrum of patterns of anatomic and functional adaptations that are related to the pathophysiology and prognosis of hypertension.

Arteries↗
PubMed1994

Left ventricular hypertrophy and geometric remodeling in hypertension: stimuli, functional consequences and prognostic implications.

OBJECTIVE: To provide a coherent overview of the stimuli to development of abnormal left ventricular geometric patterns, their impact on cardiac function and their relationship to the prognosis of hypertension, studies performed by the authors and other investigators are reviewed. RESULTS: Clinical and experimental studies have shown that an elevated left ventricular mass reflects the additive effects on the heart of higher arterial pressure over time, increased cardiac volume load related to obesity, sodium intake or other stimuli, reduced contractile efficiency of the myocardium and altered arterial hemodynamics related to vascular hypertrophy and atherosclerosis. The heart may adapt to hypertension by developing concentric or eccentric left ventricular hypertrophy, or the newly described pattern of concentric left ventricular remodeling, or by retaining normal left ventricular geometry. Each geometric pattern is associated with a distinct combination of pressure and volume stimuli, contractile efficiency (reduced in those with concentric left ventricular hypertrophy or remodeling) and prognosis (worst with concentric hypertrophy and best with normal left ventricular geometry). An appraisal of left ventricular mechanics by a physiologically appropriate midwall-shortening/end-systolic stress relationship can identify impaired contractility in an appreciable proportion of hypertensive patients. Numerous studies have shown that increased left ventricular mass and abnormal geometry have a strong predictive value for cardiovascular death, myocardial infarction and stroke. CONCLUSIONS: Increasing evidence has demonstrated the central importance of left ventricular mass and geometry in the pathophysiology and prognosis of hypertension. These measures of preclinical disease can aid clinical decision-making by separating patients into those with a high or a relatively low risk, and hence a need for pharmacological treatment or its intensification, as well as providing useful bioassays for a spectrum of clinical and experimental research.

Humans↗
PubMed1994

Evaluation of left ventricular hypertrophy by M-mode echocardiography in patients and experimental animals.

In validation studies, M-mode echocardiography has been shown to measure left ventricular (LV) mass with reasonable accuracy (r > or = .90 v necropsy measurements) in species ranging in body size from humans to rats. The sensitivity of antemortem echocardiography for the detection of necropsy LV hypertrophy as a qualitative abnormality has also been high (85% to 100%). Increased LV mass is strongly related to both increased blood pressure and to being overweight or to other causes of increased cardiac volume work. LV mass is also increased in the presence of exaggerated blood pressure responses to everyday activity, high sodium intake and blood viscosity, and genetic factors predisposing to hypertension. Indexation of LV mass by body surface area or height has advantages for the detection of hypertrophy related to hypertension or obesity. Indexation of LV mass for the power of its relation to height (2.7) revealed by analysis of growth (allometric) relations may accomplish both these goals. Recent research indicates that the level of LV mass measured by M-mode echocardiography is a stronger predictor of subsequent morbid events and death than blood pressure or other conventional risk factors except age. Preliminary findings of close relations between LV mass and arterial disease and between the change in LV mass during antihypertensive treatment and subsequent events contribute to explaining the strong predictive value of LV mass.

Adult↗
PubMed1993

Ambulatory blood pressure monitoring in offspring of hypertensive patients. Relation to left ventricular structure and function.

The relation between 24-h ambulatory blood pressure monitoring and echocardiographic left ventricular (LV) anatomy and function was examined in 30 young, normotensive offspring (16 men, 14 women) of hypertensive, parents and in 20 offspring (12 men, 8 women) of normotensive parents, comparable for age, clinical blood pressure, and gender. Offspring of hypertensive subjects exhibited higher body mass index (P < .01), relative wall thickness, and LV mass/height (both P < .001). No significant difference was found in LV chamber dimensions and in either systolic or diastolic function. The 24-h systolic and diastolic blood pressures were higher in offspring of hypertensive subjects than in controls (P < .001 and P < .0001, respectively), as was the coefficient of variation of 24 h systolic blood pressure (P < .01). In pooled groups, LV mass was positively related to daytime systolic blood pressure (r = 0.48), daytime diastolic blood pressure (r = 0.47) (both P < .001), and the coefficient of variation of 24 h diastolic blood pressure (r = 0.37, P < .01). In a multiple regression model, including as variables, body mass index, daytime systolic and diastolic blood pressures, male gender, and family history of hypertension were the major independent predictors of LV mass (both P < .0001), with an additional contribution of the coefficient of variation of 24 h diastolic blood pressure (P < .05). We conclude that male gender and a family history of hypertension are stronger determinants of early changes in cardiac structure than hemodynamic load in a group of young, normotensive adults.

Adolescent↗
PubMed1993

Methods for detection of left ventricular hypertrophy: application to hypertensive heart disease.

Left ventricular hypertrophy (LVH) detected by electrocardiography (ECG) and, more recently, by echocardiography has been shown to be an extremely strong predictor of morbidity and mortality in patients with essential hypertension and in members of the general population. Increased left ventricular mass (LVM) is strongly related to both increased blood pressure and overweight. Indexation of LVM by body surface or height has advantages for the detection of LVH related to hypertension or obesity. Indexation of LVM for height to the power 2.7 revealed by analysis of growth (allometric) relations may accomplish both these goals. In validation studies, the sensitivity of echocardiography to detect LVH has been reasonably high (85-100%), whereas that of ECG has ranged from as high as 50% in severely diseased necropsy populations to as low as 6-17% in recent studies in Cornell and Framingham. ECG sensitivity can be improved by using Cornell multivariate regression equations or by consideration of the Cornell voltage-QRS duration product. Obesity dramatically decreases the sensitivity of the ECG for detection of LVH, and recent research suggests a lower specificity and a higher rate of false-positive ECG diagnoses of LVH in black than in white subjects. Standard criteria for ECG LVH are less useful than echocardiographic findings for stratifying populations into high- and low-risk subgroups because of lower sensitivity, but improved ECG criteria need further evaluation in this respect.

Echocardiography↗
PubMed1993

Left ventricular hypertrophy associated with hypertension and its relevance as a risk factor for complications.

Recent research indicates that the level of left ventricular (LV) mass, commonly measured by echocardiography, reflects the combined effects of a variety of factors involved in the pathophysiology of hypertension, including obesity, blood pressure responses to everyday activity, high sodium intake and blood viscosity, the volume work load of the heart, and genetic factors predisposing to hypertension. Prospective studies indicate that LV mass is a stronger predictor of subsequent morbid events and death than blood pressure or other conventional risk factors except age. Preliminary findings of close relations between LV mass and arterial disease and between the change in LV mass during antihypertensive treatment and subsequent events contribute to explaining the strong predictive value of LV mass. Further research is needed to clarify the biologic basis of these observations and to determine whether stratification of hypertensive patients based on their level of LV mass can improve the treatment of hypertension.

Cardiovascular Diseases↗
PubMed1993

Influence of sodium intake on in vivo left ventricular anatomy in experimental renovascular hypertension.

The effect of different dietary salt contents (0.0035, 0.4, and 4%) on in vivo left ventricular (LV) geometry was studied by necropsy-validated echocardiographic methods in groups of 30 two-kidney, one-clip (2K, 1C) and one-kidney, one-clip (1K, 1C) male Wistar rats and two-kidney (2K) and one-kidney (1K) shams 9 wk after surgery. The salt-deficient diet was associated with lower body weight, higher plasma renin activity in both 2K,1C and 2K shams (P < 0.004) and higher hematocrit in 2K,1C (P < 0.02). Blood pressure was increased by high-salt diet in experimental groups but not in shams (P < 0.01). Increase in dietary sodium content was associated with increased cross-sectional area index (CSAI) and LV mass index in 2K rats independently of renal artery stenosis (P < 0.0007) and also in 1K shams (P < 0.01). LV end-diastolic dimension was greater in 1K,1C and 1K shams than in 2K,1C and 2K shams at every level of sodium intake and was directly related to atrial natriuretic factor levels in both 1K,1C (r = 0.68) and 2K,1C (r = 0.59). LV hypertrophy was independently predicted by blood pressure (P < 0.0006) and high-sodium diet (P < 0.05) in 1K rats (multiple r = 0.57, P < 0.001) and by high-sodium diet (P < 0.0001) and low hematocrit (P < 0.05) in 2K rats (multiple r = 0.76, P < 0.0001). Thus provision of normal or high sodium content in the diet was a more consistent stimulus to LV hypertrophy than the level of blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Left ventricular hypertrophy and hypertension.

The level of left ventricular (LV) mass as measured by echocardiography or other techniques in hypertensive patients reflects the integrated effects of the level of arterial pressure, the concomitant volume load imposed on the heart, and of alterations in arterial waveform morphology as well as of body size and non-hemodynamic variables. The LV may respond to these stimuli by concentric or eccentric hypertrophy or by the recently-described pattern of concentric remodeling, in which LV mass is normal but relative wall thickness is increased. The are strong parallelisms between increases in cardiac and systemic arterial wall thicknesses, and patients with discrete atheromas detectable by carotid ultrasound have elevated LV masses. Patients with eccentric and concentric LV hypertrophy have two to four-fold increases in the incidence of cardiovascular morbid events compared to hypertensive patients with normal LV geometry, and the change in LV mass during treatment has been associated with the risk of subsequent morbidity in initial studies. In contrast to the strong predictive power of LV geometric assessment, use of indirect measures of target organ status in the WHO system for classification of the severity of hypertension does not improve on the prediction of prognosis that can be obtained by consideration of the level of arterial pressure. Current evidence suggests that evaluation of LV geometry may contribute to improved clinical decision-making in situations where more precise stratification of risk would clarify whether or not to institute treatment, or whether it should be with drugs or non-pharmacologic measures.

Adaptation, Physiological↗
PubMed1992

Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight.

OBJECTIVES: This study was designed to determine the most appropriate method to normalize left ventricular mass for body size. BACKGROUND: Left ventricular mass has been normalized for body weight, surface area or height in experimental and clinical studies, but it is uncertain which of these approaches is most appropriate. METHODS: Three normotensive population samples--in New York City (127 adults), Naples, Italy (114 adults) and Cincinnati, Ohio (444 infants to young adults)--were studied by echocardiography. Relations of left ventricular mass to body size were similar in all normal weight groups, as assessed by linear and nonlinear regression analysis, and results were pooled (n = 611). RESULTS: Left ventricular mass was related to body weight to the first power (r = 0.88), to body surface area to the 1.5 power (r = 0.88) and to height to the 2.7 power (r = 0.84), consistent with expected allometric (growth) relations between variables with linear (height), second-power (body surface area) and volumetric (left ventricular mass and body weight) dimensions. Strong residual relations of left ventricular mass/body surface area to body surface area (r = 0.54) and of ventricular mass/height to height (r = 0.72) were markedly reduced by normalization of ventricular mass for height2.7 and body surface area1.5. The variability among subjects of ventricular mass was also reduced (p < 0.01 to p < 0.002) by normalization for body weight, body surface area, body surface area1.5 or height2.7 but not for height. In 20% of adults who were overweight, ventricular mass was 14% higher (p < 0.001) than ideal mass predicted from observed height and ideal weight; this increase was identified as 14% by left ventricular mass/height2.7 and 9% by ventricular mass/height, whereas indexation for body surface area, body surface area1.5 and body weight erroneously identified left ventricular mass as reduced in overweight adults. CONCLUSIONS: Normalizations of left ventricular mass for height or body surface area introduce artifactual relations of indexed ventricular mass to body size and errors in estimating the impact of overweight. These problems are avoided and variability among normal subjects is reduced by using left ventricular mass/height2.7. Simple nomograms of the normal relation between height and left ventricular mass allow detection of ventricular hypertrophy in children and adults.

Adult↗
PubMed1992

Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension.

The spectrum of left ventricular geometric adaptation to hypertension was investigated in 165 patients with untreated essential hypertension and 125 age- and gender-matched normal adults studied by two-dimensional and M-mode echocardiography. Among hypertensive patients, left ventricular mass index and relative wall thickness were normal in 52%, whereas 13% had increased relative wall thickness with normal ventricular mass ("concentric remodeling"), 27% had increased mass with normal relative wall thickness (eccentric hypertrophy) and only 8% had "typical" hypertensive concentric hypertrophy (increase in both variables). Systemic hemodynamics paralleled ventricular geometry, with the highest peripheral resistance in the groups with concentric remodeling and hypertrophy, whereas cardiac index was super-normal in those with eccentric hypertrophy and low normal in patients with concentric remodeling. The left ventricular short-axis/long-axis ratio was positively related to stroke volume (r = 0.45, p less than 0.001), with cavity shape most elliptic in patients with concentric remodeling and most spheric in those with eccentric hypertrophy. Normality of left ventricular mass in concentric remodeling appeared to reflect offsetting by volume "underload" of the effects of pressure overload, whereas eccentric hypertrophy was associated with concomitant pressure and volume overload. Thus, arterial hypertension is associated with a spectrum of cardiac geometric adaptation matched to systemic hemodynamics and ventricular load. Concentric left ventricular remodeling and eccentric hypertrophy are more common than the typical pattern of concentric hypertrophy in untreated hypertensive patients.

Adaptation, Physiological↗
PubMed1992

Relation of left ventricular hypertrophy, afterload, and contractility to left ventricular performance in Goldblatt hypertension.

To analyze the determinants of left ventricular (LV) performance (myocardial afterload, chamber size, mass, and contractility) in Goldblatt hypertension, 19 anesthetized one-kidney, one-clip (1K1C) and 28 two-kidney, one-clip (2K1C) male Wistar rats were studied 58 to 62 days after clipping, together with 19 sham-operated and 13 normal rats (controls), by M-mode echocardiography using necropsy-validated methods of measurement. The LV fractional shortening was inversely related to end-systolic stress in all groups (r = -0.89 to -0.95, all P less than .00001): 7 2K1C (25%) and 9 1K1C (47%) had fractional shortening above the upper confidence limit in control animals. Both 1K1C and 2K1C with high LV performance had severe hypertension, inadequate LV hypertrophy, with resultant high wall stress (both P less than .005), increased LV chamber dimension (P less than .005 and P less than .05, respectively) and high afterload-corrected fractional shortening (both P less than .001); 2K1C also had high plasma renin activity and atrial natriuretic factor levels (both P less than .01). Rats with normal LV performance exhibited mild hypertension, adequate LV hypertrophy (normalizing wall stress), and normal LV chamber size and afterload-corrected fractional shortening. Thus, 8 1/2 weeks after clipping, adequate LV hypertrophy allows maintenance of normal LV function by normalizing myocardial afterload in a majority of rats with Goldblatt hypertension, whereas increased LV contractility (and possibly use of preload reserve in 1K1C) maintains normal LV function in the presence of inadequate LV hypertrophy and elevated wall stress, in a substantial minority of rats that developed more severe Goldblatt hypertension.

Animals↗
PubMed1992

Left ventricular mass as a measure of preclinical hypertensive disease.

The ability to identify the hypertensive patient who is destined to suffer a morbid or fatal complication in the long presymptomatic phase of this condition, when its natural history would be most subject to amelioration, is limited by the weak relation between the level of blood pressure and the occurrence of complications. Recent research indicates that the level of left ventricular (LV) mass--most conveniently measured by echocardiography--reflects the combined effects of a variety of factors involved in the pathophysiology of hypertension, including obesity, exaggerated blood pressure responses to everyday activity, high sodium intake and blood viscosity, and genetic factors predisposing to hypertension. Prospective studies indicate that LV mass is a stronger predictor of subsequent morbid events and death than blood pressure or other conventional risk factors except age. Preliminary findings of close relations between LV mass and arterial disease and between the change in LV mass during antihypertensive treatment and subsequent events contribute to explaining the strong predictive value of LV mass. Further research is needed to clarify the biologic basis of these observations and to determine whether stratification of hypertensive patients based on their level of LV mass can improve the treatment of hypertension.

Echocardiography↗