Left ventricular function response to exercise in normotensive obese subjects: influence of degree and duration of obesity

Licata, Giuseppe; Scaglione, Rosario; Paterna, Salvatore; Parrinello, Giovanni; Indovina, A; Dichiara, M. A.; Alaimo, Giuseppe; Merlino, Giovanni

doi:10.1016/0167-5273(92)90212-l

Cited by 28 publications

(28 citation statements)

References 15 publications

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“…47,48 For LVH a different explanation is possible; subjects with increased prevalence of LVH at 1 y were older, were hypertensive, and had a longer duration of obesity, and hypertension 5,6,39,42 and duration of obesity 49 are risk factors Obesity, hypertension, LVH, QT interval AE Pontiroli et al for LVH. Reversibility of hypertension is possible with prolonged treatment with various antihypertensive drugs that lead to sustained reduction of the haemodynamic impact; 50 Fagerberg et al 51 found that reduced sodium intake coupled with reduced energy intake is more effective than reduced energy intake alone in reducing blood pressure in obese-hypertensive patients; finally, we should recall that, with all surgical techniques such as bilio-pancreatic diversion, gastric by pass, and gastric banding, many subjects remain hypertensive, whatever the amount of weight loss; 32,52-54 even more important, in the Swedish obesity study it was shown that surgery does not prevent development of arterial hypertension.…”

Section: Discussionmentioning

confidence: 99%

Left ventricular hypertrophy and QT interval in obesity and in hypertension: effects of weight loss and of normalisation of blood pressure

et al. 2004

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BACKGROUND: Left ventricular hypertrophy (LVH) and prolonged QT interval at ECG (QTc) are common in both obesity and arterial hypertension (AH), and are risk factors for cardiovascular disease and sudden death. METHODS: We compared the frequencies of LVH (ECG criteria) and QTc in obese-AH (n ¼ 41), in normotensive obese (n ¼ 75), in lean-AH (n ¼ 30), and in lean controls (n ¼ 68) comparable for age and sex; in obese patients, LVH and QTc were evaluated under basal conditions and 1 y later, that is, after a significant weight loss induced by bariatric surgery. RESULTS: LVH was more frequent, and QTc was longer, in obese-AH, in normotensive obese, and in lean-AH than in lean controls; after weight loss, frequency of LVH decreased in obese subjects becoming normotensive (n ¼ 87), not in obese subjects remaining hypertensive (n ¼ 29), while QTc decreased in all obese subjects. CONCLUSION: Weight loss can effectively reduce QTc; when concomitant AH disappears, weight loss can also reduce the prevalence of LVH. In obese patients remaining hypertensive, aggressive pharmacological treatment is therefore indicated to correct LVH.

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Section: Discussionmentioning

confidence: 99%

Left ventricular hypertrophy and QT interval in obesity and in hypertension: effects of weight loss and of normalisation of blood pressure

et al. 2004

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“…Abnormalities of left-ventricular diastolic filling have been observed in asymptomatic pathologically obese patients at rest compared to lean subjects [10]. On the other hand, an increased left-ventricular ejection fraction has been described at peak exercise in the majority of a group of overweight subjects [11].…”

Section: Introductionmentioning

confidence: 94%

Oxygen Uptake and Cardiac Performance in Obese and Normal Subjects during Exercise

et al. 1999

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Work capacity and cardiopulmonary performance were studied in a group of 11 young obese subjects (BMI 39.9 kg/m²) and a group of 10 young normal subjects (BMI 22 kg/m²). First of all they underwent an incremental cycle ergometer test up to exhaustion. Subsequently, every subject of the two groups performed a constant work rate test at different work loads to estimate cardiac output (q̇) below anaerobic threshold (AT) by a 20-second CO₂ rebreathing method. Obese subjects had a significantly lower AT (79 vs. 109 W). The ratio between oxygen uptake and heart rate (v̇O₂/HR) (O₂ pulse) was higher in the obese group; nevertheless, this variable became significantly lower if we took into consideration the ratio between O₂ pulse and kilogram fat-free body mass or kilogram body weight. Both these observations suggest that their reduced work tolerance is linked with a reduced oxygen supply to the muscles in activity. q̇ increased in similar ways in obese and normal subjects at the preset work rates. The ratio q̇/body surface (cardiac index; CI) that we considered in order to try to minimize the differences in body sizes between the two groups, increased less in response to increasing work rates in our obese subjects than in normal subjects. As a whole, these data appear to be in line with a relatively less efficient cardiac performance during progressive work rates in obese subjects.

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“…Overweight and obesity are associated with changes in cardiac structure and function (Licata et al 1992;Morricone et al 2002;Powell et al 2006;Rowland 2007) which may contribute to an increased risk of cardiovascular disease (Melanson et al 2001). In the early stages of obesity, there is an increase in blood volume which is accompanied by ventricular remodeling (Alaud-din et al 1990; Morricone et al 2002;Peterson et al 2004;Powell et al 2006) and diastolic dysfunction (Ferraro et al 1996;Licata et al 1992;Powell et al 2006;Sasso et al 2005).…”

Section: Introductionmentioning

confidence: 98%

Cardiac response to exercise in young, normal weight and overweight men and women

et al. 2008

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Overweight and obesity are associated with hemodynamic changes at rest. Whether these changes are mirrored during exercise is uncertain. We compared cardiac output (Q) and stroke volume (SV) in 12 overweight (OW) and 12 normal weight (NW) adults at rest and during exercise. Participants were assessed for body composition, peak oxygen consumption, and Q and SV at rest and during cycling exercise at 50, 75 and 100 W. Cardiac output was significantly higher at rest and during exercise in OW than NW when fat mass and ethnicity were used as covariates. When fat free mass was added as a covariate, Q was no longer different between groups. Stroke volume tended to be higher in OW than NW when fat mass and ethnicity were used as covariates (P = 0.055) with no differences in heart rate observed. Although the total change in Q and SV was similar between groups with each exercise intensity, overall Q was higher in the OW than NW participants. The higher Q is likely explained by a higher SV, secondary to a greater blood volume in the OW. The elevated hemodynamic response in OW may reflect the early cardiac adaptations of excess body mass.

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Left ventricular function response to exercise in normotensive obese subjects: influence of degree and duration of obesity

Cited by 28 publications

References 15 publications

Left ventricular hypertrophy and QT interval in obesity and in hypertension: effects of weight loss and of normalisation of blood pressure

Left ventricular hypertrophy and QT interval in obesity and in hypertension: effects of weight loss and of normalisation of blood pressure

Oxygen Uptake and Cardiac Performance in Obese and Normal Subjects during Exercise

Cardiac response to exercise in young, normal weight and overweight men and women

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