Cardiac mechanics and function in obese normotensive persons with normal coronary arteries

Carabello, Blasé A.; Gittens, Lisa

doi:10.1016/0002-9149(87)90958-1

Cited by 20 publications

(11 citation statements)

References 24 publications

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“…Left ventricular contractile function was assessed using the afterload-corrected mean velocity of circumferential fiber shortening method (Vd-stress) (21)(22)(23)(24). This method corrects a preload independent ejection phase index (mean VCf) (25) where Hb = hemoglobin concentration, and (LV -RA) = oxygen saturation of the left ventricle -oxygen saturation in right atrium.…”

Section: Patient Studiesmentioning

confidence: 99%

“…Because Emax can be affected by cardiac size independent of inotropic state (35,36), we also evaluated contractility using Emax corrected for end-diastolic volume. Contractile function was also analyzed using the afterloadcorrected velocity of circumferential fiber shortening (Vdrstress relationship) (21)(22)(23)(24). This relationship has an advantage of being dimensionless and therefore is independent of cardiac size.…”

Section: Patient Studiesmentioning

confidence: 99%

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Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Corin¹,

Swindle²,

Spann³

et al. 1988

J. Clin. Invest.

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Children with ventricular septal defect (VSD) often demonstrate failure to thrive (Ff1'). Such patients usually have reduced systemic cardiac output which has been postulated as a cause for their growth retardation. This study was conducted to ascertain the mechanism of the reduced cardiac output in children with VSD and FT1'1 and also in a porcine model of VSD. Forward stroke volume was reduced in VSD-F'IT children, 31±8 ml/m2, compared to normal children, 49±15 ml/m2 (P < 0.05), but was not reduced in children with VSD and normal growth and development (41±16 ml/m2). Forward stroke volume was also reduced in swine with VSD compared to controls. Contractility assessed by mean velocity of circumferential shortening (Vd) corrected for afterload was similar in normals and VSD-FT'I children. Contractile performance was also similar in normal and VSD swine. Afterload assessed as systolic stress was similar in FIT-VSD children and normal subjects. Preload assessed as end-diastolic stress was increased in the VSD-FI' group. End-diastolic volume was not larger in the VSD-FTI' group. We conclude that the reduced stroke volume seen in VSD-FT'I children and VSD-swine was not due to reduced contractility, increased afterload or reduced preload. The reduced stroke volume may have been due to failure of end-diastolic volume to increase adequately.

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Section: Patient Studiesmentioning

confidence: 99%

Section: Patient Studiesmentioning

confidence: 99%

Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Corin¹,

Swindle²,

Spann³

et al. 1988

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Consistent with this there are several studies using loaddependent measures demonstrating the detrimental effects of excess body weight on diastolic function as measured using traditional echocardiographic Doppler imaging [50][51][52][53]. There is also evidence that there are direct, load-independent effects of obesity on cardiac function.…”

Section: Obesity and Cardiac Functionmentioning

confidence: 54%

“…The effects of obesity on LV systolic function are less clear-cut, with some studies demonstrating decreased, some showing increased, and some showing no effect on LV systolic function [48,53,54]. Part of the explanation for these discordant results is likely due to the loaddependent nature of many of the measurement methods, since an obesity-related increase in plasma volume may increase cardiac output via the Frank-Starling mechanism.…”

Section: Obesity and Cardiac Functionmentioning

confidence: 99%

Cardiovascular consequences of obesity and targets for treatment

Mittendorfer

Peterson

2008

Drug Discovery Today: Therapeutic Strategies

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Obesity is a risk factor for cardiovascular disease, including coronary artery disease and heart failure, but the mechanisms by which it may cause them are not completely clear. Currently, therapies aimed at obesity-related cardiovascular disease include weight loss strategies and reduction of the other risk factors that are associated with obesity and cardiovascular disease. Other pathways with for potential drug development for obesity-related CVD are also discussed. Keywordsobesity; myocardium; metabolism; systolic function; diastolic function; coronary artery disease Cardiovascular disease (CVD) is still the leading cause of death in developed countries, despite a recent decline in coronary artery disease-related deaths. In the United States approximately 35% of all deaths are due to CVD [1]. Obesity (defined as a body mass index [BMI] of ≥ 30 kg/m 2 ) is a risk factor for CVD, especially coronary heart disease and heart failure. It is estimated that the relative risk of coronary heart disease in obesity is approximately 1.5 even after adjusting for all other traditional coronary heart disease risk factors that often co-migrate with obesity (e.g. hyperlipidemia, hypertension) [2]. Obesity also is associated with an increased risk of heart failure, with ~11 -14% of all heart failure thought to be attributable to obesity [3]. Given that excess body weight now affects more than 300 million persons worldwide, prevention and treatment of obesity should be considered one of the cornerstones for the prevention of CVD (http://www.who.int/dietphysicalactivity/publications/facts/obesity/en/). This review will focus on the impact of obesity on CVD, particularly atherosclerotic coronary artery disease and heart failure and treatment of obesity-related heart disease.

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“…Hypertension, diabetes, and obesity are three well-known causes of DD and probably represent the largest component of patients with DD outside of ischemic heart disease. [12][13][14][15] Most studies of isolated DD (i.e., without associated structural heart disease) have included patients older than the mean age of 58 years reported in our study. However, in a recent report by Klapholz et al, attention was called to a black cohort making up 30% of their urban registry population.…”

Section: Discussionmentioning

confidence: 96%

Prognosis of patients with left ventricular diastolic pressure abnormality: A long-term survival study in patients without coronary artery disease

Brady¹,

Dwyer²

2006

Clin Cardiol

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SummaryBackground: Given that an elevated left ventricular (LV) end-diastolic pressure reflects an abnormality of diastolic function, we analyzed the outcome of this finding in patients without coronary artery disease (CAD).Hypothesis: The degree to which diastolic dysfunction influences mortality has been confounded in most studies by CAD and advanced age.Methods: We performed a retrospective study of 876 patients with normal coronary arteries on arteriography. Of these, 115 patients had a left ventricular end-diastolic pressure of ≥ 15 mmHg with an ejection fraction (EF) ≥ 50%. We compared the mortality in this group (Group A) with the reported outcome in the general population, adjusted for age, gender, and race, as well as the mortality of a group of patients from the same cohort (Group B) with both diastolic and systolic dysfunction (n = 60), defined as a LVEF < 50%.Results: Follow-up was for a mean of 63 months. In Group A, all-cause mortality was 5% (six patients); two deaths were from cardiac causes. The mean annual mortality in this group (1.2%) was similar to the adjusted annual mortality of the general population (1.1%), and it was significantly lower than the annual mortality (6%) in Group B (p < 0.03).Conclusions: Our study results indicate that diastolic dysfunction with a normal EF, in the absence of CAD and systolic dysfunction, has an excellent prognosis over a long period (5-6 years).

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Cardiac mechanics and function in obese normotensive persons with normal coronary arteries

Cited by 20 publications

References 24 publications

Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.

Cardiovascular consequences of obesity and targets for treatment

Prognosis of patients with left ventricular diastolic pressure abnormality: A long-term survival study in patients without coronary artery disease

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