Abstract
Background
Notwithstanding its clinical use as a reliable measure of left ventricular performance, little is known about whether myocardial performing index (MPI) is influenced by increased left ventricular mass (LVM) in healthy obese individuals.
Aim
The present study was targeted at investigating the impact of increased LVM on the LV MPI in healthy obese men.
Subjects and Method
Sixty-six normal male subjects were involved in this study. The subjects were divided according to their body mass index (BMI), into group I (BMI = 20–24.9, n = 37, mean age 33.405 ± 10.277 years) which served as the control group, and group II (BMI = ≥ 30, n = 29, mean age 39.208 ± 10.214 years). The MPI was determined in all subjects using the following formula proposed by Tei: MPI = IVCT + IVRT/ET. LVM was calculated according to the following Devereux formula as: LVM = 0.8[1.04(IVSd + PWTd + LVIDd)ᶟ−(LVIDd)ᶟ] + 0.6.
Results
There were no significant differences in MPI between control subjects and obese subjects with increased LVM (p > 0.05). Additionally, there was no linear correlation between MPI and LVM (R 2 = 0.0003, p = 0.89).
Conclusion
MPI is a simple and accurate tool for the quantitative assessment of left ventricular function. Because of its ease of application, cost effectiveness, and reproducibility, this tool could be regarded as a principal measurement for comprehensive hemodynamic studies. MPI values (according to the Tei index) did not vary significantly between healthy obese and morbidly obese individuals, and therefore may have limited utility for predicting cardiac diseases in at-risk obese individuals.
1
Introduction
Obesity is a chronic and progressive disease that predisposes individuals to an increased risk of mortality, as demonstrated by several population studies . The significance of obesity has increased with its considerable increase in prevalence, in developed as well as developing countries. Furthermore, obesity represents an independent risk factor for cardiovascular disease, which is defined as the incidence of coronary disease, sudden death or congestive cardiac failure . The association between obesity and cardiovascular disease is independent of the levels of arterial blood pressure, cholesterol, smoking, the presence of left ventricular hypertrophy and glucose intolerance, although there is an important association between excess weight and left ventricular hypertrophy . In the heart of an obese individual, the left ventricular filling pressure and volume both increase, thereby shifting the Frank-Starling curve to the left, and inducing chamber dilation. The volume of the dilated chamber also inappropriately increases left ventricular wall stress, and the ventricle adapts by augmenting the contractile elements and myocardial mass. The final product of this adaptation is hypertrophy, generally of the eccentric type . The excess fat mass associated with obesity is known to increase metabolic demand, thus both cardiac output and total blood volume are elevated in obese individuals. These circulatory changes cause left ventricular geometric remodeling in the form of cavity dilatation, a structural change commonly observed in obesity, which is then thought to lead to a compensatory left ventricular hypertrophic response in response to increased wall stress . In addition, advances in the understanding of hormonal changes in obesity have highlighted several alternative mechanisms. Increased visceral and subcutaneous adiposity is known to cause higher levels of serum leptin, the hallmark of human obesity, and hyperinsulinaemia, both of which have been linked to ventricular hypertrophy in humans and animal models .
The Doppler-derived myocardial performance index (MPI), also known as the Tei Doppler index, which is a fairly new index of combined systolic and diastolic function, can be defined as the sum of the isovolumic contraction time and isovolumic relaxation time divided by the ejection time , with a reported normal mean ± SD value for the LV of 0.39 ± 0.05 . In a cross-sectional study MPI was previously shown to be a sensitive indicator for symptomatic heart failure , although it remains to be examined whether MPI can predict the future development of heart failure independently of other echocardiographic measurements. However, the Tei index has shown clinical usefulness for assessing LV function and outcomes in a wide range of clinical conditions, including congestive heart failure, myocardial infarction, cardiac transplant, and amyloidosis .
1.1
Aim
The goal of this study was to investigate the impact of increased LVM on the LV MPI in healthy obese men.
2
Subjects and methods
A total of 66 healthy male individuals recruited for this study, after obtaining verbal and written consent and approval from the local ethical committee at Kufa College of Medicine. The study began on the 9th of November 2010 and ended on the 4th of May 2011. To exclude conditions that may influence the results, the following participant criteria were required:
- a)
No previous history or clinical evidence of hypertension, diabetes mellitus, coronary artery disease, heart failure, cardiac valve disease, abnormal ECG, or respiratory disease.
- b)
Not taking any drugs that could affect the heart.
- c)
Not involved in competitive sports.
All participants provided information on their age, family history, and personal habits (alcohol intake, tobacco consumption, type and level of physical exercise, drug ingestion, and known pathological conditions). A detailed physical examination was conducted to exclude endocrine and cardiac co-morbidities. The subjects were divided according to BMI into group I (BMI = 20–24.9, n = 37, mean age 33.405 ± 10.277 years) which served as the control group, and group II (BMI = ≥ 30, n = 29, mean age 39.208 ± 10.214 years). The subject’s height in cm and weight in kg were measured in light clothing, using a measuring tape and digital scale, respectively. BMI was calculated using the following equation: weight (kg) / height (m) 2 .
All participants were subjected to an Echo-Doppler study ( Figs. 1 and 2 ), using the Sonos 7500 echo-Doppler equipment (M2424A Ultrasound system, Andover Masssachuses 01810, Philips, made in USA) with a 2.5 MHz phased array cardiac probe, a pulse-wave Doppler, and a built-in ECG. The MPI was calculated by placing a pulse-wave Doppler sample volume on the left ventricular out tract to record both the mitral inflow and LV outflow. The IVCT was then measured from the end of the A wave of the mitral inflow (under guidance of simultaneous ECG recording) to the commencement of AV opening. The ET was measured from the opening of the AV to the closure of AV. IVRT was measured from closure of AV to commencement of the E wave .
To guard against inter observer and intra observer errors and to verify accuracy of these measurements with the Doppler technique, the measurements need to be repeated five to seven times . In our study, the average of at least five Doppler waveform intervals was used.
We adopted M-mode estimation of LV mass ( Fig. 3 ), because most epidemiological studies use this imaging modality. The inclination for M-mode is based on its technical feasibility and availability at the time when most studies are performed. Moreover, Devereux and colleagues proposed a new adjusted equation, which was validated by necropsy findings (Devereux et al., 1986).
LVM = 0.8[1.04(IVSd + PWTd + LVIDd)ᶟ-(LVIDd)ᶟ] + 0.6 9Devereux formula).
2.1
Statistical analysis
Data were analyzed according to differences between the BMI groups (BMI = 20–24.9 and BMI = ≥ 30 kg/m 2 ). The mean and standard deviations were calculated. Independent t- tests and correlation regression tests (using SPSS version 18) were applied to compare the study groups. The correlation coefficient (r) was obtained to study the correlation between LVM and the LV Tei index. A value of p less than 0.05 was considered statistically significant (α = 0.05).
3
Results
As shown in Tables 1 and 2 , the mean ± SD values for MPI, IVCT, IVRT and ET, in relation to BMI for group I (control) and group II (obese), were (0.379 ± 6.625; 0.371 ± 5.696), (40.24 ± 12.945; 36.56 ± 7.561), (72.162 ± 19.37; 74.14 ± 16.528), and (294.721 ± 22.977; 293.407 ± 27.559), respectively.
| Group I(control), N = 37 | Group II(obese), N = 29 | p value | |
|---|---|---|---|
| LVM (M ± SD) | 201.679 ± 36.653 | 148.689 ± 34.112 | significant |
| IVSTd(M ± SD) | 1.09 ± 0.144 | 0.95 ± 0.14 | significant |
| PWTd(M ± SD) | 0.947 ± 0.109 | 0.807 ± 0.172 | significant |
| LVIDd(M ± SD) | 5.094 ± 0.334 | 4.815 ± 0.42 | significant |
| Parameters | Group I(control), N = 37 | Group II(obese), N = 29 | P value |
|---|---|---|---|
| MPI | 0.379 ± 6.625 | 0.371 ± 5.696 | Not significant |
| IVCT | 40.24 ± 12.945 | 36.56 ± 7.561 | Not significant |
| IVRT | 72.162 ± 19.37 | 74.14 ± 16.528 | Not significant |
| ET | 294.721 ± 22.977 | 293.407 ± 27.559 | Not significant |
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
