Possible diverse contribution of coronary risk factors to left ventricular systolic and diastolic cavity sizes

Abstract

It is generally believed that risk factors damage the coronary arteries, cause myocardial ischemia, and consequently change the shape of the heart. On the other hand, each of the risk factors may also have a negative effect on the heart. However, it is very difficult to examine the effects of each of these risk factors independently. Therefore, it is necessary to select an appropriate statistical method and apply it efficiently. In this study, the effects of coronary risk factors on left ventricular size and cardiac function were investigated using structure equation modeling (SEM), and were shown as Bayesian SEM-based frequency polygons using selected two-dimensional contours. This study showed that each risk factor directly affected the shape of the heart. Because vascular risk and heart failure risk are likely to evolve at the same time, managing risk factors is very important in reducing the heart failure pandemic.

Figure 1

Associations and comparison of LV cavity volume with HbA1c, BMI, Age, gender and number of diseased vessels. (A) HbA1c, (B) BMI, (C) Age, (D) Gender, (E) Number of diseased vessels. The LV cavity volume and coronary risk factors are represented as scatter plots (A–C). The gray plots are LVESVI and the black plots are LVEDVI. The solid gray or black line indicates the regression curve for the logarithmic fitted equation. The bar chart of LV cavity size is shown by gender, or by number of diseased vessels (D,E). *P < 0.05, **P < 0.01 versus 0 vessel disease at another vessel disease group. ^#P < 0.05, versus 1 vessel disease at another vessel disease group. BMI body mass index, HbA1c hemoglobin A1c, LVESVI left ventricular end-systolic volume index, LVEDVI left ventricular end-diastolic volume index.

Figure 2

Path model (A): An association of the coronary risk factors with LVESVI and LVEDVI with explanatory drawing of possible cascade from the respective risk factors. This path shows the standardized coefficient of regressing independent variables on the dependent variable of the relevant path. These variables indicate standardized regression coefficients, squared multiple correlations (italic capitals), and correlations among exogenous variables (capitals upper side of the two-way arrowhead curves). BMI body mass index, HT hypertension, HbA1c hemoglobin A1c, HL hyperlipidemia, LVESVI left ventricular end-systolic volume index, LVEDVI left ventricular end-diastolic volume index.

Figure 3

Path model (B): An association of the coronary risk factors with LVEF with explanatory drawing of possible cascade from the respective risk factors. This path shows the standardized coefficient of regressing independent variables on the dependent variable of the relevant path. These variables indicate standardized regression coefficients, squared multiple correlations (italic capitals), and correlations among exogenous variables (capitals upper side of the two-way arrowhead curves). BMI body mass index, HT hypertension, HbA1c hemoglobin A1c, HL hyperlipidemia.

Figure 4

Bayesian SEM documented by 2D contour line. The frequency polygon was described with the marginal posterior distributions of the estimands. The selected 2D contour line was applied in this study. In each figure, the effect of one risk factor on LVESVI is shows on the longitudinal axis. The effect of one risk factor on LVEDVI is shows on the horizontal axis. (I) Age reduced LVESVI and LVEDVI. (II) Male sex increased LVESVI and LVEDVI. (III) BMI reduced LVESVI and LVEDVI. (IV) Vessel disease (severely stenosed coronary arteries) increased LVESVI and LVEDVI. (V) HbA1c decreased LVEDVI but not LVESVI. SEM structure equation modeling, LVESVI left ventricular end-systolic volume index, LVEDVI left ventricular end-diastolic volume index, BMI body mass index, HbA1c hemoglobin A1c.

Figure 5

Conceptual scheme. Aging and obesity reduced LV cavity sizes at the systolic and diastolic phases, respectively. Male sex and the severity of coronary artery disease increased the LV cavity size at the systolic and diastolic phases, respectively. Diabetes reduced the LV cavity size only at the diastolic phase but not at the systolic phase, which is a unique property. As for systolic function, female sex, aging, and obesity increased LVEF, and male sex, severity of coronary artery disease, and diabetes reduced LVEF. LVEF left ventricular ejection fraction.