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When the heart is predisposed to hemodynamic stress, it is able to compensate the load by increasing its mass (Kehat et al., 2010). As myocytes are only able to proliferate for a short time after birth, increased pressure or volume load leads to hypertrophy of existing myocytes. LVM is also strongly associated with somatic growth with LVM increasing 10-fold from childhood to adulthood (Lorell et al., 2000). Physiological and exercise-induced growth of the LV is mainly mediated through growth factors while the pathological pathway is mostly stimulated by neurohormones (Dorn et al., 2005).

In obese adolescents, the increase in LVM is suggested to relate not only to the increase in hemodynamic load, but also to neurohormonal alterations due to metabolic disturbances of obesity (Chinali et al., 2006).

The first studies investigating the association between LVM and CHD were performed using the electrocardiography (ECG) method. Using this method, the Framingham Heart Study (FHS) was the first to show the association between higher LVM and increased risk of CHD (Kannel et al., 1970). Later, the association was replicated by another study of the FHS that used echocardiography as an indicator of LVM (Levy et al., 1989). The study found that LVM of elderly people free of clinical CHD was prognostic for CHD events over a 4-year follow-up. The prognostic value remained significant after adjustment for age, systolic blood pressure, smoking and the ratio of total/HDL cholesterol. Similar results were later shown in a cohort of middle-aged participants (Levy et al., 1990). Higher LVM was associated with higher risk of cardiovascular events and deaths after adjustment for several conventional cardiovascular risk factors. Moreover, results of the Cardiovascular Health Study’s elderly cohort showed that those in the highest LVM quarter had over 3-fold higher risk for coronary disease in comparison to the lowest quarter (Gardin et al., 2001).

Furthermore, LVM is an independent predictor of heart failure not related to previous myocardial infarction in elderly population (de Simone et al., 2008).

LVM is also shown to associate with increased risk of sudden cardiac death, possibly due to higher incidence of ventricular arrhythmias in patients with left ventricular hypertrophy (LVH), describing markedly increased LVM (Haider et al., 1998; Levy et al., 1987a). A study comparing the utility of LVH, LV ejection fraction and the number of stenosed vessels to predict survival in cardiac patients found that LVH was a stronger predictor of death than the other two more traditional markers of CHD (Liao et al., 1995). Furthermore, regression of LVH due to antihypertensive treatment is suggested to reduce risk for sudden cardiac death, independent of blood pressure and other cardiovascular risk factors (Wachtell et al., 2007).

Strong independent clinical determinants of LVM include age, height, systolic blood pressure and BMI (Savage et al., 1990). Among men, there was also a weak association between higher physical activity and higher LVM, but hypertrophy due to physical exercise is considered to be physiological, since it is associated with normal systolic and diastolic function (Colan, 1997). Of the clinical risk factors, BMI has been shown to have the strongest effect on LVM in childhood (Daniels et al., 1995). However, the major part of the variance in childhood was explained by lean body mass and the role of fat mass was minor.

To measure LVM, the most commonly used methods are ECG, echocardiography and magnetic resonance imaging. The sensitivity of ECG is depending on the assessment standard and varies between different populations. However, when ECG was compared to echocardiogram in the FHS cohort, the prevalence of hypertrophy was markedly lower (<1%) than using echocardiography (16–21%) (Levy et al., 1990).

The accuracy of echocardiography in detecting LVH is shown also in a necropsy study (Devereux et al., 1986). Magnetic resonance imaging is suggested to have even better

accuracy and reproducibility, but echocardiography has the advantage of lower costs and better availability making it the most practical method clinically (Armstrong et al., 2012). The most commonly used method to estimate LVM by echocardiography is to measure the interventricular septum, LV inferolateral wall thickness and LV internal diameter from 2D-guided M-mode or from direct 2D echocardiography (Figure 3) (Lang et al., 2015). The measurements are used to calculate the myocardial volume, which is converted to mass by multiplying by myocardial density. When increased LVM reaches a certain cut-off-level, it is denoted as LVH. Although this term has particular importance in the clinical setting, several different criteria have been proposed to define LVH. According to the most commonly used criterion in echocardiography, to have LVH, LVM should be two standard deviations (SD) above the mean value of the healthy population sample of the FHS (Levy et al., 1987b).

Figure 3. M-mode ultrasound image obtained during measurement of cardiac left ventricular mass. Reproduced with permission from the thesis by Mikola, (2018).

Inverse associations of SES with LVM (Medenwald et al., 2016; Murray et al., 2016;

Rodriguez et al., 2004) and the prevalence of LVH (Christensen et al., 2011; Kubota et al., 2017) have been shown. A study from the U.S. suggested that low SES measured as years of education was associated with higher LVM that remained after adjustment for age, sex, systolic blood pressure, diabetes, physical activity and BMI (Rodriguez et al., 2004). Race-ethnic comparisons of the study revealed that SES

was inversely associated with LVM among blacks but not among whites or Hispanics. A British cohort study investigating the association between occupational SES and LVM at multiple time points from childhood to adulthood found that time spent in manual socioeconomic position in any of the 3 studied time points (childhood, young adulthood, later adulthood) increased LVM index by 2.5 g/m^2.7 (Murray et al., 2016). Adjustment for current BMI attenuated the association by 32%, suggesting the mediating role of adult BMI. In contrast, adjustment for several other cardiometabolic risk factors had only small effects on estimates. Similarly, a German study showed that more than 50% of the association between educational SES and LVM was explained by BMI but that other potential mediators had no significant effects on the association (Medenwald et al., 2016).

Prior results have suggested a potential pathway from low childhood SES to increased LVM and finally to LVH in adulthood, but the evidence is limited. This pathway might be strongly mediated by adulthood obesity, a well-established risk factor for LVH. However, not all of the association is explained by higher BMI among low SES individuals and studies have shown that other conventional risk factors of cardiometabolic health have no significant effects on the association between SES and LVM (Medenwald et al., 2016; Murray et al., 2016). Researchers propose the possible role of sympathetic stimulation due to higher chronic stress among low SES people, but studies are lacking. Regardless of the detailed mechanisms, the possible pathways between low child SES and increased LVM are complex and intertwined with the pathways that are explaining the associations between child SES and other outcomes of cardiometabolic disease.