with an increased incidence of cardiovascular disease in both men and women, after adjustment for traditional cardiovascular risk factors (Levy et al., 1990). The 5-year mortality for electrocardiographic left ventricular hypertrophy was 33 percent for men and 21 percent for women (Kannel, 1991).
Increased left ventricular mass is thought to be, in part, a structural adaptation of the heart as a compensatory mechanism for increased blood pressure and wall stress. Increased blood pressure is one of the strongest correlates of left ventricular mass (Liebson et al., 1993). Not surprisingly, factors associated with elevated blood pressure are also associated with increased left ventricular mass, including obesity (de Simone et al., 1994; Schmieder and Messerli, 1993), aging (Alderman et al., 1995; Ghali et al., 1997), African-American race (Harshfield et al., 1992), and, as discussed subsequently, sodium intake.
Several cross-sectional studies have examined the relationship between sodium intake, typically as measured by urinary sodium excretion, and left ventricular mass or hypertrophy, as measured by echocardiography. Other cross-sectional studies have documented associations between sodium intake and cardiac function, such as impaired diastolic filling (Langenfeld et al., 1998).
Most reports used correlation or regression analyses and did not report left ventricular mass by level of urinary sodium excretion. Available studies predominantly enrolled hypertensive adults, but some enrolled nonhypertensive individuals (du Cailar et al., 2002; Kupari et al., 1994) or children (Daniels et al., 1990; Harshfield et al., 1994). With the exception of the study by Alderman and colleagues, which assessed left ventricular hypertrophy by electrocardiography and did not detect an association, each study documented a statistically significant, positive relationship between urinary sodium excretion and left ventricular mass (Daniels et al., 1990; du Cailar et al., 1989, 1992, 2002; Gerdts et al., 1996; Kupari et al., 1994; Langenfeld et al., 1998; Liebson et al., 1993; Schmieder et al., 1988, 1990, 1996). Figure 6-6 displays results from the report of Schmieder and coworkers (1988), who were the first to report an association between sodium intake and left ventricular hypertrophy. The only two studies that reported left ventricular mass by level of dietary sodium are included in Table 6-18.
In most studies, the association between urinary sodium excretion and left ventricular mass persisted after adjustment for other determinants of left ventricular mass, including blood pressure (du Cailar et al., 2002; Liebson et al., 1993). Such findings, in conjunction with animal studies, raise the possibility that sodium may have a