Does subclinical hypothyroidism affect cardiac pump performance? Evidence from a magnetic resonance imaging study.

Abstract

We sought to assess the effects of subclinical hypothyroidism (SHT) on the cardiac volumes and function. The cardiovascular system is one of the principal targets of thyroid hormones. Subclinical hypothyroidism is a common disorder that may represent "early" thyroid failure. Thyroid profile was evaluated in 30 females with SHT and 20 matched control subjects. Left ventricular end-diastolic volume (EDV) and end-systolic volume (ESV), stroke volume (SV), cardiac index (CI), and systemic vascular resistance (SVR) were calculated by cardiac magnetic resonance (CMR). Regional greatest systolic lengthening (E1) and greatest systolic shortening (E2) were calculated by tagging CMR. EDV was lower in SHT than in controls (64.3 +/- 8.7 ml/m(2) vs. 81.4 +/- 11.3 ml/m(2), p < 0.001), as well as SV [corrected] (38.9 +/- 7.5 ml/m(2) vs. 52.5 +/- 6.1 ml/m(2), p < 0.001) and CI (2.6 +/- 0.5 l/[min.m(2)] vs. 3.7 +/- 0.4 l/[min.m(2)], p < 0.001). SVR [corrected] was higher in SHT (12.5 +/- 2.5 mm Hg.min/[l.m(2)] vs. 8.6 +/- 1.1 mm Hg.min/[l.m(2)], p = 0.003). The E1 was higher in controls than in SHT at the basal (p = 0.007), equatorial (p = 0.05), and apical (p = 0.008) levels, as well as E2 at the equatorial (p = 0.001) and apical (p = 0.001) levels. All parameters normalized after replacement therapy. A negative correlation between TSH and EDV (p < 0.001), SV (p < 0.001), CI (p < 0.001), and E1 at the apical level (p < 0.001) and a positive correlation between TSH and SVR (p < 0.001) and E2 at the apical level (p < 0.001) were found. Subclinical hypothyroidism significantly decreased cardiac preload, whereas it increased afterload with a consequent reduction in SV and cardiac output. Replacement therapy fully normalized the hemodynamic alterations.