title: Does subclinical hypothyroidism affect cardiac pump performance? Evidence from a magnetic resonance imaging study.
abstract: OBJECTIVE
  We sought to assess the effects of subclinical hypothyroidism (SHT) on the cardiac volumes and function.
  
  
  BACKGROUND
  The cardiovascular system is one of the principal targets of thyroid hormones. Subclinical hypothyroidism is a common disorder that may represent "early" thyroid failure.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: C.N.R. Institute of Clinical Physiology, S. Cataldo Research Campus, Via G. Moruzzi 1, 56124 Pisa, Italy.
authors.forename: Andrea
authors.initials: A
authors.lastname: Ripoli
authors.forename: Alessandro
authors.initials: A
authors.lastname: Pingitore
authors.forename: Brunella
authors.initials: B
authors.lastname: Favilli
authors.forename: Antonio
authors.initials: A
authors.lastname: Bottoni
authors.forename: Stefano
authors.initials: S
authors.lastname: Turchi
authors.forename: Nael F
authors.initials: NF
authors.lastname: Osman
authors.forename: Daniele
authors.initials: D
authors.lastname: De Marchi
authors.forename: Massimo
authors.initials: M
authors.lastname: Lombardi
authors.forename: Antonio
authors.initials: A
authors.lastname: L'Abbate
authors.forename: Giorgio
authors.initials: G
authors.lastname: Iervasi
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D005260:Female; D006352:Heart Ventricles / Q000473:pathology* / Q000503:physiopathology*; D020249:Hormone Replacement Therapy; D006801:Humans; D007037:Hypothyroidism / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D019028:Magnetic Resonance Imaging, Cine; D008875:Middle Aged; D013318:Stroke Volume / Q000502:physiology*; D013963:Thyroid Hormones / Q000097:blood; D014655:Vascular Resistance / Q000502:physiology*
chemical_list: D013963:Thyroid Hormones