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CLINICAL RESEARCH: CARDIAC MAGNETIC RESONANCE

Does subclinical hypothyroidism affect cardiac pump performance?

Evidence from a magnetic resonance imaging study

Andrea Ripoli, PhD^*, Alessandro Pingitore, MD, PhD^*,*, Brunella Favilli, MSc^*, Antonio Bottoni, MD^*, Stefano Turchi, BSc^*, Nael F. Osman, PhD, Daniele De Marchi, RT^*, Massimo Lombardi, MD^*, Antonio L'Abbate, MD and Giorgio Iervasi, MD^*

^* Institute of Clinical Physiology, C.N.R., Pisa, Italy
Johns Hopkins University, Baltimore, Maryland
Scuola Superiore S. Anna and Institute of Clinical Physiology, C.N.R., Pisa, Italy

Manuscript received March 2, 2004; revised manuscript received October 1, 2004, accepted October 18, 2004.

^* Reprint requests and correspondence: Dr. Alessandro Pingitore, C.N.R. Clinical Physiology Institute, S. Cataldo Research Campus, Via G. Moruzzi 1, 56124, Pisa Italy (Email: pingi{at}ifc.cnr.it).

OBJECTIVES: 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/m² vs. 81.4 ± 11.3 ml/m², p < 0.001), as well as SVR (38.9 ± 7.5 ml/m² vs. 52.5 ± 6.1 ml/m², p < 0.001) and CI (2.6 ± 0.5 l/[min·m²] vs. 3.7 ± 0.4 l/[min·m²], p < 0.001). Systemic vascular resistance was higher in SHT (12.5 ± 2.5 mm Hg·min/[l·m²] vs. 8.6 ± 1.1 mm Hg·min/[l·m²], 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.

Abbreviations and Acronyms   CI = cardiac index   CMR = cardiac magnetic resonance   DWT = diastolic wall thickness   E1 = greatest systolic lengthening   E2 = greatest systolic shortening   EDV = end-diastolic volume   ESV = end-systolic volume   FT3 = free tri-iodothyronine   FT4 = free thyroxine   LV = left ventricular   SHT = subclinical hypothyroidism   SV = stroke volume   SVR = systemic vascular resistance   TSH = thyroid-stimulating hormone

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