Myocardial contractility and total arterial stiffness in patients with overt hyperthyroidism: acute effects of beta1-adrenergic blockade.
OBJECTIVE
To ascertain whether myocardial contractility and total arterial stiffness are significantly altered in human thyrotoxicosis, and to what extent they are affected by acute beta(1)-adrenergic blockade.


METHODS
Doppler-echocardiography was used to assess left ventricular (LV) structure and function, hemodynamics and total arterial stiffness in untreated overt hyperthyroid patients before and 2 h after 5 mg bisoprolol given orally compared with age- and sex-matched healthy euthyroid controls.


RESULTS
Compared with controls, untreated patients (n=20) had a higher heart rate (HR) and LV stroke index (SI), which were associated with higher pulse pressure (PP), larger LV end-diastolic volume index (EDVI, an index of preload,+11%, P<0.05), marginally increased stress-corrected LV midwall fractional shortening (MWS, an index of myocardial contractility,+5%; P=0.066), and shorter isovolumic relaxation time (IVRT). These changes resulted in a higher cardiac index (CI) and a lower systemic vascular resistance (SVR), which were associated with fairly normal mean blood pressure (BP) but higher PP/stroke volume (an index of total arterial stiffness,+29%; P<0.01). After bisoprolol, compared with controls, the randomly treated patients (n=10) had comparable HR but additionally increased SI; PP remained enhanced, EDVI was further enlarged (+26%, P<0.001), stress-corrected MWS was substantially unchanged, and IVRT remained shorter. Overall, these effects attenuated the high-output state, which was associated with normalization of PP/stroke volume without changes of mean BP.


CONCLUSIONS
In human overt hyperthyroidism, myocardial contractility does not play a major role in increasing LV performance, which is instead predominantly sustained by increased preload with enhanced LV diastolic function. In addition, human thyrotoxicosis is associated with increased total arterial stiffness despite fairly normal mean BP. In this scenario, acute beta(1)-adrenergic blockade blunts the cardiovascular hyperkinesia predominantly by slowing HR - a process that is associated with normalization of total arterial stiffness.
Palmieri
E A
EA
Department of Clinical Medicine and Cardiovascular Sciences, University Federico II School of Medicine, Napoli, Italy. eapalmieri@ciaoweb.it
Fazio
S
S
Palmieri
V
V
Lombardi
G
G
Biondi
B
B
D058671:Adrenergic beta-1 Receptor Antagonists; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000328:Adult; D001158:Arteries / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D017298:Bisoprolol / Q000008:administration & dosage; D001794:Blood Pressure; D016022:Case-Control Studies; D003971:Diastole; D004452:Echocardiography; D005260:Female; D006339:Heart Rate; D006801:Humans; D006980:Hyperthyroidism / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D009200:Myocardial Contraction; D018342:Receptors, Adrenergic, beta-1 / Q000502:physiology; D013318:Stroke Volume; D016277:Ventricular Function, Left
D058671:Adrenergic beta-1 Receptor Antagonists; D000319:Adrenergic beta-Antagonists; D018342:Receptors, Adrenergic, beta-1; D017298:Bisoprolol