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Thyroid disease produces characteristic changes in cardiovascular hemodynamics.
They arise from effects of T3 both on the heart and on the systemic
vasculature. H may be associated with as much as a 50% decline in systemic
vascular resistance (SVR) and T3 is capable of causing rapid
relaxation of vascular smooth muscle cells in culture (33). Since the vascular
smooth muscle of resistance arterioles primarily determine SVR, T3
may directly regulate SVR which in turn reflexly causes alterations in
blood pressure (BP) and cardiac output. This postulate is supported by
another study where a significant decrease in cardiac output after administration
of phenylephrine to H but not to normal subjects was noted (34). The ability
to block the elevated cardiac output by pharmacologically reversing the
changes in SVR of H reinforces the possibility that many of the cardiovascular
changes of H occur in response to changes in peripheral tissues. H markedly
increases oxygen consumption in the periphery and increases metabolic demands
which requires increased blood supply and pumping action of the heart.
Arterial resistance decreases and venous tone increases in H animals leading
to an augmented return of blood to the heart. The effects of T3
on venous compliance and blood volume displayed in H calves an increase
in mean circulatory filling pressure, no change in blood volume, and a
decrease in venous compliance, whereas hypo animals showed a decrease in
mean circulatory filling pressure and blood volume but no change in venous
compliance (35-37). This hemodynamic effect of T3 in the periphery
markedly contributes to the increased cardiac contraction. Studies using
heterotropic cardiac isographs have shown that T3-induced changes
in protein synthesis and cardiac growth primarily result from secondary
changes in cardiac work (38). In contrast, T3-induced changes
in myosin isoenzyme predominance occur to the same extent in the heart
in situ and in the heterotropic isograft (39-41). Thus, increases in total
protein synthesis and cardiac hypertrophy may be influenced by T3-induced
hemodynamic effects originating in the periphery.
In contrast, hypo is characterised by a low cardiac index, decreased stroke volume, decreased vascular volume, and increased SVR. Total blood volume is decreased in hypo and varies directly as a function of basal metabolic rate. Renal perfusion, when measured by glomerular filtration, is also decreased. Although sodium excretion is normal, free water clearance is impaired and can lead to hyponatremia (5). Total-body albumin distribution is expanded in hypo, in keeping with the development of high-protein-content effusions in many body cavities (42). Thyroid dysfunction alters BP: H has only minor effects on mean arterial BP, because increases in systolic BP, caused by increased stroke volume, are offset by decreases in diastolic BP, due to peripheral vasodilatation (43). Conversely hypo is associated with increases in diastolic BP. In a study of 40 H patients overtreatment that resulted in hypo was associated with an increase in diastolic BP that was reversible when thyroid function returned to normal (44). In a survey of 688 consecutive hypertensive patients, 3.6% were found to be hypo, and in this subset, diastolic BP fell significantly after adequate T4 replacement suggesting a cause-and-effect relation (45). Renin, angiotensin, and aldosterone play a minor role in this form of hypertension. T3 also modifies the secretory activity of the heart: T3 increases mRNA and protein levels of the atrial natriuretic factor (46). |
