Yet again, cardiac people seem ahead of too many endocrinologists.
The last sentence of this abstract says so much:
The implications for the identification of the effects of thyroid disease on acute myocardial infarction include the observation that restoration of normal thyroid function repeatedly reverses abnormalities in cardiovascular hemodynamics.
Which should be an absolute fundamental of treatment of thyroid disorders. Yet, as we know all too well, inappropriate treatment seems very common. I wouldn't be at all surprised if the percentage who are under- or over-treated, and with an inappropriate choice of thyroid hormones, and poor dosing regimens, after diagnosis is greater than all the undiagnosed (but needing to be diagnosed) and well-treated by a large margin. It should come to be seen a major scandal.
Dose right and people get better. Isn't that the fundamental of all disease treated by medicines? (Rather than surgery, diet, physical measures, etc.)
That we see patient after patient who can't get the contributory factors (iron deficiency, multiple vitamin deficiencies, etc.) tested, let alone adequately treated, is horrific.
Just adding that they cannot hope to get the dosing right while they continue not to understand how our thyroid systems work. Which is very much where diogenes and associates come in.
Curr Cardiol Rev. 2022 Apr 28.
doi: 10.2174/1573403X18666220428121431. Online ahead of print.
A Role of Thyroid Hormones in Acute Myocardial Infarction: An Update
Rabia Rasool Rasool 1 , Ahsanullah Unar 2 , Tassadaq Hussain Jafar 2 , Ghulam Qadir Chanihoon 3 , Bismillah Mubeen 1
PMID: 35657286 DOI: 10.2174/1573403X18666220428121431
Abstract
Acute coronary syndrome is one of the commonest life-threatening illnesses. It encompasses the clinical spectrum of acute myocardial ischemia and includes unstable angina and acute myocardial infarction both with and without ST segment elevation. Acute coronary syndrome can be attributed to a significant hemodynamic insult that leads to atherosclerosis of the epicardial coronary arteries. The main causative risk factors, such as obesity, smoking, and alcohol intake, increase the burden of acute coronary syndrome. Owing to an increase in the utilization of antioxidants, the antioxidant capacity decreases with regard to the scavenging of lipid peroxides. Moreover, the thyroid hormones are important regulators of the expression of cardiac genes, and many of the cardiac manifestations of thyroid dysfunction are associated with alterations in triiodothyronine-mediated gene expression. Cardiovascular signs and symptoms of thyroid disease are among the most acute clinically relevant findings that occur in combination with both hypothyroidism and hyperthyroidism. By understanding the cellular mechanism of the action of thyroid hormones on the heart and cardiovascular system, it is possible to explain rhythm disturbances and alterations in cardiac output, blood pressure, cardiac contractility, and vascular resistance that result from thyroid dysfunction. Oxidative stress is thereby induced, together with a decrease in antioxidant capacity for overcoming oxidative stress, which leads to endothelial dysfunction, subsequent atherosclerosis, and, ultimately, acute myocardial infarction. The implications for the identification of the effects of thyroid disease on acute myocardial infarction include the observation that restoration of normal thyroid function repeatedly reverses abnormalities in cardiovascular hemodynamics.
Keywords: Cardiovascular; Hyperthyroidism Oxidative Stress.; Hypothyroidism; Thyroid Hormone.
Rest of paper behind a very expensive paywall: