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Nathan Goodyear

Early long-term L-T3 replacement rescues mitochondria and prevents ischemic cardiac rem... - 0 views

onlinelibrary.wiley.com/...abstract

T3 thyroid hormone hormones MI mitochondria HIF-1alpha

shared by Nathan Goodyear on 29 Jun 13 - No Cached
  • Nathan Goodyear on 29 Jun 13
     
    T3 in the post MI individual decreases the MI infarct size and the progression to heart failure. What is really  interesting about this study is that the T3 induced mitochondrial biogenesis and activity which is a great thing in recovery of MI and also in disease i.e. cancer.  However, it appears to increase HIF-1alpha and angiogenesis which is stimulated by retrograde signaling.  There is a muddied picture here.  Because T3 stimulates oxidative phosphorylation and mitochondria biogenesis which is favorable for health.  However, in this study of rats, it induced HIF-1alpha and angiogenesis in post MI, which is favorable to recovery, yet this is unfavorable for cancer.    Yet oxidative phosphorylation is favorable to cancer prevention/elimination and MI recovery.
Nathan Goodyear

Rebuilding the post-infarcted myocardium by a... [Heart Fail Rev. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...18773293

thyroid MI myocardial infarction heart attack hormone hormones post-MI heart cardiac remodeling

shared by Nathan Goodyear on 03 Jul 12 - No Cached
  • Nathan Goodyear on 03 Jul 12
     
    Wow, thyroid hormones play a significant role in cardiac remodeling post MI.  Thyroid hormones, "promotes tissue growth and differentiation and favorably remodels cardiac cell while increases cellular survival..."  How many people post-MI are having their thyroid evaluated, let alone correctly evaluated?
Nathan Goodyear

Thyroid Replacement Therapy and Heart Failure - 0 views

circ.ahajournals.org/...385.full

thyroid T3 hormone hormones cardiovascular disease heart health failure CHF MI myocardial infarction heart attack heart disease

shared by Nathan Goodyear on 24 Sep 14 - No Cached
  • A good biomarker of intracardiac TH signaling would be helpful but has not been identified. In the absence of such a marker, a rational, cautious therapeutic approach might be to restore and maintain over time biochemical euthyroidism as documented by normal circulating levels of TSH, FT4, and FT3.
  • a low-T3 state resulting from altered peripheral TH metabolism secondary to caloric restriction is associated with impaired cardiac contractility
  • Low-T3 syndrome is the central finding and defines the illness in a variety of acute and chronic severe nonthyroidal illnesses with cardiac origin, including MI, HF, and surgically treated cardiac disease.1 Low circulating levels of T3 in the absence of primary thyroid hypofunction have been found in 20% to 30% of patients with dilated cardiomyopathy.
  • ...1 more annotation...
  • FT3 levels were inversely correlated to coronary artery disease
  • Nathan Goodyear on 24 Sep 14
     
    Great review of the current understanding of thyroid hormone metabolism in cardiac tissue.  Low T3 and increased rT3 (via increased D3 activity) is CLEARLY associated with poor cardiac performance and post MI and CHF is associated with poor outcomes.  T3 is critical in cardiac remodeling and recovery post MI.  T3 is actually a vasodilatory in the coronary arteries.   Why a endocrinologist would call rT3 useless only points to their ignorance of the literature.
Nathan Goodyear

Thyroid Hormone and Cardiac Disease: From Basic Concepts to Clinical Application - 0 views

www.ncbi.nlm.nih.gov/...PMC3134399

T3 cardiovascular death disease heart health MI myocardial infarction CHF heart failure thyroid hormone hormones hypothyroid hypothyroidism CVD

shared by Nathan Goodyear on 24 Sep 14 - No Cached
  • Nathan Goodyear on 24 Sep 14
     
    Low T3 post MI is associated with increased CHF, morbidity and mortality.  Article discusses thyroid hormones and cardiac function/remodeling post infarct.  The article also lays the ground work for a new study of T3 in patients post MI to be followed for 6 months.
Nathan Goodyear

Estradiol Enhances Recovery After Myocardial Infarction by Augmenting Incorporation of ... - 0 views

circ.ahajournals.org/...1605.long

estradiol estrogen EPCs MI CVD endothelial progenitor cells hormone hormones

shared by Nathan Goodyear on 11 Jul 12 - No Cached
  • Nathan Goodyear on 11 Jul 12
     
    Estradiol shown to increase EPC activity post MI in female MI rat model
Nathan Goodyear

PLOS ONE: Increased Risk of Non-Fatal Myocardial Infarction Following Testosterone Ther... - 0 views

www.plosone.org/...10.1371%2Fjournal.pone.0085805

Testosterone therapy cardiovascular disease men male hormones

shared by Nathan Goodyear on 30 Jan 14 - No Cached
  • For all TT prescription subjects combined, the post/pre prescription rate ratio for MI (RR)was 1.36
  • In men aged 65 years and older the RR was 2.19 (1.27, 3.77), while in men under age 65 years the RR was 1.17
  • increasing RR with increasing age.
  • ...20 more annotations...
  • The RRs were 0.95 (0.54, 1.67) under 55 years
  • 1.35 (0.77, 2.38) at 55–59
  • 1.29 (0.71, 2.35) at 60–64,
  • 1.35 (0.44, 4.18) at 65–69, 1.62
  • 3.43 (1.54, 7.66) at 75 years and older
  • The adjusted post/pre RR for PDE5I across all ages was 1.08
  • For TT prescription, in men under age 65 years, the RR was 2.90 (1.49, 5.62) for those with a history of heart disease and 0.90 (0.61, 1.34) for those without
  • In men aged 65 year and older, the RR was 2.16 (0.92, 5.10) for those with a history of heart disease and 2.21 (1.09, 4.45) for those without.
  • Among men aged 65 years and older, we observed a two-fold increase in the risk of MI in the 90 days after filling an initial TT prescription
  • Among younger men with a history of heart disease, we observed a two to three-fold increased risk of MI in the 90 days following an initial TT prescription and no excess risk in younger men without such a history
  • Among older men, the two-fold increased risk was associated with TT prescription regardless of cardiovascular disease history
  • our own findings appear consistent with a higher frequency of thrombotic events following TT prescription among men with more extensive coronary vascular disease.
  • Our findings are consistent with a recent meta-analysis of placebo-controlled randomized trials of testosterone therapy lasting 12 or more weeks among mainly older men, which reported that testosterone therapy increased the risk of adverse cardiovascular-related events (OR = 1.54, 95%CI:1.09, 2.18), as well as serious adverse cardiovascular-related events (OR = 1.61, 95%CI:1.01, 2.56) which included myocardial infarction along with other conditions
  • This association appeared unrelated to average baseline testosterone level (p = 0.70) but varied by source of funding (p = 0.03), with a stronger summary effect in a meta-analysis of studies not funded by the pharmaceutical industry (OR = 2.06, 95%CI:1.34, 3.17) compared with studies funded by the pharmaceutical industry
    • Nathan Goodyear
      Nathan Goodyear on 30 Jan 14
       
      This supports prior analysis that studies done by pharmaceutical corps will be more favorable to their product(s) than those independently funded.  This is called bias.
  • the evidence supports an association between testosterone therapy and risk of serious, adverse cardiovascular-related events–including non-fatal myocardial infarction–in men
  • there is some evidence that low endogenous testosterone levels may also be positively associated with cardiovascular events
  • effects of endogenous and exogenous testosterone may differ. Exogenous testosterone (TT) is associated with physiologic changes that predispose to clotting and thrombotic disorders including increased blood pressure [18], polycythemia [19], reductions in HDL cholesterol [18], [20], and hyperviscosity of the blood and platelet aggregation. [20]–[23]; TT also increases circulating estrogens [24], [25] which may play a role in the observed excess of adverse cardiovascular-related events, given that estrogen therapy has been associated with this excess in both men and women
  • did not include information on the serologic or diagnostic indications for treatment.
  • no association between PDE5I prescriptions and the risk of MI
  • Recently TT has been increasing extraordinarily rapidly, including among younger men and among those without hormone measurement
  • Nathan Goodyear on 30 Jan 14
     
    New cohort study finds increased risk of Testosterone in men > 65 and those : these are based in marketing-based medicine not evidence based medicine.
Nathan Goodyear

Thyroid Hormone Treatment to Mend a Broken Heart - 0 views

jcem.endojournals.org/...1172.full

free T3 fT3 heart cardiac MI myocardial infarction hypothyroidism hypothyroid CHF congestive heart failure hormone hormones thyroid

shared by Nathan Goodyear on 03 Jul 12 - No Cached
  • Nathan Goodyear on 03 Jul 12
     
    free T3 is critical in the heart healing post MI.  Hypothyroidism and CHF share many hemodynamic and cardiovascular similarities.
Nathan Goodyear

Acute myocardial infarction and thyroid function: New pathophysiological and therapeuti... - 0 views

informahealthcare.com/...07853890.2011.573501

thyroid hormone hormones T3 heart attack heart health myocardial infarction MI

shared by Nathan Goodyear on 24 Sep 14 - No Cached
  • Nathan Goodyear on 24 Sep 14
     
    Thyroid hormone plays significant role in cardiac remodeling after acute myocardial infarction.  Thyroid hormone, particularly T3 as the vast majority of T3 is produced in heart tissue via D1 enzymatic activity, improves cardiac contractility, reduces systemic vascular resistance, reduces cardiac work load, decreases blood pressure, improves cardiac metabolism, and thus improves outcomes post MI.
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