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Prescribing levels of Testosterone is lower in the UK versus US.

In this study, flu vaccine is found to reduce MI risk by 45%.  Now, the take home point here is that those with cardiovascular compromise need to avoid the flu--not, that the flu vaccine by itself reduces the risk. The authors of this study fail to state the low success of the flu vaccine in the prevention of the flu.  They also fail to state the increased inflammation as a result of the vaccine itself.  A better approach would be to use natural therapies i.e.. vitamin D that have been shown to prevent the flu. 

Study finds increased risk of sudden MI in men with low Testosterone and elevated Estradiol.  In converse, increased risk is associated with elevated Estradiol in women.

This study appears to fly in the face of the recent studies on the dangers of Testosterone therapy in those with comorbidities.  This study was a retrospective cohort.  The study found that men in the highest risk for MI, had a reduced MI risk with Testosterone therapy.  Men in the lower risk quartiles had no such benefit.  Of note, the frequency of injections suggests inadequate dosing i.e. 4.4 in first year and 8.2 in follow up.  Most injection regimens will require at least monthly injections, though Testosterone pellets were used.  Of special note, no mention of level testing of Testosterone prior to study and/or during study and follow up.

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.

reverse T3 predictive of increased mortality in people with myocardial infarctions

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.

Animal model finds that Testosterone improves ventricular remodeling and function following myocardial infarction in male rats.  This similar finding has been found in human studies as well.   Testosterone therapy was found to lower BNP in this rat study.

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This is simply a public release prior to publication.  Study found that Testosterone therapy in men with existing CAD did not increased adverse events; in fact, it appeared to decrease the adverse events when compared to that of the non-treatment group.  Study not yet available to read the specific design, stats, and results which would be required to better analyze the actually results.

Only abstract available here, but EDTA chelation found to reduce risk of death, reinfarction, stroke, hospitalization, angina in individuals with diabetes and prior MI from 38% to 25%.

My heart attack is a life changing event. I am always aware of this fact that when I am speaking to a loved one, it could be the last conversation that I have with them. My coronary arteriography present that I have three vessel diseases. Please support me for getting heart treatment.

Comprehensive review of hyperthemic therapy.

Surgery induced metastasis: it is real and steered by NETosis.