Nuclear Imaging raises concerns about radiation and cancer. But what if Nuclear Imaging could be done exposing you to the same amount of radiation as a chest x-ray?

When I entered by Cardiovascular Disease Fellowship (Cardiology) in 1989, I entered as a Faculty member from the Iowa American Heart Association. At that time I was known for being a lipid specialist, and a specialist in Advanced Cardiac Life Support - where I helped write the protocols for both.

My cardiology pathway would soon take two twists.

The first would be my entry into heart failure where I would be trained by Goldstein and Dougherty. Goldstein had secured grants and funding for research and treatment of patients with various forms of heart failure. Goldstein was also known as an expert in post partum cardiomyopathy - or heart failure occurring in women after delivering their babies.

Dougherty was known as a world expert in diastolic dysfunction - heart failure associated with a stiff heart resulting in the inability of the heart to relax to fill with blood, so the blood could then be pumped throughout the body.

Goldstein and Dougherty would be instrumental in my training as a heart failure specialist. This would allow me to both take care of these patients in the clinic, be part of the phosphodiesterase inhibitor (PDE) research and given the assignment of writing the first comprehensive chapter on the use of PDEs for heart failure.

This work also opened the doorway to working with Taegtmeyer (Krebs last PhD student) using glucose-insulin-potassium (GIK) treatments for heart failure patients.

The second cardiology pathway would be nuclear imaging.

Here I would once again be trained by Goldstein, who had a grant for a new nuclear isotope named Teboroxime. Teboroxime was a research drug, not yet available for use and it would compete with the other Technetium-99m (Tc-99m; the "m" means metastable) research drug, Sestamibi.

I wrote the first single photon emission computed tomography (SPECT) paper on Teboroxime which was later compared with Sestamibi. [My later exposure of the lies perpetuated by Lantheus and subsequent Big Pharma companies owning Sestamibi, would later lead to Big Pharma coming after me. You can read more about that here: https://www.flemingmethod.com/about if interested.]

I had selected UTHSCH for my cardiology fellowship after learning that Merhage was conducting positron emission tomography (PET) imaging. I was particularly interested in PET, as this coupled my previous PhD research of anti-matter with my current position as a Cardiology Fellow.

Upon my arrival I discovered that Merhage had left. Gould who was running the PET research facility was also engaged in research with Ornish, using Ornish dietary study patients to demonstrate the clinical effectiveness of PET.

The PET laboratory was carrying out research on several isotopes, including ammonia, glucose and the rubidium-82 (Rb-82) generator.

The prior group of cardiology fellows had accidentally released strontium (parent compound for the rubidium) after bypassing a safety mechanism. As a result, I was treated to a rather liberal dose of strontium after the prior cardiology fellows left their contaminated shoes in what became my research office. This was detected by me after experimenting with the Geiger counter in my laboratory.

This work with PET imaging of the Ornish patients brought full circle my investigations as it included research into the effect of diets, lipids and heart disease. The actual Fleming Unified Theory of Vascular Disease (FUTVD; later called ITIRD) presented first at the 1994 American Heart Association Conference in Dallas, TX, would evolved out of these investigations and other research resulting in my determining that there were multiple other factors that played a role in the development of chronic InflammoThrombotic Immunologic Response Diseases (ITIRDs).

The following papers show some of my earlier research in nuclear cardiac imaging as I sought to increase the abiltiy to separate regional blood flow changes between the different coronary arteries and their vascular beds (angina) and find heart disease - the earlier the better for diagnosing and treating patients.

The involvement with pharmacologically stressing the heart to enhance these differences between diseased and non-diseased, or less diseased arteries stemmed from the approach we used in the PET imaging laboratory, where there is insufficient time to take a patient from a treadmill to the PET (positron emission tomography) imaging table given the short half-life of the isotopes being used.

The use of pharmacologic stress instead of stressing the heart by using a treadmilll, a method developed by Bruce, also became desireable as I investigated differences in outcomes between patients pharmacologically stressed and those stress by Bruce's treadmill test.

It is important to emphasize here, that Gould had been trained by both Ter-Pogossian and Bruce. Subsequently, Gould trained me in both and my investigations further demonstrated that patients were placed at increased risk of adverse outcomes (strokes-CVAs, heart attacks-MIs) when placed on the treatdmill, while using pharmacologic stress did not produce this risk. The use of pharmacologic stress also allowed for further determination of differences in flow reserve compared with treadmill stress.

The following papers provide some of the research I conducted and published, along with papers from the last section, laying the foundation for this improvement diagnostic testing with reduced risk to the person being stressed. It would lay the foundation for the development of FMTVDM.