A cardiac lesion begins to form from oxidized or damaged lipids that cause arterial injury. Atherosclerosis is a process of chronic endothelial injury that increases permeability of the arterial wall, allowing oxidized lipid particles to bind and aggregate on the arterial surface - contributing to the formation of lesions (atheroma).

The presence of such compounds stimulates the vessel cells to produce molecules and recruit leukocytes (monocytes, granulocytes, and T-cells) to the arterial walls, and stimulates the proliferation of smooth muscle cells.

The recruited leukocytes are transformed into lipid-laden foam cells and are responsible for the growth of the lesion.4 Growth factors then are released and stimulate the generation of new capillaries through the process of angiogenesis, providing the growing lesion with an adequate blood supply.

Expression of adhesion molecules and chemokines (MCP-1 and others) participate in platelet aggregation, lymphocyte, and monocyte adhesion - further activating the lesion injury.

A physical change in the smooth muscle cells, and the process of cell turnover (apoptosis) produces excessive amounts of collagen, elastin and proteoglycans. This transforms the endothelial injury into a lesion comprised of a thin fibrous cap and lipid core (plaque) that is unstable and prone to rupture.

1. MCP-3: Guides immune cell direction & activity
2. sFas: Prevents cell death
3. Fas Ligand: Initiates cell death and recycling
4. Eotaxin: Activates immune cells at areas of damage
5. CTACK: Helps clean up damaged tissue
6. IL-16: Recruits & activates immune cells
7. HGF: Stimulates tissue and repair
8. HDL: Helps remove bad cholesterol
9. HbA1c: Diabetes marker

Fifty-percent of Heart Attack victims have normal cholesterol. As such, cholesterol testing alone doesn’t provide a complete picture of cardiac health, and in fact, the role of dietary cholesterol in relation to CHD has been called into question in recent years as the US dietary guidelines are reevaluated.

Many other methods, such as the CAC test and more invasive methods of vascular imaging require strong presentation of symptoms before a physician will recommend them.

The PULS Test bridges this gap by providing unprecedented diagnostic information that includes and expands upon lipid profiling without the invasiveness of other methods. The PULS Test aims to identify vulnerable, asymptomatic patients with active, yet undetected CHD, and for whom early intervention can help.

The PULS Cardiac Test identifies patients that may not be identified as high-risk using other tests, as well as patients who are at low risk for heart attack, ensuring that interventions are focused only on those patients who actually need them. Unlike traditional tests for Heart Disease, the PULS Test can detect the early stages of endothelial or arterial injury, diagnose disease stage, and predict how likely the disease will cause an unstable cardiac lesion rupture (myocardial infarction). The PULS Test is:

• Validated in a multi-ethnic population
• Outcome data demonstrates clinical utility in identifying patients in danger of developing disease
• Conforms to current ACC/AHA (ATP IV) guidelines
• Motivates patients to adhere to physician recommendations

The test results will include:

• Your patient’s complete Cardiac Profile with individual measurements for each of the 9 protein biomarkers that contribute to their cumulative 5-year unstable cardiac lesion diagnosis and likelihood of rupture. This score will then be categorized into a low, borderline, or elevated category.
• Your patient’s “Heart Age” which shows your Cardiac Score relative to your Age and Gender group.
• Recommended lifestyle modifications that may help maintain or reduce your chances of a Heart Attack.

PULS Test results will allow you to then determine the most appropriate course of action for the patient based on the latest clinical guidelines.