If you knew you were at risk of a heart attack within the next five years because of unstable plaque in the arteries, would you do something to stop it? You bet you would! But how do we know if that risk exists?
Your doctor will do a risk assessment on you if you fall into one or more of the ‘at risk’ categories, but sometimes you need more than that. Happily, technology has now emerged which enables us to specifically look for protein markers released when plaques formed during the process of atherosclerosis are unstable. This is major because forewarned is forearmed and you can do a lot to lower the risk of a heart attack occurring in the next few years IF you know!
I have listed the new Cleveland Labs PULS Cardiac Test to enable you to test for those markers should you need to.
In a large clinical trial, the PULS Cardiac Test identified 61% of patients who went on to have a cardiac event who otherwise would have been missed using established risk factors alone (5).
That is really important! I’ve included some info on the test itself below for you, but first here is my general advice on Cardiovascular testing, and you can also see my Heart Disease factsheet here.
With heart tests, you can look at what risk factors you may have and offset those risks very specifically to prevent problems developing or progressing in future. You can also test to see if you already have active heart disease as plaques formed during atherosclerosis release specific markers which can now be measured. It is so much more sophisticated nowadays than just looking at your cholesterol and blood pressure levels, if you know what to look for!
My advice if you fall into an ‘at risk’ category (familial history, high LDL cholesterol, blood pressure or diabetes, poor diet/lifestyle, smoke or are obese) is to do EITHER the Genova CV Health or the Doctors Data Comprehensive Cardiovascular Risk test (the former has a great report and lipid fractionation and the latter includes a diabetes HBA1c test along with some really important protective markers like CoQ10 and red blood cell magnesium) AND the PULS Cardiac Test to look for the specific protein markers released in active heart disease. You can see a PULS sample report here. Check which test gives you what you need to know. Shame one test doesn’t do all of it really but it is highly specialised stuff! Once you have some info to work with, you can get started on reducing those risks and reversing the issue!
Follow the links there to see sample reports and test info etc. Now, some info from the lab on the new PULS test itself. I have to say, if you are an ‘at risk’ person, it seems like a no brainer to me. Talk to your doctors and, if they do not look for these markers, then I now can!
An Elevated PULS Cardiac Test May Identify:
- Coronary heart disease development
- Presence of unstable/vulnerable arterial plaque
- Increased near-term risk of a heart attack
Atherosclerotic disease progression is characterised by chronic endothelial damage and an accumulation of fatty plaque within the arterial wall. Unstable plaque can rupture and lead to arterial blockage causing a heart attack. The first steps in prevention are the identification of individuals at near-term risk of a heart attack, and allowing for more aggressive therapy to potentially avoid a future event.
The PULS (Protein Unstable Lesion Signature) Cardiac Test measures key clinical risk factors including age, sex, diabetic status, family history of heart attack, and distinct protein biomarkers. These markers are associated with the biological pathways underlying cardiac lesion formation, progression and rupture. This refined methodology of cardiac risk assessment provides an improved calculation of a patient’s near-term (5 year) risk for a heart attack.
The PULS Cardiac Test may be performed on individuals at intermediate risk with one or more risk factors for coronary heart disease.
- Cardiovascular risk prediction models such as the Framingham Risk Score calculate risk of a cardiovascular event within the next 10 years. When used, these calculations rely heavily on established clinical risk factors (1) which may not fully estimate the prevalence of cardiovascular disease in the general population (2, 3)
- The PULS Cardiac Test measures clinically significant proteins in the blood associated with active unstable lesion formation and when combined with established clinical risk factors, predicts whether a cardiac lesion could rupture within a 5 year period (4).
- In the Multi-Ethnic Study of Atherosclerosis (MESA), the PULS Cardiac Test outperformed a common risk calculator, yielding a net reclassification index of 42.7% in individuals defined as intermediate risk by the Framingham Risk Score (4). Reclassification of those initially defined as intermediate risk to high risk may result in more appropriate therapeutic intervention.
- In a large clinical trial, the PULS Cardiac Test identified 61% of patients who went on to have a cardiac event who otherwise would have been missed using established risk factors alone (5).
The frequency of ordering The PULS Test is determined by an individual’s medical history, but may be monitored more frequently in those at moderate to high risk for cardiovascular disease.
The PULS Cardiac Test should be performed on a serum and EDTA whole blood sample. Patients do not need to fast for the test.
1. Wilson PW et al. Prediction of coronary heart disease using risk factor categories. Circulation. 1998; 97: 1837-1847.
2. Greenland P et al. Major risk factors as antecedents of fatal and nonfatal coronary heart disease events. JAMA. 2003; 290: 891-897.
3. Khot UN et al. Prevalence of conventional risk factors in patients with coronary heart disease. JAMA. 2003; 290: 898-904.
4. Cross DS et al. Coronary risk assessment among intermediate risk patients using a clinical and biomarker based algorithm developed and validated in two population cohorts. Curr Med Res Opin. 2012; 28: 1819-1830.
5. Simonini A and Harrington DS. Early detection of unstable cardiac lesions in asymptomatic individuals at risk of acute coronary syndrome. Cardiology. 2015; 131: 148.