New diagnostic blood test predicts risk of sudden heart attack
There is a difference between the atherosclerosis that kills a 42-year-old with sudden cardiac arrest and the kind that gives a 76-year-old relatively benign chest pain. Unfortunately, doctors lack a definitive way to tell what that difference is.
A new blood test, invented by a team of doctors and scientists at the University of Nebraska Medical Center, can tell the difference and predicts sudden heart attack risk in an ongoing clinical study.
The new test evaluated patients’ inflammatory response to atherosclerosis, the accumulation of fatty plaques in the arteries and the process that drives coronary artery disease. In 400 patients at UNMC the new test reliably differentiated heart attack victims from those with stable disease, regardless of heart attack symptoms. Using nationwide samples from the Veterans Administration, the inventors were able to repeat the results.
The new test is poised to completely change the management of the most pervasive chronic disease in the world, perhaps even supplant tests like blood cholesterol. The new blood test will differentiate if coronary atherosclerosis will progress to cardiac arrest or stable angina.
Additionally, the new blood test will provide a better basis to manage the disease. If a patient knows their atherosclerosis is more likely to progress to a heart attack then management can be more conservative, focusing on lifestyle and less on medicines like statins. The test may allow for more beneficial use of statin drugs.
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MAA is a titer for atherosclerotic disease
There is an emerging consensus in the study of atherosclerotic disease: it is an inflammatory disease. The progression of atherosclerosis is closely associated with the progression of a sustained inflammatory response. The driving mechanisms of the inflammatory response, especially associated with heart attack is unclear.
Malondiahadehyde (MDA) is a product of lid peroxidation. MDA is a mediator or marker of inflammation but no study has ever correlated MDA titer to atherosclerosis of cardiovascular disease. Malondialdehyde–acetaldehyde (MAA) is a further product of preoccupation and, unlike MDA, its concentration in serum correlates to progression of coronary artery disease and risk of sudden heart attack.
In an ongoing study at the University of Nebraska Medical Center, the inventors segregated patients presenting to the emergency room into four groups:
1) “Controls” – Patients without any history of CAD;
2) “Non-Obstructive CAD” – Patients that presented for cardiac catheterization with chest pain and CAD, but no evidence of an AMI;
3) “Acute MI” – Patients with CAD who presented with an AMI; and,
4) “Multi-Vessel Obstructive CAD” – Patients with severe CAD who presented for CABG surgery.
Patients with acute MI had significantly higher levels of serum anti-MAA IgM titers (961.2 mg/L) (p<0.01) compared to control patients (427.3 mg/L). The Multi-Vessel Obstructive group (689.4 mg/L) was increased over controls, yet significance was not present. Acute MI samples had increased IgM levels compared to the Non-Obstructive group (358.1 mg/L) (p=0.026). Patients with Non-Obstructive, Acute MI and Multi-Vessel Obstructive CAD had significantly higher levels of serum anti-MAA IgG titers (183.4 mg/L; 244.9 mg/L; 124.2 mg/L, respectively) (p<0.001) compared to control patients (97.4 mg/L). Acutely after AMI (within 60 minutes of chest pain), anti-MAA IgG antibodies are present in the serum and were significantly different from Non-Obstructive (p=0.027) or Multi-Vessel Obstructive CAD (p=0.003).
Patients with Non-Obstructive, Acute MI and Multi-Vessel Obstructive CAD had significantly higher levels of serum anti-MAA IgA titers (367.5 mg/L; 361.1 mg/L; 2495.5 mg/L, respectively) (p<0.001) compared to control patients (82.6 mg/L). Most dramatic was the large increase in anti-MAA serum IgA in the Multi-Vessel Obstructive group, which was significant (p<0.001) compared to both the acute MI and Non-Obstructive patient groups. Importantly, anti-MAA antibody isotype evaluation reveals a pathogenic association of IgM and IgG isotypes with AMI, while serum IgA (not secretory IgA) is associated with chronic stable progressive CAD. On a sub-group of AMI patients (n=10) serum was collected 24 hours post-AMI and assayed for serum anti-MAA IgG levels. 24 hours post-AMI, anti-MAA IgG antibody titers decreased 72.6% (p=0.015), anti-MAA IgM titers decreased 71.6% (p=0.81), and anti-MAA IgA