The MESA website has some useful online tools for estimating arterial age and age and sex percentile calcium scores. Check them out here.
The UK's NICE committee has also produced a PDF that explains the concept of using calcium scoring in subjects with chest pain of recent onset.
Lifetime cardiovascular risk (as opposed to 10 year risk) is another approach, suggested by Berry and colleagues in the NEJM.
A lifetime risk calculator can be found here - QRisk website.
Useful tool from the Confirm CT registry that integrates coronary CTa findings with clinical risk factors and demographic data - Confirm Tool.
I'm not sure exactly how this intriguing graph was constructed, but it demonstrates that nearly half of the reduction in CHD deaths over the past 50 years is due to new therapies, whilst most of the remainder stems from better risk factor control.
From the ESC Guidelines
Another approach to understanding the changes in CVD mortality and incidence rates is by applying models such as the IMPACT mortality model. Based on information on changes in coronary risk factors and in treatment as obtained from the results of RCTs regarding the effectiveness of different treatment modalities, it estimates the expected influence on CHD mortality by age and gender. This model has been applied in different countries; the results from these studies are rather consistent and similar to what has been observed in other studies of the same subject, as summarised in Figure 1. Beneficial reductions in major risk factors—in particular smoking, BP, and cholesterol—accounted for more than half of the decrease in CHD deaths, although they were counteracted by an increase in the prevalence of obesity and type 2 diabetes; 40% of the decline in CHD death rates is attributed to better treatments of acute myocardial infarction, heart failure, and other cardiac conditions. Results from clinical trials and natural experiments also show that a decline in CHD mortality can happen rapidly after individual or population-wide changes in diet or smoking.
Percentage of the decrease in deaths from coronary heart disease attributed to treatments and risk factor changes in different populations (adapted from Di Chiara et al. Does surveillance impact on cardiovascular prevention? Eur Heart J 2009;30:1027–1029.)
ACCF/AHA guidelines - nice summary of current thoughts.
Similar guidelines were published recently by the European Society of Cardiology.
Images above show non-invasive cardiac imaging using CT, compared (bottom) to invasive coronary angiography - 'A'. Note the distal left main stem 'soft' plaque visible on the contrast CT - 'C', invisible on the non-contrast calcium scoring CT scan in 'B'.
Dangerous plaques are missed by calcium scoring alone in maybe 5% scans in symptomatic subjects.
A multi-biomarker blood and urine test designed to estimate future cardiovascular risk is in the news at present, having been featured at the prestigious TedMed conference and written up on theheart.org.
The test comprises a panel of five biomarkers, each focussing on different phases on the atherosclerotic plaque development and rupture process. This seems to me to be an interesting and novel approach.
The company that provides the test, Cleveland Heart Lab, suggests that the F2-Isoprostane/Creatinine urinary ratio highlights oxidation and unhealthy lifestyles such as smoking, lack of exercise and obesity, apparently representing a long-term marker of cardiovascular risk.
The next two of the markers estimate intermediate cardiovascular risk. These are hS-CRP and urinary microalbumin.
Finally, in terms of assessing very near-term risk of cardiovascular events, myeloperoxidase and Lipoprotein-Associated Phospholipase-A2 are markers of a vulnerable plaque phenotype.
On the company's website there are several supportive studies.
On the whole I think this is an interesting approach, but of course much remains to be done. Generally, with the biomarker approach, only small incremental benefits over and above Framingham scoring have been demonstrated. I am more of an advocate for atherosclerosis imaging which is generally associated with a far higher relative risk of cardiovascular events if the test is positive.
Whilst the idea of a simple, relatively inexpensive blood test is appealing to both patients and their doctors, be positive and negative predictive values of the test must be known. It must also (or they must also) provide added value to Framingham risk scoring if it is to be of any use.
Does the biomarker panel change with either lifestyle modification or drug therapy?
Although not directly testing this particular panel of biomarkers, the HRP Bioimage study should hopefully provide some firm ground for the recommendation of either blood biomarkers, structural atherosclerosis imaging tests or both in the asymptomatic high-risk population.
If you have any thoughts on this please feel free to jot them down below.
HDL research must continue (via the heart.org)
> After a series of negative trial results, the concept of raising high-density lipoprotein (HDL) as a therapeutic approach to reducing cardiovascular risk looks to be in a sorry state. But lipid experts at the recent European Atherosclerosis Society (EAS) 2012 Congress were adamant that the HDL hypothesis was not yet dead and that it is imperative that research in this direction continue.
What do you think? Do you hold out any hope for this method of lowering CV risk? Should we wait for the results of the phase 3 anacetrapib study? What about the HPS2-thrive study with Niacin? Do we have to wait until 2013 or should we withdraw Niacin today?
As a change, I thought I'd cover this Day in Stockholm using Twitter feeds. This will give you multiple opinions from a cross section of delegates. Simply click on the links to read more!
Safety of 2 intravenous heparin doses with PCI in ACS patients treated with fondaparinux - here.
ISAR REACT 3A: Reduced dose of unfractionated heparin in patients undergoing percutaneous coronary interventions - here.
Today's hotline press releases - here.
Nurses can reduce the risk of recurrent complications in heart patients: results from the RESPONSE trial - here.
REACH: Comparative Determinants of 4-Yr CV Event Rates in Stable Outpatients at Risk of or with Atherothrombosis - here.
A pill costing less than £1.50 a day has the potential to save thousands of heart failure patients - here.
Hot arteries: Marion Hoffman, Chicago - Vascular muscle cell factor implicated in aortic aneurysms - here.
Future of myocardial perfusion imaging - here.
This post on HeartWire caught my eye. At the recent EAS meeting, it was announced that a statement is forthcoming, supporting a screening blood test for Lp(a) - and then therapy with nicotinic acid to lower levels below 50mg/dL. This recommendation is aimed at those at intermediate and high risk of CV disease.
However, as the authors state further down the page:
"Since lifestyle appears to have little impact on an individual's Lp(a) level, the EAS consensus panel recommends that 1 to 3 g of niacin (nicotinic acid) daily is the best treatment for lowering Lp(a) levels. However, the group acknowledges that there have not been randomized, controlled trials selectively targeting plasma levels of Lp(a) and calls for further studies in both primary- and secondary-prevention settings to better define which patients should be targeted for treatment and what the target level of Lp(a) should be."
Where do you stand on this? Are you comfortable to screen and treat this 'risk factor' in the absence of clinical end point evidence?
Let us know your plans regarding Lp(a) below!