Age could be modifiable risk factor in heart disease

Age could be modifiable risk factor in heart disease

Age is currently considered an unmodifiable risk factor in the development of cardiovascular disease -- but it might not need to be. According to the authors of a Viewpoint published on March 4, 2008 in The Lancet, age can be broken down into factors which are indeed "unstoppable," but also into factors that can be modified if tackled early enough.

Dr Allan Sniderman, Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University, Montreal, Quebec, Canada, and Dr Curt Furberg, Wake Forest University School of Medicine, North Carolina, USA, say: "Age is not considered to be a modifiable risk factor but unfortunately it outranks all those that are -- eg, lipids, blood pressure and smoking -- as a predictor of clinical events. If so, a tight limit exists on how much prevention can be achieved. But is conventional wisdom correct? Are all the effects of age immutable?"

Epidemiological studies show contradictory results in this vein. Some analyses show that the major determinants of risk are the classic modifiable risk factors: abnormal levels of circulating fats, smoking, and high blood pressure. Others indicate that age and gender make the strongest effects. This paradox, according to the article, is essential to effective prevention.

Atherosclerosis, the building up of hard plaques in the arteries, can lead to blockage that slows or completely stops blood flow, leading to death of the tissue fed by this artery, called infarction. A heart attack due to plaques in the coronary artery is a classical example of this scenario. The authors point out a challenge related to this when they ask: "How do we deal with the dilemma that atherosclerosis is often well underway before middle age whereas clinical complications are common only after middle age?"

Risk factors such as abnormal levels of circulating fats on disease progression is related to both the condition's magnitude and duration. For instance, certain fats like high LDLs increase risk more than others like low LDLs. However, raised concentrations of high LDL over many years would be expected lead to more vascular disease than the same exposure over only a few years. The authors highlight this: "This last point is key. Conventional analyses do not distinguish between the biological changes within arteries - the non-modifiable effects of disintegration of tissues over time - and those produced by exposure over time to risk factors such as atherogenic dyslipoproteinaemia."

A number of studies are referenced by the authors, including INTERHEART and AMORIS, that show that abnormal levels of circulating fats, along with high blood pressure and smoking, actually cause vascular disease rather than simply being risk factors. It is emphasized that factors such as these should be taken seriously outside of the standard calculations of risk, which can involve complex statistical analysis and might obscure their importance. Additionally, epidemiological studies often focus on populations for short periods of time, when long periods will help elucidate which factors are truly modifiable risks.

Even in people as young as their twenties can have serious coronary disease, so early intervention can be extremely beneficial. "Success is more probable if we prevent atherosclerosis from diffusely invading and completely distorting the arterial tree than if we attempt to intervene in only the final stages," say the authors.

For this population especially, lifestyle changes can be helpful, but can be inadequate if someone has abnormal blood pressure or blood fats for other reasons. The authors discuss pharmaceutical options: benefits, costs, side effects, and of course, the timing. For instance, statins are used to lower cholesterol levels and have few side effects. The identification of key risk factors, such as an abnormal LDL value, could allow high risk populations to be targeted earlier, while others can wait for treatment.

In conclusion, the authors propose that age perhaps need not be considered an unmodifiable risk factor for cardiovascular disease. Rather, they say: "Age can be deconstructed into time-related effects of disintegration that affect all of us versus time-related effects of exposure to the modifiable causal factors that affect some of us more than others. This crucial distinction is not taken into account by the methods we use to predict risk.

"The natural history of coronary disease can be likened to a three-act tragedy. The first act introduces and develops the main characters - namely, atherogenic dyslipoproteinaemia, high blood pressure, and smoking - that appear as we mature and unless something is done, persist during our lifetime. During the second act, which also takes place over decades, these villains incessantly attack and progressively deform the innocent arterial wall. Finally, the third act, which can be tragically brief: in an instant, the plaque ruptures, the artery thromboses, and the hero or heroine dies, all too frequently unaware of the drama that was enacted within their arteries. What is the difference, you ask? In the drama of coronary disease, the ending is not fixed; if some of the characters are edited out of the play as soon as they appear, the third act need never take place."

Age as a modifiable risk factor for cardiovascular disease

Allan D Sniderman, Curt D Furberg

The Lancet, March 4, 2008


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