Coronary heart disease (CHD) remains one of the leading causes of death worldwide despite significant advances in its diagnosis and management. Since over half of first presentations of CHD are either sudden death or a heart attack, by which time the underlying process causing CHD have been in place for many years, there is an obvious need for more effective prevention measures to be introduced at earlier point in its course. With the advent of modern imaging techniques and computer assisted image analysis, all people should be aware of the choices on what level of preventative care they wish to invest in, as it is certainly true that while the advanced technology required to assess ones individual risk of CHD is truly amazing, it comes at a hefty price.
This article will outline our individualised approach that includes early identification of those at risk, coupled with tailored preventive strategies, based on four principles:
Identify the individual patient’s risk.
Identify risk factors.
Implement a holistic package of recommendations that addresses the four main ‘layers’ of risk.
Design a recall programme for those at the highest risk.
Identifying the Patient’s Risk of future Coronary events
The first step in preventing coronary disease events is to identify the individual patient’s risk.
There are several ways that this can be done:
i. population-based statistical datasets, used by many GPs such as QRISK, where a calculator, based on large population studies, is used that takes into account age, gender, blood cholesterol, weight blood pressure and presence of diabetes. This is the widely used and low cost option.
ii. Individualised risk assessment; by taking the QRISK and then using advanced imaging techniques to discover, for an individual person, whether they are actually developing coronary artery disease. The techniques range from undertaking a CT Coronary Artery Calcium (CAC) and/or a CT Coronary Angiogram with or without a fat attenuation index (FAI), a marker of active coronary inflammation and risk of future fatal myocardial infarction (MI).
Clearly the first approach, based on a risk factor analysis is a great deal lower cost than the latter, perhaps explaining why, at present, its remains outside the scope of most state funded healthcare systems (such as the NHS) to provide for a whole population.
At SCVC, we believe that the choice of which system we use to identify one’s personal risk of future heart symptoms needs to be made by each patient on an informed basis, since risk scoring systems are not infallible, and the facts are that in around 50% of all presentation of coronary artery disease, the first sign of a heart issue is a heart attack or sudden death. Many coronary events occur every year in patients who were deemed to be at ‘low’ or ‘intermediate’ risk using the QRISK calculators.
Identifying Risk Factors
The second step is to identify risk factors such as raised LDL cholesterol, raised blood pressure, sedentary lifestyle, inflammatory conditions, family history of CHD, diabetes, or impaired glucose tolerance.
Implementing a Holistic Package of Recommendations
The third step is to implement a holistic package of recommendations that addresses the four main ‘layers’ of risk, as set out in the table below:
Worse (bigger holes)
Better (smaller holes)
Goal to reduce heart attack risk
Plaque burden and location
Large volumes of liquid plaque in proximal location that are more prone to rupture. A ruptured plaque in a proximal position is an ‘accident waiting to happen’.
Absent or low volume plaque, plaque in distal position. Scarred and/or calcified plaque is better than non-calcified plaque as it is then ‘stable’ and less likely to rupture.
Lower LDL Cholesterol long-term to help lower plaque volume and harden existing non-calcified plaque. Address other risk factors such as raised HbA1C, minimising pro-inflammatory diet (carbs, including gluten in sensitive individuals, and other inflammatory conditions associated with an increase in LDL ‘escape’ from the arterial circulation.
Plaque cap vulnerability and triggers for plaque rupture
Active inflammation, thinned cap, one or more therefore is prone to rupture. High blood pressure, sudden changes in blood pressure producing peaks in shear forces that can initiate plaque rupture
Healed and no longer vulnerable to rupture. Good blood pressure control, dampening of sudden changes in blood pressure that produce shear stress.
By reducing LDL and ‘hardening’ the plaque contents, thinning of the cap becomes less important. Statins through a pleomorphic effect, may reduce plaque inflammation. Avoidance of activities that cause sudden rise in blood pressure such as isometric strain (eg heavy weight lifting). Use of beta blockers to dampen sudden major changes in BP. Ongoing research into ‘anti-inflammatory’ drugs will help establish if these may also help protect against plaque rupture.
Vigour of platelet activation and coagulation system
Sedentary lifestyle. Unexpected extreme exercise may activate these pathways in part explaining the association between extreme exercise and cardiac events.
Regular exercise, antiplatelet drugs such as Aspirin and Clopidogrel, possibly DOACs.
By promoting graded and regular exercise and, in high-risk cases, use of antiplatelet drugs such as Aspirin or Clopidogrel, there will be a lower grade thrombotic reaction to plaque rupture. Dampened effect of exercise induced prothrombotic activity by using beta blockers and appropriately graded exercise programme. Statins may reduce adrenaline-induced prothrombotic platelet aggregation.
Effectiveness of natural clot buster systems
Sedentary lifestyle. Unexpected extreme exercise may supress these pathways in part explaining the association between extreme exercise and cardiac events.
Regular exercise improves natural thrombolysis. No current drug therapy directly affects the pathway however statins may have an indirect beneficial effect.
Regular exercise in high-risk patients can be protective. Its protective effect is lost after a few weeks of sedentary lifestyle, so it really is a case of “If you don’t use it you lose it”. If Triglycerides are raised then consideration of Fibrates that reduce PAI-1 levels which enhances fibrinolysis. Statins may also enhance fibrinolytic potential.
The identifiable ‘risk’ layers that contribute to a fatal heart attack are: i. location and volume of cholesterol-rich deposits (known as atheroma or ‘plaque’) in and around focal points in the wall of the artery – where the exact position of this plaque build-up matters, since an accumulation in a position closer to the coronary artery’s origin supplies a larger part of the heart, and is clearly potentially more important than a build-up in the more distant smaller branches supplying less of the heart muscle; ii. changes in the fibrous cap that separates the cholesterol-rich plaque from circulating blood; most of the time the fibrous cap is effective in preventing blood components from being exposed to this atheroma, however an inflammatory process, like that involved with the formation of skin pustules, occurs, which leads to episodic and on occasion major thinning of the fibrous cap. Once thinned, the cap becomes prone to ‘fracture’- initiating the plaque rupture that heralds a heart attack; iii. blood ‘stickiness’ which affects the propensity to form a large and biologically active plug at the point of any injury including plaque rupture which can, if overly intense can then be massively amplified by the coagulation cascade leading to a large clot or thrombus which blocks the arterial blood flow at the point of the plaque rupture; iv. the effectiveness and vigour of our innate ‘clot buster’ systems built into all arteries to protect from inappropriate and dangerous arterial clots. Plaque rupture may occur multiple times without triggering a heart attack because of these protective systems and, it is the additional failure of the protective ‘clot buster system’ that must happen before a heart attack occurs.
Designing a Recall Programme
Finally, for those at highest risk, it is important to design a recall programme to periodically recheck status, to ensure that the goals have been reached, and to reconsider using functional testing or CT techniques to assess whether additional measures, including coronary revascularization may be required.
In conclusion, the prevention of coronary disease events requires a multifaceted approach that includes identifying the individual patient’s risk, identifying risk factors, implementing a holistic package of recommendations that addresses the four main ‘layers’ of risk, and designing a recall programme for those at the highest risk. It is important to take a proactive and individualized approach to the prevention of coronary disease events, and to address all aspects of risk in a comprehensive and holistic manner.