Dr. Qaadri

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Heart Disease and Cardiovascular Risk Reduction

By Dr. Shafiq Qaadri, MD

What is cardiovascular risk reduction?
Cardiovascular risk reduction refers to pharmacological and non-pharmacological interventions that reduce the risk of coronary and cerebrovascular atherosclerotic events.

We often forget how much lifestyle modification can help. Diet (low in fat and salt), aerobic exercise, smoking cessation, and weight loss have an important effect on lowering cardiovascular risk.

In high-risk patients, those with known atherosclerosis or diabetes, emphasis must be placed on aggressive pharmacotherapy with aspirin, ramipril, and statin therapy to lower LDL-cholesterol.

Prevention of cardiovascular disease is now a possibility: The combination of lifestyle modification and pharmacotherapy can prevent about 70% of heart attacks and strokes.

The challenge today is putting the knowledge we have gained from landmark clinical trials into practice. It is a legitimate expectation of each patient and our professional responsibility to ensure that every high-risk atherosclerosis patient be treated with these agents.

Does Peripheral Artery Disease equal Coronary Artery Disease?
Yes, PAD equals CAD, definitely. There is overwhelming evidence that patients with peripheral artery disease carry the same risk of developing a heart attack or stroke as patients with known coronary or cerebrovascular disease.

In other words, a patient with peripheral artery disease who has no cardiac symptoms, is in fact at greater risk of losing life than limb.

Because atherosclerosis is a systemic process, the presence of peripheral disease indicates that vascular decompensation and atherosclerosis has begun, potentially leading to coronary and cerebrovascular events.

Can family physicians identify such patients?
Yes. Though most patients with peripheral atherosclerosis are asymptomatic, measuring the ankle-brachial index can easily identify them. This is the ratio of blood pressure measured in the posterior tibial artery to the brachial artery, measured by using a handheld Doppler.

About 15% of Canadians over 55 may have asymptomatic peripheral insufficiency, placing them at very high-risk for coronary and cerebrovascular events…about a 30% risk of developing a heart attack or stroke over 10 years.

Once these asymptomatic patients have been identified by the ankle-brachial index, targeted risk reduction therapy can begin.

Dr. Ramgoolam in Winnipeg recently conducted the first Canadian primary care study to assess this problem, and demonstrated that ankle-brachial index can be easily incorporated into a FP’s routine physical examination.

So, yes: Painful legs equal an aching heart. PAD equals CAD. We must make this connection.

Then should patients with PAD be treated with risk reduction therapies to prevent heart disease and stroke?
Undoubtedly. This is an area that we often overlook, and unfortunately results in suboptimal risk reduction for very high-risk patients.

In a large number of patients who undergo peripheral vascular surgery, clinicians may forget to initiate risk reduction therapy. Yet the landmark HOPE study showed that patients with PAD derived greater cardiovascular benefit with ramipril treatment.

How can family physicians improve cardiovascular risk identification and reduction?
Canadian family physicians should be commended for their excellent efforts towards identifying high-risk patients. The use of the Framingham risk calculator is a very valuable tool in the primary prevention setting, which incorporates age, sex, cholesterol, smoking, and blood pressure. This calculation is not required for patients with diabetes, who are by definition, at very high risk.

Likewise, patients with known atherosclerosis--coronary, cerebrovascular or peripheral--by definition are in the very high risk category. We should be very aggressive with all these patients.

Other inflammatory markers, such as C-reactive protein, may become very useful in the identification of high risk patients.

How low should LDL Cholesterol be lowered?
The landmark Heart Protection Study published earlier this year has clearly defined this concept. In high risk patients, irrespective of their starting LDL-C and other lipid parameters, lowering LDL-C by 1 mmol/L is associated with a 30% cardiovascular risk reduction.

In a high-risk patient, irrespective of their starting LDL-C level, therapy with a statin should be initiated.

Going from 3.5 to 2.5 carries the same benefit as going from 2.5 to 1.5. Lower is better, and there are no more cut-offs.

Should a diabetic patient who has normal blood pressure and kidney function be treated with an ACE inhibitor?
Definitely, for both cardiovascular risk reduction and renal protection. Cardiovascular risk reduction with the ACEI ramipril is a distinct indication, different from heart failure, renal dysfunction, and hypertension.
The ACEI is for reducing the risk of future cardiovascular events, and the effects are mediated in part through improving endothelial function and retarding atherosclerosis, and are independent of blood pressure lowering. Even if the patient is not diabetic, but a high-risk patient over the age of 55, this therapy would be evidence-based practice.

How is the metabolic syndrome linked to cardiovascular disease?
The metabolic syndrome of insulin resistance affects about 90% of type II diabetic patients. It is a collection of multiple cardiovascular and metabolic risks, including diabetes, obesity, small dense LDL, low HDL, hypertension, inflammation, impaired fibrinolysis, and atherosclerosis.

Insulin resistance is the common denominator of the metabolic syndrome, and has emerged as an independent risk factor for cardiovascular events. An important concept is that you do not need to be diabetic to be called a “metabolic patient.” Someone who has central obesity, with high triglycerides and low HDL but normal glucose, also has a cardiovascular dysmetabolic state, and is at high risk of future events.

What is C-reactive protein and why is it getting so much media attention?
Over the past few years our understanding of how atherosclerosis develops has changed. We are identifying novel markers of atherosclerosis, and the high sensitivity C-reactive protein (CRP) is one of the most important.

The role of CRP as a key predictor of atherosclerosis stems from a fundamental paradigm shift in our understanding of the disease process: Inflammation plays a central role in the genesis of atherosclerosis and its complications.

Inflammatory cascades closely modulate each stage of atherosclerosis--plaque formation, propagation and rupture. Indeed, the inflammatory marker CRP has been shown to be the most powerful predictor of myocardial infarction, stroke, and vascular death in a variety of settings.

Just recently CRP has been demonstrated to be a more sensitive marker of cardiovascular risk than LDL-C. It is believed that routine assessments of high sensitivity CRP will enter routine cardiovascular risk algorithms within the next few years.

Do medications within the same class—such as statins or the ACEs—have the same effects? Are medications interchangeable?
Class effect refers to medications that share the same mechanism of action, yet are chemically different. The assumption that they are chemically interchangeable is not valid without clinical validation.

As a result, we carefully use medications that have been shown to be beneficial in a particular setting, and try as much as possible to avoid extrapolation. Both the therapeutic effectiveness, and side effect profile of medications of the same class can be markedly different, further reinforcing the concept that these drugs should be used for the specific indication, duration, dose and patient population employed when they were studied.

For example, metformin and phenformin are medications of the same class, yet phenformin causes marked lactic acidosis and was withdrawn from the market many years ago.

What does the future hold?
The future holds great promise. We will see the translation of CRP into routine clinical practice for cardiovascular risk reduction. We will also see family physicians use the ankle-brachial index to target high-risk patients, and there are national programs being planned for this.

The use of stem cells and gene therapy to repair damaged myocardium will become routine. Instead of pharmacotherapy, we will have cell-therapy for cardiovascular disease. The use of ventricular assist devices as a bridge to transplant will become more readily available in Canada, and we may even get closer to gene knockout and overexpression strategies to retard future cardiovascular events.

It is an exciting time, though we should not forget the large impact on cardiovascular disease that we can make today, by simply putting our current knowledge of risk reduction into practice.

Your final message to family physicians about risk reduction?
The last decade has empowered us with information and tools that have made prevention a distinct possibility. The challenge is to aggressively translate this vast body of evidence into the primary care setting. As physicians, we must all strive to continuously seek out better ways of risk identification, while building upon our current knowledge, in an effort to conquer cardiovascular disease, which is still the number one cause of death in Canada.

Dr. Shafiq Qaadri is a family physician and CME lecturer in Toronto. This column appears monthly.

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