Atherothrombosis a Focus on PAD
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Hello, I am Mark Robbins, the director of the Peripheral Vascular Program at Vanderbilt Heart and Vascular Institute. Itâs my pleasure on behalf of e-learning systems to bring to you a lecture on Atherothrombosis.
Atherothrombosis manifests primarily as three distinct clinical syndromes involving the cerebral, cardiac, and peripheral vasculature. The prevalence of each are depicted in this slide with the prevalence of Cerebral Vasculature Disease, Cordial Heart Disease, and Peripheral Artery Disease; being 4.8, 13.2, and 8 million respectively as we will see later in the presentation. The stated prevalence of Peripheral Artery Disease is likely a significant underestimate. More importantly is the fact that patients with a history of Atherothrombosis are more likely to die from a future atherothrombotic event.
Data from the Framingham Health Study strengthened the relationship with history of atherothrombosis and reduced life expectancy. In this study, healthy individualâs age 60 years who do not have atherothrombosis were expected to live a further 20 years to the age of 80. Comparatively, patients with a history of micro infarction lived 9.2 fewer years and those with a history of stroke live 12 fewer years.
Atherothrombosis is not limited to the United States. Data in 2004 from the World Health Organization places atherothrombosis as the leading cause of death worldwide, exceeding infectious disease, cancer, injuries, pulmonary disease, and aids.
This at combined a direct and indirect cost of $403.1 billion doubling the cost attributed to cancer and 13 times the cost attributed to HIV.
To help better understand the history of atherothrombosis, Bristol Myers Squibb and Sanofil Aventous partnered to bring us to Reach Registry.
The reduction of atherothrombosis for continued health registry had the following objectives: to identify comparable patterns in atherosclerosis risk factor prevalence and treatment in many countries around the world; they enrolled over 70,000 patients from 44 different countries. The design of the registry was for outpatients aged 45 years or older with established coronary artery disease, cerebrovascular disease, and peripheral arterial disease or with at least three atherosclerotic risk factors, which were enrolled over an initial seven month recruitment period on a worldwide basis and followed for up to two years. Outcomes measures or baseline prevalence of atherosclerosis risk factors, medication use, and degree of risk factor control.
One finding in the Reach Registry should not be a surprise is a significant overlapping manifestations of atherothrombosis. You should be well established the atherothrombosis is a systemic disease and once the diagnosis is made in one location, there is a high probability of other vascular territories being involved.
If we look at the manifestations of atherothrombosis on the x-axis of this slide including death, nonfatal myocardial infarction, non-fatal stroke, and the composite end point; it makes the price some equals with the highest mortality for patients with a history of peripheral arterial disease, exceeding the mortality associated with coronary artery disease and cerebrovascular disease. Another point to be made from this slide, if your initial event was a myocardial infarction you're most likely next event in the future would be another myocardial infarction with stroke following suit or simply put if a patient has a past event within a certain vascular bed, future events will more than likely affect the same vascular bed.
In my opinion, one of the most striking findings within the Reach Registry was the association between the escalating risk of cardiovascular event and the number of vascular beds involved. If for example, we look at cardiovascular death the one-year rate of death was 1.4% when only one vascular territory was involved climbing to 2.4% and then 3.8% for two and three vascular locations involved respectively.
Focusing on the diagnosis of peripheral arterial disease, which was associated with the worst outcomes in the Reach Registry. How are we doing as primary care physicians, cardiologists, vascular surgeons, and vascular medicine specialists in the diagnosis and treatment of peripheral vascular disease? The next two trials we will cover try to determine the answers to these questions.
McIafferty et al published the following data in 2000 in the Journal of Vascular Surgery. They mailed an anonymous survey to 843 internal medicine physicians in central and southern Illinois with the following question: how often parts of a health and physical exam for peripheral arterial disease would be performed in the following hypothetical patient: a 65-year-old with a history of hypertension. They receive a response from 360 physicians, 230 physicians completed the questionnaire from a varied practice distribution.
Within the survey, which likely reflects a common practice pattern, a history of claudication was taken by less than 40% of physicians. In addition, a history of foot ulcers was taken by less than 30% of physicians. This is clearly demonstrating a deficit in respect to peripheral arterial disease.
Additional data on how we are doing in the diagnosis and treatment of peripheral arterial disease was gathered by Hirsh et al published in Jama in 2001. They enrolled close to 7,000 patients who were either 70 years or older or were 50 to 69 years of age with diabete meltas or had ever smoked; in other words, patients at risk for peripheral arterial disease. Patients were enrolled within 350 primary care practices and each patient was evaluated by history and measurement by an ankle brachial index. A history of peripheral arterial disease was made either by a known history of peripheral arterial disease or at the ankle brachial index was less than 0.9. Peripheral arterial disease was found in an amazing 1,865 patients were 29% of the cohort.
In addition, overlapping manifestations of atherosclerosis mainly confined to coronary artery disease or present in 56% of these patients diagnosed with peripheral arterial disease.
Keep in mind the significance of overlapping manifestations of atherosclerosis again illustrated by the Reach Registry; the escalating risk of major adverse events of the more atherosclerotic locations being involved.
When Hirsh et al evaluated their treatment data a sobering trend emerged. Although, hypertension was treated in over 80% of patients with a peripheral arterial disease; treatment of hyperlipidemia was found in less than 50% of patients. In less than 40% of patients with peripheral arterial disease as their sole diagnosis received anti-platelet therapy. This again demonstrating the lack of awareness and significance the diagnosis of peripheral arterial disease currently has within our medical community.
This under treatment of peripheral arterial disease could explain in part the high event rate in those with a history of peripheral arterial disease is outlined again. This slide from the Reach Registry again focusing on cardiovascular death, those patients with a history of peripheral arterial disease at a higher event rate than patients with a history of previous myocardial infarction and stroke.
The partnerâs trial outlined the various holes that we have in our evaluations with patients with peripheral arterial disease. Although, the majority of the patients are aware of their diagnosis less than 50% of physicians within the partnerâs trial were aware that their patient had a diagnosis of peripheral arterial disease. In addition, it is highly unlikely that all patients with significant peripheral arterial disease will present with classic claudication as only 11% of the patients diagnosed with peripheral arterial disease had classic claudication within the partners trial. That means that within the partnerâs trial 85 to 95% of patients would have been missed if we waited for them to describe a pattern of classic claudication.
How can we ensure that we make the diagnosis of peripheral arterial disease in our office so that we can initiate appropriate therapy to prevent the mortality and morbidity associated with the cardiovascular and cerebrovascular risks?
The first thing we must do is recognize the patients at highest risk. Newman et al found that independent of age that four risk factors emerged as major factors associated with peripheral arterial disease. These are diabetes, which evades a fourfold risk of peripheral arterial disease compared to the general population; as well as smoking, hypertension, and hypercholesterolemia.
Once we find those at risk, a good view of systems and a follow-up exam is necessary. We should concentrate on the detail limb exam looking for absent or diminished femoral or pedal pulses; arterial brutis; hair loss; poor nail growth; dry, scaly, atrophic skin; dependent rubor; pallor with leg extension after one minute at 60 degrees at which time normal color should return when placing the leg in a dependant position after 10 to 15 seconds, longer than 40 seconds indicates severe ischemia; and inspection of a shoeless and sockless foot with ischemia tissue ulcerations.
If we suspect peripheral arterial disease based on the history and physical exam, the next step is obtain an ankle brachial index. The concept of ankle brachial index is as follows: this systolic blood pressure in the leg should be approximately the same as the systolic blood pressure in the arm. Therefore, the ratio of systolic blood pressure in the leg versus the arm should be approximately 1 or slightly higher. Ankle brachial index has been found to be 95% sensitive and 99% specific for angiographically diagnosed peripheral arterial disease. Any value less than 0.9 confirms the diagnosis of peripheral arterial disease. Just as important as making the diagnosis with an abnormal ankle brachial index is to realize that the lower the value, the higher the future risk for cardiovascular events. There are published reports that for every 0.1 decrease in ankle brachial index, there is an associated 10.2% relative risk increase in three-year cardiovascular events.
For those who have automated blood pressure cuffs in their office Beckman et al established a correlation between Doppler measured ankle brachial index and what could be obtained with an automated cuff, making it easier for primary care physicians to perform ankle brachial indices within their day-to-day practice.
With each accumulation of data concerning peripheral arterial disease with its associated risks of future cardiovascular events independent of symptomatic status the ACC and AHA published their guidelines for the management approach for peripheral arterial disease in 2005.
the ACC and AHA established class one indications were the following: a history of walking impairment, claudication, ischemic rest pain, and/or non-healing wounds is recommended as a required component of a standard review of systems for adults 50 years or older who have atherosclerotic risk factors or adults 70 years and older. In addition, individuals with asymptomatic lower extremity peripheral arterial disease should be identified by examination and/or measurement of an ankle brachial index so that therapeutic interventions known to diminish their increased risk of myocardial infarction, stroke and death may be offered.
In summing up the recommendations, The ACC and AHA â For the purpose of this guideline asymptomatic lower extremity peripheral arterial disease implies the absence of classic leg claudication symptomsâ¦ data demonstrate that lower extremity peripheral arterial disease even without classic claudication is often associated with leg dysfunction, diminished functional capacity and an increased cardiovascular ischemic risk.
Now letâs turn our attention to managing patients with peripheral arterial disease.
Treatment of peripheral arterial disease requires two distinct strategies. In my opinion by far the most important is risk reduction of atherothrombotic events. We must recognize patients with peripheral arterial disease are at high risk for future strokes and heart attacks. We are decreasing those risks by adequately control your risk factors. These include smoking, hyperlipidemia, hypertension, and diabetes. In addition to controlling risk factors, these patients must be on anti-platelet therapy.
With respect to specific goals the risk factor measured, lack of proteins, the LDL goal should be at minimum less than 100. In my opinion, as close to 70 as you obtain safely. The first line of therapy in these patients should be stat drugs. There is an overwhelming wealth of knowledge concerning status of these future risks for cardiovascular events. Again anti-platelet therapy is mandatory. We will discuss it later in the presentation. The role of single or dual anti-platelet therapy. Blood pressure goal should be less than 130 over 80, especially in patients with diabetes or history of mineral insufficiency. Based on the HOPE trial and others, ACE-inhibitors should be the first line of drugs. People should not be concerned about using beta blockers in patients with peripheral arterial disease. With respect to glycemic control, hemoglobin A1C should be managed as close below 7 as safe and absolutely complete cessation of tobacco smoking is again mandatory. Emerging risk factors although not associated with good clinical benefit with treatment, are homocysteine, hyperprotein delay, CRP, and Apolipoprotein E .
Once there is adequate control of risk factors we can turn to symptomatic treatment of claudication. Exercise is one of the most effective but underutilized treatments for claudication. To be effective it does take the triad of frequency, intensity and duration. An exercise program should be performed at least 4 times per week for the duration of oneâs life. Intensity is defined by a pace that elicits claudication within 5 minutes. Each salvable claudication is then followed by rest until a minimum of 4 repetitions are performed. As compared to pharmacological therapy, exercise has been shown to be more beneficial with claudication free walking time.
Once our patients have been adequately treated from a risk factor stand point and have established an adequate exercise program, but remain symptomatic, pharmacologic therapy is likely warranted. Cilostazol has been found to be superior to the other forms of pharmacologic therapy on this page and is my first drug of choice. I have to be careful in patients with a history of coronary disease because it cannot be used in patients with established congestive heart failure due to the possibility of pro-arrhythmia.
Lastly is there is refractory claudication use of interventional therapy may be warranted. In recap again the most important aspect of the treatment strategies for peripheral arterial disease are risk reduction for future, cardiac, and cerebral vascular events. Both of which drive the morbidity and mortality associated with peripheral arterial disease. Secondary goals are symptom relief. This should first start with an exercise program which is then followed by pharmacologic therapy if necessary and then ultimately with interventional therapy if there is refractory claudication.
There are well established goals for the treatment of risk factors for peripheral arterial disease and atherothrombosis in general. The goal for the use of anti-platelet therapy is less well established. Over the next few slides, we will try to make some sense and come up with some regimens and goals for therapy for single or dual anti-platelet therapy with patients with known atherothrombosis.
There are three main groups of anti-platelets available for use in patients with atherothrombosis. Aspirin with its wealth of data, in cyclooxygenace, it prevents the production of thrompoxinate. Two, Dipyridamole inhibits phosphodiesterase effecting the production of cyclic-amp and clopidogrel and ticlopidine are both non-competitive inhibitors of ADP receptor. Therefore effective platelet irrigation through inhibit of the glycoprotein 2b3A receptor.
Letâs turn our attention at this point to clinical evidence of clopidogrel.
One of the first studies to evaluate Plavix or clopidogrel was the Caprie trial. This study enrolled patients with documented atherothrombosis in equal numbers with respect mycartilagen, peripheral arterial disease and cerebral vascular disease. These patients were randomized to Aspirin or Plavix and their primary endpoint was myocardial infarction, stroke, or vascular death.
In over 19,000 patients studied. Treatment with clopidogrel was associated with a significant 8.7% relative risk reduction in primary end-point over aspirin mono-therapy. These results were primarily pushed by the over 20% relative risk-reduction in patients were enrolled with peripheral arterial disease.
The CURE, COMMIT and CLARITY trials all evaluated patients with established and unstable acute coronary syndromes. Simply stated all three trials compared Aspirin versus Aspirin plus Plavix in this high risk group. Across the board the combination of Aspirin and Plavix was significantly more beneficial in reduction of primary end points as the mono-therapy with Aspirin alone.
The most recent trial published was the CHARISMA trial; which in a similar design to CAPRIE with some notable exceptions. CHARISMA enrolled not only patients with documented atherothrombosis but also patients at risk for atherothrombosis but no documentation of disease. Additionally patients were randomized to either Aspirin versus Aspirin plus Plavix.
The major findings of the CHARISMA trial are outlined in this slide. It is apparently that asymptomatic patients drive little benefit from dual anti-platelet therapy and did somewhat better with Aspirin alone. For those with symptomatic peripheral arterial disease, cerebral vascular disease or coronary artery disease had significant benefit from dual anti-platelet therapy. The primary end point of the trial although did not meet statistical significance and when we looked at all patients in over 15,000 studied there was no net benefit for patients who received dual anti-platelet therapy versus those who received Aspirin alone.
In conclusion, the CHARISMA data suggests the following. Symptomatic patients experience a 12% reduction in the primary end point significant with no significant increase in severe bleeding. Asymptomatic patients experience a 20% increase in the primary end point which did not reach significance with no significant increase in severe bleeding. Overall clopidogrel plus aspirin was not significantly more effective than Aspirin alone in reducing the primary end point in all patients studied.
Focusing on coronary disease, results in the CURE, COMMIT, and CLARITY point to a clear cut strategy that would favor dual-anti-platelet therapy. The ACC and AHA in 2007 published their guidelines for the use of clopidogrel in patients with unstable angina and non-ST segment myocardial infarction. In the initial management strategy, when an invasive strategy is used, Aspirin is initialed with clopidogrel loading followed by daily maintenance dose and this should be initiated before diagnostic angiography. If the plan is for conservative therapy, clopidogrel loading dose followed by daily maintenance dose added to Aspirin in anti-coagulate therapy is recommended. Clopedogrel administration should be for at least one month and ideally up to one year. Again the timing of dosing should be as soon as possible after admission. If the strategy initially is conservative therapy with subsequent diagnostic angiography, only in the event of recurrent symptoms ischemia, heart failure or serious arrhythmia post conservative management, they recommend clopidogrel loading dose followed by daily maintenance dose added to Aspirin anticoagulant therapy. Again, being initiated before diagnostic angiography.
Class one selected recommendations by patient management strategies post-angiography are as follows. In patients undergoing percutaneous coronary intervention, recommendation is to administer a loading dose of clopidogrel if not started before angiography and to continue Aspirin. In the medical therapy group if coronary artery disease was found on angiography, a loading dose of clopidogrel if not given before the diagnostic angiography should be given at this time and continue with Aspirin. If there is no significant coronary disease found, the recommendation is anti-platelet therapy. To plan for coronary bypass grafting, you should continue your Aspirin but discontinue clopidogrel 5 to 7 before elective coronary artery bypass graft.
Class I selective recommendations for clopidogrel for use in long term medical therapy is secondary prevention. In patients who presented with unstable angina or non-ST segment elevation myocardial infarction and they are going to be treated medically without stinting, the recommended therapy is clopidogrel 75 mg a day prescribed for at least one month and ideally up to a year. In addition, Aspirin of 75 up to 162 mg per day indefinitely. If a bare metal stint was used, in these patients, recommended therapy is going to be clopidogrel described in a dose of 75 mg a day for a minimum of one month and ideally for up to one year unless the patient is of increased risk of bleeding and is given for a minimum of two weeks. Aspirin at a dose of 162 to 325 mg per day for at least one month then this can be reduced to 75-163 mg per day indefinitely.
My overall synopsis to anti-platelet therapy in patients with atherothrombosis is as follows: For patients with coronary disease it is rather straight forward. In patients who have unstable coronary syndromes who have undergone percutaneous coronary intervention, or are high risk medical therapy only patients, we should follow ACC AHA guidelines for dual anti-platelet therapy and clopidogrel. There are no strict guidelines at this time for patients with a previous history of TAA or stroke. They definitely need anti-platelet therapy but whether this is sole therapy with Plavix or sole therapy with Aspirin or dual therapy with Aspirin and clopidogrel is still in question. Patients with peripheral arterial disease, anti-platelet therapy is mandatory. Whether or not you use single or dual therapy hinges on the overlapping manifestations of disease. The more overlapping manifestations that a patient has, such as they have combined peripheral arterial disease, cerebral vascular disease and a history of coronary artery disease in this patient more than likely will benefit from dual anti-platelet therapy with Aspirin and Plavix. The patient who presents with sole claudication, with no documented events from a coronary stand point or super vascular standpoint may benefit more from Plavix as outlined in the CAPRIE trial. The CHARISMA trial clearly states in its findings that patients at risk for atherothrombosis but no documented events do better with Aspirin alone. I want to thank you for your time.
|Goals and Objectives|
After participating in this activity, the viewer should be better able to:
1. Describe atherothrombosis manifestations and mortality rates
2. Identify physical exam findings and risk factors of PVD
3. Describe PVD risk factor modification and treatment
4. Describe oral antiplatelet therapies
5. Identify when monotherapy vs. combination antiplatelet therapy is indicated with atherothrombosis
Estimated time to complete this activity is 38 minutes.
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