In this video, from our Percutaneous Coronary Intervention Essentials course, you'll learn how to identify non-obstructive coronary artery disease (CAD) and obstructive (severe) CAD. We'll talk about the eyeball assessment, or QCA, and introduce other modalities of imaging.
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[00:00:00] In this lesson, we're going to talk a little more specifically about peri-procedural medication and what that might include. It's essential to ensure the patient is on the correct medication before they undergo a PCI procedure. The first thing we're going to consider is antianginal therapy. As previously mentioned, one of the prerequisites for recommending PCI in most guidelines for stable patients is optimal antianginal therapy.
[00:00:30] To be considered for a PCI procedure, the patient should have symptoms of angina despite being on optimal medical therapy. Antianginal therapy is usually considered to be two different drugs at optimal dose or specifically, the highest dose the patient is able to tolerate without side effects. This is also going to be important long term for the patient. Even if PCI improve symptoms, it's naive to think that revascularization via stenting a single part of a coronary artery
[00:01:00] will render the patient completely free of angina particularly if the patient has a distal, diffuse or small vessel disease unsuitable for revascularization. As noted previously, it's also very important that patients have their risk factors for cardiovascular disease fully assessed. Irrespective of whether the patient undergoes a PCI procedure. It's important to address their lipid profile, blood glucose, and blood pressure, not only to manage their current but also their future cardiovascular risk.
[00:01:30] This will hopefully have the additional benefit of reducing the risk of progressive coronary artery disease and the need for future revascularization. There is some evidence to suggest that high-intensity statin therapy used before PCI may reduce the complication rates of PCI-related procedures where the mechanism of this is poorly understood. Antiplatelet therapy is crucial when considering PCI. Exactly which `antiplatelet therapy to use and for how long
[00:02:00] depends on a number of factors that we will discuss in relation to several clinical cases throughout the course. For patients with chronic stable angina undergoing elective PCI, most guidelines recommend aspirin in combination with one other antiplatelet therapy. This second agent is conventionally clopidogrel in most interventional practice. In patients with acute coronary syndromes, aspirin plus the addition of a more potent antiplatelets agents such as ticagrelor or prasugrel
[00:02:30] are recommended by most guidelines as these agents are recognized to be more efficacious than their antiplatelet activity. These agents also have a more rapid onset of action than clopidogrel which is helpful in time-critical ACS presentations. In addition, a percentage of patients are paired genetically resistant to the antiplatelet action of clopidogrel with estimates of up to 30% of the population affected. This is not apparent without formally testing for platelet inhibition which is not widely done in routine clinical practice. These new agents
[00:03:00] may provide a potential mitigation to this concern. All patients undergoing a PCI procedure will require heparin. Recommended amounts vary from guideline to guideline and individual operator preference but a rough rule of thumb for dosing patients is that 70 or 100 units per kilogram is generally required. The aim of heparin is to prevent coronary artery thrombosis due to instrumentation with equipment used for PCI. Anticoagulation is a dynamic process with significant inter-patient
[00:03:30] variability. We decide whether the patient is adequately anticoagulated with heparin based on an activated clotting time or ACT which is normally performed in the cath lab during the PCI procedure. Once we normally start with a standard dose of heparin, we then decide on any additional heparin based on the measured ACT. The anticoagulant effects of heparin will wear off during the procedure and then particularly long or complex procedures, it's mandatory to recheck ACT levels periodically to ensure that the levels
[00:04:00] remain therapeutic and decide if another dose of heparin is indicated. As a standard of care, we would usually expect an activated clotting time between 250 and 350 seconds when taken about 10 minutes after heparin administration. It is sometimes necessary during a procedure to use more powerful antiplatelet drugs. As oral antiplatelet therapy becomes more efficacious, there is a decrease need for these supplemental intravenous agents.
[00:04:30] The most commonly used intravenous antiplatelet agents in the cath lab are glycoproteins IIb/IIIa receptor antagonists. These agents essentially prevent cross-linking of activated platelets. Glycoprotein IIb/IIIa inhibitors are very powerful agents and can cause significant bleeding complications particularly in the elderly and those with other comorbidities. They can also be associated with a significant drop in platelet count and consequent bleeding in some individuals.
[00:05:00] It is very important that when these agents are used, a platelet count is checked shortly after initiation and regularly for the duration of the infusion to ensure that the patient is not becoming thrombocytopenic. Like a protein IIb/IIIa receptor antagonist and now ordinarily used only in high-risk patients with large amounts of visible thrombus on the angiogram and during the PCI procedure. Commonly used available agents are abciximab, known as ReoPro;
[00:05:30] eptifibatide, known as Integrilin; or tirofiban, known as Aggrastat. The specific indications for using these agents, doses, and side effect profile are available for each on the respective drug information sheets and are outside the scope of this lesson.