One of your patients has discrete angiographically significant lesions in the mid right coronary artery and the mid left anterior descending coronary artery. He is 60 years old and is not diabetic. He has ongoing class 2 anginal symptoms despite optimal dose of a beta-blocker and a long-acting nitrate.
What do you recommend?
The benefits of revascularization and the comparison of modalities depend on the patient’s background and coronary anatomy. With this anatomy revascularization is for symptoms and not prognosis. Both modalities are equally effective in this respect. Revascularization should be considered for stable angina refractory to two oral antianginals in preference to a third agent. The risk of stroke is similar. Although PCI has the advantage of rapid recovery, the probability of repeat revascularization is statistically higher.
A 45-year-old diabetic male patient has returned to clinic following a recent angiogram. He has stable class 2 angina and is currently on aspirin 75 mg od, atorvastatin 40 mg nocte, and bisoprolol 2.5 mg as antianginal treatment. His symptoms have improved since starting the beta-blocker. The angiogram showed severe plaque in the proximal left anterior descending artery and discrete simple lesions in the mid circumflex and right coronary arteries. The echocardiogram has shown moderate LV impairment.
This question tests an understanding of patterns of stable coronary disease where revascularization is associated with prognostic benefit. The evidence generally favours bypass surgery as the mode of revascularization in these cases. The key features are (1) left main stem disease or (2) multivessel disease with (i) proximal LAD involvement or (ii) LV impairment/ large territory of proven ischaemia or (iii) in a diabetic patient. The main PCI prognostic indication for stable coronary disease is proven ischaemia with frequent daily symptoms.
Which one of the following is true of atherosclerotic plaque formation?
Endothelial injury and dysfunction result from a number of insults. Decreased nitric oxide (NO), which is antiatherogenic, results from endothelial dysfunction. Branch points are vulnerable. Modified cholesterol esters (oxidized LDL) accumulate in the subendothelial space and are phagocytosed by macrophages to form foam cells. Abnormal vascular smooth muscle proliferation at points of atherosclerosis contributes to plaque formation and also determines the stability of the lesions (fibrous cap–thin caps = vulnerability to shear stress).
Atherosclerotic plaque rupture is the most common event leading to clinically relevant ischaemia.
Which one of the following statements regarding this process is not true?
Clinically silent plaque rupture with spontaneous healing is well recognized. If a patient presents with an ACS, and a ruptured culprit plaque is identified without luminal stenosis (i.e. ongoing ischaemia), it is reasonable to continue medical therapy without stenting as long as the event has stabilized.
Which one of the following statements regarding the new generation of antiplatelet drugs is not true?
Clopidogrel and prasugrel are both pro-drugs, irreversible inhibitors, and once-daily regimes. The maintenance dose of prasugrel is halved for weight <60 kg or age >75 years. Clopidogrel is converted to its active metabolite by the cytochrome enzyme pathway; this accounts for the variability of action in some patients (hyporesponders) which can lead to stent thrombosis. Prasugrel is converted to its active form faster and more consistently. Ticagrelor is reversible and direct acting and therefore is again faster acting and more predictable than copidogrel. All inhibit the P2Y12 ADP platelet receptor.
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