Antithrombotic therapy is imperative in the management of patients presenting with an acute coronary syndrome (ACS). The combination of antiplatelet therapy in conjunction with antithrombotic therapy has become the standard of care in improving the morbidity and mortality of patients with an ACS and in reducing ischemic complications of percutaneous coronary intervention. Patients with an ACS are at increased risk for a recurrent event, both in-hospital and for several months afterward. Secondary prevention to reduce these events is accomplished through the establishment of appropriate medical therapy. Dual antiplatelet therapy with aspirin and adenosine 5'-diphosphate P2Y(12) receptor blockers such as ticlopidine or clopidogrel are integral components of this regimen; however, both of these thienopyridines have a relatively slow onset of action and variable bioavailability. Prasugrel, a third-generation thienopyridine approved by the US FDA in 2009, has a more rapid onset of platelet inhibition than clopidogrel and ticlopidine because of increased efficiency of prodrug-to-active metabolite conversion. The result is higher and less variable concentration of the active metabolite within 60 minutes following oral dosing. Phase II and III trials assessing the safety and efficacy of prasugrel have been completed, including JUMBO-TIMI 26, PRINCIPLE-TIMI 44, and TRITON-TIMI 38. These trials demonstrated greater inhibition of platelet aggregation and lower rates of the composite endpoint of death, non-fatal myocardial infarction, and stroke compared with clopidogrel. However, major bleeding occurred more frequently with prasugrel treatment than with clopidogrel. This review highlights the current state of evidence-based antiplatelet therapy and provides guidance on appropriate use of prasugrel in cardiovascular medicine.
We present the case of a retrograde dissection of a right coronary artery (RCA) into the coronary sinus of Valsalva (CSV) attributed to a high-pressure jet extruding from a ruptured angioplasty balloon. The dissection was further complicated by an acute stent thrombosis. Both the CSV dissection and the acute stent thrombosis were successfully treated percutaneously using a combination of a Jo-Med Covered Stent and three bare metal stents. Case PresentationAn 83-year-old female developed chest pain and shortness of breath on postoperative day 3 after a total knee replacement. Her electrocardiogram revealed new-onset atrial fibrillation with a rapid ventricular rate and inferolateral ST segment depressions. She was treated with intravenous metoprolol for rate control and spontaneously converted to normal sinus rhythm after a few hours. She ruled in for a myocardial infarction with mildly positive Troponin I of 0.09 ng/dL. Her spiral computed tomography scan was negative for pulmonary emboli. The patient had a nuclear stress test that revealed inferior ischemia, and she was referred for coronary angiography.The patient's left coronary system revealed no significant disease, but her RCA coronary had an 80% to 90% stenosis in the ostial portion, followed by a 70% to 80% stenosis in the proximal vessel and a 40% to 50% stenosis in the mid vessel. The 4-French catheter dampened with each engagement of the RCA. The ostium of the RCA was calcified and highly angulated (Figures 1 and 2). Because of the patient's high-risk clinical and angiographic presentation, she was referred for a percutaneous coronary intervention (PCI).A 6-F JR4 Cordis guiding catheter was placed near the ostium of the RCA, which could not be engaged due to damping. A .014-in. PT2 wire was manipulated past the RCA lesions into the distal posterior descending coronary artery. The ostial and proximal RCA lesions were predilated with a 2.5 mm × 12 mm Sprinter balloon to 8 atm. A 70% to 80% residual stenosis remained in the ostial lesion, with a 60% to 70% residual in the proximal lesion; therefore, provisional stenting was employed. Because of the patient's advanced age, atrial fibrillation, and history of gastrointestinal bleeding, we decided to use overlapping bare metal stents. A 3.0 mm × 20 mm Liberte stent was deployed in the proximal RCA at 12 atm, and a second 3.0 mm × 20 mm Liberte stent was deployed at 14 atm in the proximal portion of the first stent, extending 2 to 3 mm out of the ostium of the RCA (Figure 3). A 3.0 mm × 15 mm Quantum Maverick balloon was used for high-pressure postdilatation. The Quantum Maverick was first inflated to 16 atm in the distal stent and then inflated to 16 atm in the ostial stent. After these first two inflations, no contrast was seen in the CSV (Figure 4). A third inflation to 14 atm was performed with the Quantum Maverick extending outside the ostial stent, in order to ensure the ostium was fully dilated. During this third inflation, the balloon was noted to lose pressure at approximately 14 atm, and was quickly...
Background: Nonaspirin, nonsteroidal anti-inflammatory drugs (NANSAIDs) have been associated with arterial thromboembolic events in the general population. Our objective was to determine the prevalence of NANSAID use in patients diagnosed with cryptogenic emboli or paradoxical embolic events from a patent foramen ovale (PFO) or atrial septal defect (ASD) compared with a control population with an incidental PFO/ASD and no history of embolic events. Methods: We performed a retrospective case-control study of 90 age-matched patients to assess the association of NANSAIDs with cryptogenic arterial embolic events in patients with and without a history of PFO/ASD. Odds ratios (ORs) were obtained by χ2 analysis. Multivariate analysis was conducted with a logistical regression method. Results: Patients with cryptogenic embolic events had a high prevalence of prescription NANSAID use regardless of the presence of a PFO/ASD and were far more likely to have a history of NANSAID use than those with an incidentally discovered PFO/ASD and no history of arterial emboli (OR 4.30, 95% confidence interval 1.14–13.07, p = 0.01). Conclusions: Many patients previously diagnosed with paradoxical emboli may be experiencing the prothrombotic effects of NANSAIDs rather than a paradoxical mechanism for their arterial embolic event.
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