Delayed-onset eptifibatide-induced thrombocytopenia.

PURPOSE: We present a unique case of delayed-onset, profound eptifibatide-induced thrombocytopenia that occurred 5 days after initiation of the drug. SUMMARY: Eptifibatide is a platelet glycoprotein IIb/IIIa receptor inhibitor with indications for use in patients with acute coronary syndromes. Eptifibatide-induced thrombocytopenia is uncommon but well studied and typically occurs within 24 hours of initiation of the drug. In the case described here, a 62-year-old male with a past history of coronary artery disease (including percutaneous coronary intervention within the past 12 months) was started on eptifibatide at a dosage of 2 µg/kg per minute for management of significant thrombus burden prior to a planned cardiac revascularization procedure; heparin for anticoagulation was also initiated. About 5 days after initiation of eptifibatide, the patient developed severe thrombocytopenia, with the platelet count dropping precipitously from 249 × 103/µL on admission to less than 1 × 103/µL. After eptifibatide and heparin therapy were discontinued and the patient was switched to argatroban, the platelet count recovered to 38 × 103/µL over the next 2 days. An eptifibatide platelet antibody assay was positive for IgG-mediated reactions consistent with eptifibatide-induced thrombocytopenia. Scoring of this case with the Naranjo scale yielded a score of 4, suggesting a possible adverse reaction to eptifibatide. CONCLUSION: This is the first published case report of profound eptifibatide-induced thrombocytopenia occurring more than 24 hours after eptifibatide initiation and serves to bring awareness that a delayed reaction can occur.

A Case of Cardiac Arrest Due to Transcatheter Aortic Valve Infolding.

Prosthetic valvular infolding during transcatheter aortic valve implantation (TAVI) is an under-recognized yet significant complication that can occur. Here, we describe the case of a 61-year-old male with a history of heart failure with reduced ejection fraction (HFrEF) and low-flow, low-gradient severe aortic valve stenosis of a bicuspid aortic valve who presented to undergo TAVI. During the procedure, repositioning of the valve resulted in prosthetic valvular infolding and resultant severe aortic regurgitation (AR), culminating in cardiac arrest. Swift balloon valvuloplasty corrected the valve geometry and eliminated any AR, allowing hemodynamic recovery and completion of the procedure. Our case and review highlight methods, both angiographic and echocardiographic, to recognize prosthetic valvular infolding the moment it presents, as well as strategies to correct the infolding with minimal detriment to the patient.

Exhaustion of coronary vasodilatory reserve in the resting state: Clinical characteristics and long-term outcomes after intervention.

OBJECTIVES/BACKGROUND: Resting coronary blood flow approximates flow with maximal vasodilation in very severe coronary stenosis. We studied the incidence of exhausted vasodilatory reserve by FFR, its clinical characteristics and long-term prognosis after FFR guided percutaneous coronary intervention (PCI). METHODS: Consecutive patients undergoing FFR-guided PCI for coronary stenosis with reduced resting blood flow (baseline Pd/Pa < 0.8) were included. Basal maximal vasodilation (BMV) was defined as less than 5% difference between resting Pd/Pa and FFR, that is, FFR-baseline Pd/Pa < 0.05. RESULTS: Of 658 vessels that underwent FFR-guided PCI in 602 patients, 151 vessels had resting blood flow in the ischemic range (baseline Pd/Pa ≤ 0.8) and were included in the analysis. Of these, 28 lesions in 28 patients met criteria for BMV (4.25% of the entire registry and 18.5% of those with the reduced basal coronary flow). Stenosis severity was a significant predictor of the presence of BMV. In long term follow-up (median 106 ± 3.6 months), BMV was not associated with increased target vessel revascularization (TVR) or major adverse cardiac event compared to non-BMV(OR 1.9, 95% CI 0.7-4.8, p-value 0.2 and OR 1.3, 95% CI 0.75-2.5, p = 0.3, respectively). CONCLUSION: Low baseline Pd/Pa that approximates fractional flow reserve (exhausted vasodilatory reserve) defines a subgroup of patients with severe coronary artery stenosis. Prognosis, when treated with PCI along with medical therapy, appears similar to those with intact vasodilatory reserve.

Giant Coronary Artery Aneurysms.

We present the case of a patient with giant coronary artery aneurysm. He has underlying severe coronary atherosclerosis and concomitant aneurysms of the abdominal aorta and popliteal artery. Our patient was treated surgically in the past due to underlying severe atherosclerosis. Despite bypass, his coronary aneurysms continued to enlarge. There is a lack of randomized trials regarding management to guide the decision-making process. Our case describes the work-up and treatment of a patient with giant coronary artery aneurysm requiring urgent orthopedic surgery.

Use of "super-glue" to seal a perforation during chronic total occlusion coronary intervention and the potential to "unglue" it.

Coronary perforation remains a dreaded complication of chronic total occlusion (CTO) percutaneous coronary intervention (PCI). We present a case of successful CTO recanalization complicated by a perforation treated by n-butyl-cyanoacrylate (medical "super-glue"). We also present an in vitro experiment showing that a glue plug in a plastic tube can acutely be passed by a low tip load guide wire and undergo balloon angioplasty recreating a lumen. These results suggest that n-butyl-cyanoacrylate glue may be an alternative for treating perforation during CTO PCI with the possibility of recanalizing the vessel through the glue plug at a later time.

Leadless solution for arrhythmia-related sudden unexpected death in epilepsy.

A leadless pacemaker is a recently approved pacing technology that helps mitigate lead-related complications, but it has several limitations. Careful candidate selection is needed. Here, we demonstrate leadless pacing as the solution for prolonged postictal bradycardia/asystole; there is no consensus regarding pacemaker implantation for seizure patients with such a risk of sudden cardiac death.

Right ventricular failure following placement of a percutaneous left ventricular assist device.

Right ventricular (RV) dysfunction following surgical implantation of a left ventricular assist device (LVAD) is a well-documented phenomenon, and it is associated with poor outcomes. We are reporting a 25-year-old male patient who presented to the hospital with flu-like symptoms, hypotension and acute hypoxic respiratory failure. The patient's Laboratory data was significant for elevated troponin, and his Chest X-ray showed acute pulmonary edema. Echocardiogram revealed reduced left ventricular (LV) ejection fraction and normal RV function. Coronary angiography was normal, and the cardiac index was 1.3 L/min/m2. Impella 5.0 (Abiomed, MA) was placed through the left axillary artery graft and 4.5 L/min flow was achieved with an improvement in blood pressure. Thirty minutes later, he developed hypotension, the device flow dropped to 3.0 L/min, and right atrial pressure increased. The Pulmonary artery pulsatility index was consistent with RV failure. Possible causes of RV failure include unmasking of RV dysfunction with high LVAD flow and altered RV geometry due to ventricular septum shift. Impella RP (Abiomed, MA) was placed for RV support achieving a flow of 3.8 L/min with a significant improvement in impella LV flow, cardiac output and blood pressure (mean 90 mmHg). Ventricular support devices were weaned off on day 9. The patient was discharged on day 15. Conclusion: our case highlights the risk of RV failure following percutaneous LVAD placement. Early identification and appropriate mechanical support is imperative.

Novel antiplatelet agents in cardiovascular medicine.

OPINION STATEMENT: Dual antiplatelet therapy with aspirin and a P2Y12 receptor blocker, particularly clopidogrel, has been the standard of therapy for secondary prevention in patients with acute coronary syndromes and patients treated with percutaneous coronary intervention. More potent P2Y12 inhibitors such as ticagrelor and prasugrel are associated with better pharmacodynamic effect and improved clinical outcomes but are associated with an increased risk of bleeding compared to clopidogrel. In addition, the observation of treatment failure in ~10 % of high-risk patients treated with aspirin and a potent P2Y12 inhibitor is another major concern. Personalized antiplatelet therapy based on therapeutic winnow concept for P2Y12 receptor blocker may facilitate the balance between reducing ischemic events and avoiding bleeding events, thereby improving net clinical outcome. New class of agents like vorapaxar has been approved by the FDA to reduce thrombotic events in patients with a history of myocardial infarction or with peripheral arterial disease. In addition, new P2Y12 receptor and protease-activated receptor (PAR)-1 receptor antagonists and agents targeting intracellular signaling downstream from G protein-coupled receptors are among the novel strategies under investigation to prevent arterial ischemic event occurrences.

Review of pharmacokinetic and pharmacodynamic modeling and safety of proton pump inhibitors and aspirin.

The efficacy of aspirin in primary and secondary prevention of cardiovascular diseases has been convincingly demonstrated. Gastrointestinal (GI) adverse effects with aspirin may lead to poor adherence and/or discontinuation of treatment. Proton pump inhibitors (PPIs) have been used for more than 20 years as the first choice for treating peptic ulcers and their bleeding complications, gastroesophageal reflux disease, non-steroidal anti-inflammatory drug-induced GI lesions and dyspepsia. Adherence becomes a major concern when aspirin is co-prescribed with PPIs to prevent GI adverse effects. Combining aspirin and PPIs into one tablet is an effective approach to address aspirin-related GI adverse effects and increase adherence to aspirin therapy for the prevention of cardiovascular diseases.

Tratamiento antiagregante plaquetario personalizado / Personalized Antiplatelet Therapy

Actualmente está bien establecido que la alta reactividad plaquetaria a la adenosina difosfato durante el tratamiento con clopidogrel es un factor independiente predictivo del riesgo de eventos isquémicos en pacientes a los que se ha practicado una intervención coronaria percutánea. Sin embargo, el papel exacto de las pruebas de la función plaquetaria sigue siendo objeto de controversia. Las pruebas de la función plaquetaria para asegurar una inhibición plaquetaria óptima han sido recomendadas por algunos autores para mejorar los resultados en los pacientes tratados con clopidogrel. En ensayos prospectivos y aleatorizados recientes sobre tratamiento antiagregante plaquetario personalizado, no se ha podido demostrar un efecto favorable de las pruebas de la función plaquetaria en cuanto a mejora de los resultados clínicos. En este artículo se analizan los mecanismos de la falta de respuesta a clopidogrel, los ensayos recientes de las pruebas de la función plaquetaria y otros nuevos avances en el campo del tratamiento antiagregante plaquetario personalizado (AU)

It is well established that high on-treatment platelet reactivity to adenosine diphosphate during clopidogrel therapy is an independent risk factor for ischemic event occurrences in a postpercutaneous coronary intervention patients. However, the precise role of platelet function testing remains debated. Platelet function testing to ensure optimal platelet inhibition has been recommended by some authorities to improve outcomes in patients treated with clopidogrel. Recent prospective, randomized trials of personalized antiplatelet therapy have failed to demonstrate a benefit of platelet function testing in improving outcomes. In this review article, we discuss the mechanisms responsible for clopidogrel non reponsiveness, recent trials of platelet function testing, and other new developments in the field of personalized antiplatelet therapy (AU)

Update: Acute coronary syndromes (V). Personalized antiplatelet therapy.

It is well established that high on-treatment platelet reactivity to adenosine diphosphate during clopidogrel therapy is an independent risk factor for ischemic event occurrences in a postpercutaneous coronary intervention patients. However, the precise role of platelet function testing remains debated. Platelet function testing to ensure optimal platelet inhibition has been recommended by some authorities to improve outcomes in patients treated with clopidogrel. Recent prospective, randomized trials of personalized antiplatelet therapy have failed to demonstrate a benefit of platelet function testing in improving outcomes. In this review article, we discuss the mechanisms responsible for clopidogrel nonreponsiveness, recent trials of platelet function testing, and other new developments in the field of personalized antiplatelet therapy.