No abstract

The interaction of platelets with the polymeric surface of drug eluting stents has not been fully described in the literature. Our aim was to analyze the patterns of activation and deposition of platelets exposed to two different stent platforms; (a) the polymeric surface of the paclitaxel eluting stent (Taxus((R)) stent, PES,) and (b) the metallic surface of a stent with identical structural design (Express((R)) stent, BMS). Platelet activation was tested by deploying stents in an in vitro flow chamber model. Anticoagulated blood of 25 healthy volunteers was circulated (flow rate 10 ml/min for 60 min) into the flow chamber system. P-selectin expression, glycoprotein IIb/IIIa activation (PAC-1 binding) and platelet-monocyte complexes (PMC) formation were evaluated at 0, 10, 30 and 60 min. Surface platelet deposition was assessed by surface electron microscopy in stents implanted in the in vitro system for 60 min and in stents implanted in normal porcine coronary arteries for 24 h. Platelet activation evaluation showed a higher P-Selectin expression (92.9% of baseline in PES versus 68.3 % in BMS, P = 0.01) and higher PMC formation (125.7 % of baseline in PES versus 75.6% in BMS, P < 0.01) in the PES compared to the BMS control group. PAC-1 binding levels did not differ among groups. In the in vitro study, SEM analysis of the stent surface showed no statistical differences on platelet deposition between the groups. In addition, presence of proteinaceous material was more frequently seen on the BMS group (moderate to complete coverage = 80% in BMS versus 26% in PES, P < 0.01). In the in vivo study, complete platelet coverage was similar between groups (PES = 7% versus BMS = 8%, P = NS). However, there was an overall trend towards less platelet deposition on the BMS surface (mild and moderate coverage = 83%, 9% in BMS versus 49%, 44% in PES, P < 0.001 for both) but thrombus formation was not observed in either group. The polymeric surface of the PES appears to induce a higher degree of platelet activation and deposition compared to the BMS surface. The biological implications of these findings on the patterns of vascular healing need to be further studied in vivo. Condensed Abstract The interaction of human platelets with the surface of drug eluting stents has not been fully characterized. Patterns of platelet activation and adhesion were evaluated in vitro and in vivo after exposing platelets to the surface of the paclitaxel-eluting stent and identical bare metal stent. The degree of PMC formation and P-selectin expression was increased in PES compared to BMS. In the in vivo study, complete platelet coverage was similar between groups. There was an overall trend towards less platelet deposition on the BMS surface, however, thrombus formation was not observed on either surface. The polymeric surface of the PES appears to induce a higher degree of platelet activation and deposition compared to the BMS surface.

Over the last decade, one group of neurohormonal markers, including atrial natriuretic peptide (ANP), N-terminal pro-ANP, B-type natriuretic peptide (BNP), and N-terminal proBNP, has generated much interest in the evaluation and management of heart failure and acute coronary syndrome. There has been so much literature on the subject, especially concerning BNP and proBNP, that it leaves us confused at times about what the literature has to say about these markers. In this article, we have made an honest attempt to examine all the available literature in relation to the impact of BNP and proBNP on cardiovascular disease and present it to the reader in an assimilated fashion.

Learning Objective: Recognize nonspecific and delayed presentations of malignant hyperthermia (MH). Case: A 22-year-old male was admitted with drug overdose. He was found to be afebrile and drowsy with shallow respirations in the ER and was intubated for airway protection. CXR showed a right lower lobe infiltrate. Five hours later in the MICU, he was noted to be flushed and tachycardic with a temperature of 104.8ЊC. Cultures were obtained; Tylenol and antibiotics administered with a cooling blanket applied later. A review of medications given in the ER revealed succinylcholine. A CPK level of 37,789 U/L, elevated urine myoglobin, and high fever suggested malignant hyperthermia with rhabdomyolysis. The patient became normothermic after two doses of dantrolene. He was counseled about MH on discharge. Discussion: MH is a rare genetic disorder due to the mutations of ryanodine receptor in skeletal muscles. It usually occurs after administration of inhaled anesthetics or depolarizing muscle relaxants. Clinical features include marked fever, muscle rigidity, metabolic acidosis, rhabdomyolysis and hemodynamic instability. Hyperthermia develops within minutes to hours following exposure to disease-inducing medications. Many of the early signs are nonspecific and can mimic those of other etiologies. In our case, delayed diagnosis of MH was due to not only late-onset hyperthermia, but also initial attribution of his fever to aspiration pneumonia. Treatment includes discontinuation of triggering agents, oxygenation and use of dantrolene along with cooling measures. This case demonstrates the variability of presentation and underscores the need for continuous monitoring whether in a surgical or medical setting.

No abstract