Atherosclerotic Cardiovascular Disease in Individuals with Hepatitis C Viral Infection.

PURPOSE OF REVIEW: Hepatitis C virus (HCV) and atherosclerotic cardiovascular disease (ASCVD) are two diseases that affect millions around the globe. Hepatitis C affects more than 70 million individuals globally. ASCVD is commonly encountered and remains the top cause of death worldwide. A link has been identified between HCV and atherosclerosis. RECENT FINDINGS: A review of recent studies which define the association between HCV infection and an increased risk of subclinical ASCVD and experiencing cardiovascular (CV) events. It is now recognized that there is an increased burden of atherosclerosis in individuals infected with HCV that translates into increased cardiovascular events. An increase in the number of diagnosed cases of HCV is expected as screening recommendations for the virus have expanded. Strategies to educate healthcare professionals about this increased CV risk will need to be considered as well as the optimal strategy to lower CV risk in this growing population.

Use of a Modified Cardiopulmonary Bypass Circuit for Suction Embolectomy with the AngioVac Device.

The AngioVac suction cannula and circuit were designed for the percutaneous removal of soft thrombus and emboli in procedures requiring extracorporeal circulatory support. We describe a modification of the AngioVac suction catheter and cardiopulmonary bypass (CPB) circuit to effectively remove thrombus while maintaining the ability to rapidly initiate full CPBs during a medical crisis. This article will discuss the design concepts of the modified circuit as well as procedural protocols and considerations. The design modifications of incorporating an oxygenator, reservoir, and bridge allow for an increased flexibility that allows adaption to veno-venous extracorporeal membrane oxygenation or full CPB support when required for oxygenation or hemodynamic support.

Platelet protease-activated receptor antagonism in cardiovascular medicine.

Ischemic heart disease remains the number one cause of death in the world despite advances in invasive and pharmacologic therapies. An ongoing area of research is the central role of platelets in atherothrombosis. Many therapeutic strategies have been developed over the last few decades affecting different platelet receptors to alter platelet-mediated thrombosis including targeting the receptors for thromboxane A(2), adenosine diphosphate, and fibrinogen. However, despite the use of pharmacologic agents directed at these pathways, residual morbidity and mortality still exist. Therefore, identifying agents that more favorably balance a reduction in ischemic events while minimizing bleeding events is an ongoing mission. Thrombin is known to be the most potent stimulant of platelet-mediated thrombosis whose action on the platelet is through a family of receptors known as the protease-activated receptors (PARs). Activation through the PAR-1 receptor, in particular, results in an early and intense response by the platelet to thrombin, and it is the primary thrombin receptor on platelets, thus making it a potentially desirable target for therapy. Most recently, two PAR-1 antagonists, atopaxar and vorapaxar, have been tested in clinical trials. Generally, the results show a reduction in ischemic event rates, but an increase in bleeding event rates. This article will summarize the current state of the literature and consider the role these drugs might play in the future for the prevention of ischemic heart disease events.

Drug-eluting stents versus bare-metal stents in saphenous vein graft interventions: a systematic review and meta-analysis.

OBJECTIVES: We sought to review the published data and perform a meta-analysis to reach robust conclusions in the comparison between bare-metal stents (BMS) and drug-eluting stents (DES) in saphenous vein graft (SVG) percutaneous coronary interventions (PCIs). BACKGROUND: Drug-eluting stents are superior to BMS in reducing major adverse cardiac events (MACE) after PCI in native coronary arteries. However, studies comparing BMS with DES in PCI of SVG have had mixed results, probably due to smaller numbers and the nonrandomized nature of most of them. METHODS: The published reports search identified 4 randomized controlled trials and 19 cohort studies comparing BMS with DES in SVG interventions. Clinical end point data were abstracted and analyzed in aggregate and in subgroup analyses with random-effects model. RESULTS: Patients receiving DES had a lower risk of mortality (odds ratio [OR]: 0.75; confidence interval [CI]: 0.59 to 0.96), target lesion revascularization (TLR) (OR: 0.57; CI: 0.40 to 0.82), target vessel revascularization (TVR) (OR: 0.56; CI: 0.40 to 0.77), and MACE (OR: 0.61; CI: 0.42 to 0.79). Drug-eluting stent use resulted in a significant absolute risk reduction in TLR (-0.07; CI: -0.11 to -0.03), TVR (-0.10; CI: -0.15 to -0.05), and MACE (-0.12; CI: -0.18 to -0.06). There was no significant difference between the groups in recurrent myocardial infarction (OR: 0.99; CI: 0.65 to 1.51) or stent thrombosis (OR: 0.78; CI: 0.40 to 1.52). CONCLUSIONS: In this meta-analysis comparing DES with BMS use in PCI of SVG lesions, DES use was associated with improved mortality, MACE, TLR, and TVR. There was no evidence of increased risk of myocardial infarction or stent thrombosis.

Acquired Fanconi syndrome after treatment with capecitabine, irinotecan, and bevacizumab.

OBJECTIVE: To describe a case of acquired Fanconi syndrome after treatment with capecitabine, irinotecan, and bevacizumab. CASE SUMMARY: A 77-year-old female with metastatic colon cancer presented with vomiting and diarrhea. The patient had been diagnosed with stage IIIC (T3, N2, M0) colon cancer 18 months earlier and was initially treated with FOLFOX6 (regimen of oxaliplatin, fluorouracil, and leucovorin) after her hemicolectomy. She was switched to a capecitabine/oxaliplatin regimen after 4 cycles due to central access problems. She did well until 10 months after her cancer diagnosis, when metastasis was discovered. She was started on reduced doses of capecitabine, irinotecan, and bevacizumab. After her eleventh cycle, she presented to the hospital with the above symptoms. Laboratory test results showed hypokalemia, hypocalcemia, hypophosphatemia, and hypouricemia. The patient had not been started on any new medications other than chemotherapy for over 1 year. The electrolyte derangements were new, since the patient had laboratory values checked every 3 weeks. Despite daily intravenous replacements, the electrolyte abnormalities persisted. Laboratory evaluations demonstrated the presence of euglycemic glucosuria and a high fractional excretion of phosphorus in the setting of hypophosphatemia. Fanconi syndrome was confirmed by demonstration of aminoaciduria. DISCUSSION: Fanconi syndrome is a disorder characterized by proximal tubular dysfunction resulting in electrolyte wasting. In the acquired form, medications and multiple myeloma are the most common causes. Based on the Naranjo probability scale, a drug was the probable cause of Fanconi syndrome in our patient. However, because multiple drugs were involved, it was not possible to determine which one was the culprit. CONCLUSIONS: This is the first case of Fanconi syndrome reported after the administration of capecitabine, irinotecan, and bevacizumab. More studies are needed to confirm this association.