Role of Monotherapy with a P2Y12 Inhibitor for Secondary Prevention in Patients with Established Atherosclerosis.

PURPOSE OF REVIEW: The role of monotherapy with a P2Y12 inhibitor for secondary prevention of cardiovascular diseases has been assessed in several randomized trials. In this article, we summarize the evidence regarding P2Y12 monotherapy for secondary prevention in each one of the major vascular territories. RECENT FINDINGS: Available data including a large recent meta-analysis show no differences in terms of all-cause death, vascular death, stroke, and a minor difference of the risk of myocardial infarction with P2Y12 monotherapy as compared to dual antiplatelet therapy. Overall, mono antiplatelet therapy with aspirin and the P2Y12 inhibitors appear similar in efficacy. However, there are clinical conditions that may suggest one drug regimen over another in secondary prevention. The risk of bleeding must always be weighed in each patient individually for the optimal choice of the antiplatelet regimen.

Impact and role of pulmonary embolism response teams in venous thromboembolism associated with COVID-19.

Venous thromboembolism associated with COVID-19, particularly acute pulmonary embolism, may represent a challenging and complex clinical scenario. The benefits of having a multidisciplinary pulmonary embolism response team (PERT) can be important during such a pandemic. The aim of PERT in the care of such patients is to provide fast, appropriate, multidisciplinary, team-based approach, with the common goal to tailor the best therapeutic decision making, prioritizing always optimal patient care, especially given lack of evidence-based clinical practice guidelines in the setting of COVID-19, which potentially confers a significant prothrombotic state. Herein, we would like to briefly emphasize the importance and potential critical role of PERT in the care of patients in which these two devastating illnesses are present together.

Thromboembolic Complications in Severe COVID-19: Current Antithrombotic Strategies and Future Perspectives.

The coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus (SARS- CoV-2) is our latest pandemic and has turned out to be a global public health crisis. One of the special characteristics of this disease is that it may predispose patients to thrombotic disease both in the venous and arterial circulation. We review arterial and venous thromboembolic complications in patients with COVID-19, epidemiology, pathogenesis, hematologic biomarkers, and current antithrombotic strategies. Future perspectives and clinical trials are ongoing to determine the best thromboprophylaxis strategies in the hospitalized patients with severe COVID-19.

Current Role of Ivabradine in Stable Coronary Artery Disease Without Heart Failure.

Increase in heart rate represents a significant contribution in the pathophysiology of coronary artery disease and heart failure, by promoting atherosclerotic process and endothelial dysfunction. Thus, it negatively influences cardiovascular risk in the general population. The aim of this review is to analyze the current, controversial, and future role of ivabradine as an anti-anginal agent in the setting of coronary artery disease without heart failure. Ivabradine represents a selective heart rate-lowering agent that increased diastolic perfusion time and improving energetics in the ischemic myocardium.

Successful pharmacomechanical intervention with ultrasonic-accelerated thrombolytic catheter for massive pulmonary embolism.

An 86-year-old male with history of metastatic prostate carcinoma and hypertension was admitted due to acute onset dyspnea and lower extremity pain and swelling. Transthoracic echocardiography revealed a large right atrial thrombus extending in to the right ventricle. Within 12 h, the patient developed severe hypoxemia, tachypnea with sustained hypotension and cardiogenic shock due to presumed massive pulmonary embolism. The patient underwent emergency pulmonary angiography which showed large emboli in the right main pulmonary artery extending in to the middle and lower lobe branches. An ultrasonic-accelerated thrombolytic catheter was placed in the right main pulmonary artery for continuous infusion of alteplase for 20 h. Repeat pulmonary angiogram showed resolution of the large pulmonary emboli, with normal flow in to the distal pulmonary arteries. Significant improvement of hemodynamics, symptoms and hypoxemia occurred as well.

Emergency intervention for unprotected left main coronary artery stenosis: case report and review of the literature.

Left main coronary artery stenosis is an important cause of symptomatic coronary artery disease, although relatively infrequent. The current guidelines recommend coronary artery bypass grafting as the first line treatment and standard of care, but percutaneous coronary intervention is likely to lead to faster reperfusion of coronary flow, avoiding the delays of a major surgical intervention. Our patient overcame cardiogenic shock after the flow of the left main coronary artery was rapidly restored through percutaneous coronary intervention and 6 days later, when hemodynamically stable, he underwent elective coronary artery bypass graft surgery. One year after the intervention, the patient has a normal functional status and an ejection fraction of 52%. This result is compatible with several small studies showing that percutaneous coronary intervention in left main coronary artery occlusions is feasible and effective, with a good short- and mid-term prognosis.

Successful percutaneous mechanical thrombectomy in a haemodynamically unstable patient with massive pulmonary embolism.

Massive pulmonary embolism with haemodynamic instability has a high mortality. Traditionally these patients are treated with i.v. thrombolytic therapy. When this therapeutic approach is contraindicated, surgical embolectomy and most recently, percutaneous mechanical interventions are alternative treatment options. This case report presents a 73-year-old female with a residual hemiparesis secondary to a meningioma resection 45 days previously, who presented with progressive shortness of breath, accompanied by oppressive chest pain, hypotension, tachycardia and severe hypoxaemia. CT pulmonary angiogram confirmed a massive pulmonary embolism extending into the lobar branches bilaterally. The patient was treated with percutaneous mechanical thrombectomy with excellent haemodynamic and clinical outcomes.

Proliferation and beta-tubulin for human aortic endothelial cells within gas-plasma scaffolds.

PURPOSE: We determined if human aortic endothelial cells (HAEC) enhanced proliferative and angiogenic phenotypes within gas-plasma treated bioresorbable D,L-polylactic acid (D,L-PLA) three-dimensional scaffolds. METHOD: 6 x 10(3) HAEC (N=120) were incubated for 6, 12 or 18 days within either non-treated control or treated scaffolds. Before removing media, unstained wells were observed for apparent cell densities. Quantitative colorimetric WST-1 mitochondrial assays were determined for pooled conditioned media from both HAEC attached to wells and their respective HAEC-containing scaffolds. Fixed HAEC in scaffolds were examined using non-quantitative laser confocal microcopy with FITC-conjugated consensus, Types-I/II or Type-III beta-tubulin. RESULTS: WST-1 indicated that significantly (p<0.05) less mitochondria were on cell culture plates than inside scaffolds but for different reasons. For example, a 12-18 days comparison between WST-1 and beta-tubulin indicated that wells decreased because of overgrowth apotosis; whereas, mitochondrial activity inside treated scaffolds decreased with increased tubulogenesis. Observed with consensus and Type-I/II beta-tubulin, HAEC-treated scaffolds exhibited increased cell-cell interconnections and angiogenic cords undergoing tubulogenesis to form vessels with central lumens as well as increased Type-III beta-tubulin, predominantly in cells of smaller surface areas. Moreover, beta-tubulin inside HAEC-treated scaffolds appeared in discrete cytoskeletal and podial regions; yet, beta-tubulin for HAEC-control scaffolds was located in more diffuse cytoplasmic regions especially at 18 days. CONCLUSIONS: HAEC-treated scaffolds undergo increased migration, proliferation, beta-tubulin expression and quiescent cord formation. HAEC in scaffolds represent a potential model to study mechanisms for vascular cord progression into tubes. WST-1 does not represent accurate cell densities in three-dimensional scaffold matrices.