Open repair for thoracoabdominal aortic aneurysms precipitated by chronic aortic dissection

Chronic dissection of the thoracoabdominal aorta may require surgical repair for aneurysm, malperfusion, or rupture. Endovascular repair is made difficult by a noncompliant dissection septum, visceral vessels arising from different lumens, and the common use of diseased aortic landing zones. Thus, open repair remains the gold standard in terms of favorable outcomes and durability. During thoracoabdominal aortic repair, we use a multimodal strategy to prevent spinal cord and visceral or renal artery ischemia; key modalities include cerebrospinal fluid drainage, left heart bypass with and without visceral protection, cold renal protection, and aggressive reimplantation of intercostal or lumbar arteries. Patients with chronic dissection require lifelong surveillance, as there is a significant risk for subsequent intervention on unrepaired aortic segments.

Clinico-pathophysiological considerations in coronary microvascular disorders

Around half of the patients undergoing an elective coronary angiogram to investigate typical stable angina symptoms are found to have non-obstructive coronary arteries (defined as < 50% stenosis). These patients are younger with a female predilection. While underlying mechanisms responsible for these presentations are heterogeneous, structural and functional abnormalities of the coronary microvasculature are highly prevalent. Thus, coronary microvascular dysfunction (CMD) is increasingly recognised as an important consideration in patients with non-obstructive coronary arteries. This review will focus on primary coronary microvascular disorders and summarise the four common clinical presentation pictures which can be considered as endotypes - Microvascular Ischaemia (formerly “Syndrome X”), Microvascular Angina, Microvascular Spasm, and Coronary Slow Flow. Furthermore, the pathophysiological mechanisms associated with CMD are also heterogenous. CMD may arise from an increased microvascular resistance, impaired microvascular dilation, and/or inducible microvascular spasm, ultimately causing myocardial ischaemia and angina. Alternatively, chest pain may arise from hypersensitivity of myocardial pain receptors rather than myocardial ischaemia. These two major abnormalities should be considered when assessing an individual clinical picture, and ultimately, the question arises whether to target the heart or the pain perception to treat the anginal symptoms.

Percutaneous catheter-based repeat revascularization in patients with previous PCI or CABG: a comprehensive review of the evidence

Repeat revascularization after percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) is one of the most common long-term complications which warrants continuous clinical follow up. Re-interventions negatively impact long-term survival in patients with coronary artery disease. The repeat revascularization after PCI can be either a target lesion revascularization (stent thrombosis/in-stent restenosis) or a revascularization of native coronary artery after PCI (target vessel revascularization/non-target vessel revascularization). The EVENT registry reports that repeat revascularization rates in patients undergoing PCI is 12% in the first year of follow up. Repeat revascularization with additional stent deployment increases the rate of stent thrombosis and restenosis, thereby leading to recurrent ischemic events. Repeat revascularization after CABG can be either in the early postoperative period or later due to native disease progression or late graft stenosis. The need for re-intervention after surgical or percutaneous revascularization is inevitable and is dependent on modifiable and non-modifiable risk factors.

Histological analysis of thrombi retrieved after acute ischemic stroke from large vessel occlusion: from research to clinical practice

Emergent reperfusion therapies have improved acute ischemic stroke prognosis, but many patients are still bound to bad clinical outcome, probably because of our incomplete knowledge of its pathophysiology. Thanks to mechanical thrombectomy, occluding material is available for histological analysis. Several studies investigated the possible relationship between thrombus composition and clinical, procedural, and radiological variables of acute ischemic stroke. The potential value of thrombus analysis as a tool for clinical practice and research is still not defined, as data from the literature are heterogeneous and sometimes conflicting. We propose a review of the existing literature regarding histological analysis of thrombi in acute ischemic stroke. We classified articles on clot composition according to the clinical variable explored in each study. We first distinguished articles about etiology, procedural, and radiological variables, and then we performed a subclassification for each group. This review could help both in the interpretation of thrombus analysis in clinical practice and in its usage for future research.

Pharmacologic therapies for the low cardiac output syndrome in children after cardiac surgery: evidence of their efficacy and trends in their use

The low cardiac output syndrome describes the phenomenon of the reduction of cardiac output that can occur following cardiac surgery requiring cardiopulmonary bypass. If unrecognized or untreated, this condition can result in significant morbidity and mortality. Along with non-pharmacologic therapies, pharmacologic agents used to help manage the low cardiac output syndrome include catecholamine inotropes, inodilators, systemic vasodilators, pulmonary vasodilators, and other classes of medications. We summarize the rationale and key evidence supporting the use of these therapies in children. In addition, utilizing provider surveys and registry reviews, we describe the current trends in the use of these medications and the variation demonstrated between providers and centers. Given the heterogeneous etiology of low cardiac output syndrome, successful management requires that pharmacologic therapies be tailored to the physiologic derangements of each patient.