OBJECTIVES Current guidelines recommend prophylactic replacement of the ascending aorta at an aneurysmal diameter of >55 mm to prevent acute Type A aortic dissection (TAAD) in non-Marfan patients. Several publications have challenged this threshold, suggesting that surgery should be performed in smaller aneurysms to prevent this devastating disease. We reviewed our experience with measuring aortic size at the time of TAAD to validate the existing recommendation for prophylactic ascending aorta replacement. METHODS All patients who had been admitted for TAAD to our emergency department from 2014 to 2019 and underwent ascending aorta replacement were included. Marfan patients were excluded. The maximum diameter of the dissected aorta was measured preoperatively using CT scan. We estimated the aortic diameter at the time of dissection to be 7 mm smaller than the measured maximum diameter of the dissected aorta (modelled pre-dissection diameter). RESULTS Overall, 102 patients were included. Of these, 67 were male (65.6%) and 35 were female (34.4%), and the cohort’s mean age was 65 ± 12.1 years. In addition, 66% were treated for arterial hypertension. The mean maximum modelled pre-dissection diameter was 39.6 ± 4.8 mm: 39.1 ± 5.1 mm in men and 40.7 ± 2.8 mm in women (P = 0.1). The cumulative 30-day mortality rate was 19.6% (20/102). CONCLUSIONS TAAD occurred at a modelled aortic diameter below 45 mm in 87.7% of our patients. Therefore, the current aortic diameter threshold of 55 mm excludes ∼99% of patients with TAAD from prophylactic replacement of the ascending aorta. The maximum diameter of the ascending aorta warrants reappraisal and this parameter should be a distinct part of a personalized decision-making process that also takes into account age, gender and body surface area to establish the surgical indication for preventive aorta replacement aimed to improve the survival benefit of this procedure.
Vasoplegic syndrome (VS) is a common complication following cardiovascular surgery with cardiopulmonary bypass (CPB), and its incidence varies from 5 to 44%. It is defined as a distributive form of shock due to a significant drop in vascular resistance after CPB. Risk factors of VS include heart failure with low ejection fraction, renal failure, pre-operative use of angiotensin-converting enzyme inhibitors, prolonged aortic cross-clamp and left ventricular assist device surgery. The pathophysiology of VS after CPB is multi-factorial. Surgical trauma, exposure to the elements of the CPB circuit and ischemia-reperfusion promote a systemic inflammatory response with the release of cytokines (IL-1β, IL-6, IL-8, and TNF-α) with vasodilating properties, both direct and indirect through the expression of inducible nitric oxide (NO) synthase. The resulting increase in NO production fosters a decrease in vascular resistance and a reduced responsiveness to vasopressor agents. Further mechanisms of vasodilation include the lowering of plasma vasopressin, the desensitization of adrenergic receptors, and the activation of ATP-dependent potassium (KATP) channels. Patients developing VS experience more complications and have increased mortality. Management includes primarily fluid resuscitation and conventional vasopressors (catecholamines and vasopressin), while alternative vasopressors (angiotensin 2, methylene blue, hydroxocobalamin) and anti-inflammatory strategies (corticosteroids) may be used as a rescue therapy in deteriorating patients, albeit with insufficient evidence to provide any strong recommendation. In this review, we present an update of the pathophysiological mechanisms of vasoplegic syndrome complicating CPB and discuss available therapeutic options.
Background: The COVID-19 (coronavirus disease 2019) pandemic is reducing health care accessibility to non–life-threatening diseases, thus hiding their real incidence. Moreover, the incidence of potentially fatal conditions such as acute type A aortic dissection seems to have decreased since the pandemic began, whereas the number of cases of chronic ascending aortic dissections dramatically increased. We present two patients whose management has been affected by the exceptional sanitary situation we are dealing with.Case report: A 70-year-old man with chest pain and an aortic regurgitation murmur had his cardiac workup delayed (4 months) because of sanitary restrictions. He was then diagnosed with chronic type A aortic dissection and underwent urgent replacement of ascending aorta and aortic root. The delay in surgical treatment made the intervention technically challenging because the ascending aorta grew up to 80 mm inducing strong adhesions and chronic inflammation. The second case report concerns a 68-year-old woman with right lower-limb pain who was diagnosed with deep vein thrombosis. However, a CT scan to exclude a pulmonary embolism could not be realized until 5 months later because of sanitary restrictions. When she eventually got the CT scan, it fortuitously showed a chronic dissection of the ascending aorta. She underwent urgent surgery, and the intervention was challenging because of adhesions and severe inflammation.Conclusion: Delayed treatment due to sanitary restrictions related to COVID-19 pandemic is having a significant impact on the management of potentially life-threatening conditions including type A aortic dissection. We should remain careful to avoid COVID-19 also hitting patients who are not infected with the virus.
Heparin-induced thrombocytopenia (HIT) is a major issue in cardiac surgery requiring cardiopulmonary bypass (CPB). HIT represents a severe adverse drug reaction after heparin administration. It consists of immune-mediated thrombocytopenia paradoxically leading to thrombotic events. Detection of antibodies against platelets factor 4/heparin (anti-PF4/H) and aggregation of platelets in the presence of heparin in functional in vitro tests confirm the diagnosis. Patients suffering from HIT and requiring cardiac surgery are at high risk of lethal complications and present specific challenges. Four distinct phases are described in the usual HIT timeline, and the anticoagulation strategy chosen for CPB depends on the phase in which the patient is categorized. In this sense, we developed an institutional protocol covering each phase. It consisted of the use of a non-heparin anticoagulant such as bivalirudin, or the association of unfractionated heparin (UFH) with a potent antiplatelet drug such as tirofiban or cangrelor. Temporary reduction of anti-PF4 with intravenous immunoglobulins (IvIg) has recently been described as a complementary strategy. In this article, we briefly described the pathophysiology of HIT and focused on the various strategies that can be applied to safely manage CPB in these patients.
Introduction: The choice of Cardiac Preservation Solution (CPS) for myocardial protection at the time of heart procurement remains controversial and uncertainties persist regarding its effect on the early and midterm Heart Transplantation (HTx) outcomes. Thus, we retrospectively analyzed our adult HTx performed with two different CPS, during a period of 12 years, in terms of hospital mortality, mid-term survival, inotropic score, primary graft dysfunction and rejection score. Methods: From January 2009 to December 2020, 154 adult HT were performed in our hospital. Patients were divided in two groups according to the CPS used: St. Thomas (n=75, group P 1) and HTK-Custodiol (n=79, group P 2). The choice of CPS was related to an institutional policy; from 2009 to 2015, St. Thomas solution was exclusively used, and after that, HTK-Custodiol alone. Results: There was no significant difference between the two groups in terms of preoperative and intraoperative features. Postoperatively, the Custodiol group showed significantly lower inotropic score (p<0.0001), mean rejection score (p= 0.036) and 30 days mortality (p=0.0068). The use of HTK-Custodiol was the only variable that improved midterm survival (HTK-Custodiol vs St Thomas, HR= 0.20 (95% CI: 0.069 -0.6) p=0.0039). Conclusion: In our single center experience, using HTK-Custodiol as myocardial protection during heart procurement leads to improved outcomes after HTx, including postoperative inotropic score, rejection score, 30-days mortality and midterm survival.
Background To compare mid-term clinical outcomes and hemodynamic performance of the stented pericardial Trifecta bioprosthesis for surgical aortic valve replacement (AVR) with a technically comparable commonly used surgical bioprosthesis. Methods Data from consecutive patients implanted with the TF or the Carpentier Edwards Magna Ease valve were retrospectively analyzed. Primary analysis was performed on a propensity score–matched cohort. Primary endpoints included the composite of death or reoperation and structural valve deterioration. The comparison also included echocardiographic assessments at one-week post-AVR and at the last documented follow-up. Results Two propensity score–matched groups of 170 patients each were identified from the overall population ( n = 486). Incidence of postoperative mortality (2.9% vs. 7.1%, respectively, p = 0.08), and patient prosthesis mismatch (1.2% and 2.4%, p = 0.41) were similar. At mean follow-up of 5.84 (Trifecta) and 6.1 (Carpentier Edwards) years, the incidence of all-cause death/reoperation (15.3% vs. 15.9%, p = 0.88 for Trifecta and Carpentier Edwards, respectively) and structural valve disease (1.8% vs. 2.9%, p = 0.47) were similar. Overall, postoperative mean transvalvular pressure gradients were significantly lower in the Trifecta group than in the Carpentier Edwards group (7.7 ± 3.3 vs. 11.3 ± 3.6 mmHg, p < 0.01). Mean transvalvular gradient remained significantly lower through the last follow-up for small-sized Trifecta valves (19/21 mm; 10.5 ± 4.2 vs. 13.8 ± 5.9 mmHg, p = 0.039) but not for larger valves (10.3 ± 4.8 vs. 9.4 ± 3.5 mmHg, p = 0.31). Conclusion The Trifecta valve is a valuable alternative to the Carpentier Edwards valve in terms of safety, hemodynamic performance, and mid-term durability. Smaller-sized valves provide additional clinical benefits, given their persistent hemodynamic advantages through mid-term follow-up.
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