Baroreflex Function in Cardiovascular Disease.

The baroreflex system is involved in modulating several physiological functions of the cardiovascular system and can modulate cardiac output, blood pressure, and cardiac electrophysiology directly and indirectly. In addition, it is involved in regulating neurohormonal pathways involved in the cardiovascular function, such as the renin-angiotensin-aldosterone system and vasopressin release. Baroreflex dysfunction is characterized by sympathetic overactivation and parasympathetic withdrawal and is associated with several cardiovascular diseases, such as hypertension, heart failure, and coronary artery disease. Targeting the baroreflex system via invasive (eg, baroreflex activation therapy and endovascular baroreceptor amplification) and noninvasive approaches (eg, slow breathing exercises and exercise training) has emerged as a novel pathway to manage cardiovascular diseases. Studies examining the long-term safety and efficacy of such interventions in various cardiovascular diseases are needed.

Bilateral sympathectomy for treatment of refractory ventricular tachycardia.

Ventricular tachycardia (VT) commonly occurs in patients with ischemic or nonischemic cardiomyopathy and requires antiarrhythmic drugs, ablation, or advanced circulatory support. However, life-threatening VT may be refractory to these therapies, and may cause frequent implantable cardioverter defibrillator (ICD) discharges. Left cardiac sympathetic denervation reduces the occurrence of these fatal arrhythmias by inhibiting the sympathetic outflow to the cardiac tissue. We present a 69-year-old man with nonischemic cardiomyopathy, life-threatening VT, and hemodynamic instability with numerous ICD discharges, who remained refractory to antiarrhythmic drug therapy and ablation attempts. He was effectively treated with bilateral cardiac sympathectomy. Six months later, he remained free of VT with no ICD discharges.

Arrhythmogenic Right Ventricular Dysplasia: An Under-recognized Form of Inherited Cardiomyopathy.

We report a case of arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD) in order to evaluate the course of an under-recognized form of cardiomyopathy with a vast array of clinical manifestations. The patient is a 49-year-old white woman transferred from an outside hospital due to dyspnea and persistent hypoxia. She had a pertinent family history that included a sister who died suddenly in her 30s from unexplained heart failure. Initial work-up for hypoxia was unrevealing. Transthoracic echocardiography revealed isolated right ventricular dysfunction with dilation and multiple trabeculations. Further investigation, including cardiac computed tomography and magnetic resonance imaging, revealed fatty infiltration into the right ventricular wall suggestive of ARVD.

Fusion of Bovine Tissue Aortic Valve Leaflets in a Patient With Left Ventricular Assist Device.

Patients with both a prosthetic aortic valve and prolonged left ventricular assist device support can develop rapid deterioration of their valve prosthesis. In patients with myocardial recovery who are undergoing explantation of their ventricular assist device, preoperative and intraoperative evaluation of the valve prosthesis should be performed to ensure adequate function. (Level of Difficulty: Advanced.).

Relation of Vasoplegia in the Absence of Primary Graft Dysfunction to Mortality Following Cardiac Transplantation.

Vasoplegia following cardiac transplantation is associated with increased morbidity and mortality. Previous studies have not accounted for primary graft dysfunction (PGD). The definition of vasoplegia is based on pressor requirement at 48 hours, many PGD parameters may have normalized after the initial 24 hours on inotropes. We surmised that the purported negative effects of vasoplegia following transplantation may in part be driven by PGD. We reviewed 240 consecutive adult cardiac transplants at our center between 2012 and 2016. The severity of vasoplegia was evaluated as a risk factor for 1-year survival, and the analysis was repeated for the subgroup of 177 patients who did not develop PGD. Overall, 63 (26%) of patients developed mild, moderate, or severe PGD. In those without PGD, vasoplegia was associated with length of stay but not with short- or long-term mortality. Moderate and/or severe vasoplegia occurred in 35 (15%) patients and was associated with higher short-term mortality, length of stay, and PGD. Multivariate logistic regression identified body mass index ≥35 kg/m2, left ventricular assist device before transplantation, and use of extracorporeal membrane oxygenation as joint risk factors for vasoplegia. In patients without PGD, only left ventricular assist device before transplantation was associated with vasoplegia. In conclusion, our results show that, in the sizeable subgroup of patients with no signs of PGD, vasoplegia had a much more modest impact on post-transplant morbidity and no significant effect on 1- and 3-year survival. This suggests that PGD may be a confounder when assessing vasoplegia as a risk factor for adverse outcomes.