Treatment Strategies for Hypertrophic Cardiomyopathy: Alcohol Septal Ablation and Procedural Step-by-Step Technique.

Alcohol septal ablation (ASA) is a well-established procedure for septal reduction therapy in patients with obstructive hypertrophic cardiomyopathy, significant at rest or provocable outflow tract gradients, and medically refractory symptoms. This percutaneous approach to relief of obstruction and eventual cardiac remodeling involves the infusion of a small quantity of ethanol into an appropriately targeted septal artery that is feeding the basal septum to create an iatrogenic and controlled focal infarction. Early akinesia is followed by subsequent thinning and remodeling, which widens the outflow tract, reducing or eliminating the obstruction. Historically, the use of ASA was reserved primarily for high-risk surgical candidates; however, more contemporary data suggest similar outcomes in the short-term and long-term safety of the procedure and overall effectiveness in relieving obstructive symptoms when it is performed in broader populations at experienced centers. Therefore, the current guidelines published in 2020 support ASA as a class 1 indication, similar to its open-heart surgical counterpart, surgical myectomy, when no concomitant significant coronary or valve surgical indication exists. This article summarizes contemporary management of patients with hypertrophic cardiomyopathy who were selected for ASA and details procedural methods and outcomes.

Catheter thrombectomy for basilar artery stroke immediately after insertion of durable left ventricular assist device.

Background: Acute ischemic stroke (AIS) following left ventricular assist device (LVAD) implantation is a serious complication associated with device morbidity. AIS development following LVAD placement typically presents between 6- and 24-months post implantation.Case/Results: We report a case of a 67-year-old male who initially presented with reduced ejection fraction and severe coronary vessel disease. Following coronary artery bypass graft surgery, the patient remained in a low output state necessitating placement of an LVAD device. Approximately 4.5 hours following LVAD implantation, a severe acute decrease in mental status revealed new development of ischemic stroke of the basilar artery, which was successfully treated in one pass with catheter endovascular thrombectomy.Conclusion: While embolic stroke management in these cases remains difficult as patients are usually anticoagulated, our case demonstrates the utilization of endovascular thrombectomy as a viable therapeutic option in the setting of an uncommon occurrence of embolic stroke in the hours following LVAD implantation.

Escalation from impella 5.5 to ECPELLA support as a bridge to mitral valve surgery in a patient with degenerative mitral regurgitation.

Severe mitral regurgitation (MR) is an important cause of acute heart failure and significant contributor to morbidity and mortality. Mechanical circulatory support (MCS) devices such as Impella are readily used to hemodynamically stabilize patients with cardiogenic shock (CS) secondary to this valvular pathology. Impella can also be combined with VA-ECMO to an "ECPELLA" configuration if further escalation of hemodynamic support is needed. We report a case of a 57-year-old female who presented with CS secondary to a perforated anterior mitral valve leaflet and non-ischemic cardiomyopathy that did not stabilize with initial choice of Impella 5.5. She required further escalation from axillary Impella 5.5 to the combined ECPELLA configuration, which allowed hemodynamic stabilization and ultimately a successful high-risk isolated mitral valve replacement. Despite adequate Impella flow, escalation to a combined MCS configuration, such as ECPELLA, may need to be considered upfront for acute valvular insufficiency in the setting of pre-existing cardiomyopathy.

Dual antiplatelet therapy with concomitant anticoagulation: current perspectives on triple therapy.

Anticoagulation and antiplatelet therapy are individually mainstays of treatment for multiple cardiovascular conditions. Antiplatelet therapy, most commonly with dual agents, is vital in the setting of coronary artery disease with acute coronary syndrome requiring percutaneous coronary intervention to prevent in-stent complications. A multitude of cardiovascular conditions with increased thromboembolic risk also require anticoagulation, including atrial fibrillation, venous or arterial thrombosis, and prosthetic heart valves to name a few. There is often an overlap in comorbidities as our patient population ages and becomes more complex, frequently necessitating a combination of both anticoagulation and antiplatelet agents, known as "triple therapy". To reduce or treat thromboembolic disease states as well as reduce platelet aggregation for coronary stent protection, many patients are placed at an increased bleeding risk without compelling evidence of reduction in major adverse cardiac events. With this comprehensive review of the existing literature, we aim to analyse different strategies and durations of triple therapy medication regimens.

Nonalcoholic Fatty Liver Disease and Cardiovascular Disease: Causation or Association.

Nonalcoholic fatty liver disease (NAFLD) is a disease process that is gaining increasing recognition. The global prevalence of NAFLD is increasing in parallel with growing rates of risk factors for NAFLD such as hypertension, obesity, diabetes, and metabolic syndrome. NAFLD has been referred to as a risk factor for cardiovascular disease (CVD). As CVD is the leading cause of morbidity and mortality worldwide, there are constant efforts to describe and alleviate its risk factors. Although there is conflicting data supporting NAFLD as a causative or associative factor for CVD, NAFLD has been shown to be associated with structural, electrical, and atherosclerotic disease processes of the heart. Shared risk factors and pathophysiologic mechanisms between NAFLD and CVD warrant further explication. Pathologic mechanisms such as endothelial dysfunction, oxidative stress, insulin resistance, genetic underpinnings, and gut microbiota dysregulation have been described in both CVD and NAFLD. The mainstay of treatment for NAFLD is lifestyle intervention including physical exercise and hypocaloric intake in addition to bariatric surgery. Investigations into various therapeutic targets to alleviate hepatic steatosis and fibrosis by way of maintaining the balance between lipid synthesis and breakdown. A major obstacle preventing the success of many pharmacologic approaches has been the effects of these medications on CVD risk. The future of pharmacologic treatment of NAFLD is promising as effective medications with limited CVD harm are being investigated.