Preintervention imaging and intraoperative management care of the hypertrophic obstructive cardiomyopathy patient

With an estimated overall mortality of less than 1 percent per year, hypertrophic cardiomyopathy, is the most common genetic cardiomyopathy. Intraoperative transesophageal echocardiography is the standard of care for assessing patients with hypertrophic obstructive cardiomyopathy undergoing surgical septal myectomy, allowing surgical planning, intraoperative hemodynamic monitoring, and postprocedural assessment of the repair, including detection of immediate complications. At various phases during surgical septal myectomy, the changing hemodynamic conditions may lead to worsening or improvement in left ventricle outflow tract obstruction by change in preload or afterload, systolic anterior motion of the mitral valve, or sympathetic stimulation. These characteristics represent unique challenges in the management of these patients, requiring a comprehensive understanding of the management of all the conditions required to decrease the left ventricle outflow tract gradient avoiding obstruction, which include the maintenance of sinus rhythm, adequate rate avoiding tachycardia and bradycardia, and avoidance of systemic hypotension preserving preload and afterload, with adequate vasoactive agents. The aim of this review is to summarize the perioperative assessment and management of patients undergoing hypertrophic obstructive myopathy surgery.

An antibody against L1 cell adhesion molecule inhibits cardiotoxicity by regulating persistent DNA damage

Targeting the molecular pathways underlying the cardiotoxicity associated with thoracic irradiation and doxorubicin (Dox) could reduce the morbidity and mortality associated with these anticancer treatments. Here, we find that vascular endothelial cells (ECs) with persistent DNA damage induced by irradiation and Dox treatment exhibit a fibrotic phenotype (endothelial–mesenchymal transition, EndMT) correlating with the colocalization of L1CAM and persistent DNA damage foci. We demonstrate that treatment with the anti-L1CAM antibody Ab417 decreases L1CAM overexpression and nuclear translocation and persistent DNA damage foci. We show that in whole-heart–irradiated mice, EC-specific p53 deletion increases vascular fibrosis and the colocalization of L1CAM and DNA damage foci, while Ab417 attenuates these effects. We also demonstrate that Ab417 prevents cardiac dysfunction-related decrease in fractional shortening and prolongs survival after whole-heart irradiation or Dox treatment. We show that cardiomyopathy patient-derived cardiovascular ECs with persistent DNA damage show upregulated L1CAM and EndMT, indicating clinical applicability of Ab417. We conclude that controlling vascular DNA damage by inhibiting nuclear L1CAM translocation might effectively prevent anticancer therapy-associated cardiotoxicity.

Acute Ischemic Stroke in a Young Patient with Left Ventricular Thrombus Attributed to Doxorubicin Cardiomyopathy

We report a case of acute middle cerebral territory ischemic infarction caused by left ventricular thrombus (LVT) in a doxorubicin cardiomyopathy patient. A major adverse effect of doxorubicin is cardiotoxicity. In doxorubicin cardiomyopathy, as the ventricular contractility decreases, LVT can occur and lead to systemic embolic events such as stroke.