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Kenny Howell posted an update 5 months, 4 weeks ago
The Gerbode defect is a rare abnormal communication between the left ventricle (LV) and right atrium (RA). The lesion is either congenital or acquired. Acquired defects are largely iatrogenic or infective in origin. We present two cases of acquired Gerbode defects with similar clinical presentations but very different outcomes.
Patient 1 A 64-year-old male presented with features of decompensated cardiac failure and a low-grade temperature. Dehiscence of a recently implanted bioprosthetic aortic valve and high-velocity LV to RA jet (Gerbode defect) was found on echocardiography. Blood cultures grew
and the diagnosis of infective endocarditis was established. The patient was treated with intravenous antibiotics and the aortic valve and Gerbode defect were successfully surgically repaired.Patient 2 An 81-year-old male presented after being found on the floor at home. On admission, he was clinically septic with evidence of decompensated heart failure. No clear infective focus was initially found. Transthoracic echocardiography revealed severe left ventricular impairment, with a normal bioprosthetic aortic valve. He was treated with intravenous antibiotics, but later deteriorated with evidence of embolic phenomena. Repeat echocardiography revealed a complex infective aortic root lesion with bioprosthetic valve dehiscence and flow demonstrated from the LV to RA. Unfortunately, the patient succumbed to the infection and cardiac complications.
The Gerbode defect is a rare but important complication of infective endocarditis and valve surgery. Care needs to be taken to assess for Gerbode defect shunts on echocardiogram, especially in the context of previous cardiac surgery.
The Gerbode defect is a rare but important complication of infective endocarditis and valve surgery. Care needs to be taken to assess for Gerbode defect shunts on echocardiogram, especially in the context of previous cardiac surgery.
The SelectSecure lumenless 3830 pacing lead is often considered to be the pacing lead of choice for transvenous pacing in children because of its small diameter, lead strength, and reliable long-term sensing and pacing characteristics. One of the potential long-term pitfalls of a sturdy pacing lead is relative retraction with growth in children resulting in late lead dislodgement.
We report two cases of late SelectSecure 3830 lead dislodgement at 11.8 years (Case 1) and 8.8 years (Case 2), respectively, post the initial implantation. Case 1 was diagnosed with congenital complete heart block (CHB) at 9 months old when he presented with unconfirmed diphtheria infection. Case 2 was diagnosed with CHB at 14 weeks of age with positive maternal anti-Ro antibodies. Both patients underwent implantation of a transvenous permanent pacemaker implantation with Medtronic SelectSecure 3830 lead due to symptomatic bradycardia. Apart from a pulse generator change at 8.5 years (Case 1) and 7 years (Case 2), respectively, post-implant due to normal battery depletion, both patients are well in the interim.
As part of the pacemaker follow-up for rapidly growing children, we recommend more frequent surveillance of lead ‘tautness’ by chest radiography especially in children with CHB with no underlying heart rhythm.
As part of the pacemaker follow-up for rapidly growing children, we recommend more frequent surveillance of lead ‘tautness’ by chest radiography especially in children with CHB with no underlying heart rhythm.
Primary percutaneous coronary intervention (PCI) for acute coronary syndrome has significantly contributed to improvements in overall outcomes. However, clinical challenges exist when performing urgent PCI for patients with a history of coronary artery bypass grafting (CABG).
An 83-year-old man with a history of CABG presented with an inferior ST-elevation myocardial infarction (STEMI). Emergent coronary angiography showed an occlusion of the right coronary artery that had been previously grafted with the right gastroepiploic artery. Primary PCI for the native coronary artery was performed on the assumption that the bypass graft had been occluded. We were unable to attain angiographic antegrade flow after balloon angioplasty, and intravascular ultrasound revealed a ruptured plaque with a thrombus proximally and a patent bypass graft with complete recanalization distally. These findings suggested that the plaque rupture with resultant thrombus formation proximal to the anastomosis eventually overlay the paimportance of a multifaceted approach in such an urgent situation.
The European Society of Cardiology guidelines for the diagnosis and management of acute pulmonary embolism (PE) developed in collaboration with the European Respiratory Society (ERS) has been updated in 2019. Recommendations were added or updated on all stages of the evaluation and management of pulmonary embolism, encompassing diagnosis, early treatment, and long-term management.
We illustrate an exemplary case, assembled for the purposes of this review, of a 70-year-old woman who presented at the emergency department with dyspnoea and thoracic pain. She was diagnosed with intermediate-high-risk acute PE and promptly treated with low molecular weight heparin. After 24 h of stay in intensive care unit, she was transferred to the cardiology department and switched to non-vitamin K-dependent oral anticoagulant apixaban 10 mg b.i.d. for 7 days and then 5 mg b.i.d. After discharge from the hospital 8 days later, she received standard-dose apixaban 5 mg b.i.d. for 6 months; the dose was reduced to 2.5 mg b.i.dof chronic sequelae in the long-term follow-up.
Anderson-Fabry disease (AFD) is an X-linked lysosomal storage disorder resulting from a mutation of alpha-galactosidase A gene (
), causing deficiency in alpha-galactosidase activity. RO5126766 The enzyme deficit can lead to storage of globotriaosylceramide in various organs including heart. Studies suggest that vasospastic angina (VSA) is associated with AFD.
This clinical case series aimed to present two female patients with AFD, including progressive cardiac involvement a 50-year-old woman (patient number 1) and a 39-year-old woman (patient number 2) who are siblings with a male AFD patient harbouring p. Arg342Glu missense variant in alpha-galactosidase A gene (
), who suffered VSA and subsequent ventricular fibrillation. Enzymatic tests and genetic analysis confirmed AFD in both female patients and histological tests revealed globotriaosylceramide deposits in their hearts. In patient number 1, a 12-lead electrocardiography and transthoracic echocardiography revealed cardiac hypertrophy. Coronary angiography revealed no organic coronary artery stenosis and vasospasms was induced by spasm provocation test.
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