Acute Ischemic Stroke Due to Incomplete Endothelialization of a Left Atrial Appendage Occluder.

Left atrial appendage occlusion (LAAO) has become a preferred alternative for ischemic stroke prophylaxis in patients with a high risk of cardioembolic stroke but who are contraindicated for long-term anticoagulation. While the intervention has been successful in reducing bleeding events when compared to using anticoagulation, some stroke risk still persists. We present a case of stroke related to the failure of a left atrial appendage occluder, which was found to have a peri-device leak and incomplete endothelialization. In our case, we also believe these may have been exacerbated by comorbid severe mitral regurgitation. While current post-procedural protocols do address management of specific findings predictive of device failure, our patient still suffered from ischemic stroke despite following guidelines. Based on current outcome studies on LAAO, he may have been at higher risk than appreciated. His surveillance imaging at post-operative day 45 revealed a small peri-device leak of < 5 mm, which is now found to be associated with a higher embolic stroke risk than larger leaks of > 5 mm. Moreover, his mitral regurgitation, which was severe and borderline symptomatic, remained undertreated for a prolonged period. In cases of similar comorbidities, one might consider exploring the role of concomitant endovascular mitral repair and LAAO to optimize outcomes.

Multiple Recurrent Infective Endocarditis Secondary to Streptococcus mitis Bacteremia Despite Proper Antibiotic and Surgical Treatment.

Infective endocarditis (IE) is a rare and potentially fatal disease. It is an infection of the endocardium of the heart and heart valves. One of the major complications faced by patients who have recovered from a first episode of IE is recurrent IE. Risk factors for recurrent IE include intravenous (IV) drug use, prior episodes of IE, poor dentition, recent dental procedures, male gender, age over 65, prosthetic heart valve endocarditis, chronic dialysis, positive valve culture(s) obtained at the time of surgical intervention, and persistent postoperative fever. We present a case of a 40-year-old male with a history of former IV heroin use who experienced multiple episodes of recurrent IE caused by the same pathogen, Streptococcus mitis. This recurrence occurred despite the patient completing the appropriate course of antibiotic therapy, undergoing valvular replacement, and maintaining drug abstinence for two years. This case highlights the challenges associated with identifying the source of infection and emphasizes the need to develop guidelines for surveillance and prophylaxis against recurrent IE.

A Case of Myocardial Infarction in a Patient With Spontaneous Spinal Subdural Hematoma.

Spontaneous spinal subdural hematoma (SSDH) is an extremely rare clinical condition and a neurologic emergency that is most commonly associated with anticoagulation therapy and coagulopathy. We present a case of myocardial infarction (MI) with an unusually high troponin level in the setting of SSDH. This case underscores the challenges and importance of properly differentiating type 1 MI from type 2 MI as the management is different. It also presents challenges in managing MI in the setting of recent bleeding in the context of desired anticoagulation and antiplatelet therapy.

Unexpected Case of Cardiac Sarcoidosis in a Caucasian Male.

Cardiac sarcoidosis (CS) is an underappreciated diagnosis in healthy patients presenting with recurrent syncope. This may be particularly limited in patients who do not meet common epidemiology and manifestations of sarcoidosis, which are typically African American women and pulmonary, respectively. In our case, we have a previously healthy middle-aged Caucasian American male who presented with recurrent syncope for one week. Initial electrocardiogram showed a right bundle branch block with a normal P-R interval. A few days into the admission, the patient suffered another episode of syncope precipitated by micturition, and repeat electrocardiogram revealed evolution to complete atrioventricular block, necessitating emergent placement of a temporary permanent pacemaker. Transthoracic echocardiogram showed preserved left ventricular ejection fraction of 55%-60% with normal heart valves. Chest computerized tomography revealed few pulmonary nodules, prompting a weak concern for infiltrative disease, e.g., sarcoidosis. To evaluate for possible cardiac structural abnormalities, a cardiac magnetic resonance imaging (MRI) study was considered but precluded by the presence of MRI-incompatible temporary pacemaker. Despite low suspicion, a fluorodeoxyglucose-positron emission tomography was obtained which unexpectedly revealed hypermetabolic lymph nodes in the perihilar, supraclavicular, and mediastinal regions as well as an area along the interventricular septum, consistent with atrioventricular (AV) conduction pathways. As the patient met major criteria for CS per Japanese Circulation Society guidelines, a tentative diagnosis was made, and a Biotronik single-chamber implantable cardiac defibrillator was ultimately placed. On outpatient follow-up, endobronchial ultrasound-guided fine-needle biopsy of perihilar lymph nodes revealed only rare epithelioid histiocytes, rare alveolar macrophages, and benign bronchial cells, consistent with benign nodal tissue. Further attempts for histological confirmation were aborted due to profound calcification and location of affected lymph nodes. A decision was made to defer further biopsy, including the gold standard of diagnosis endomyocardial biopsy, due to the risks outweighing the benefits. He initiated medical therapy with prednisone and mycophenolate, as well as trimethoprim-sulfamethoxazole for Pneumocystis prophylaxis. Unlike general sarcoidosis, which is often considered a benign systemic disease, CS has high potential for severe complications including arrhythmia, systolic heart failure, and sudden cardiac death. In general, males carry a higher risk of CS than females, especially those who are of African American descent as they carry a higher incidence of nonspecific sarcoidosis. Expectations related to our patient's demographic initially delayed diagnostic workup for infiltrative disease, primarily focusing on intracranial, orthostatic, and infectious causes. This case report serves to inform clinicians on early manifestations of CS, raise awareness of its incidence in unexpected demographics, and encourage them to consider infiltrative diseases when presented with patients of similar symptoms.

Akt activation improves microregional oxygen supply/consumption balance after cerebral ischemia-reperfusion.

There have been reports that activation of Akt may provide neuroprotection after cerebral ischemia-reperfusion. We tested the hypothesis that activation of Akt would decrease infarct size and improve microregional O2 supply/consumption balance after cerebral ischemia-reperfusion. This hypothesis was tested in isoflurane-anesthetized rats with middle cerebral artery blockade for 1 h and reperfusion for 2 h with or without SC-79 (Akt activator, 0.05 mg/kg, three doses). Regional cerebral blood flow was determined using a C14-iodoantipyrine autoradiographic technique. Regional small vessel (20-60 µm diameter) arterial and venous oxygen saturations were determined microspectrophotometrically. Akt phosphorylation was determined by Western blot. There were no significant hemodynamic or blood gas differences between groups. The control ischemic-reperfused cortex had a similar O2 consumption, but lower blood flow and higher O2 extraction compared to the contralateral cortex. However, microregional O2 supply/consumption balance was significantly reduced in the ischemic-reperfused cortex with many areas of low O2 saturation (42 of 80 veins with O2 saturation below 50%). SC-79 did not significantly affect cerebral O2 consumption, but significantly improved O2 supply/consumption balance in the reperfused area (18 of 80 veins with O2 saturation below 50%). This was associated with a reduced cortical infarct size (13.3 ±â€¯0.5% control vs 6.7 ±â€¯0.3% SC-79). In control, Akt phosphorylation was elevated at 2 h after ischemia. With SC-79, Akt was activated at 15 min but not at 2 h in the ischemic reperfused area. These results suggest that early Akt activation is important for not only cell survival, but also for the control of local oxygen balance after cerebral ischemia-reperfusion.

Effects of rapamycin pretreatment on blood-brain barrier disruption in cerebral ischemia-reperfusion.

The mammalian target of rapamycin (mTOR) pathway is essential in neuronal survival and repair in cerebral ischemia. Decreases in blood-brain barrier (BBB) disruption are associated with a decrease in neuronal damage in cerebral ischemia. This study was performed to investigate how pre-inhibition of the mTOR pathway with rapamycin would affect BBB disruption and the size of the infarcted cortical area in the early stage of focal cerebral ischemia-reperfusion using quantitative analysis of BBB disruption. Rats were treated with 20mg/kg of rapamycin i.p. once a day for 2days (Rapamycin Group) or vehicle (Control Group) before transient middle cerebral artery (MCA) occlusion. After one hour of MCA occlusion and two hours of reperfusion, the transfer coefficient (Ki) of (14)C-α-aminoisobutyric acid ((14)C-AIB) to measure the degree of BBB disruption and the size of the cortical infarct were determined. Ischemia-reperfusion increased the Ki in the Rapamycin treated (+15%) as well as in the untreated control group (+13%). However, rapamycin pretreatment moderately decreased Ki in the contralateral (-30%) as well as in the ischemic-reperfused (-29%) cortex when compared with the untreated control group. Rapamycin pretreatment substantially increased the percentage of cortical infarct compared with the control group (+56%). Our data suggest that activation of mTOR pathway is necessary for neuronal survival in the early stage of cerebral ischemia-perfusion and that the reason for the enlarged cortical infarct by rapamycin pretreatment may be related to its non-BBB effects on the mTOR pathway.