Fifty-four year-old man with recent history of myocardial infarction and a percutaneous coronary intervention who suffered a ventricular fibrillation arrest at home. He was resuscitated in the field. His heart rhythm was in atrial fibrillation. The cardiac catheterization showed a patent stent from his previous myocardial infarction and no new occlusions. He subsequently underwent hypothermia protocol using the Alsius CoolGard 3000 Temperature Control System and Icy Catheter. Heparin drip was started for atrial fibrillation 36 hours after catheter insertion and became therapeutic 2 hours before the end of cooling maintenance phase. Heparin drip was stopped 4 hours into the rewarming phase because of spontaneous conversion to sinus rhythm. Subcutaneous heparin was resumed for deep venous thrombosis prophylaxis. He was extubated to room air after hypothermia protocol. The cooling catheter was removed 88 hours after insertion. Within 1 minute of catheter removal, his oxygen saturation dropped to 80%. Transthoracic echocardiogram showed a mobile thrombus in the right atrium prolapsing into the right ventricle. Computer tomography angiography of the chest confirmed a large saddle embolus. Ninety minutes later, patient went into cardiac arrest with pulseless electrical activity while he was being considered for surgical embolectomy, but he could not be resuscitated. The temporal relationship of the catheter removal and his acute clinical decompensation led to believe that this was an intravascular cooling catheter (ICC)-related event. Providers should be cognizant of the complications of central venous catheters such as thrombosis formation, as it could lead to fatal pulmonary embolism. Physicians should promote frequent assessment of the access site(s) during routine physical examinations and potentially use point of care vascular ultrasound in high-risk cases to rule out a catheter-associated thrombus before catheter removal.
Therapeutic hypothermia (TH) improves neurological outcomes after cardiac arrest by mitigating cerebral reperfusion injury. Serum magnesium (Mg) inhibits glutamate release, restores blood-brain barrier integrity, and decreases brain edema. The neuroprotective role of Mg in cardiac arrest patients undergoing TH is not well established. We analyzed 438 survivors of cardiac arrest who completed a TH protocol from 2008 through 2016. Multivariate and receiver operating characteristic (ROC) analyses examined the association between Mg supplementation and Mg levels before, during, and after TH with neurologic outcomes. Participants were 65.5 ± 15.9 years old, 47% received bystander cardiopulmonary resuscitation, and time to target temperature was 286 ± 196 minutes. Patients with favorable neurologic outcomes had lower Mg levels at presentation (2.1 mg/dL vs. 2.2 mg/dL, p = 0.010; OR [95% CI] = 0.531 [0.329-0.857]) and more frequently received Mg supplementation (39% vs. 25%, p = 0.009; OR [95% CI] = 1.936 [1.171-3.202]). Mg levels on presentation inversely correlated with favorable neurologic outcomes (r = -0.134, p = 0.036). Stratification of patients based on Mg levels demonstrated trends toward worse neurological outcomes at the extremes of the range, though sample sizes were small and the point estimate was not significant. ROC analysis showed no significant Mg level determining favorable outcomes. Mg levels at presentation inversely correlated with neurologic outcomes in cardiac arrest survivors undergoing TH. Intracellular shift and increased renal excretion of Mg may be responsible for the low Mg levels seen in some patients undergoing TH. Whether Mg supplementation could potentiate the beneficial effects of TH remains unclear and deserves further investigation.
Aortic regurgitation is a frequently encountered condition, in which traditional measurements of severity have proven to be of limited value in identifying those who would be best served by aortic valve replacement. Novel methods of assessing severity are vital, particularly as an entirely new paradigm of aortic regurgitation has surfaced, with the advent of transcatheter aortic valve replacement (TAVR), and the adverse events that are being observed with varying degrees of aortic regurgitation. With that in mind, a comprehensive assessment of aortic regurgitation should now include indexed left ventricular systolic volumes and a comprehensive assessment of right ventricular function, in addition to the quantitative measures that are currently recommended. Cardiac MRI also provides valuable information and should be strongly considered, particularly in challenging cases. The incremental value of additional echocardiographic parameters such as strain imaging, speckle tracking imaging, and tissue Doppler imaging remains unclear, and evidence for their utility is not, as yet, compelling. However, the field of aortic regurgitation assessment has been reinvigorated by the prevalence of paravalvular regurgitation post-TAVR, and many of the abovementioned parameters may need to be re-visited so that we can more accurately determine prognosis and risk stratify patients in a more reliable and evidence-based manner.
Introduction:
Sudden cardiac arrest is a major cause of mortality in the United States and globally. Therapeutic hypothermia (TH) has demonstrated success in improving neurological outcomes in post-cardiac arrest patients. TH causes several physiologic ECG changes, including QTc prolongation. TH also decreases serum magnesium levels. These changes may lead to malignant ventricular arrhythmia and poor neurological outcome. We aimed to evaluate the association between the QTc interval during TH, magnesium levels, and neurologic outcomes.
Methods:
We reviewed the electrocardiograms of 366 patients who underwent TH at various intervals corresponding to pre-cooling, maintenance of targeted temperature management, and rewarming periods. We reviewed the change in the corrected QT segment (QTc) and evaluated their relationship with the patients’ magnesium levels and neurologic outcomes.
Results:
71.3% of the patients had a significant increase in QTc interval defined as >60 ms or any QTc>500 ms during TH. Patients with persistent prolongation of QTc after rewarming had poor neurological outcomes (p<0.05). Magnesium level showed a positive correlation with QTc interval at presentation (R=0.240, p<0.05) and at 48 hours (R=0.225, p= <0.05). Patients who had poor neurological outcomes tended to have higher magnesium levels at presentation (p<0.05). The majority of patients who received supplemental Mg did not have any significant change in their QTc.
Conclusion:
TH is independently associated with QTc prolongation. Patients with a persistent increase in QTc interval during the rewarming phase should be promptly evaluated for QTc-prolonging factors given its association with worse neurological outcomes. The inverse correlation between magnesium levels and poor neurological outcomes deserves further investigation.
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