RESUMEN
Brugada syndrome is a rare cardiac condition characterized by distinctive electrocardiogram patterns, predisposing individuals to fatal arrhythmias. While primarily linked to a loss-of-function mutation in the SCN5A gene, acquired forms of the syndrome have been associated with various factors, including drug use. We present a case of a 31-year-old female who presented to the emergency department unresponsive following cocaine use and developed type 1 Brugada ECG patterns alongside an incomplete right bundle branch block in V1-V3, ST elevations with biphasic waves, and diffuse repolarization abnormalities with J point deviations while in the intensive care unit. This study aimed to discuss the complexity of managing drug-induced Brugada-like findings and highlights the need for further research into the mechanisms underlying cocaine-induced cardiac effects. We aimed to discuss potential mechanisms for the impact of cocaine as its role as a sodium channel blocker and its potential effects on connexin 43 in the context of Brugada syndrome. This study also reinforced the importance of differentiating between true Brugada syndrome and other similar ECG changes for appropriate care management.
RESUMEN
This is a case of a 20-year-old pregnant female presenting EKG abnormalities associated with an overdose of bupropion. These ECG abnormalities are prolongation of the QRS, prolongation of the corrected QT interval (QTc), right axis deviation, and a terminal R wave. The propagation of electricity through the myocardium is dependent on many factors. It is dependent on the flow of sodium from the extracellular to intracellular space, flow of potassium from intracellular to extracellular space, and ultimately the propagation of the signal at the gap junction by Connexin 43 (Cx-43). We postulate that the ECG abnormalities in this case are secondary to bupropion's effect on the potassium rectifier channels (Kir) and or Cx-43 at the gap junction.
RESUMEN
In the United States, tricyclic antidepressants (TCA) are commonly prescribed to treat psychiatric illnesses and neuropathic pain. This class of antidepressants has been found to cause pathognomonic electrocardiogram (ECG) changes in cases of overdose.1 Specifically, TCA's cause a dominant terminal R wave in aVR and widening of the QRS complex due to their sodium channel blocking effect. Diphenhydramine, better known as Benadryl, is known to disrupt sodium channels in the same manner. In this case report, a 13-year-old female was brought into the emergency department (ED) after attempted suicide by diphenhydramine overdose. The patient presented with palpitations, nausea and confusion. She was agitated, tachycardic and exhibited opsoclonus. An ECG was performed upon the patient's arrival which showed large terminal R waves in aVR along with large S waves in lead I indicating right axis deviation. Given the patient's age and reported ingestion, it was highly suspicious that her symptoms and ECG changes were the result of a sodium channel blockade. Sodium bicarbonate was given, which resulted in notable ECG changes as well as symptomatic improvement. TCA's, and similarly diphenhydramine, have sodium channel blocking properties which can be revealed by performing an ECG. Administration of sodium bicarbonate in the ED has been shown to be a successful treatment by reversing this sodium channel blockade. Topics: Tricyclic antidepressants, diphenhydramine, overdose, sodium channel blockage, sodium bicarbonate administration.
RESUMEN
This case report discusses a patient who had subtle EKG abnormalities that were indicative of a pathological amount of coronary artery disease resulting in occlusion of the right coronary artery (RCA) even though ST-elevation criteria for STEMI were not initially present. In the proper clinical setting, focal repolarization abnormalities in conjunction with cardiac risk factors and cardiac symptoms may indicate a high probability of a pathological amount of coronary disease that warrants emergent intervention. We report a case of a 54-year-old male with cardiac risk factors and cardiac symptoms who presented to the emergency department (ED). Initial EKG, while technically abnormal, was not diagnostic. The point of care troponin was elevated at 0.10 ng/mL. Patient ultimately went to the catheterization lab where he was found to have an occlusion of the RCA and left circumflex artery which required stenting. Topics: Electrocardiogram, ECG, cardiology, myocardial infarction.
RESUMEN
Current guidelines to detect for myocardial infarction (MI) are not sufficient to triage patients requiring immediate cardiac catheterization, with at least 25% of non-ST elevation myocardial infarction (NSTEMI) patients found to have acute coronary occlusion (ACO) only on delayed catheterization, and up to 35% of perceived ST-elevation myocardial infarction (STEMI) ACOs found as false positives at catheterization. There has been a call for an integration of a new paradigm: occlusion/non-occlusion MI (OMI/NOMI). Here we discuss a 51-year-old female who presented to the emergency department with subtle electrocardiogram (ECG) abnormalities not adherent to the current MI guidelines. However, the subtle abnormalities when combined with her history and risk factors point to a high probability of a pathological amount of coronary disease that required immediate catheterization. This case report illustrates the importance in revisiting current guidelines and the need to integrate OMI/NOMI alongside current guidelines to guide decision making for immediate reperfusion needs. Topics: Occlusion, myocardial infarction, ST elevation myocardial infarction, acute coronary syndromes, electrocardiography.
RESUMEN
Electrocardiograms (EKGs) are rapid, non-invasive tests that provide invaluable insight into the pathologic processes plaguing our patients. We present a case of a two-year-old child found to have ingested cocaine whose EKG mimicked that of Brugada Syndrome. However, given the differences, we propose that the reason for this pattern was more likely a sodium channel toxicity secondary to the sodium channel blocking effects of cocaine, resulting in a brugada phenotype rather than a brugada genotype. Topics: Brugada, brugada phenotype, sodium channel blocker.
RESUMEN
The progression of normal cells from G2 into mitosis is stably blocked when their DNA is damaged. Tumor cells lacking p53 arrest only transiently in G2, but eventually enter mitosis. We show that an important component of the stable G2 arrest in normal cells is the transcriptional repression of more than 20 genes encoding proteins needed to enter into and progress through mitosis. Studies from a number of labs including our own have shown that, by inducing p53 and p21/WAF1, DNA damage can trigger RB-family-dependent transcriptional repression. Our studies reported here show that p130 and p107 play a key role in transcriptional repression of genes required for G2 and M in response to DNA damage. For plk1, repression is partially abrogated by loss of p130 and p107, and is completely abrogated by loss of all three RB-family proteins. Mouse cells lacking RB-family proteins do not accumulate with a 4N content of DNA when exposed to adriamycin, suggesting that all three RB-family proteins contribute to G2 arrest in response to DNA damage. Stable arrest in the presence of functional p53-to-RB signaling is probably due to the ability of cells to exit the cell cycle from G2, a conclusion supported by our observation that KI67, a marker of cell-cycle entry, is downregulated in both G1 and G2 in a p53-dependent manner.