Presentation Type
Poster
Discipline Track
Patient Care
Abstract Type
Case Report
Abstract
Introduction: Takotsubo cardiomyopathy (TSCM) or broken heart syndrome was first described in Japan in the 1990s, the syndrome has gained worldwide attention within the scientific community in the past few decades. The disease manifests predominantly in postmenopausal females in the presence of stressful triggers such as severe physical or emotional stress. Initially thought to be a benign condition, recent reports have demonstrated that TSCM may be associated with severe complications and mortality similar to acute coronary syndrome. Concerted efforts have been made to define various pathophysiologic aspects of TSCM; however, the precise etiologic understanding remains unclear. Some of the mechanisms proposed for the development of Takotsubo syndrome include elevated levels of circulating plasma catecholamines and their metabolites, microvascular dysfunction, inflammation, estrogen deficiency, spasms of the epicardial coronary vessels, and aborted myocardial infarction. In our patient, there was no acute stressor factor identified.
Case Report: A 69-year-old lady with OSA, Vit D deficiency, venous insufficiency, and sick sinus syndrome (s/p pacemaker in 2006). The patient presented to the ED referred by her PCP for evaluation of chest pain and dyspnea on exertion that started while she was dancing on a Saturday night. Initially, the pain was severe 9/10, accompanied by chest pressure and diaphoresis, with no radiation. She denied stressing factors. Her symptoms improved with rest, and she went to bed, the next morning the patient woke up with chest pain and mild dyspnea, so she decided to consult with her PCP. On her way to the ER, she was given nitroglycerin by EMS which subsided her chest pain. In the ER her symptoms were mild, with no respiratory distress, on room air, and speaking in full sentences, her MAP was around 66-70, her HR was in the low 60’s, and her RR was 18. On physical exam no JVD, clear lungs, and unremarkable S1 and S2 without pedal edema. Her EKG showed new T wave inversion in anterolateral leads, and elevated HS troponin (186). Negative UDS. 2D Echocardiogram showed LVEF 50% with apical akinesis and basal septal hyperkinesis. Left heart catheterization was done and revealed widely patent LAD, LCX, and RCA (dominant). The patient’s symptoms resolved and was started on DGMT before discharge.
Academic/Professional Position
Resident
Mentor/PI Department
Internal Medicine
Recommended Citation
Abarca Guzman, Oliverio Jose and Gonzalez Morales, Elimar, "Sick Sinus Syndrome and Takotsubo Cardiomyopathy" (2024). Research Symposium. 1.
https://scholarworks.utrgv.edu/somrs/2024/posters/1
Included in
Sick Sinus Syndrome and Takotsubo Cardiomyopathy
Introduction: Takotsubo cardiomyopathy (TSCM) or broken heart syndrome was first described in Japan in the 1990s, the syndrome has gained worldwide attention within the scientific community in the past few decades. The disease manifests predominantly in postmenopausal females in the presence of stressful triggers such as severe physical or emotional stress. Initially thought to be a benign condition, recent reports have demonstrated that TSCM may be associated with severe complications and mortality similar to acute coronary syndrome. Concerted efforts have been made to define various pathophysiologic aspects of TSCM; however, the precise etiologic understanding remains unclear. Some of the mechanisms proposed for the development of Takotsubo syndrome include elevated levels of circulating plasma catecholamines and their metabolites, microvascular dysfunction, inflammation, estrogen deficiency, spasms of the epicardial coronary vessels, and aborted myocardial infarction. In our patient, there was no acute stressor factor identified.
Case Report: A 69-year-old lady with OSA, Vit D deficiency, venous insufficiency, and sick sinus syndrome (s/p pacemaker in 2006). The patient presented to the ED referred by her PCP for evaluation of chest pain and dyspnea on exertion that started while she was dancing on a Saturday night. Initially, the pain was severe 9/10, accompanied by chest pressure and diaphoresis, with no radiation. She denied stressing factors. Her symptoms improved with rest, and she went to bed, the next morning the patient woke up with chest pain and mild dyspnea, so she decided to consult with her PCP. On her way to the ER, she was given nitroglycerin by EMS which subsided her chest pain. In the ER her symptoms were mild, with no respiratory distress, on room air, and speaking in full sentences, her MAP was around 66-70, her HR was in the low 60’s, and her RR was 18. On physical exam no JVD, clear lungs, and unremarkable S1 and S2 without pedal edema. Her EKG showed new T wave inversion in anterolateral leads, and elevated HS troponin (186). Negative UDS. 2D Echocardiogram showed LVEF 50% with apical akinesis and basal septal hyperkinesis. Left heart catheterization was done and revealed widely patent LAD, LCX, and RCA (dominant). The patient’s symptoms resolved and was started on DGMT before discharge.