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DKA-Induced Takotsubo Cardiomyopathy in Patient with Known HOCM
Ayla Gordon1, Gina LaCapra1, Roberto Roberti1
1Overlook Medical Center, Summit, NJ, USA.
Insights
Diabetic Ketoacidosis can induce Takotsubo cardiomyopathy, especially in patients with hypertrophic cardiomyopathy. This case highlights the complex interplay between DKA, TC, and HOCM, leading to syncope due to reduced brain perfusion.
Area of Science:
- Cardiology
- Endocrinology
- Medical Case Reports
Background:
- Diabetic Ketoacidosis (DKA) is a serious complication of diabetes.
- Takotsubo cardiomyopathy (TC) is a temporary heart condition.
- Hypertrophic cardiomyopathy (HOCM) is a genetic heart muscle disease.
Observation:
- This report details the first case in the US of DKA-induced TC in a patient with known HOCM.
- The patient presented with new-onset DKA and subsequent TC.
- The interaction between DKA, TC, and HOCM presented unique clinical challenges.
Findings:
- DKA precipitated TC in a patient with pre-existing HOCM.
- The reduced ejection fraction (EF) from TC exacerbated the outflow tract obstruction in HOCM.
- This led to transiently decreased cerebral perfusion, resulting in syncope.
Implications:
- This case underscores the critical need to recognize DKA as a potential trigger for TC, particularly in patients with HOCM.
- Understanding the biochemical and physiological mechanisms is crucial for managing these complex cases.
- Early diagnosis and intervention are vital to prevent adverse outcomes like syncope and potential cardiac events.
Abstract:
The first published case of Diabetic Ketoacidosis-induced Takotsubo cardiomyopathy was in 2009. Our patient is the 1st reported case of Diabetic Ketoacidosis- (DKA-) induced Takotsubo cardiomyopathy (TC) in a patient with known hypertrophic cardiomyopathy (HOCM) in the United States. In the literature, there are only two examples linking DKA to TC; however, this report focuses on the biochemical and physiological causes of TC in a patient with known HOCM and new-onset DKA. TC in previously diagnosed HOCM poses particular complications. With the above patient's baseline outflow tract obstruction due to septal hypertrophy, the acute reduction in EF due to TC resulted in transient drop in brain perfusion and, therefore, syncope.
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