Talks
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Resident
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Internal Medicine
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Resident
Discipline/Specialty (Author 2)
Internal Medicine
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Resident
Discipline/Specialty (Author 3)
Internal Medicine
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Resident
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Internal Medicine
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Resident
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Internal Medicine
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Faculty
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Internal Medicine
Discipline Track
Clinical Science
Abstract
Background: 1 out of 3 substance abuse emergency department visits are related to cocaine. In the US (United States), >5.5 million people consume cocaine. Hospitalizations for heart failure have a similar amount, with 5.7 million. Cocaine's cardiovascular adverse effects arise secondary to sympathetic nervous system stimulation, including decreased myocardial oxygen supply, coronary vasoconstriction, acceleration of atherosclerosis and thrombus formation. Studies have demonstrated contradictory information regarding cardiac anatomical changes (dilation/hypertrophy) secondary to chronic cocaine use. Cocaine cessation and guideline- directed medical therapy (GDMT) for HF are mainstay management. We present a case of a patient with HF and cocaine abuse.
Case: 38-year-old female with end stage renal disease (ESRD) on hemodialysis, systolic HF, and chronic cocaine abuse, who has been recurrently admitted for acute on chronic diastolic heart failure. Presenting with shortness of breath, orthopnea, bilateral lower extremity pitting edema. Drug screen test has demonstrated cocaine in multiple occasions. Within a year, three 2d echocardiograms demonstrated significant progression of HF even after cocaine cessation. Initial echo demonstrated left ventricular hypertrophy and preserved LVEF. 2nd echo with mild diastolic dysfunction, however the last echo demonstrated LVEF 35%. Her comorbidities presented a challenge for GDMT administration, she was initially started on carvedilol and later optimized with the addition of sacubitril/valsartan.
Discussion: This case illustrates HF cardiomyopathy progression in the setting of cocaine abuse, and its challenges for GDMT compliance. It underscores the need for comprehensive, patient-centered approaches to manage the interplay between HF, and cocaine abuse. Social determinants, particularly stimulant drug use, adds layers of complexity to an already intricate healthcare landscape.
Conclusion: These challenges mandate a multidisciplinary effort, including research to understand pathophysiology, dose relationship, disease progression and management; and an emphasis on patient education to mitigate the progression of these intertwined conditions
Presentation Type
Talk
Recommended Citation
Othon Martinez, Diana; Ali, Kashif; Gonzalez Morales, Elimar; Malaga-Espinoza, Barbara; Garcia, Jian; and Gutierrez, Cesar, "Heart Failure in the setting of cocaine abuse… cause or progression? A case report." (2024). Research Colloquium. 16.
https://scholarworks.utrgv.edu/colloquium/2024/talks/16
Included in
Heart Failure in the setting of cocaine abuse… cause or progression? A case report.
Background: 1 out of 3 substance abuse emergency department visits are related to cocaine. In the US (United States), >5.5 million people consume cocaine. Hospitalizations for heart failure have a similar amount, with 5.7 million. Cocaine's cardiovascular adverse effects arise secondary to sympathetic nervous system stimulation, including decreased myocardial oxygen supply, coronary vasoconstriction, acceleration of atherosclerosis and thrombus formation. Studies have demonstrated contradictory information regarding cardiac anatomical changes (dilation/hypertrophy) secondary to chronic cocaine use. Cocaine cessation and guideline- directed medical therapy (GDMT) for HF are mainstay management. We present a case of a patient with HF and cocaine abuse.
Case: 38-year-old female with end stage renal disease (ESRD) on hemodialysis, systolic HF, and chronic cocaine abuse, who has been recurrently admitted for acute on chronic diastolic heart failure. Presenting with shortness of breath, orthopnea, bilateral lower extremity pitting edema. Drug screen test has demonstrated cocaine in multiple occasions. Within a year, three 2d echocardiograms demonstrated significant progression of HF even after cocaine cessation. Initial echo demonstrated left ventricular hypertrophy and preserved LVEF. 2nd echo with mild diastolic dysfunction, however the last echo demonstrated LVEF 35%. Her comorbidities presented a challenge for GDMT administration, she was initially started on carvedilol and later optimized with the addition of sacubitril/valsartan.
Discussion: This case illustrates HF cardiomyopathy progression in the setting of cocaine abuse, and its challenges for GDMT compliance. It underscores the need for comprehensive, patient-centered approaches to manage the interplay between HF, and cocaine abuse. Social determinants, particularly stimulant drug use, adds layers of complexity to an already intricate healthcare landscape.
Conclusion: These challenges mandate a multidisciplinary effort, including research to understand pathophysiology, dose relationship, disease progression and management; and an emphasis on patient education to mitigate the progression of these intertwined conditions