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Abstract
Introduction: Cocaine, a significant source of morbidity and mortality in the United States, is one of the most frequently consumed recreational substances worldwide. Long-term use of cocaine is known to cause irreversible cardiotoxic effects, such as structural damage to the heart, electrical irregularities, diastolic heart failure, and myocardial infarctions. Cocaine-induced cardiomyopathy is associated with concentric ventricular hypertrophy alongside decreased ventricular compliance. However, recent research has hypothesized that patients who already have symptomatic cardiovascular disease are at an increased risk of developing an impairment in systolic ventricular function following chronic cocaine use, which is hypothesized to be caused by either direct cocaine-induced myocardial damage or small vessel coronary artery disease. We present an unusual case in which a patient developed systolic dysfunction alongside a left ventricular apical aneurysm following long-term cocaine use.
Case Presentation: A 53-year-old lady with a known history of type 2 diabetes mellitus, hypertension, hyperlipidemia, prior cerebrovascular accident with left-sided weakness, and chronic cocaine use presented to emergency after she developed dyspnea at rest and orthopnea. She reported that her symptoms began at rest, which improved slightly with positional changes but worsened over a short course of time, prompting her to consult medical help. She endorsed that she was told about having a “weak heart” when she was hospitalized for a stroke. She denied chest pain, pressure, palpitations, dizziness, syncope, or near syncope. Despite these comorbidities, she continued with cocaine usage, snorting cocaine at least two times a week. Upon admission, apart from tachycardia at 95 beats per minute, no other abnormalities were noted on physical examination. Admission labs were positive for an elevated brain natriuretic peptide at 284.07 pg/ml and high sensitivity troponins, which were trended at 61, 52, and 51 ng/L, with no other abnormalities noted on the complete metabolic profile. Complete blood count was notable for anemia with hemoglobin at 9.7g/dl, mean corpuscular volume 85.2fL, and hematocrit of 29.4%. Chest x-ray demonstrated pulmonary vascular congestion. EKG revealed sinus tachycardia. She was admitted for acute heart failure exacerbation potentiated by cocaine usage. The echocardiogram showed moderated ischemic cardiomyopathy with an ejection fraction of 40%, old inferior apical myocardial ischemia, inner apical thinning, apical aneurysm, and akinesis. She was diuresed and initiated on guideline-directed medical therapy with plans for cardiac catheterization. Unfortunately, despite counseling, she left against medical advice before further interventions could be performed
Discussion: This case demonstrates the impact on heart health caused by long-term cocaine use in individuals with underlying conditions. The development of weakened heart function and a bulging area in the ventricle shows how cocaine can affect the heart in multiple ways, like those seen in ischemic disease Despite being aware of the risks involved, continued cocaine use worsened her heart failure, resulting in Fluid accumulation in her lungs requiring hospitalization.
This case emphasizes the importance of educating patients and consistently warning them about the dangers of cocaine use. The patient's decision to leave care prematurely before completing treatments sheds light on the difficulties faced when managing substance abuse issues within healthcare settings.
Presentation Type
Poster
Recommended Citation
Olson, Kennedy; Reckley, William; Kondapavuluru, Roy; Abarca, Oliverio; Durazo, Yareli; and Suarez Parraga, Andres, "Cocaine-Induced Left Ventricular Apical Aneurysm: A Case Report" (2024). Research Colloquium. 77.
https://scholarworks.utrgv.edu/colloquium/2024/posters/77
Cocaine-Induced Left Ventricular Apical Aneurysm: A Case Report
Introduction: Cocaine, a significant source of morbidity and mortality in the United States, is one of the most frequently consumed recreational substances worldwide. Long-term use of cocaine is known to cause irreversible cardiotoxic effects, such as structural damage to the heart, electrical irregularities, diastolic heart failure, and myocardial infarctions. Cocaine-induced cardiomyopathy is associated with concentric ventricular hypertrophy alongside decreased ventricular compliance. However, recent research has hypothesized that patients who already have symptomatic cardiovascular disease are at an increased risk of developing an impairment in systolic ventricular function following chronic cocaine use, which is hypothesized to be caused by either direct cocaine-induced myocardial damage or small vessel coronary artery disease. We present an unusual case in which a patient developed systolic dysfunction alongside a left ventricular apical aneurysm following long-term cocaine use.
Case Presentation: A 53-year-old lady with a known history of type 2 diabetes mellitus, hypertension, hyperlipidemia, prior cerebrovascular accident with left-sided weakness, and chronic cocaine use presented to emergency after she developed dyspnea at rest and orthopnea. She reported that her symptoms began at rest, which improved slightly with positional changes but worsened over a short course of time, prompting her to consult medical help. She endorsed that she was told about having a “weak heart” when she was hospitalized for a stroke. She denied chest pain, pressure, palpitations, dizziness, syncope, or near syncope. Despite these comorbidities, she continued with cocaine usage, snorting cocaine at least two times a week. Upon admission, apart from tachycardia at 95 beats per minute, no other abnormalities were noted on physical examination. Admission labs were positive for an elevated brain natriuretic peptide at 284.07 pg/ml and high sensitivity troponins, which were trended at 61, 52, and 51 ng/L, with no other abnormalities noted on the complete metabolic profile. Complete blood count was notable for anemia with hemoglobin at 9.7g/dl, mean corpuscular volume 85.2fL, and hematocrit of 29.4%. Chest x-ray demonstrated pulmonary vascular congestion. EKG revealed sinus tachycardia. She was admitted for acute heart failure exacerbation potentiated by cocaine usage. The echocardiogram showed moderated ischemic cardiomyopathy with an ejection fraction of 40%, old inferior apical myocardial ischemia, inner apical thinning, apical aneurysm, and akinesis. She was diuresed and initiated on guideline-directed medical therapy with plans for cardiac catheterization. Unfortunately, despite counseling, she left against medical advice before further interventions could be performed
Discussion: This case demonstrates the impact on heart health caused by long-term cocaine use in individuals with underlying conditions. The development of weakened heart function and a bulging area in the ventricle shows how cocaine can affect the heart in multiple ways, like those seen in ischemic disease Despite being aware of the risks involved, continued cocaine use worsened her heart failure, resulting in Fluid accumulation in her lungs requiring hospitalization.
This case emphasizes the importance of educating patients and consistently warning them about the dangers of cocaine use. The patient's decision to leave care prematurely before completing treatments sheds light on the difficulties faced when managing substance abuse issues within healthcare settings.