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  • Oral presentation
  • Open Access

Cocaine use as an independent predictor of cardiac steatosis: initial experience by 1H spectroscopy

  • 1,
  • 1,
  • 2,
  • 1,
  • 3 and
  • 4
Journal of Cardiovascular Magnetic Resonance201012 (Suppl 1) :O90

https://doi.org/10.1186/1532-429X-12-S1-O90

  • Published:

Keywords

  • Cocaine
  • Left Ventricular Filling
  • Cocaine User
  • Exact Logistic Regression
  • TrueFisp Sequence

Introduction

Elevated myocardial triglyceride levels have been observed within the myocardium of diabetic and obese individuals. Use of cocaine leads to cardiomyopathy and precipitation of cardiovascular disease such as myocardial infarction, ventricular arrhythmias, and left ventricular dysfunction. Proton magnetic resonance spectroscopy (1H-MRS) has been applied to measure lipid overload in the human heart [1].

Purpose

The primary goal of the present study was to evaluate the myocardial fat in cocaine abusers. We applied 1H-MRS to quantify myocardial septal triglyceride content compared to the non-cocaine users to ascertain the prevalence and severity of cardiac steatosis among cocaine-use patients.

Methods

MRI/MRS studies were performed using a 3.0 T scanner (Tim Trio, Siemens) on 44 participants (32 cocaine users, and 12 non-users) with informed content. To measure left ventricular function, the entire heart was imaged in short-axis orientation using a retrospectively gated TrueFisp sequence. The short-axis along with the two and four chamber views were used to position the spectroscopic volume (6-8 ml voxel) within the interventricular septum. Myocardial 1H-MRS spectra were obtained with ECG and navigator gated with water suppressed (32 averages) and unsuppressed (4 averages) PRESS, TR/TE = 1-RR/30 ms. Fat content was quantified with Amares/MRUI and related to water in unsuppressed spectra and expressed as fat/water percent ratios.

Results

The characteristics of study participants are presented in Table 1. Using a 1% cut-off for cardiac steatosis, the overall prevalence of cardiac steatosis was 32% (14/44). The prevalence of cardiac steatosis in cocaine users was significantly higher than that in those who did not use cocaine (65.7% in cocaine users, and 16.7% in cocaine non-users, p < 0.004). Exact logistic regression analysis indicated that after controlling for age, gender, glucose, triglycerides, and systolic blood pressure, cocaine use was associated with a 14-fold risk of cardiac steatosis (adjusted OR 13.8, 95% CI:1.1,169).
Table 1

Characteristics of Study Participants of the Pilot Study

 

Cocaine use N = 32

never use N = 12

Female gender

45.7 ± 6.7

42.8 ± 9.5

Smoking/Diabetes

39.4%/9.1%

46.2%/0.0%

Systolic/Diastolic bp (mmhg)

130 ± 18/81 ± 12

123 ± 37/79 ± 18

Cholesterol (mg/dL)

174 ± 36

168 ± 35

Fasting glucose/Triglycerides (mg/dL)

97 ± 36/131 ± 103

84 ± 10/62 ± 25

Body Mass Index

27.5 ± 5.5

28.5 ± 6.7

LV end systolic/diastolic volume (mL)

61 ± 17/152 ± 34

69 ± 18/166 ± 27

Ejection Fraction (%)

60 ± 5

58 ± 8

LV mass (gm)

114 ± 28

118 ± 21

Conclusion

This pilot study demonstrated that cocaine use is significantly associated with cardiac steatosis. Human studies indicate that cardiac steatosis is associated with impaired left ventricular filling dynamics and diastolic dysfunction [2]. However, we cannot discriminate whether there is a causal relationship between increased myocardial TG content and reduced left ventricular function in our current study due to limited number of participants. Further studies are under way to make these distinctions.

Authors’ Affiliations

(1)
The Johns Hopkins Hospital, Baltimore, MD, USA
(2)
The National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA
(3)
Radiology and Imaging Sciences, National Institutes of Health, NIH, Bethesda, Bethesda, MD, USA
(4)
Department of Epidemiology, Johns Hopkins School of Hygiene and Public health, Baltimore, MD, USA

References

  1. Szczepaniak LS, et al.: Circ Res. 2007, 101: 759-767. 10.1161/CIRCRESAHA.107.160457.View ArticlePubMedGoogle Scholar
  2. Meer van der RW, et al.: European Heart Journal. 2008, 29: 1516-1522. 10.1093/eurheartj/ehn207.View ArticlePubMedGoogle Scholar

Copyright

© Liu et al; licensee BioMed Central Ltd. 2010

This article is published under license to BioMed Central Ltd.

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