Cardiac manifestations of cocaine abuse: a cross-sectional study of asymptomatic men with a history of long-term abuse of “crack” cocaine

Chakko, Simon; Fernandez, Aland; Mellman, Thomas A.; Milanes, Fernando; Kessler, Kenneth M.; Myerburg, Robert J.

doi:10.1016/0735-1097(92)90374-v

Cited by 54 publications

(20 citation statements)

References 31 publications

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“…We also observed global LV systolic dysfunction in 34% of our series. This prevalence was higher than in previous echocardiographic reports on asymptomatic patients, in which it ranged from 0% to 14% [7,13,32,36]. Still, we only found mild systolic dysfunction, with the lowest LVEF being 48%, probably because we assessed the chronic effect of cocaine and not the acute phase effect, and also because our cocaine abusers were asymptomatic and likely to have less severe cardiac involvement.…”

Section: Discussioncontrasting

confidence: 71%

Long term effects of cocaine on the heart assessed by cardiovascular magnetic resonance at 3T

Maceira

Ripoll

Cosı́n-Sales

et al. 2014

Journal of Cardiovascular Magnetic Resonance

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BackgroundCocaine is an addictive, sympathomimetic drug with potentially lethal effects. The prevalence and features of cocaine cardiotoxicity are not well known. We aimed to assess these effects using a comprehensive cardiovascular magnetic resonance (CMR) protocol in a large group of asymptomatic cocaine users.MethodsConsecutive (n = 94, 81 males, 36.6 ±7 years), non-selected, cocaine abusers were recruited and had a medical history, examination, ECG, blood test and CMR. The CMR study included measurement of left and right ventricular (LV, RV) dimensions and ejection fraction (EF), sequences for detection of myocardial oedema and late gadolinium enhancement (LGE). Images were compared to a cohort of healthy controls.ResultsYears of regular cocaine use were 13.9 ± 9. When compared to the age-matched healthy cohort, the cocaine abusers had increased LV end-systolic volume, LV mass index and RV end-systolic volume, with decreased LVEF and RVEF. No subject had myocardial oedema, but 30% had myocardial LGE indicating myocardial damage.ConclusionsCMR detected cardiovascular disease in 71% of this cohort of consecutive asymptomatic cocaine abusers and mean duration of abuse was related to probability of LV systolic dysfunction.

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Section: Discussioncontrasting

confidence: 71%

Long term effects of cocaine on the heart assessed by cardiovascular magnetic resonance at 3T

Maceira

Ripoll

Cosı́n-Sales

et al. 2014

Journal of Cardiovascular Magnetic Resonance

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“…Patients who chronically abuse cocaine may have various ECG findings, including "early repolarization" with f-point and ST-segment elevation in the midprecordialleads as well as increased QRS voltage and a prolonged QT interval, but Brugada-type ECG changes have not previously been reported in this group of patients. [19][20][21] In addition, the specificity of the described ECG abnormalities has been questioned. "…”

Section: Discussionmentioning

confidence: 96%

Brugada-Type Electrocardiographic Pattern Induced by Cocaine

Littmann

Monroe

Svenson

2000

Mayo Clinic Proceedings

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Right bundle branch block with coved ST-segment elevation in leads V1 through V3 is the electrocardiographic (ECG) marker of the Brugada syndrome. We describe a healthy young man with a normal baseline ECG in whom a transient Brugada pattern was observed repeatedly after recreational cocaine use. Intravenous administration of procainamide and subsequent intravenous propranolol followed by noradrenaline failed to reproduce the Brugada sign. An electrophysiologic study performed in the presence of the Brugada ECG pattern showed no inducible arrhythmias. This case illustrates that, in susceptible individuals, cocaine may provoke the Brugada sign. The clinical importance of this cocaine-induced ECG abnormality is currently unknown.

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“…A number of human case reports have noted an association of CC abuse with cardiac hypertrophy [36]. Increases in left ventricular mass measured with an echocardiogram were documented in human CC abusers when compared to age-matched control subjects [37]. Cocaine use is also known to cause increased plasma concentration of atrial natriuretic peptide, indicative of circulatory overload and pump failure [38].…”

Section: Morphological Findingsmentioning

confidence: 97%

Markers of cardiac oxidative stress and altered morphology after intraperitoneal cocaine injection in a rat model

Fineschi¹,

Baroldi

Centini

et al. 2001

International Journal of Legal Medicine

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This study was designed to assess the parameters of myocardial oxidative stress and related cardiac morphological changes following intraperitoneal cocaine exposure in rats. The cardiac levels of reduced glutathione(GSH), oxidised glutathione(GSSG), ascorbic acid (AA), and the production of malondialdehyde (MDA) were measured, as well as the variations of activity in the enzyme systems involved in cell antioxidant defence, glutathione peroxidase (GSH-Px), glutathione reductase (GR) and superoxide dismutase (SOD). After chronic cocaine administration for 30 days GSH was significantly depleted in the heart from 30 min (P < 0.001) to 24 h (P < 0.001) after exposure, and GSSG was increased for a similar time (P < 0.05 at 30 min and P < 0.01 at 24 h). SOD increased during the first hour (P < 0.001), GR and GSH-Px both increased from 30 min to 24 h, and these increases were statistically significant (P < 0.01 and P < 0.001 at 30 min and P < 0.01 and P < 0.001 at 24 h, respectively). The AA levels increased after 1 h (P < 0.01), remaining significantly so for 24 h (P < 0.001) and MDA increased from 30 min to 24 h, all values being highly significant (P < 0.001). The body weight was significantly (P < 0.001) reduced in both cocaine groups (40 mg/kg x 30 days and 40 mg/kg x 10 days + 60 mg/kg x 20 days). The heart weight (P < 0.01) and its percentage of the body weight (P < 0.001) were significantly higher in these two groups than in the controls. Similarly, in the noradrenaline 4 mg/ kg x 30 days group, the body weight was significantly (P < 0.001) reduced and the heart weight (P < 0.01) and its percentage of body weight (P < 0.001) were significantly higher than in the controls. In comparing the cocaine and noradrenaline experiments, the frequency and extent of cardiac lesions obtained with 40 mg/kg x 10 days + 60 mg/kg x 20 days of cocaine were similar to those with 8 mg/kg of noradrenaline at 24 h. In this experimental model, cocaine administration compromised the antioxidant defence system of the heart associated with a significant increase of heart weight and the percentage of body weight.

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Cardiac manifestations of cocaine abuse: a cross-sectional study of asymptomatic men with a history of long-term abuse of “crack” cocaine

Cited by 54 publications

References 31 publications

Long term effects of cocaine on the heart assessed by cardiovascular magnetic resonance at 3T

Long term effects of cocaine on the heart assessed by cardiovascular magnetic resonance at 3T

Brugada-Type Electrocardiographic Pattern Induced by Cocaine

Markers of cardiac oxidative stress and altered morphology after intraperitoneal cocaine injection in a rat model

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