Author + information
- aSection of Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut
- bDivision of Cardiothoracic Surgery, Duke University School of Medicine, Durham, North Carolina
- cDivision of Cardiology, Massachusetts General Hospital, Boston, Massachusetts
- ↵∗Address for correspondence:
Dr. James L. Januzzi Jr., Department of Cardiology/Internal Medicine, Massachusetts General Hospital, Yawkey 5984, 32 Fruit Street, Boston, Massachusetts, 02114.
“Because a mainline into my vein,
Leads to a center in my head,
And then I’m better off than dead.”
—The Velvet Underground (1)Self-congratulatory press releases from cardiovascular centers across the country have had a similar message: 2016 was a banner year for heart transplantation. The norm of approximately 2,200 transplants a year across the United States was dramatically upended with 3,191 in the last year (Figures 1A and 1B). This increase in heart transplantation was particularly felt in areas with the longest wait times for available hearts, and it allowed for significantly more patients to undergo this potentially lifesaving procedure.
The abrupt rise in graft availability leads to an inevitable question: why was there such a dramatic spike in the number of organs from otherwise young and healthy donors? With other common modes of death among donors—motor vehicle accidents, homicide, and suicide—remaining fairly constant, the answer appears to lie in the logarithmic rise in drug-related deaths (2).
The gloomy reality is that we are living amid a drug epidemic, one with wide-ranging implications across individuals and society. The impact of the growing crisis created by addiction is reflected in daily news stories and even highlighted in hugely popular television dramas, such as Breaking Bad, where the morally questionable protagonist Walter White leaves a swath of death in his path during his career cooking and selling methamphetamine.
Growth in use of drugs of abuse among young and otherwise healthy individuals has left hospitals overwhelmed with complications of addiction, including the all too common scenario of overdose and brain death, taking patients in the prime of their lives. Workers in the field of advanced heart failure must perpetually operate with conflicting emotions: on the one hand, our patients waiting for a heart are given another chance, whereas on the other hand, this opportunity is coming at a dark cost.
There are other aspects of the rise in addiction-related donor heart availability to consider. Whereas the complications that may occur from addiction-related infectious diseases such as hepatitis C and human immunodeficiency virus are well known to transplant physicians, the cardiotoxic effects of many illicit drugs are surprisingly less well understood (3). This is particularly relevant in those patients dying after using increasingly common drugs such as cathinones (“bath salts”) or combinations of drugs that include methamphetamines; both situations are increasing in incidence. Are the hearts from donors who have abused these newer intoxicants suitable for transplantation?
In this issue of JACC: Heart Failure, an interesting paper by Schürer et al. (4) examines a question we ought to know a lot more about: the cardiac effects of methamphetamine. These investigators, based out of 2 medical centers in Germany, set out to describe the clinical characteristics and histological changes in the myocardium of 30 patients with methamphetamine-associated cardiomyopathy. Importantly, these investigators describe pathological changes and clinical outcomes in patients according to whether the patients stopped (n = 23), or continued to use the drug (n = 7). Echocardiograms in these young patients (mean age 30 years) were highly abnormal, with severe systolic dysfunction and left ventricular chamber dilatation. A majority of patients had regurgitant valvular lesions, with the mitral valve the most common site of disease. Ventricular thrombi and pleural or pericardial effusions were common. At follow-up, improvements in ventricular function and symptoms were seen solely among the patients who discontinued drug abuse. Histological analysis of the myocardial tissue in these patients showed diffuse inflammation, fibrosis, and myonecrosis; fibrosis correlated with the duration of abuse and inversely predicted left ventricular function at follow-up.
How could these findings affect our care of patients? First, methamphetamines were not typically the sole culprits in the study: most of the patients profiled in this study used other substances, such as alcohol, heroin, and cocaine; each of these substances is known to have profound cardiotoxic effects, and their combined use is associated with a higher risk for death. This polysubstance abuse quite frequently involves concomitant use of a psychomotor stimulant with an opiate—often referred to as a “speed balling,” a practice that places individuals at inordinate risk for cardiorespiratory arrest. Second, this study provides objective data in support of the presumption that cardiac function will improve only after cessation of drug abuse. Therefore, rather than simply administering a cocktail of neurohormonal blockade to patients with suspected methamphetamine-associated cardiomyopathy, the majority of focus should be on helping such patients quit using methamphetamines. Third, the histological findings of inflammation, fibrosis, and myocyte damage, coupled with the low diagnostic yield and limited clinical indication for endomyocardial biopsies in these patients, raises the possibility for use of biomarkers to assist with the management of heart failure after the index hospitalization (5).
What implications do these findings have on the use of hearts from a donor pool that increasingly consists of drug-related deaths? Currently, assessment of donor hearts relies on macroscopic assessments of the heart that use transthoracic echocardiography and coronary angiography. These methods are somewhat insensitive for the purpose of capturing the degree of disease present at the level of the myocytes, dysfunction that might contribute to feared complications after transplantation such as primary graft failure. This study hints at the microscopic insults that occur at the histopathological level with long-term methamphetamine use; the magnitude of these insults might be important to quantify for the purposes of managing the recipient after transplantation. More data are needed to understand the short- and long-term implications of using donor hearts from patients with a history of methamphetamine use. Additionally, in the future, increasing knowledge of the microscopic and biochemical effects of methamphetamine use may allow us to “optimize” suboptimal donor hearts and continue to increase the donor pool from this demographic group.
The destructive nature of substance abuse ranges from its harmful effects on individual health to the tearing apart of social fabric. Schürer et al. (4) should be congratulated for taking a step toward improving our understanding of the cardiovascular toxicities of one of the most common drugs of abuse. More studies in this area are needed; this study serves to establish an important basic foundation for what will be ultimately required: a comprehensive examination of the cardiac effects of all major illicit substances that uses cutting-edge imaging technology and biomarker assessments. Patient-centered intervention studies are needed that will help us understand the efficacy of various interventions. Finally, collaboration among cardiologists, mental health professionals, epidemiologists, and public health officials across the world is essential to contend with this intensifying international crisis. If lessons from Breaking Bad are to be believed, the devastation caused by the drug problem does not leave a single person unscathed.
↵∗ Editorials published in JACC: Heart Failure reflect the views of the author and do not necessarily represent the views of JACC: Heart Failure or the American College of Cardiology.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2017 American College of Cardiology Foundation
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