The concept of high-risk plaque emerged from pathologic and epidemiologic studies 3 decades ago that demonstrated plaque rupture with thrombosis as the predominant mechanism of acute coronary syndrome and sudden cardiac death. Thin-cap fibroatheroma, a plaque with a large lipidic core covered by a thin fibrous cap, is the prototype of the rupture-prone plaque and has been traditionally defined as “vulnerable plaque.” Although knowledge on the pathophysiology of plaque instability continues to grow, the risk profile of our patients has shifted and the character of atherosclerotic disease has evolved, partly because of widespread use of lipid-lowering therapies and other preventive measures. In vivo intracoronary imaging studies indicate that superficial erosion causes up to 40% of acute coronary syndromes. This changing landscape calls for broader perspective, expanding the concept of high-risk plaque to the precursors of all major substrates of coronary thrombosis beyond plaque rupture. Other factors to take into consideration include dynamic changes in plaque composition, the importance of plaque burden, inflammatory activation (both local and systemic), healing mechanisms, regional hemodynamic pattern, properties of the fluid phase of blood, and the amount of myocardium at risk subtended by a lesion. Rather than the traditional focus limited to the thin-cap fibroatheroma, the authors advocate a more comprehensive approach that considers both morphologic features and biological activity of plaques and blood. This position paper highlights the challenges to the usual concept of high-risk plaque, proposes a broader definition, and analyzes its key morphologic features, the technological progress of plaque imaging (particularly using intracoronary imaging techniques), advances in pharmacologic therapies for plaque regression and stabilization, and the feasibility and efficacy of focal interventional treatments including preemptive plaque sealing.

Data continue to accumulate demonstrating the benefits of intravascular imaging guidance to improve patient outcomes after percutaneous coronary intervention (PCI)1 and the potential of intravascular imaging to identify high-risk vulnerable plaques.2 Optical coherence tomography (OCT) and near-infrared spectroscopy (NIRS) have been established as useful modalities for intravascular imaging in the catheterization laboratory. While the high resolution of OCT enables accurate identification of many plaque morphologies3 and precise quantitative measurements of plaque and stent dimensions, limited penetration remains a limitation.

Intravascular ultrasound and optical coherence tomography are used with increasing frequency for the care of coronary patients and in research studies. These imaging tools can identify culprit lesions in acute coronary syndromes, assess coronary stenosis severity, guide percutaneous coronary intervention (PCI), and detect vulnerable plaques and patients. However, they have significant limitations that have stimulated the development of multimodality intracoronary imaging catheters, which provide improvements in assessing vessel wall pathology and guiding PCI. Prototypes combining 2 or even 3 imaging probes with complementary attributes have been developed, and several multimodality systems have already been used in patients, with near-infrared spectroscopy intravascular ultrasound-based studies showing promising results for the identification of high-risk plaques. Moreover, postmortem histology studies have documented that hybrid imaging catheters can enable more accurate characterization of plaque morphology than standalone imaging. This review describes the evolution in the field of hybrid intracoronary imaging; presents the available multimodality catheters; and discusses their potential role in PCI guidance, vulnerable plaque detection, and the assessment of endovascular devices and emerging pharmacotherapies targeting atherosclerosis.

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Cardiology HomeNew OnlineCurrent IssueFor Authors Podcast Journals JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Cardiology journal

In the 160 years since Virchow first described atherosclerosis as an inflammatory disease, there has been ongoing debate about what initiates and drives the inflammatory process. In the last few years, several important insights have revolutionized the understanding of how atheroma transition into sclerotic plaques and why they rupture to cause sudden death, myocardial infarction, and stroke. Specifically, there is now strong evidence to support the thesis that the transition of cholesterol into its crystalline form is central to the development of atherosclerosis and plaque rupture. This chapter tells the story of the development of this elegant thesis. In addition, it summarizes the range of diseases in which cholesterol crystals have been found and highlights how understanding their central role in atherosclerosis provides a paradigm for the development of treatments for one of the most common diseases affecting humankind.

BackgroundNear-infrared spectroscopy (NIRS) and intravascular ultrasound are promising imaging modalities to identify non-obstructive plaques likely to cause coronary-related events. We aimed to assess whether combined NIRS and intravascular ultrasound can identify high-risk plaques and patients that are at risk for future major adverse cardiac events (MACEs).MethodsPROSPECT II is an investigator-sponsored, multicentre, prospective natural history study done at 14 university hospitals and two community hospitals in Denmark, Norway, and Sweden. We recruited patients of any age with recent (within past 4 weeks) myocardial infarction. After treatment of all flow-limiting coronary lesions, three-vessel imaging was done with a combined NIRS and intravascular ultrasound catheter. Untreated lesions (also known as non-culprit lesions) were identified by intravascular ultrasound and their lipid content was assessed by NIRS. The primary outcome was the covariate-adjusted rate of MACEs (the composite of cardiac death, myocardial infarction, unstable angina, or progressive angina) arising from untreated non-culprit lesions during follow-up. The relations between plaques with high lipid content, large plaque burden, and small lumen areas and patient-level and lesion-level events were determined. This trial is registered with ClinicalTrials.gov, NCT02171065.FindingsBetween June 10, 2014, and Dec 20, 2017, 3629 non-culprit lesions were characterised in 898 patients (153 [17%] women, 745 [83%] men; median age 63 [IQR 55–70] years). Median follow-up was 3·7 (IQR 3·0–4·4) years. Adverse events within 4 years occurred in 112 (13·2%, 95% CI 11·0–15·6) of 898 patients, with 66 (8·0%, 95% CI 6·2–10·0) arising from 78 untreated non-culprit lesions (mean baseline angiographic diameter stenosis 46·9% [SD 15·9]). Highly lipidic lesions (851 [24%] of 3500 lesions, present in 520 [59%] of 884 patients) were an independent predictor of patient-level non-culprit lesion-related MACEs (adjusted odds ratio 2·27, 95% CI 1·25–4·13) and non-culprit lesion-specific MACEs (7·83, 4·12–14·89). Large plaque burden (787 [22%] of 3629 lesions, present in 530 [59%] of 898 patients) was also an independent predictor of non-culprit lesion-related MACEs. Lesions with both large plaque burden by intravascular ultrasound and large lipid-rich cores by NIRS had a 4-year non-culprit lesion-related MACE rate of 7·0% (95% CI 4·0–10·0). Patients in whom one or more such lesions were identified had a 4-year non-culprit lesion-related MACE rate of 13·2% (95% CI 9·4–17·6).InterpretationCombined NIRS and intravascular ultrasound detects angiographically non-obstructive lesions with a high lipid content and large plaque burden that are at increased risk for future adverse cardiac outcomes.FundingAbbott Vascular, Infraredx, and The Medicines Company.

Dr. Robert A. Kloner from the University of Southern California, and the Heart Institute of Good Samaritan Hospital, Los Angeles moderated the topic Triggers for Cardiovascular Events with Drs. Murray Mittleman from Beth Israel Deaconess Medical Center and Harvard Medical School, James Muller from InfraReDx, Inc., and Peter H. Stone from Brigham and Women's Hospital and Harvard Medical School. The discussion focused primarily on: (1) acute risk factors as a trigger for heart disease; (2) short term physiologic factors such as a surge in arterial pressure and/or heart rate, an increase in coagulability, or vasoconstriction; (3) other triggers such as lack of sleep or overeating; (4) population stressors such as earthquakes, floods and industrial accidents; (5) psychological triggers such as anxiety, depression, frustration, anger, and bereavement; (6) chemical triggers such as cocaine and marijuana; (7) physical triggers such as moderate physical activity and sexual activity; (8) environmental exposure such as air pollution and exposure to heavy metals; (9) the rupture of vulnerable plaques and detection methods; and (10) pharmacologic approaches as a part of routine prevention (Med Roundtable Cardiovasc Ed. 2012;3(1):45-54) ©2012 FoxP2 Media, LLC

Atherosclerotic plaques prone to rupture may cause acute myocardial infarction (MI) but can also heal without causing an event. Certain common histopathological features, including inflammation, a thin fibrous cap, positive remodelling, a large necrotic core, microcalcification, and plaque haemorrhage are commonly found in plaques causing an acute event. Recent advances in imaging techniques have made it possible to detect not only luminal stenosis and overall coronary atherosclerosis burden but also to identify such adverse plaque characteristics. However, the predictive value of identifying individual adverse atherosclerotic plaques for future events has remained poor. In this Position Paper, the relationship between vulnerable plaque imaging and MI is addressed, mainly for non-invasive assessments but also for invasive imaging of adverse plaques in patients undergoing invasive coronary angiography. Dynamic changes in atherosclerotic plaque development and composition may indicate that an adverse plaque phenotype should be considered at the patient level rather than for individual plaques. Imaging of adverse plaque burden throughout the coronary vascular tree, in combination with biomarkers and biomechanical parameters, therefore holds promise for identifying subjects at increased risk of MI and for guiding medical and invasive treatment.

BACKGROUND Autopsy studies suggest that implanting stents in lipid-rich plaque (LRP) may be associated with adverse outcomes. OBJECTIVES The purpose of this study was to evaluate the association between LRP detected by near-infrared spectroscopy (NIRS) and clinical outcomes in patients with coronary artery disease treated with contemporary drug-eluting stents. METHODS In this prospective, multicenter registry, NIRS was performed in patients undergoing coronary angiography and possible percutaneous coronary intervention (PCI). Lipid core burden index (LCBI) was calculated as the fraction of pixels with the probability of LRP >0.6 within a region of interest. MaxLCBI(4mm) was defined as the maximum LCBI within any 4-mm-tong segment. Major adverse cardiac events (MACE) included cardiac death, myocardial infarction, definite or probable stent thrombosis, or unplanned revascularization or rehospitalization for progressive angina or unstable angina. Events were subcategorized as culprit (treated) lesion-related, nonculprit (untreated) lesion-related, or indeterminate. RESULTS Among 1,999 patients who were enrolled in the COLOR (Chemometric Observations of Lipid Core Plaques of Interest in Native Coronary Arteries Registry), PCI was performed in 1,621 patients and MACE occurred in 18.0% of patients, of which 8.3% were culprit lesion-related, 10.7% were nonculprit lesion-related, and 31% were indeterminate during 2-year follow-up. Complications from NIRS imaging occurred in 9 patients (0.45%), which resulted in 1 peri-procedural myocardial infarction and 1 emergent coronary bypass. Pre-PCI NIRS imaging was obtained in 1,189 patients, and the 2-year rate of culprit lesion-related MACE was not significantly associated with maxLCBI(4mm) (hazard ratio of maxLCBI(4mm) per 100: 1.06; 95% confidence interval: 0.96 to 1.17; p = 0.28) after adjusting clinical and procedural factors. CONCLUSIONS Following PCI with contemporary drug-eluting stents, stent implantation in NIRS-defined LRPs was not associated with increased periprocedural or late adverse outcomes compared with those without significant lipid. (C) 2020 by the American College of Cardiology Foundation.

Immunity to fungal infections is mediated by cells of the innate and adaptive immune system including Th17 cells. Ca(2+)influx in immune cells is regulated by stromal interaction molecule 1 (STIM1) and its activation of the Ca(2+)channelORAI1. We here identify patients with a novel mutation inSTIM1 (p.L374P) that abolished Ca(2+)influx and resulted in increased susceptibility to fungal and other infections. In mice, deletion ofSTIM1 in all immune cells enhanced susceptibility to mucosalC. albicansinfection, whereas T cell-specific deletion ofSTIM1 impaired immunity to systemicC. albicansinfection.STIM1 deletion impaired the production of Th17 cytokines essential for antifungal immunity and compromised the expression of genes in several metabolic pathways including Foxo andHIF1 alpha signaling that regulate glycolysis and oxidative phosphorylation (OXPHOS). Our study further revealed distinct roles ofSTIM1 in regulating transcription and metabolic programs in non-pathogenic Th17 cells compared to pathogenic, proinflammatory Th17 cells, a finding that may potentially be exploited for the treatment of Th17 cell-mediated inflammatory diseases.

Tobacco consumption (predominantly cigarettes) is the leading preventable cause of mortality worldwide. Although the major focus of strategies to reduce mortality from tobacco must include prevention of future generations from initially gaining access, some smokers are unwilling or unable to quit. Can the higher risk chronic smoker be identified and can their risk be reduced? The risk of adverse events in cigarette smokers is influenced by the intensity and duration of cigarette smoking or secondhand exposure, associated conventional risk factors, environmental stressors, and certain genetic variants and epigenetic modifiers. Recent data suggest that inflammatory markers such as high-sensitivity C-reactive protein (hs CRP) and targeted imaging can identify some smokers at higher risk. As smoking is prothrombotic, aspirin initiation and expanded statin use might reduce cardiovascular risk in those who do not presently meet criteria for these therapies, but further study is required. Thus, although advocacy for smoking cessation should always be the primary approach, increased efforts are needed to identify and potentially treat those who are unable or unwilling to quit.

OBJECTIVE:Inform coronavirus disease 2019 (COVID-19) infection prevention measures by identifying and assessing risk and possible vectors of infection in nursing homes (NHs) using a machine-learning approach.DESIGN:This retrospective cohort study used a gradient boosting algorithm to evaluate risk of COVID-19 infection (ie, presence of at least 1 confirmed COVID-19 resident) in NHs.SETTING AND PARTICIPANTS:The model was trained on outcomes from 1146 NHs in Massachusetts, Georgia, and New Jersey, reporting COVID-19 case data on April 20, 2020. Risk indices generated from the model using data from May 4 were prospectively validated against outcomes reported on May 11 from 1021 NHs in California.METHODS:Model features, pertaining to facility and community characteristics, were obtained from a self-constructed dataset based on multiple public and private sources. The model was assessed via out-of-sample area under the receiver operating characteristic curve (AUC), sensitivity, and specificity in the training (via 10-fold cross-validation) and validation datasets.RESULTS:The mean AUC, sensitivity, and specificity of the model over 10-fold cross-validation were 0.729 [95% confidence interval (CI) 0.690‒0.767], 0.670 (95% CI 0.477‒0.862), and 0.611 (95% CI 0.412‒0.809), respectively. Prospective out-of-sample validation yielded similar performance measures (AUC 0.721; sensitivity 0.622; specificity 0.713). The strongest predictors of COVID-19 infection were identified as the NH's county's infection rate and the number of separate units in the NH; other predictors included the county's population density, historical Centers of Medicare and Medicaid Services cited health deficiencies, and the NH's resident density (in persons per 1000 square feet). In addition, the NH's historical percentage of non-Hispanic white residents was identified as a protective factor.CONCLUSIONS AND IMPLICATIONS:A machine-learning model can help quantify and predict NH infection risk. The identified risk factors support the early identification and management of presymptomatic and asymptomatic individuals (eg, staff) entering the NH from the surrounding community and the development of financially sustainable staff testing initiatives in preventing COVID-19 infection.

A combination optical coherence tomography and near-infrared spectroscopy (OCT-NIRS) coronary imaging system is being developed to improve the care of coronary patients. While stenting has improved, complications continue to occur at the stented site and new events are caused by unrecognized vulnerable plaques. An OCT-NIRS device has potential to improve secondary prevention by optimizing stenting and by identifying vulnerable patients and vulnerable plaques. OCT is already in widespread use world-wide to optimize coronary artery stenting. It provides automated lumen detection and can identify features of coronary plaques not accurately identified by angiography or intravascular ultrasound. The ILUMIEN IV study, to be completed in 2022, will determine if OCT-guided stenting will yield better clinical outcomes than angiographic guidance alone. While the superb spatial resolution of OCT enables the identification of many plaque structural features, the detection by OCT of lipids, an important component of vulnerable plaques, is limited by suboptimal specificity and interobserver agreement. In contrast, NIRS has been extensively validated for lipid-rich plaque detection against the gold-standard of histology and is the only FDA-approved method to identify coronary lipids. Studies in patients have demonstrated that NIRS detects lipid in culprit lesions causing coronary events. In 2019, the positive results of the prospective Lipid-Rich Plaque Study led to FDA approval of NIRS for detection of high-risk plaques and patients. The complementarity of OCT for plaque structure and NIRS for plaque composition led to the sequential performance of NIRS and OCT imaging in patients. NIRS identified lipid while OCT determined the thickness of the cap over the lipid pool. The positive results obtained with OCT and NIRS imaging led to development of a prototype combined OCT-NIRS catheter that can provide co-registered OCT and NIRS data in a single pullback. The data will provide structural and chemical information likely to improve stenting and deliver more accurate identification of vulnerable plaques and vulnerable patients. More precise diagnosis will then lead to OCT-NIRS guided treatment trials to improve secondary prevention. Success in secondary prevention will then facilitate development of improved primary prevention with invasive imaging and effective treatment of patients identified by non-invasive methods.

Despite advanced understanding of the biology of atherosclerosis, coronary heart disease remains the leading cause of death worldwide. Progress has been challenging as half of the individuals who suffer sudden cardiac death do not experience premonitory symptoms. Furthermore, it is well-recognized that also a plaque that does not cause a haemodynamically significant stenosis can trigger a sudden cardiac event, yet the majority of ruptured or eroded plaques remain clinically silent. In the past 30 years since the term vulnerable plaque was introduced, there have been major advances in the understanding of plaque pathogenesis and pathophysiology, shifting from pursuing features of vulnerability of a specific lesion to the more comprehensive goal of identifying patient cardiovascular vulnerability. It has been also recognized that aside a thin-capped, lipid-rich plaque associated with plaque rupture, acute coronary syndromes (ACS) are also caused by plaque erosion underlying between 25% and 60% of ACS nowadays, by calcified nodule or by functional coronary alterations. While there have been advances in preventive strategies and in pharmacotherapy, with improved agents to reduce cholesterol, thrombosis, and inflammation, events continue to occur in patients receiving optimal medical treatment. Although at present the positive predictive value of imaging precursors of the culprit plaques remains too low for clinical relevance, improving coronary plaque imaging may be instrumental in guiding pharmacotherapy intensity and could facilitate optimal allocation of novel, more aggressive, and costly treatment strategies. Recent technical and diagnostic advances justify continuation of interdisciplinary research efforts to improve cardiovascular prognosis by both systemic and local diagnostics and therapies. The present state-of-the-art document aims to present and critically appraise the latest evidence, developments, and future perspectives in detection, prevention, and treatment of high-risk plaques occurring in vulnerable patients.

The COVID-19 pandemic teaches lessons we must embrace to overcome two additional existential threats: nuclear war and global warming. Health professionals need to send a message to those whose lives we have vowed to protect: all three threats result from forces of nature made dangerous by triumphs of human intelligence, and all three can be solved by human intelligence.1Ghinai I McPherson TD Hunter JC et al.First known person-to-person transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the USA.Lancet. 2020; 395: 1137-1144Summary Full Text Full Text PDF PubMed Scopus (374) Google Scholar, 2Ervin RR Glazier JB Aronow S et al.Human and ecologic effects in Massachusetts of an assumed thermonuclear attack on the United States.N Engl J Med. 1962; 266: 1127-1137Crossref PubMed Scopus (38) Google Scholar, 3Lown B Chivian E Muller J Abrams H The nuclear-arms race and the physician.N Engl J Med. 1981; 304: 726-729Crossref PubMed Scopus (32) Google Scholar, 4Abrams HL Inadvertent nuclear war.Lancet. 1988; 2: 559-560Abstract PubMed Scopus (1) Google Scholar, 5Watts N Amann M Arnell N et al.The 2019 report of The Lancet Countdown on health and climate change: ensuring that the health of a child born today is not defined by a changing climate.Lancet. 2019; 394: 1836-1878Summary Full Text Full Text PDF PubMed Scopus (877) Google Scholar Albert Einstein warned that "the unleashed power of the atom has changed everything save our modes of thinking and we thus drift toward unparalleled catastrophe".6The New York Times ArchivesThe Einstein letter that started it all; a message to President Roosevelt 25 years ago launched the atom bomb and the atomic age.https://www.nytimes.com/1964/08/02/archives/the-einstein-letter-that-started-it-all-a-message-to-president.htmlDate: Aug 2, 1964Date accessed: June 10, 2020Google Scholar The nuclear threat plus global warming led the Bulletin of the Atomic Scientists to advance the Doomsday Clock to 100 seconds before midnight—the closest ever—just before the pandemic. Although it may seem overwhelming to contemplate additional threats during COVID-19, we must address all three since they are the greatest dangers ahead. Their origins and solutions are remarkably similar. COVID-19 is the most visible. Had the outbreak happened before air travel, the mutant virus would have remained in China and spread slowly, if at all. Today, we face a permanent threat of future pandemics—genes will continue to mutate and planes will continue to fly. Nuclear war is the least visible threat, as well hidden as the virus of a bat in a cave near Wuhan. It is, however, the most likely to have an immediate, devastating impact. In a city hit with a nuclear weapon, by intent or by accident, there would be no decisions about which patient to treat with the remaining ventilator.2Ervin RR Glazier JB Aronow S et al.Human and ecologic effects in Massachusetts of an assumed thermonuclear attack on the United States.N Engl J Med. 1962; 266: 1127-1137Crossref PubMed Scopus (38) Google Scholar, 3Lown B Chivian E Muller J Abrams H The nuclear-arms race and the physician.N Engl J Med. 1981; 304: 726-729Crossref PubMed Scopus (32) Google Scholar, 4Abrams HL Inadvertent nuclear war.Lancet. 1988; 2: 559-560Abstract PubMed Scopus (1) Google Scholar Global warming is the threat most certain to generate future harm, although human suffering will spread more slowly than with nuclear war or a pandemic.5Watts N Amann M Arnell N et al.The 2019 report of The Lancet Countdown on health and climate change: ensuring that the health of a child born today is not defined by a changing climate.Lancet. 2019; 394: 1836-1878Summary Full Text Full Text PDF PubMed Scopus (877) Google Scholar The global response to COVID-19 is a source of hope. Scientists launched an inspiring counterattack on the coronavirus. Clinicians, often risking their own lives, rushed to bedsides. The struggles against these threats teach valuable lessons. First, each threat must be recognised. Second, political leaders must respect truth and defer to expertise. Third, the threats are global and require global cooperation. Fourth, we all have to focus on our collective survival, and that includes care for the least privileged. The world need not be the same after the pandemic. It can be better. A COVID-19-induced awakening can arrest our drift toward catastrophe. Health professionals, uniquely aware of the threats, have an obligation to enhance understanding of the requirements for survival in the 21st century. JEM is a co-founder of International Physicians for Prevention of Nuclear War, the organisation awarded the 1985 Nobel Peace Prize. DGN is a co-founder of Physicians for Social Responsibility. We declare no competing interests.

HomeCirculationVol. 139, No. 23Cardiac Events and Nuclear War Free AccessArticle CommentaryPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessArticle CommentaryPDF/EPUBCardiac Events and Nuclear WarPrevention by Cardiovascular Specialists James E. Muller, MD, John O. Pastore, MD and Amir Lerman, MD James E. MullerJames E. Muller James E. Muller, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. Email E-mail Address: [email protected] Brigham and Women's Hospital, Boston, MA (J.E.M.). IPPNW, Maldern, MA (J.E.M.). , John O. PastoreJohn O. Pastore Steward Health Care, Boston, MA (J.O.P.). and Amir LermanAmir Lerman Mayo Clinic, Rochester, MN (A.L.). Originally published3 Jun 2019https://doi.org/10.1161/CIRCULATIONAHA.119.039882Circulation. 2019;139:2597–2599The Bulletin of the Atomic Scientists warns that humanity faces 2 existential threats: global warming and nuclear destruction. Either could unleash unparalleled human suffering and possibly end civilization. Cardiologists, who are trained in prevention, have played a major role in addressing the second of these dual threats: the danger posed by nuclear weapons. During the Cold War, cooperative action by Soviet and American cardiologists helped reduce this threat, permitting subsequent generations to grow up without the fear of a nuclear disaster. But the nuclear threat, a permanent problem facing humanity, has risen again. Young cardiologists and their more senior colleagues are needed to meet this ongoing preventive challenge.Cardiologists at the ForefrontThe cardiovascular events we work to prevent—sudden cardiac death, myocardial infarction, rupture of an aneurysm, stent thrombosis, and stroke—are low-probability, high-consequence negative events. These catastrophic occurrences threaten our patients in much the same way that nuclear war threatens humanity. This similarity is the likely reason that cardiologists played a major role in reducing nuclear risk during the Cold War.Our colleagues in physics alert us to the degree of nuclear threat by moving the hands on the Doomsday Clock of the Bulletin of the Atomic Scientists. In 2018, they moved the hands forward to 2 minutes before midnight, the closest to disaster since 1953 when the Soviets developed a hydrogen bomb, creating the threat of a war between nuclear-armed states. The physicists attribute the current increase in nuclear risk to proliferation to 9 nations, terrorism, the increased complexity of the computer systems governing the weapons, the threat of nuclear war between North Korea and the United States, and the possible end of the United States–Russia Intermediate Nuclear Weapons treaty.Peaks in risk occur at times of national conflict and when nuclear war–fighting ideas are not counterbalanced by public opposition. As in the 1980s, the concept that a "limited" nuclear war could be won has entered the thinking of government leaders, and a new, costly United States–Russia nuclear arms race is underway.It can be argued that nuclear weapons policy is best managed by governmental leaders, leaving little role for the individual, let alone a special role for cardiovascular professionals. But cardiologists have made major contributions to reducing prior nuclear threats. In the 1960s, as the Cold War limited peaceful contacts, Dr Paul Dudley White worked closely with Dr Alexander Myasnikov to build a United States–Russia medical bridge to decrease tensions. In 1962, Dr Bernard Lown, Dr Sidney Alexander, and colleagues alerted the public to the medical consequences of the use of nuclear weapons. At the height of the Cold War, cardiologists played a major role by founding International Physicians for Prevention of Nuclear War. This work included a televised discussion from Moscow organized by Dr Eugene Chazov in 1982 in which 3 Russian and 3 US physicians spoke against the arms race to millions of Russians and Americans. Four of the 6 physicians in the video were cardiologists.The Nobel Committee awarded the 1985 Nobel Peace Prize to the International Physicians for Prevention of Nuclear War. The committee recognized the ability of physicians to help the public visualize threats and to communicate complex scientific issues in understandable terms. Since 1985, the number of nuclear weapons worldwide has decreased from >60 000 to ≈15 000. In 2007, the International Physicians for Prevention of Nuclear War cofounded the International Campaign to Abolish Nuclear Weapons, which won the 2017 Nobel Peace Prize.Although cardiac risk may be low in any given year, cardiologists act on the basis of cumulative risk over a decade or a lifetime. For the nuclear threat, which has a low annual risk, we must think in terms of the lifetime of humanity. A 1% annual risk of nuclear war, started by intention or by accident, rises to a 50% risk over a 70-year period.Prevention of cardiac events in most cases requires a change in behavior: cessation of smoking, taking medications for hypertension, weight loss. For the nuclear threat, Einstein stated that the prevention of nuclear war also requires a difficult change in high-risk and potentially modifiable behavior. We must recognize that in the nuclear era destructive force can no longer be the ultimate guarantor of security. Paradoxically, at moments of greatest danger, when the threat is most visible, the possibility of change is greatest—a linkage familiar to cardiologists when a lifelong smoker quits after having a heart attack.Reducing the Nuclear Threat in the 21st CenturyThe nuclear threat has waxed and waned over the decades (Figure). Nuclear risk, which began with the first nuclear explosion in 1945 in Alamogordo, NM, peaked with the Soviet hydrogen bomb, the Cuban Missile Crisis in 1962, and the Cold War in the 1980s. In 2017, Presidents Trump and Kim Jong Un exchanged threats of nuclear war and accurately described the devastation that would ensue. Their rhetoric broke through the widespread denial of the problem and alerted younger generations of the nuclear threat.Download figureDownload PowerPointFigure. Nuclear risk over decades. An historical summary of the estimation of nuclear risk depicted by the Doomsday Clock of the Bulletin of the Atomic Scientists from 1947 to 2017. The extreme risk experienced in 1962 during the Cuban Missile Crisis is not shown because it emerged and was resolved in the interval between settings of the clock.1 US indicates United States; and USSR, Union of Soviet Socialist Republics. Figure prepared by Noy Kaufman and James Muller, MD.Health professionals can make the unimaginable imaginable (and hence preventable), alerting the public to the chance of an accidental nuclear war and educating about the cumulative probability aspect of the threat. Now, professionals of the 21st century and beyond are needed in the struggle for survival in the nuclear era. Many college-aged students are now aware of the problem, contributing youthful energy to the successful effort by International Campaign to Abolish Nuclear Weapons to obtain a United Nations vote in favor of the Treaty on the Prohibition of Nuclear Weapons.For health professionals new to the nuclear threat, an excellent introductory book is The Seventh Decade: The New Shape of Nuclear Danger by Jonathan Schell.2 For those already committed to action, there are many ways through which to contribute: International Physicians for the Prevention of Nuclear War, Physicians for Social Responsibility, and International Campaign to Abolish Nuclear Weapons.The campaign titled Back From the Brink3 is advocating 5 steps to reduce the threat:Renounce the first use of nuclear weapons;End the sole, unchecked authority of any president to launch a nuclear attack;Take US nuclear weapons off hair-trigger alert;Cancel the trillion-dollar program to build replacement weapons with enhanced capabilities; and,Pursue an agreement with nuclear-armed states to eliminate all nuclear weapons.Although the nuclear threat to the life and health of humanity is terrible to contemplate, it is an artificial threat created by human ingenuity. We must now harness the ingenuity that brought us 21st century medical science to reduce nuclear danger. With an energetic, worldwide educational effort by health professionals on the nuclear threat, we can join our colleagues in moving the hands of the Doomsday Clock back from the midnight hour.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.James E. Muller, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. Email james.[email protected]comReferences1. Bulletin of the Atomic Scientists. Doomsday Clock: timeline.2019. https://thebulletin.org/doomsday-clock/past-announcements/. Accessed March 13, 2019.Google Scholar2. Schell J. The Seventh Decade: The New Shape of Nuclear Danger. New York, NY: Henry Holt Publishers; 2007.Google Scholar3. Back from the brink: the call to prevent nuclear war. 2018. https://www.preventnuclearwar.org. Accessed March 13, 2019.Google Scholar Previous Back to top Next FiguresReferencesRelatedDetails June 4, 2019Vol 139, Issue 23 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.119.039882PMID: 31158002 Originally publishedJune 3, 2019 Keywordsnuclear warcardiovascular specialistspreventioncardiologistsPDF download Advertisement