Introduction: From the initial report of intraoperative radiofrequency (RF) ablation causing esophageal injury,GIL01 atrioesophageal fistulas (AEF) have been reported in percutaneous atrial fibrillation RF ablations.SCA04,PAP04 Atrioesophageal fistulas have been estimated to occur in as many as 1% of AF ablationsDOL03 but a likely accepted event rate is less than 0.1%.PAP04,SCA04,CUM06 The mortality associated with AEF is devastating and was found to approach 100% in the largest published registry of AEF.CUM06 This is in stark contrast to a near zero death rate of atrial perforations during RF ablation.BUN05 An article by Müller et al (http://www.heartrhythmjournal.com/article/S1547-5271(15)00418-X/abstract) examined the high incidence of esophageal lesions after atrial fibrillation ablations related to the use of esophageal temperature probes. Multivariate analysis revealed the use of the temperature probe was the only independent predictor of esophageal lesions. Finally, data in Heart Rhythm examined the rate of atrioesophageal fistula formation with contact force (CF) sensing catheters versus non-CF-sensing catheters. Black-Maier et al found the “occurrence of atrioesophageal fistula formation accounted for a 5-fold higher proportion of all MAUDE medical device reports of injury or death with CF-sensing catheters compared with non-CF-sensing catheters.”

Value of Imaging: The value of intracardiac imaging via radial intracardiac echo (ICE) cannot be underestimated given the nonuniform thickness and variable course along the posterior wall of the left atrium.SAN05,GOO05,REN06 The proximity of the esophagus to the left pulmonary venous antrum is depicted in Figure 1. Typically, patients with AEF present a mean of 12.3days after their procedure;CUM06 however, presentation within 3-5days of the ablation has been reported.PAP04 Findings on CT scans can be non-specific but, infected pleural and pericardial effusions may suggest esophageal contamination of the pleural spaces. CT scan of the chest (without oral contrast) with the presence of intravenous contrast seen in the esophagus or surrounding posterior mediastinum would imply a fistulous connection.MAL07 Additionally, one may note a narrowed, irregular, and ulcerated pulmonary vein, posterior left atrial wall thickening, posterior mediastinal fat induration, or pneumomediastinum.MAL07

Imaging Demonstrated Proximity of Esophagus to Left Pulmonary Veins. The top left inset of the figure depicts the 3D reconstruction of the left atrium and pulmonary veins with the esophagus tagged in red. The course of the esophagus is along the posterior left atrium in contiguity to the left pulmonary vestibule. The ICE image of the left pulmonary vestibule shows the characteristic echocardiographic signature of an esophageal temperature probe in the 8 o’clock position.
Imaging Demonstrated Proximity of Esophagus to Left Pulmonary Veins. The top left inset of the figure depicts the 3D reconstruction of the left atrium and pulmonary veins with the esophagus tagged in red. The course of the esophagus is along the posterior left atrium in contiguity to the left pulmonary vestibule. The ICE image of the left pulmonary vestibule shows the characteristic echocardiographic signature of an esophageal temperature probe in the 8 o’clock position.

Mechanism of Esophageal Injury: Finite-element analysis supports that esophageal injury is exclusively due to thermal conduction from the atrium.BER05 Esophageal injury can occur despite small electrode size, low power (<30W), and low electrode temperature (34°C). There are two caveats however, irrigated electrodes and electrode-endocardial contact verification (direct visualization with ICE or force-sensing) may increase power delivery to the tissue.

Avoiding Esophageal Injury: There has been much enthusiasm to determine means by which esophageal injury can be avoided. These include echocardiographic monitoring for microbubble formation,CUM05 the use of cryoablation to lower esophageal ulceration,RIP07 plan ablations to avoid esophagus by creating virtual esophageal tube using electroanatomic mapping,SHE07 esophageal irrigation to lower esophageal temperature,TSU07 and physically deflecting the esophagus away from the ablation site.HER06 The study by Muller et alMUL15 suggests the possibility that esophageal temperature probes may increase susceptibility to esophageal lesions. Figure 2 shows ICE images before and after orogastric tube removal. One notes the signature of the OGT at 8 o’clock in the left image. There is a small indentation in the posterior left atrial wall at the site of the OGT. On the right, imaging demonstrates this indentation is resolved after removal of the OGT. I will often remove esophageal instrumentation to avoid any possible displacement of the esophagus towards the left atrium.

Intracardiac Echocardiography (ICE) of Orogastric Tube (OGT). The left image depicts the ICE signature of the OGT at ~8 o’clock. There is a small indentation in the posterior left atrial wall at the site of the OGT. On the right, ICE demonstrates the resolution of this indentation after removal of the OGT.
Intracardiac Echocardiography (ICE) of Orogastric Tube (OGT). The left image depicts the ICE signature of the OGT at ~8 o’clock. There is a small indentation in the posterior left atrial wall at the site of the OGT. On the right, ICE demonstrates the resolution of this indentation after removal of the OGT.

CF-sensing catheters have certainly enhanced ability to deliver more consistent lesions however, there are clearly limitations when the operator cannot see real-time electrode-endocardial contact. There have been many times where I have seen left and right atrial tenting due to catheter contact at less than 10g of force. Force sensing has certainly added to our armamentarium but I would caution all that there is more to ablation than contact force.

Note:  These radial ICE images would not be possible without my mentor, Dr. David Schwartzman (Pittsburgh, PA).

REFERENCES:

GIL01  Gillinov AM, Pettersson G, Rice TW, “Esophageal injury during radiofrequency ablation for atrial fibrillation,” J Thor Card Surg, V. 122, No. 6 (December 2001), pp. 1239-1240.

SCA04  Scanavacca MI, D’Avila A, Parga J, Sosa E, “Left Atrial-Esophageal Fistula Following Radiofrequency Catheter Ablation of Atrial Fibrillation,” J Cardiovasc Electrophysiol, V. 15, No. 8 (August 2004), pp. 960-962.

PAP04  Pappone C, Oral H, Santinella V, Vicedomini G, Lang CC, Manguso F, Torracca L, Benussi S, Alfieri O, Hong R, Lau W, Hirata K, Shikuma N, Hall B, Morady F, “Atrio-Esophageal Fistula as a Complication of Percutaneous Transcatheter Ablation of Atrial Fibrillation,” Circulation, V. 109 (June 8, 2004), pp. 2724-2726.

DOL03  Doll N, Borger MA, Fabricius A, Stephan S, Gummert J, Mohr FW, Hauss J, Kottkamp H, Hindricks G, “Esophageal perforation during left atrial radiofrequency ablation: Is the risk too high?” J Thor Cardiovasc Surg, V. 125, No. 4 (April 2003), pp. 836-842.

CUM06  Cummings JE, Schweikert RA, Saliba WI, Burkhardt D, Kilikaslan F, Saad E, Natale A, “Brief Communication: Atrial-Esophageal Fistulas after Radiofrequency Ablation,” Ann Int Med, V. 144, No. 8 (18 April 2006), pp. 572-574.

BUN05  Bunch TJ, Asirvatham SJ, Friedman PA, Monahan KH, Munger TM, Rea RF, Sinak LJ, Packer DL, “Outcomes After Cardiac Perforation During Radiofrequency Ablation of the Atrium,” J Cardiovasc Electrophysiol, V. 16, No. 11 (November 2005), pp. 1172-1179.

SCH06  Schwartzman DS, Nosbisch J, and Housel Debra, “Echocardiographically guided left atrial ablation: Characterization of a new technique,” Heart Rhythm, V. 3, No. 8 (August 2006), pp. 930 –938.

SAN05  Sanchez-Quintana D, Cabrera JA, Climent V, Farre J, de Mendonca MC, Ho SY, “Anatomic Relations Between the Esophagus and Left Atrium and Relevance for Ablation of Atrial Fibrillation,” Circulation, V. 112 (September 6, 2005), pp. 1400-1405.

GOO05  Good E, Oral H, Lemola K, Han J, Tamirisa K, Igic P, Elmouchi D, Tschopp D, Reich S, Chugh A, Bogun F, Pelosi F Jr, Morady F, “Movement of the Esophagus During Left Atrial Catheter Ablation for Atrial Fibrillation,” JACC, V. 46, No. 11 (December 6, 2005), pp. 2107-21190.

REN06  Ren J-F, Lin D, Marchlinski FE, Callans DJ, Patel V, “Esophageal imaging and strategies for avoiding injury during left atrial ablation for atrial fibrillation,” Heart Rhythm, V. 3, No. 10 (October 2006), pp. 1156-1161.

MAL07  Malamis AP, Kirshenbaum KJ, and Nadimpalli S, “CT Radiographic Findings: Atrio-esophageal Fistula After Transcatheter Percutaneous Ablation of Atrial Fibrillation,” J Thorac Imaging, V. 22, No. 2 (May 2007), pp. 188-191.

BER05  Berjano EJ and Hornero F, “What affects esophageal injury during radiofrequency ablation of the left atrium? An engineering study based on finite-element analysis,” Physiol Meas, V. 26 (2005), pp. 837-848.

CUM05  Cummings JE, Schweikert RA, Saliba WI, Burkhardt JD, Brachmann J, Gunther J, Schibgilla V, Verma A, Dery MA, Drago JL, Kilicaslan F, Natale A, “Assessment of Temperature, Proximity, and Course of the Esophagus During Radiofrequency Ablation Within the Left Atrium,” Circulation, V. 112 (July 26, 2005), pp. 459-464.

RIP07  Ripley KL, Gage AA, Olsen DB, Van Vleet JF, Lau C-P, Tse H-F, “Time Course of Esophageal Lesions After Catheter Ablation with Cryothermal and Radiofrequency Ablation: Implication for Atrio-Esophageal Fistula Formation After Catheter Ablation for Atrial Fibrillation,” J Cardiovasc Electrophysiol, V. 18, No. 6 (June 2006), pp. 642-646.

SHE07  Sherzer AI, Feigenblum DY, Kulkarni S, Pina JW, Casey JL, Salka KA, Simons GR, “Continuous Nonfluoroscopic Localization of the Esophagus During Radiofrequency Catheter Ablation of Atrial Fibrillation,” J Cardiovasc Electrophysiol, V. 18, No. 2 (February 2007), pp. 157-160.

TSU07  Tsuchiya T, Ashikaga K, Nakagawa S, Hayashida K, Kugimiya H, “Atrial Fibrillation Ablation with Esophageal Cooling with a Cooled Water-Irrigated Intraesophageal Balloon: A Pilot Study,” J Cardiovasc Electrophysiol, V. 18, No. 2 (February 2007), pp. 145-150.

HER06  Herweg B, Johnson N, Postler G, Curtis AB, Barold SS, Ilercil A, “Mechanical Esophageal Deflection During Ablation of Atrial Fibrillation,” PACE, V. 29 (September 2006), pp. 957-961.

MUL15  Müller P, Dietrich J-W, Halbfass P, Abouarab A, Fochler F, Szöllösi A, Nentwich K, Roos M, Krug J, Schade A, Mügge A, Deneke T, “Higher incidence of esophageal lesions after AF ablation related to the use of esophageal temperature probes,” Heart Rhythm, Published Online: April 03, 2015.

Starting 2021 with new paper! Looking at longevity of 2.1Ah biventricular defibrillators (CRT-D) and perhaps help explain high rate of complications when patients need to undergo generator changes for battery depletion. More research is needed to examine the clinical and cost effectiveness of avoiding generator changes during a vulnerable physiologic time in the lives of CRT-D patients.

2.1Ah biventricular defibrillator (CRT-D) battery longevity exceeds patient survival in HFrEF patient cohort.

Key Points:

  • These data demonstrated the first reversal in ICD battery longevity versus patient survival; the 2.1-Ah ICD battery life exceeded patient survival in a typical HFrEF cohort.
  • Our results support the hypothesis that the acceleration of device OOS during the sixth to ninth years (when it is expected that roughly 98% of 1.0-Ah and 1.4-Ah CRT-D systems reach ERI) may explain the historically high rate of complications for ICD generator changes as compared with at the initial implantation.
  • During the entire study, only 5.7% of 2.1Ah devices reached the ERI point (average time to ERI: 7.8 ±1.5 years) in up to 10.3 years of follow-up.

Read full manuscript at Journal of Innovations in Cardiac Rhythm Management.

Welcome to the 4th Annual Lakeland Regional Health Cardiovascular Symposium. Tired of CV Symposiums that focus on the procedures that can be done to your patients rather than prevention of CV disease?!? This year we’ll be focusing on the PREVENTION of CV disease. Please click to attend the Symposium for 5.5 hours of free CME on Saturday February 8, 2020. I’ll be adding links to any talks the speaker has permitted so you can follow along on day of Symposium.

7:30 – 7:55A Registration and Continental Breakfast
7:55 – 8:00A Welcome Remarks
8:00 – 8:40A: Lipid management and risk panels for cardiovascular disease, Dr. Stephen Kopecky


8:40 – 9:30A: Prevention of Sudden Cardiac Death, Williams


9:30 – 10:00A: Prevention of Cardioembolic Stroke, Dr. Khanna


10:00 – 10:20A: Ask-the-Experts Refreshment Break
10:20 – 11:00A: DM2 and CV Disease, Dr. Owen

11:00 – 11:40A: Frequent Touch Primary Care and CV Disease Prevention, Drs. Ghany and Syed

11:40A – 12:20P: Applying Evidence-Based Guidelines to Lower Heart Failure Readmissions, Dr. Navin Rajagopalan


12:20 – 12:30P: Ask-the-Experts Refreshment Break
12:30 – 1:30P: Luncheon, Plant-Based Diets and Prevention of CV Disease, Dr. Monica Aggarwal

Many thanks to the faculty of the 2019 LRH Cardiovascular Symposium! We had over 200 registrants for 6 hours of great cardiovascular CME. From left to right, Dr. Parag Patel (Mayo Clinic), Dr. Anuja Dokras (University of Pennsylvania), Dr. Jeff Williams (LRH), Dr. Carl Pepine (University of Florida), Dr. Edward Tadajweski (WellSpan Health), Dr. Philip Owen (LRH), Dr. Matthew Martinez (Lehigh Valley Health Network), and Dr. Kathryn Lindley (Washington University). Dr. Denise Edwards (University of South Florida) is not pictured.

We had over 200 registrants to this year’s CV Symposium with physicians and nurses traveling from all over Florida. Our faculty was fantastic and their lectures are included below.

Anuja Dokras, MD, PhD, Associate Professor, Penn Fertility Care, University of Pennsylvania Medical Center, Philadelphia, PA. Dr. Dokras lectured about the role of obstetric and gynecologic issues and the future risk of heart disease in women.

Denise Edwards, MD, Director, Healthy Weight Clinic, Assistant Professor of Internal Medicine and Pediatrics, USF Health. Dr. Edwards lectured about the assessment and treatment of obesity in adolescents and women.

Kathryn J. Lindley, MD, Assistant Professor of Medicine, Director, Center for Woman’s Heart Disease, Washington University School of Medicine. Dr. Lindley spoke about the risks of women’s heart disease in pregnancy.

Matthew W Martinez, MD FACC, Associate Professor of Medicine, University of South Florida, Medical Director – Sports Cardiology and Hypertrophic Cardiomyopathy Program, Lehigh Valley Health Network. Dr. Martinez discussed the current state-of-the-art in the management of cardiovascular disease in sports participation.

Phil Owen, MD, FACC, Interventional Cardiology, Lakeland Regional Health. Dr. Owen gave a nice summary on the potential risks and management of CV disease with cancer therapies.

Parag Patel, MD, Mayo Clinic, Program Director for the Advanced Heart Failure/Transplant Fellowship. Dr. Patel described issues and techniques to decrease readmission rates for congestive heart failure.

Carl J Pepine, M.D., MACC, Professor Emeritus of Medicine, University of Florida Health. Dr. Pepine discussed the management of resistant hypertension including common treatment issues.

Edward Tadajweski, MD, FACC, Director of Cardiology, WellSpan Health (Good Samaritan Hospital, Lebanon, PA). Dr. Tadajweski spoke about acute coronary syndromes in women.

Jeffrey L. Williams, MD, MS, FACC, FHRS, Co-Director, LRH Heart Rhythm Center, Course Director, 2019 Lakeland Regional Health Cardiovascular Symposium. Dr. Williams lectured on the diagnosis and treatment of common supraventricular tachycardias.

Join us on February 9, 2019 for 6 hours of free CME. You’ll have the chance to hear topics ranging from acute coronary syndromes and resistant hypertension in women to cardio-oncology as well as management of CHF. We will have speakers from Washington University, Lehigh Valley Health System, WellSpan Health, University of Florida, and others. To register, call 863-687-1190 or online at 2019cvsymposium.eventbrite.com

Atrioventricular nodal tachycardia (AVNRT) is one of the most common supra ventricular tachycardias (SVT) that we find during electrophysiology studies. Fifteen to thirty percent of the population has “dual AV-node physiology.” Most day-to-day conduction is from “fast” AV node pathway. Patients with “dual AV node physiology” may occasional use the “slow” AV node pathway and this can set up the reentrant arrhythmia.

Atrioventricular nodal tachycardia (AVNRT) is one of the most common arrhythmias. This short video gives an introduction to the mechanism and treatment options that are available.

Wondering how you as a doctor or nurse can make a difference? Join us on February 9, 2019 for 6 hours of free CME.

We are excited to have Dr. Denise Edwards (Assistant Professor of Internal Medicine and Pediatrics, Director of the Healthy Weight Clinic at USF Health) speaking about Weight Management in Women and Adolescents. To register, call 863-687-1190 or online at 2019cvsymposium.eventbrite.com


2019 Lakeland Regional Health Cardiovascular Symposium: Special Focus on Women’s and Adolescent Heart Disease

We are excited to have Dr. Anuja Dokras the Director, Penn Polycystic Ovary Syndrome Center speaking about role of obstetric and
gynecologic issues and the future risk of heart disease in women. To register, call 863-687-1190 or online at 2019cvsymposium.eventbrite.com 

A recent publication from the National Center for Health Workforce Analysis  predicted a shortage of 7080 cardiologists by 2025. Another publication reported recruitment incentives for cardiologists are at “unprecedented levels.”   I decided to revisit a paper I published in 2007 (JLW AHHJ 2007) predicting a general cardiology workforce shortage. [1]

I developed this model to project the need for general Cardiologists from 2005-2050 using Matlab (Mathworks, Inc., Natick, MA). The growth in need for General Cardiologists was estimated by incorporating the effect of retirement, prevalence of heart disease, and patient per physician load. At the peak demand in the year 2038, the model projected a need for 62,452 General Cardiologists. Current training durations would result in 29043 General Cardiologists and Fast-Tracking (e.g., third year of Internal Medicine training counted as first year of cardiology) would result in 32533 General Cardiologists. There was evidence of an impending shortage of General Cardiologists that will peak in 2038 resulting in only 46.5% of the projected need for General Cardiologists. This may result from a complex cascade of declining US medical graduates and those matching in Internal Medicine residencies, combined with an increasingly complex cardiovascular disease patient requiring the care of multiple, distinct cardiovascular specialists.

Baseline Data for Modeling the Cardiologist Workforce:

The 35th Bethesda Conference [2] revealed that only 120 of 173 Clinical Cardiac Electrophysiology (EP) spots and 229 of 269 Interventional spots are filled per year.  These baseline partial fill rates were used to assess the effect completely filling these subspecialty fellowship positions would have on overall number of General Cardiologists. In 2001, there were 2160 total trainees and 709 first year fellows.  In the baseline conditions of the model, the number of first year fellows was taken as 709, 2nd year fellows numbered 726, and 3rd year fellows numbered 725.

There are an estimated 6 cardiologists per 100,000 U.S. residents.  This was used as the basis for calculating the number of cardiologists in the US at 16800 in 2005.

Determining Growth in Need for General Cardiologists: 

Effect of Retirement:  I estimated that 10% of Cardiologists would retire by 2015.  Thus, the model uses 1%/year increase in need due to retirement.

Effect of Prevalence of Heart Disease (HD):  Heart disease deaths indicate a need for cardiologists however, prevalence of HD is more important than death in determining workforce requirements.  In this model, it was assumed the prevalence of HD will grow by 1.7%/year until 2030.  As the baby boomer population passes away, the prevalence of HD will decrease by 0.58%/year from 2030-2040 and 0.39%/year from 2040-2050.

Effect of Decreasing Physician-Patient Load:  The average physician’s patient load in cardiovascular medicine declined by over a third from 1980-1995.  There are a higher proportion of patients who require the care of more than one cardiovascular specialist (e.g., a General Cardiologist, Electrophysiologist, Interventionalist, and/or Heart Failure Specialist).    For every 10% decrease in average patient load, 20% more physicians are required. The model uses 2%/year increase in demand due to decreasing physician-patient load.

Effect of Cardiovascular Subspecialty “Fast-Tracking”:  

1.The 8th Working Group of the 35th Bethesda Conference suggested a means to allow a 5-year short-track to train general cardiologists. The trainee would complete 2 years of general internal medicine then 3 years of cardiology.  This short-track would increase the number of general cardiologists, free up more money for additional trainees, and permit trainees to begin paying on student loans.  However, they did not discuss the possibility of “Fast-Tracking” for Interventional or Electrophysiology Fellowships for those who have already completed a 3-year Internal Medicine residency.
2. In this model, “Fast-tracking” would comprise 2 years of a General Cardiology Fellowship then 2 years of either Interventional or Electrophysiology training. This concept of “Fast-Tracking” was incorporated into the model to assess its effect on the General Cardiology Workforce numbers.

Growth in Need for General Cardiologists from 2005-2050 :

Gen Cardiology Workforce Model

Projections of Cardiology Workforce from 2005-2050. This model incorporates a decrease in heart disease prevalence by 0.58%/year from 2030-2040 and 0.39%/year from 2040-2050.  Current training duration (blue line) and Fast-Track (red line) would still result in deficit when compared with model projection of need for General Cardiologists (green line).  At the peak demand in the year 2038, there is a projected need for 62,452 General Cardiologists.  Current training durations would results in 46.5% (n=29043 total cardiologists) the projected need and Fast-Tracking would result in 52.1% the projected need for General Cardiologists (n=32533).

Current training duration (blue line) and Fast-Track (red line) would still result in deficit when compared with model projection of need for General Cardiologists (green line) from 2005-2050.  See Figure.  At the peak demand in the year 2038, current training durations and Fast-Tracking would result in 46.5% (n=29043) and 52.1% (n=32533) the projected need for General Cardiologists. Doubling the number of General Fellows trained and incorporating Fast-Track for EP and Interventional fellows would help offset the predicted shortage in General Cardiologists (green line) by year 2020.  However, this would result in an oversupply in General Cardiologists by the year 2050.

 

How accurate was my model predicting the cardiology workforce as of 2015?

The Association of American Medical Colleges (AAMC) publishes a biannual report on the most current data available about active physicians and physicians in training. [3]  The AAMC estimated 22038 active cardiologists whereas my model predicted 20515 active cardiologists in 2015.  Certainly, care delivery models and market forces (e.g., 2008-2009 recession leading to decreased retirement rates) have affected the cardiology workforce projections.  My estimates of the prevalence of heart disease continue to be accurate. In 2012, The Trust for America’s Health [4] found that at present growth rates “the number of new cases of type 2 diabetes, coronary heart disease and stroke, hypertension and arthritis could increase 10 times between 2010 and 2020—and double again by 2030.”  Finally, it is difficult to get an accurate trend in cardiologist patient loads over time. The recent Medscape Cardiologist Compensation Report 2016 [5] reported that only a quarter of cardiologists have seen an influx of patients due to the Affordable Care Act (ACA) while three-quarters have not.

Is there an impending shortage of general cardiologists? I suspect my model is accurate though has overestimated the shortage of general cardiologists we can expect moving forward. Several reasons included delayed retirement of current cardiologists, the move towards primary-care directed delivery, and the use of physician extenders.  That being said, there have been a host of studies examining the cardiology workforce using a variety of analyses that all point to a shortage of cardiologists moving forward.

It is clearly difficult to place a number on any “shortage” of cardiologists however, there is a common theme to the various studies looking at the future cardiology workforce.  The most recent study [6] reported a shortage of 7080 cardiologists by the year 2025.  “Projections were developed using the Health Resources and Services Administration’s (HRSA) Health Workforce Simulation Model (HWSM), an integrated microsimulation model that estimates current and future supply and demand for health care workers in multiple professions and care settings.” The 2009 American College of Cardiology Board of Trustees Workforce Task Force [7] reported a deficit of 16000 cardiologists by 2025 and best case scenario of 8000 cardiologist deficit with pointed interventions. The CV workforce model I developed estimated a deficit of 17865 general cardiologists by the year 2025.

Summary:

It continues to be reasonable to estimate a general cardiologist shortage by the year 2025. There is consensus of a likely deficit in the general cardiologist workforce using a disparate set of studies including those looking at practice-level demand, prevalence of CV disease, and implications from recruitment incentives for general cardiologists. Regional variation is to be expected but health systems should be cognizant of the likelihood of a general cardiologist shortage in the near- to mid-term.

References:

1  Williams JL, “Projecting the General Cardiology Workforce Shortage,” American Heart Hospital Journal, V. 5 (Fall 2007), pp. 203-209.

2  Fye WB, Hirshfeld JW. Cardiology’s workforce crisis: a pragmatic approach. Presented at the 35th Bethesda Conference, Bethesda, Maryland, October 17–18, 2003. J Am Coll Cardiol 2004;44:215–75.

3  American Association of Medical Colleges, “2016 Physician Specialty Data Report,” Accessed online at https://www.aamc.org/data/workforce/reports/457712/2016-specialty-databook.html.

4  ”F as in Fat: How Obesity Threatens America’s Future”; Trust for America’s Health Issue Report, Sept 2012; Robert Wood Johnson Foundation. Accessed at http://healthyamericans.org/report/100/.

5 Peckham C, “Medscape Cardiologist Compensation Report 2016,” April 1, 2016. Accessed at: https://www.medscape.com/features/slideshow/compensation/2016/cardiology#page=15

6  U.S. Department of Health and Human Services Health Resources and Services Administration Bureau of Health Workforce National Center for Health Workforce Analysis, “National and Regional Projections of Supply and Demand for Internal Medicine Subspecialty Practitioners: 2013-2025,” December 2016. Accessed online at https://bhw.hrsa.gov/sites/default/files/bhw/health-workforce-analysis/research/projections/internal-medicine-subspecialty-report.pdf.

7  Rodgers GP, Conti JB, Feinstein JA, Griffin BP, Kennett JD, Shah S, Walsh MN, Williams ES, Williams JL. ACC 2009 survey results and recommendations: addressing the cardiology workforce crisis: a report of the ACC Board of Trustees Workforce Task Force. J Am Coll Cardiol 2009;54:1195–208.