eMedicine Specialties > Cardiology > Myocardial Disease and Cardiomyopathies

Cardiogenic Shock: Follow-up

Author: Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Coauthor(s): Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Contributor Information and Disclosures

Updated: Aug 20, 2008

Follow-up

Further Inpatient Care

Cardiogenic shock is an emergency, requiring immediate resuscitative therapy before shock irreversibly damages vital organs. Simultaneously, identifying the cause of shock is important so that therapy can be directed to amending the cause.

Transfer

Immediately transfer a patient who develops cardiogenic shock to an institution at which invasive monitoring, coronary revascularization, and skilled personnel are available to provide expert care to the patient.

Prognosis

In the absence of aggressive, highly experienced technical care, mortality rates among patients with cardiogenic shock are exceedingly high (up to 70-90%). The key to achieving a good outcome is rapid diagnosis, prompt supportive therapy, and expeditious coronary artery revascularization in patients with myocardial ischemia and infarction. The mortality rate is reduced to 40-60% if patients are treated aggressively. The prognosis for patients who survive cardiogenic shock is not well studied but may be favorable if the underlying cause of shock is expeditiously corrected.

Patient Education

For excellent patient education resources, visit eMedicine's Shock Center and Public Health Center. Also, see eMedicine's patient education articles Shock and Cardiopulmonary Resuscitation (CPR).

Miscellaneous

Medicolegal Pitfalls

  • Cardiogenic shock has a very high mortality rate (60-80%), although mortality rates have decreased over the last 2 decades.
  • Areas of nonfunctioning but viable (hibernating) myocardium can cause or contribute to the development of cardiogenic shock.
  • The key to a good outcome in patients with cardiogenic shock is an organized approach, with rapid diagnosis and prompt initiation of pharmacologic therapy to maintain blood pressure and cardiac output.
  • Early and definitive restoration of coronary blood flow is the most important intervention for producing an improvement in survival, and, at present, it represents standard therapy for patients with cardiogenic shock due to myocardial ischemia.
  • Cardiogenic shock may be prevented with early revascularization in patients with MI and with required intervention in patients with structural heart disease.
  • Patients with cardiogenic shock who are admitted to hospitals without facilities for revascularization should be immediately transferred to a tertiary care center with such facilities. If time to PCI is more than 1 hour and onset of symptoms is within 3 hours, rapid administration of thrombolytic therapy is recommended.

Special Concerns

  • RV infarction
    • RV infarction occurs in up to 30% of patients with inferior MI and becomes hemodynamically unstable in 10% of these patients. The diagnosis is made by identifying an ST-segment elevation in the right precordial leads (V3 or V4 R) and/or typical hemodynamic findings after right heart catheterization. These are elevated right atrial and RV end-diastolic pressures with normal-to-low pulmonary artery wedge pressure and low cardiac output. Echocardiography findings can also be very helpful in the diagnosis of RV infarction. Patients with cardiogenic shock due to RV infarction have a better prognosis when compared to those with cardiogenic shock due to left ventricular systolic failure.
    • Regarding the management of cardiogenic shock due to RV infarction, supportive therapy begins with the restoration and maintenance of RV preload with fluid administration. However, excessive fluid resuscitation may compromise left ventricular filling by introducing an interventricular septal shift. Inotropic therapy with dobutamine may be effective in increasing cardiac output in patients with RV infarction. Maintenance of systemic arterial pressure in order to maintain adequate coronary artery perfusion may require vasoconstricting agents, such as norepinephrine. In unstable patients, an IABP may be useful for ensuring adequate blood supply to the already compromised right ventricle. Revascularization of the occluded coronary artery, preferably by PTCA, is crucial for management and has shown to dramatically improve outcome.
  • Acute mitral regurgitation
    • Acute mitral regurgitation is usually associated with inferior MI due to ischemia or infarction of the papillary muscle. The incidence rate is approximately 1% of MI, and posteromedial papillary muscle is involved more frequently than anterolateral muscle. Acute mitral regurgitation usually occurs 2-7 days following acute MI and manifests with an abrupt onset of pulmonary edema, hypotension, and cardiogenic shock.
    • Echocardiography findings are extremely useful in making a diagnosis. The 2-dimensional echocardiogram image shows the malfunctioning mitral valve, and findings from a Doppler study can be used to document the severity of mitral regurgitation. Right heart catheterization is often required for stabilizing the patient. Tall V waves identified on pulmonary arterial and wedge pressure waveforms indicate acute mitral regurgitation. However, the diagnosis must be confirmed based on echocardiography or left ventriculography findings before definitive therapy or surgery is initiated.
    • Hemodynamic stabilization by reducing afterload, either with nitroprusside or IABP, is often instituted. Definitive therapy requires revascularization, if ischemia is present, and/or surgical valve repair or replacement, if a structural valvular lesion is present. The mortality rate in the presurgical era was 50% in the first 24 hours, with a 2-month survival rate of 6%.
  • Cardiac rupture
    • Rupture of the free wall of the left ventricle occurs within 2 weeks of the MI and may occur within the first 24 hours. The rupture may involve the anterior, posterior, or lateral wall of the ventricle.
    • Cardiac rupture often presents as sudden cardiac death. Premortem symptoms include chest pain, agitation, tachycardia, and hypotension. This diagnosis should be considered in patients with electromechanical dissociation who have a history of anginal pain. Patients rarely, if ever, survive cardiac rupture.
  • Ventricular septal rupture
    • Approximately 1-3% of acute MIs are associated with ventricular septal rupture. Most septal ruptures occur within the week following MI. Patients with acute ventricular septal rupture develop acute heart failure and/or cardiogenic shock, with physical findings of a harsh holosystolic murmur and left parasternal thrill. A left-to-right intracardiac shunt, as demonstrated by a step-up (>5% increase in oxygen saturation) between the right atrium and right ventricle, confirms the diagnosis. Alternatively, 2-dimensional and Doppler echocardiography findings can be used to identify the location and severity of the left-to-right shunt.
    • Rapid stabilization using IABP and pharmacologic measures, followed by emergent surgical repair, is life saving. The timing of surgical intervention is controversial, but most experts suggest operative repair within 48 hours of the rupture. Ventricular septal rupture portends a poor prognosis unless management is aggressive. Immediate surgical repair of patients with ventricular septal rupture is reported to be associated with survival rates of 42-75%; therefore, prompt surgical therapy is imperative as soon as possible after the diagnosis of ventricular septal rupture is confirmed.
  • Reversible myocardial dysfunction
    • Other causes of severe reversible myocardial dysfunction are sepsis-associated myocardial depression, myocardial depression following cardiopulmonary bypass, or inflammatory myocarditis. In older literature, this presentation is often referred to as cold septic shock. In these situations, myocardial dysfunction occurs from the effects of inflammatory cytokines, such as tumor necrosis factor and interleukin-1.
    • Myocardial dysfunction may vary from mild to severe and may lead to cardiogenic shock. For patients in cardiogenic shock, cardiovascular support with inotropic agents may be required until recovery, which generally occurs after the underlying disease process resolves.
 


More on Cardiogenic Shock

Overview: Cardiogenic Shock
Differential Diagnoses & Workup: Cardiogenic Shock
Treatment & Medication: Cardiogenic Shock
Follow-up: Cardiogenic Shock
Multimedia: Cardiogenic Shock
References
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References

  1. Ajani AE, Maruff P, Warren R, et al. Impact of early percutaneous coronary intervention on short- and long-term outcomes in patients with cardiogenic shock after acute myocardial infarction. Am J Cardiol. Mar 1 2001;87(5):633-5, A9-10. [Medline].

  2. Alonso DR, Scheidt S, Post M, Killip T. Pathophysiology of cardiogenic shock. Quantification of myocardial necrosis, clinical, pathologic and electrocardiographic correlations. Circulation. Sep 1973;48(3):588-96. [Medline].

  3. Ammann P, Straumann E, Naegeli B, et al. Long-term results after acute percutaneous transluminal coronary angioplasty in acute myocardial infarction and cardiogenic shock. Int J Cardiol. Feb 2002;82(2):127-31. [Medline].

  4. Antoniucci D, Valenti R, Migliorini A, et al. Relation of time to treatment and mortality in patients with acute myocardial infarction undergoing primary coronary angioplasty. Am J Cardiol. Jun 1 2002;89(11):1248-52. [Medline].

  5. Barron HV, Every NR, Parsons LS, et al. The use of intra-aortic balloon counterpulsation in patients with cardiogenic shock complicating acute myocardial infarction: data from the National Registry of Myocardial Infarction 2. Am Heart J. Jun 2001;141(6):933-9. [Medline].

  6. Bengur AR, Meliones JN. Cardiogenic shock. New Horiz. May 1998;6(2):139-49. [Medline].

  7. Berger PB, Tuttle RH, Holmes DR, et al. One-year survival among patients with acute myocardial infarction complicated by cardiogenic shock, and its relation to early revascularization: results from the GUSTO-I trial. Circulation. Feb 23 1999;99(7):873-8. [Medline].

  8. Chauhan A, Zubaid M, Ricci DR, et al. Left main intervention revisited: early and late outcome of PTCA and stenting. Cathet Cardiovasc Diagn. May 1997;41(1):21-9. [Medline].

  9. Dzavik V, Burton JR, Kee C, et al. Changing practice patterns in the management of acute myocardial infarction complicated by cardiogenic shock: elderly compared with younger patients. Can J Cardiol. Jul 1998;14(7):923-30. [Medline].

  10. Edep ME, Brown DL. Effect of early revascularization on mortality from cardiogenic shock complicating acute myocardial infarction in California. Am J Cardiol. May 15 2000;85(10):1185-8. [Medline].

  11. Fechner PU. [Diseases of the orbit]. Buch Augenarzt. 1976;67(0):136-43. [Medline].

  12. Goldberg RJ, Gore JM, Alpert JS, et al. Cardiogenic shock after acute myocardial infarction. Incidence and mortality from a community-wide perspective, 1975 to 1988. N Engl J Med. Oct 17 1991;325(16):1117-22. [Medline].

  13. Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med. Apr 15 1999;340(15):1162-8. [Medline].

  14. Hasdai D, Califf RM, Thompson TD, et al. Predictors of cardiogenic shock after thrombolytic therapy for acute myocardial infarction. J Am Coll Cardiol. Jan 2000;35(1):136-43. [Medline].

  15. Hasdai D, Holmes DR, Topol EJ, et al. Frequency and clinical outcome of cardiogenic shock during acute myocardial infarction among patients receiving reteplase or alteplase. Results from GUSTO-III. Global Use of Strategies to Open Occluded Coronary Arteries. Eur Heart J. Jan 1999;20(2):128-35. [Medline].

  16. Hasdai D, Holmes DR, Califf RM, et al. Cardiogenic shock complicating acute myocardial infarction: predictors of death. GUSTO Investigators. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries. Am Heart J. Jul 1999;138(1 Pt 1):21-31. [Medline].

  17. Ho TC, Ting CT, Liu TJ, et al. Percutaneous coronary revascularization improves the prognosis of patients with cardiogenic shock in acute coronary syndrome: a chronological study. Int J Cardiol. Jun 2003;89(2-3):135-43. [Medline].

  18. Hochman JS, Boland J, Sleeper LA, et al. Current spectrum of cardiogenic shock and effect of early revascularization on mortality. Results of an International Registry. SHOCK Registry Investigators. Circulation. Feb 1 1995;91(3):873-81. [Medline].

  19. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med. Aug 26 1999;341(9):625-34. [Medline].

  20. Hochman JS, Sleeper LA, White HD, et al. One-year survival following early revascularization for cardiogenic shock. JAMA. Jan 10 2001;285(2):190-2. [Medline].

  21. Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic shock complicating acute myocardial infarction--etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1063-70. [Medline].

  22. Hollenberg SM, Kavinsky CJ, Parrillo JE. Cardiogenic shock. Ann Intern Med. Jul 6 1999;131(1):47-59. [Medline].

  23. Holmes DR, Bates ER, Kleiman NS, et al. Contemporary reperfusion therapy for cardiogenic shock: the GUSTO-I trial experience. The GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol. Sep 1995;26(3):668-74. [Medline].

  24. Holmes DR, Berger PB, Hochman JS, et al. Cardiogenic shock in patients with acute ischemic syndromes with and without ST-segment elevation. Circulation. Nov 16 1999;100(20):2067-73. [Medline].

  25. Hsu RB, Chien CY, Wang SS, Chu SH. Survival after early surgical revascularization in patients with both acute myocardial infarction and cardiogenic shock. J Formos Med Assoc. Nov 2001;100(11):725-8. [Medline].

  26. Jacobs AK, French JK, Col J, et al. Cardiogenic shock with non-ST-segment elevation myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded coronaries for Cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1091-6. [Medline].

  27. Lehmann A, Boldt J. New pharmacologic approaches for the perioperative treatment of ischemic cardiogenic shock. J Cardiothorac Vasc Anesth. Feb 2005;19(1):97-108. [Medline].

  28. Mehta SR, Eikelboom JW, Natarajan MK, et al. Impact of right ventricular involvement on mortality and morbidity in patients with inferior myocardial infarction. J Am Coll Cardiol. Jan 2001;37(1):37-43. [Medline].

  29. Menon V, Webb JG, Hillis LD, et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1110-6. [Medline].

  30. Mueller H, Ayres SM, Conklin EF, et al. The effects of intra-aortic counterpulsation on cardiac performance and metabolism in shock associated with acute myocardial infarction. J Clin Invest. Sep 1971;50(9):1885-900. [Medline].

  31. Sanborn TA, Sleeper LA, Bates ER, et al. Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for ca. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1123-9. [Medline].

  32. Scheidt S, Wilner G, Mueller H, et al. Intra-aortic balloon counterpulsation in cardiogenic shock. Report of a co-operative clinical trial. N Engl J Med. May 10 1973;288(19):979-84. [Medline].

  33. Slater J, Brown RJ, Antonelli TA, et al. Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a report from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1117-22. [Medline].

  34. Srimahachota S, Boonyaratavej S, Udayachalerm W, et al. Percutaneous coronary intervention in acute myocardial infarction with cardiogenic shock: immediate and late outcomes. J Med Assoc Thai. Oct 2001;84(10):1449-54. [Medline].

  35. Sutton AG, Finn P, Hall JA, et al. Predictors of outcome after percutaneous treatment for cardiogenic shock. Heart. Mar 2005;91(3):339-44. [Medline].

  36. Thiele H, Lauer B, Hambrecht R, et al. Reversal of cardiogenic shock by percutaneous left atrial-to-femoral arterial bypass assistance. Circulation. Dec 11 2001;104(24):2917-22. [Medline].

  37. Thompson CR, Buller CE, Sleeper LA, et al. Cardiogenic shock due to acute severe mitral regurgitation complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we use emergently revascularize Occluded Coronaries in cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1104-9. [Medline].

  38. Urban P, Stauffer JC, Bleed D, et al. A randomized evaluation of early revascularization to treat shock complicating acute myocardial infarction. The (Swiss) Multicenter Trial of Angioplasty for Shock-(S)MASH. Eur Heart J. Jul 1999;20(14):1030-8. [Medline].

  39. Webb JG, Sleeper LA, Buller CE, et al. Implications of the timing of onset of cardiogenic shock after acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1084-90. [Medline].

  40. Webb JG, Sanborn TA, Sleeper LA, et al. Percutaneous coronary intervention for cardiogenic shock in the SHOCK Trial Registry. Am Heart J. Jun 2001;141(6):964-70. [Medline].

  41. Wong SC, Sanborn T, Sleeper LA, et al. Angiographic findings and clinical correlates in patients with cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?. J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1077-83. [Medline].

  42. Gowda RM, Fox JT, Khan IA. Cardiogenic shock: Basics and clinical considerations. Int J Cardiol. Nov 23 2007;[Medline].

  43. Windecker S. Percutaneous left ventricular assist devices for treatment of patients with cardiogenic shock. Curr Opin Crit Care. Oct 2007;13(5):521-7. [Medline].

  44. Singh M, White J, Hasdai D, Hodgson PK, Berger PB, Topol EJ. Long-term outcome and its predictors among patients with ST-segment elevation myocardial infarction complicated by shock: insights from the GUSTO-I trial. J Am Coll Cardiol. Oct 30 2007;50(18):1752-8. [Medline].

  45. Singh M, White J, Hasdai D, Hodgson PK, Berger PB, Topol EJ. Long-term outcome and its predictors among patients with ST-segment elevation myocardial infarction complicated by shock: insights from the GUSTO-I trial. J Am Coll Cardiol. Oct 30 2007;50(18):1752-8. [Medline].

  46. Bailey A, Pope TW, Moore SA, Campbell CL. The tragedy of TRIUMPH for nitric oxide synthesis inhibition in cardiogenic shock: where do we go from here?. Am J Cardiovasc Drugs. 2007;7(5):337-45. [Medline].

  47. Jeger RV, Lowe AM, Buller CE, Pfisterer ME, Dzavik V, Webb JG. Hemodynamic parameters are prognostically important in cardiogenic shock but similar following early revascularization or initial medical stabilization - A report from the SHOCK Trial. Chest. Oct 20 2007;[Medline].

  48. Farrar DJ, Lawson JH, Litwak P, Cederwall G. Thoratec VAD system as a bridge to heart transplantation. J Heart Transplant. Jul-Aug 1990;9(4):415-22; discussion 422-3. [Medline].

  49. Rose EA, Gelijns AC, Moskowitz AJ, Heitjan DF, Stevenson LW, Dembitsky W. Long-term mechanical left ventricular assistance for end-stage heart failure. N Engl J Med. Nov 15 2001;345(20):1435-43. [Medline].

  50. Damme L, Heatley J, Radovancevic B. Clinical results with the HeartMate LVAD: Worldwide Registry update. J Congestive Heart Failure Circ Support. 2001;2,:5-7(3).

  51. Rose EA, Gelijns AC, Moskowitz AJ, Heitjan DF, Stevenson LW, Dembitsky W. Long-term mechanical left ventricular assistance for end-stage heart failure. N Engl J Med. Nov 15 2001;345(20):1435-43. [Medline].

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Further Reading

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Keywords

cardiogenic shock, cardiac failure, heart failure, myocardial infarction, MI, ST-elevation MI, ST-elevation myocardial infarction, STEMI, non–ST-elevation acute coronary syndrome, NSTEMI, unstable angina, myocardial ischemia, heart attack, cardiac dysfunction, acute myocarditis, sustained arrhythmia, acute valvular catastrophe, end-stage cardiomyopathy, coronary artery disease, CAD, myocardial pathology, myocardial stunning, hibernating myocardium, systolic dysfunction, diastolic dysfunction, valvular dysfunction, cardiac arrhythmias, mechanical heart complications, left ventricular end-systolic pressure-volume curve, curvilinear diastolic pressure-volume curve, shock state, hemodynamic support, vasopressor supportive therapy, inotropic supportive therapy, thrombolytic therapy, intra-aortic balloon pump, ventricular assist device, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting, coronary artery bypass grafting, shock trial

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Contributor Information and Disclosures

Author

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Russell F Kelly, MD, Program Director, Assistant Professor, Department of Internal Medicine, Division of Cardiology, Cook County Hospital, Rush Medical College
Russell F Kelly, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Ronald J Oudiz, MD, FACP, FACC, Associate Professor of Medicine, Division of Cardiology, The David Geffen School of Medicine at UCLA; Director, Liu Center for Pulmonary Hypertension, LA Biomedical Research Institute at Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx  Clinical Trials + honoraria

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Thomas G Di Salvo, MD, Associate Professor of Medicine, Medical Director, Vanderbilt Heart and Vascular Institute, Vanderbilt University Medical Center
Disclosure: Nothing to disclose.

 
 
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