Technology at the crossroads with care and costs: the implantation of the automatic internal cardiac defibrillator.

The automatic internal cardiac defibrillator (AICD, ACD or ICD) represents one of the biggest challenges in medical practice in these days of reduced reimbursements, increased financial pressures, increasingly complex technology, and growing malpractice litigation. It has been proved most valuable in aborting sudden cardiac death (SCD), and has saved thousands of lives. SCD is a threat in every patient with heart disease, so theoretically every cardiac patient is a candidate for an AICD. SCD is responsible for more than 250,000 deaths in this country annually, the incidence being highest in those with congestive heart failure. (1) Proper use of the AICD requires careful patient selection. Medicare will reimburse for this device if certain criteria are met. The majority of patients at highest risk for SCD are those with coronary artery disease with or without prior myocardial infarction, especially if there has been congestive failure (CHF). The criteria for Medicare reimbursement have been changing year by year, and lately include an ejection fraction (EF) at or below 30% and a left ventricular activation time (QRS) of more than 120 ms. These criteria are unduly restrictive and arbitrary, as Drs. Ashwath and Sogade have shown in their report in this issue of the Southern Medical Journal. (2) The implication is that those who meet the criteria are at high risk and those who do not meet them are at low risk. Unfortunately, nothing could be farther from the truth.

The EF is not always a precise number and represents the ratio of end-systolic volume to the end-diastolic volume X 100. It is estimated in an echocardiogram by careful measurements or simply "eye-balling" by the reader. Experience and competence are important here, and variations by as much as 5 to 10% between readers are not unusual. EF can be evaluated by cardiac catheterization, either by careful planimetry or by "eyeballing," again subject to individual variability. Nuclear study may be more accurate, but again, marked variability may occur. The state of the patient is important (over- or under-hydration, a recent bout of ischemia, or angina, and so forth). If there is significant mitral regurgitation (even transiently), a significant volume of blood may go "backward," emptying the ventricle, reducing its systolic volume, and improving the apparent EF but not cardiac output. Anginal episodes are commonly associated with this phenomenon. Hence, if a patient has a 31% EF, he does not meet the criteria, although there may be a very high-risk situation for SCD. A prolonged QRS duration is clear, but there are many who are at high risk with a "normal" QRS. This is the gist of the paper by Drs. Ashwath and Sogade. SCD is an electrical phenomenon usually caused by ventricular fibrillation (VF). (3) There is no question that those with low EF and long QRS are at high risk of VF, but many with normal EF and QRS are at significant risk of SCD. Patients with low EF have systolic dysfunction; however, about 40% of patients with CHF have diastolic dysfunction, and one of the definitions of diastolic dysfunction is a normal or increased EF. They too are at risk for SCD. (4) What is the conscientious physician to do? The answer is judgment.

Runs of ventricular tachycardia, increasing ventricular ectopy on Holter monitor or during or immediately after a stress test, cardiomegaly, episodes of unexplained syncope, and recurrent episodes of CHF, especially in a smoker, are all clues to an electrically unstable myocardium. Certain families have genetic predisposition to SCD. (5,6) Frequent monitoring only occasionally reveals a high-risk problem. Electrophysiologic testing for VF inducibility frequently identifies the vulnerable patient. Other markers of vulnerability include QT prolongation, reduced heart rate variability, and T-wave alternans. (7-9) Those with these markers have greater than 20% annual risk of SCD. (10) Elevated levels of brain natriuretic peptide have been shown to be a predictor of SCD among 45% of 452 patients with CHF followed for 1.6 years. (11) The SCD-heft study of 45.5 months has shown that in patients with an EF less than 35%, the SCD rate was 25% with anti-arrhythmic drugs, 37.9% with no antiarrhythmia medications, and 9% in those with an AICD. (12) Drugs used in high-risk cases have their hazards, as shown by the CAST studies, with more deaths with the medications than without. (13,14) Amiodarone and sotalol are widely used here, but their side effects are daunting, compliance is a problem, and the results were better with an AICD. (15) In patients with an old myocardial infarction, an EF of less than 40%, and ventricular ectopy, the 5-year death rate was 32% with drugs and 28% untreated, but with an AICD, the SCD rate was 10%. (15) Lipid-lowering drugs (statins) have been reported to reduce arrhythmias and mortality rates by 19%, but this requires more study for confirmation. (16)

If one is convinced that the risk is significant, frank discussion with the patient and family are mandatory, and a consensus is reached. It takes great courage to prescribe this expensive device ($30,000.00). There are hospital costs, physician charges, and a long, complex lifetime follow-up for "reprogramming," for battery replacement, for lead repositioning, for review of manufacturers' advisories, and to manage the not-so-rare "inappropriate" shocks that can be rather painful and frightening. (17) AICD implantation adds another complex medical problem to an already ill patient. These patients have multiple other problems with multiple medications (hypertension, diabetes, impaired renal function, and so forth), and electrolyte disorders are common. Abnormal electrolyte levels (especially hypokalemia) make VF more likely and more difficult to defibrillate. With these caveats, the AICD can be lifesaving and worthwhile. There must be a deep commitment for follow-up by both the physician and the patient. It is clearly indicated when there is significant risk of SCD.

Accepted October 20, 2004.

References

1. Moss AJ, Zareba W, Hall WJ, et al. Multicenter Automatic Defibrillator Implantation Trial II Investigators: prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002;346:877-883.

2. Ashwath ML, Sogade FO. Ejection fraction and QRS width as predictors of Event Rates in Implantable Cardioverter Defibrillator Patients. S Med J 2005;98:513-517.

3. Ellison KE, Stevenson WG, Sweeney MO, et al. Management of arrhythmias in heart failure. Congest Heart Fail 2003;9:91-99.

4. Jones RC, Francis GS, Lauer MS. Predictors of mortality in patients with heart failure and preserved systolic function in the digitalis investigation group trial. J Am Coll Cardiol 2004;44:1025-1029.

5. Ackerman MJ, Tester DJ, Jones GS, et al. Ethnic differences in cardiac potassium channel variants: implications for genetic susceptibility to sudden cardiac death and genetic testing for long QT syndrome. Mayo Clinic Proc 2003;78:1479-1487.

6. Snapir A, Mikkelsson S, Perola M, et al. Variation in the alpha2B adrenoceptor gene as a risk factor for prehospital fatal myocardial infarction and sudden cardiac death. J Am Coll Cardiol 2003;41:190-194.

7. Klingenhaben T, Zabel M, D'Agostino RB, et al. Predictive value of T wave alternans for arrhythmic events in patients with congestive heart failure. Lancet 2000;356:651-652.

8. Zabel M, Malik M, Hnatkova K, et al. Analysis of the T wave morphology from the 12-lead ECG for prediction of long term prognosis in male US veterans. Circulation 2002;105:1066-1070.

9. La Rovere MT, Pinna GD, Maestri R, et al. Short-term heart rate variability strongly predicts sudden cardiac death in chronic heart

failure patients. Circulation 2003;107:565-570.

10. Myerberg RJ, Castellenos A. Cardiovascular collapse, cardiac arrest and sudden cardiac death, in Braunwald E, Fauci AS. Kasper DL (eds): Harrison's Principles of Internal Medicine. New York, NY, McGraw-Hill, 1998, pp 228-233.

11. Berger R, Huelsman M, Strecker K, et al. B type natriuretic peptide predicts sudden death in patients with chronic heart failure. Circulation 2003;103:2392-2397.

12. Hammill SC. Cardiac arrhythmias: report of a late breaking trial. J Am Coll Cardiol 2004;(Suppl 2A):16A-18A.

13. CAST Study, Cast II Investigators. Effect of antiarrhythmic agent morieizine on survival after myocardial infarction: the Cardiac Arrhythmia Suppression Trial II Investigators. N Engl J Med 1992;327:227-233.

14. CAST Investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction: the Cardiac Arrhythmia Suppression Trial (CAST) Investigators. N Engl J Med 1989;321:406-412.

15. Buxton AE, Lee KL, Fisher JD, et al. A randomized study of the prevention of sudden death in patients with coronary artery disease: Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med 1999;341:1882-1890.

16. Mitchell LB, Powell JL, Gillis AM, et al, and the AVID Investigators. Are lipid lowering drugs also antiarrhythmic drugs? An Analysis of the Antiarrhythmics Versus Implantable Defibrillators (AVID Trial). J Am Coll Cardiol 2003;42:81-87.

17. Rosenquist M, Beyer T, Block M, et al. Adverse events with intravenous implantable cardioverter defibrillators: a prospective multicenter study: European 7219 Jewel ICD Investigators. Circulation 1998;98:663-670.

George Ritter, MD, FACP, FACC 

Reprint requests to Dr. George Ritter, 28420 Sunset Blvd., West, Lathrup Village, MI 48076-2659. Email: [e-mail]