Latest Therapeutic Approaches in Congestive Heart Failure

Majdi Ashchi, D.O., FACC, FCCP, Interventional Cardiologist,
Memorial Medical Center, Jacksonville, FL

 

Introduction

Congestive Heart Failure is a complex clinical syndrome that results from any structural or functional cardiac disorder that impairs the ability of the ventricle/ s to fill with or eject blood. It is a major cause of death and suffering throughout the world. In the USA, there are nearly 5 million patients with Heart Failure (HF) and nearly 500,000 patients are diagnosed each year for the first time with HF. There are between 12-15 million office visits for HF and and nearly 6.5 million hospital days each year 1. Over the past decade, the annual hospitalizations for HF have increased from 550,000 to nearly 900,000 as a primary diagnosis and from 1.7 to 2.6 million as a primary or secondary diagnosis 2.

HF is primarily a disease of the elderly and approximately 6-10% of men or women older than 65 years have HF 3,4. More than 80% of patients hospitalized with HF are more than 65 years old. HF is not only the most common Medicare diagnosis, but also more Medicare dollars are spent on it than any other diagnosis 5.

The main clinical manifestations of HF includes dyspnea and fatigue which limits exercise tolerance, causes fluid retention, and possibly lead to pulmonary and peripheral edema. Coronary artery disease is the leading cause of systolic heart failure (2/3 cases) and the remaining are due to nonischemic causes of systolic dysfunction and may or may not have identifiable cause (e.g. hypertension, valve disease, myocarditis, idiopathic dilated cardiomyopathy).

In the latest (12/2001) ACC/AHA Guidelines for the Evaluation and Management of Chronic HF in the Adult: Executive Summary, a new classification scheme for HF was recommended to complement and not to replace the New York Heart Association (NYHA) functional classification which primarily gauges the severity of symptoms in patients who are in stages C or D 6 (Table 1).

Table 1. Stages Of Heart Failure (HF)
Stage Description
A. Patients at high risk of developing HF because of the presence of conditions that are strongly associated with the development of HF. Such patients have no identified structural or functional abnormalities of the pericardium, myocardium, or cardiac valves and have never shown signs or symptoms of HF.
B. Patients who have developed structural heart disease that is strongly associated with the develop ment of HF but who have never shown signs or symptoms of HF.
C. Patients who have current or prior symptoms of HF associated with underlying structural heart disease.
D. Patients with advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy and who require specialized interventions.

This new classification of HF emphasized both the evolution and progression of disease. This classification emphasizes the importance of the established risk factors in the development of HF and that medical intervention performed even prior to appearance of left ventricular dysfunction or symptoms may reduce morbidity and or mortality from HF.

The recommendations by the ACC/AHA 6 follow previous ACC/AHA guidelines and they are based on evidenced based medicine whenever possible:

Class I: Conditions for which there is evidence and/or general agreement that a given procedure/therapy is useful and effective.

Class II: Conditions for which there is conflicting evidence and /or a divergence of opinion about the useful ness/efficacy of performing the procedure/therapy.

Class II a: Weight of evidence/opinion is in favor of usefulness/efficacy.

Class II b: Usefulness/efficacy is less well established by evidence/opinion.

Class III: Conditions for which there are evidence and /or general agreement that a procedure/therapy is not useful/effective and in some cases may be harm- ful.

Diagnosis of HF

The assessment of patients with HF includes the initial evaluation and the detection of predisposing factors. A thorough history and physical examination to identify cardiac and noncardiac risk factors that might lead or accelerate HF is of paramount basic importance. Basic laboratory work up would include 12-lead electro cardiogram; chest radiograph, 2-dimentional echocardiography or radionulcide ventriculography to assess left ventricular systolic function. Other work up includes complete blood count, serum electrolytes, liver function test, and thyroid profile. Noninvasive imaging to define likelihood of coronary artery disease is done based on clinical history and more invasive testing including cardiac catheterization may be necessary.

Heart Failure Therapy 10

There are three goals in the treatment of HF patients. These goals include improvement in symptoms and quality of life, improvement in survival and elimination or lessening of the complications of HF.

The treatment of HF encompasses many therapies and methodologies. There are general therapies atop of pharmacological and interventional therapies all of which could be aided by ancillary data-guided therapies.

  1. Basic methods and treatment of HF ( *Non FDA approved and or new therapy )
  1. Fluid restriction (if congestion persists despite diuretic therapy)
  2. Weight loss in obese patients
  3. Education
  4. Sodium restriction in all patients
  5. Treatment of underlying disease or precipitating factor
  6. Respiratory therapy*
  1. Pharmacological Treatment of HF
  1. Diuretics. Thiazides, loop diuretics, spironolac tone (RALS trial given for class IV HF for neuro hormonal effect). Adenosine a1 receptor blockers BG9719 * 7, Vasopressin receptor blockers*
  2. Inotropic agents which could be also vasodilator agent or in combination of: Dobutamine, dopam ine, milrinone, epinephrine, amrinone, levosimendan*, enoximone*.
  3. Vasodilators.
  1. ACE inhibitors, angiotensin receptor blockers (ARB),hydralazine, and oral nitrates.
  2. Natriuretic peptide (Intravenous): Natrecor (Nesiritide)8.
  3. Endothelin Receptor Blockrs; Tezosentan*, Bosentan*.
  1. Beta-Blockers 10: Coreg, Lopressor, etc.
  2. Antiarrhythmic agents
  3. Anticoagulation
  1. Interventional Therapy
  1. Revascularization: PCI (percutaneous coronary intervention), surgical, TMR (transmyocardial laser) 9 *.
  2. Electrical Conduction ablation,therapeutic
  3. Cardiac pacing either by AV pacing or by cardiac resynchronization (atrial and biventricular pac- ing)*.
  4. Ventricular assist devices (IABP)
  5. Hemofiltration *
  6. Total heart replacement: Abiocor*
  7. Heart Transplantation : allograft,cellular
  8. Ventricular wall stress reduction therapy
  1. Infarct Exclusion patch-plasty * (Dor procedure, SAVER trial)
  2. Partial Ventriculectomy (Batista operation)*
  3. Myosplint* & CardioCasp*
  4. Vetricular end-diastolic support: Dynamic cardiomyoplasty* and CorCap*, Acorn*.

Therapy of the HF patient could be guided by serum hBNP level, hemodynamic invasive monitoring i.e. Swan Ganz catheterization or by an implanted hemodynamic monitor (Chronicle)*.In the recent past, HF patients have been monitored in a relatively effective noninvasive fashion and in an out patient basis using bioimpedance (Bio-Z, SORBA, IQ).

The ACC/AHA recommendations for treatment of chronic HF follows their new chronic HF classification. Each of the four stages (A-D) has recommendations based on their weight of medical evidence.

In Stage A, patients at high risk of development of HF (normal LV systolic function), treatment is directed towards aggressively controlling risk factors e.g. patients with hypertension (systolic or diastolic), diabetes, hyperlipidemia, alcohol consumption, illicit drug abuse, atherosclerotic vascular disease, thyroid disease, family history of cardiomyopathy and in patients with supraventricular tachyarrhhmias that need heart rate control. Angiotensin converting enzyme (ACE) inhibition in-patients with diabetes mellitus, hypertension or history of atherosclerotic disease is recommended.

In Stage B, patients with left ventricular dysfunction who have not developed symptoms, treatment is directed to stage A but adds treatment to patients who have suffered from myocardial infarction and or patients with valve disease ( stenosis or regurgitation). ACE inhibition is recommended for all myocardial infarction patients regardless of left ventricular ejection fraction and all patients with low ejection fraction. Beta-blocker therapy is recommended in all patients with recent myocardial infarction regardless of left ventricular ejection fraction and in patients with low ejection fraction regardless of myocardial infraction. Treatment of valve disease (surgical or percutaneous) is recommended when it is hemodynamically significant.

In Stage C, patients with left ventricular dysfunction with current or prior symptoms, treatment measures listed in stages A& B are also appropriate however, there will be a need for the addition of diuretics, moderate salt restriction and use of digoxin when appropriate to reduce symptoms and enhance exercise tolerance. Patients with fluid evidence of fluid retention would benefit from diuretics. Spironolactone (Aldactone) who recommended if patients have recently or currently had symptoms of class IV heart failure. Angiotensin receptor blockade (ARB) could be substituted for ACEI due ACEI contraindications (angioedema, cough). Hydralazine and nitrate combination could be substituted for patients with contraindications to both ARB and ACEI (hypertension, renal insufficiency, angioedema, and cough). Calcium channel blocker use is still controversial at best. Long term continuous or intermittent infusion of positive inotropic drugs is not recommended. These patients should be discouraged and recommend withdrawal of drugs that may adversely affect their clinical status i.e. nonsteroidal anti-inflammatory drugs, most antiarrhythmic drugs, most calcium channel blockers. Immunization for both pneumococcal and influenza vaccines is highly recommended to reduce their respiratory infections. Physical activity is encouraged and restriction is only during periods of exacerbation and suspected myocarditis 11-12.

In Stage D, patients with refractory End-Stage Heart Failure, treatment becomes more specialized and more intense and has to be done in a hospital. Also, surgical treatment may be of warranted and or of benefit. Meticulous control of fluid and hemodynamics becomes very important. Euvolemia is the goal. Atop of all the previous stage recommendations (A-C), treatment may need to be guided with invasive monitoring (swan-ganz catheter), referral to a HF program with expertise in treatment of refractory HF and that has access to a cardiac transplant team or a surgical team that can deal with high risk surgical patients.

In the past decade, diastolic dysfunction has been recognized as a major cause of heart failure. It is estimated that 20-40% of patients with HF has normal or preserved left ventricular systolic function but have impairment of ventricular relaxation leading to HF symptoms 13-14. Many disorders cause diastolic dysfunction include but not limited to restrictive cardiomyopathy, obstructive and nonobstructive hypertrophic cardiomyopathy, infiltrative cardiomyopathy. (See Dr.M.Koren's paper in this issue for more details about diastolic dysfunction).

Summary

HF is a major health problem. Not much has changed in the last decade in terms of diagnosis except the recognition of the effect of diastolic dysfunction. Treatment has improved dramatically resulting in improvement in both morbidity and mortality. The poly-pharmacy in treatment of HF is targeting not only the mechanics and volume of HF but also the neurohormonal changes of HF. Two new modalities have been recently approved for clinical use which includes cardiac resynchronization therapy (biventricular pacing) and the intravenous vasodilator, nesiridide.

The treatment modalities of HF is growing but not keeping up with the very high and growing prevalence of HF and its morbidity and mortality.Therapy is expensive and becoming more expensive. Our society will have to decide through our leaders and medical societies on the efficacy and cost-effectiveness of these therapeutic treatments and modalities.

References

  1. O'Connell JB, Bristow M. Economic Impact of heart failure in the United States: time for a different approach. J Heart Lung Transplant 1993; 13:S107-12.
  2. Haldeman GA, Croft JB, Giles WH, Rashidee A. Hospitalization of patients with HF: National Hospital Discharge Survey, 1985 to 1995. Am Heart J 1999; 137; 352-60.
  3. Kannel WB, Belanger AJ. Epidemiology of Heart Failure. Am Heart J 1991; 121:951-7.
  4. Kannel WB. Epidemilogy and prevention of cardiac failure: Framingham Study insights. Eur Heart J 1987; 8 Supll F: 23-6.
  5. Massie BM,Shah NB.Evolving trends in the epidemiologic factors of heart failure: rationale for preventive strategies and comprehensive disease management.Am Heart J 1997; 133:703-12.
  6. Hunt As et al., ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: Executive Summary.JACC 2001; 38:2101-2113.
  7. Gottlieb SS,Brater DC, Thomas I, et al. BG9719 (CVT-124), an A1 adenosine receptor antagonist, protects against the decline in renal function observed with standard congestive heart failure therapy (abstract) .J Am Coll Cardiol 2001; 37:172A.
  8. Colucci WS,Elkayan U, Horton DP, et al for the Nesiritide Study Group. Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure.N Engl J Med 2000; 343:246-253.
  9. Oesterle Sn, Sanborn Ta,Ali N, et al. Percuatneous transmyocardial laser revascularization for severe angina: The PACIFIC randomized trial. Lancet 2000; 356:1705-1710.
  10. Young J. In Topol EJ, ed. Texbook of cardiovascular medicine. Philadelphia: Lippincott-Raven, 1998:2273.
  11. Chati Z, Zannad F, Jeandel C, et al. Physical deconditioning may be a mechanism for the skeletal muscle energy phosphate metablolism abnormalities in chronic heart failure. Am Heart J 1996;131:560-6.
  12. Sinoway LI. Effect of conditioning and deconditioning stimuli on metablically determined blood flow in humans and implications for congestive heart failure. Am J Cardiol 1988;62:45E-8E.
  13. Litwin SE, Grossman W. Diastolic dysfunction as a cause of heart failure. J Am Coll Cardiol 1993;22:49A-55A.
  14. Daughtery AH,Naccarelli GV, Gray EL, Hicks CH, Goldstein RA. Congestive Heart Failure with normal systolic function. Am J Cardiol 1984;54:778-82.
Jacksonville Medicine / February, 2002

What's New · Northeast Florida Medicine Journal · Know Your Physician · Legal & Legislative
· DCMS Alliance · Academy of Medicine · Member Websites · Community Health
About the DCMS · Meetings Calendar · Member Benefits · Employment Connection · Home

Duval County Medical Society   ·   555 Bishopgate Lane  ·   Jacksonville, FL  32204
Phone: (904) 355-6561   ·     FAX:  (904) 353-5848   
General Email: dcms@dcmsonline.org    ·   Webmaster's Email: mdoran@dcmsonline.org
Privacy Policy and Disclaimers