Surgical Innovations for Chronic Heart Failure in the Context of Cardiopulmonary Rehabilitation.

In recent years, pharmacological management of CHF has benefited from the addition of angiotensin- converting enzyme (ACE) inhibitors and adrenergic beta-blockers, providing major symptomatic improvement in people with mild to moderate heart failure.[2] Physical activity is likewise gaining acceptance as an important intervention.[3] Structured exercise programs for people with cardiovascular and pulmonary disease have existed in the United States for nearly 3 decades, and the outcomes are well documented in the literature.[4,5] In recent years, the emphasis and direction of research have shifted to the beneficial effects of both endurance training and resistive exercise for clinical and behavioral outcomes for patients with CHF. Exercise for patients with CHF is safe[3] and results in physiological and psychological changes that lead to improved functional status. These improvements include improvements in control of heart rate,[6-10] measures of quality of life,[11-15] exercise capacity,[16-27] left ventricular function,[28-33] skeletal muscle physiology,[34,35] and peripheral blood flow and endothelial function.[36-38] Squires[39] has provided an extensive summary of the evidence-based benefits of endurance and resistive exercise training for people with CHF (Tab. 1).

Table 1. Demonstrated Changes Due to Endurance or Resistive Exercise Training for Patients With Chronic Heart Failure(a)

Increases or improvements:
* Peak oxygen consumption, ventilatory anaerobic threshold, and
  maximal cardiac output
* Physical work capacity and submaximal exercise endurance
* Leg blood flow and arterial oxygen content
* Skeletal muscle aerobic enzyme activity, phosphocreatine, and
  adenosine triphosphate
* Muscle fiber size, skeletal muscle strength and endurance
* Parasympathetic nervous system activity
* Diastolic function
* Respiratory muscle function (with specific training)
* Morbidity and mortality in patients with coronary artery disease
* Spontaneous daily activity and quality-of-life indexes

Decreases:
* Symptoms of dyspnea, fatigue, and weakness
* Submaximal exercise ventilation, carbon dioxide and
  respiratory exchange ratio
* Neurohormonal activation and sympathetic nervous system
  activity
* Resting and submaximal exercise heart rate and blood lactate
  level
* Ventricular arrhythmias
* New York Heart Association functional class
* Phosphocreatine depletion during isometric exercise

No change:
* Submaximal exercise oxygen consumption
* Pulmonary artery or pulmonary capillary wedge pressure
* Mean arterial pressure during exercise
* Left ventricular end-systolic and diastolic volumes
* Left ventricular ejection fraction

(a) Adapted by permission from Squires RW. Exercise Prescription for the High-Risk Cardiac Patient. Champaign, Ill: Human Kinetics Inc; 1998:149-151.

The physiological adaptation to exercise training for people with CHF warrants attention because these individuals were historically exempted from exercise programs due to the presumption that poor left ventricular function prohibited improvement, increased the risk of an exercise-induced cardiovascular event, and might even be worsened by exercise. Although strongly associated with mortality, ejection fraction is poorly related to exercise performance as measured by oxygen consumption ([VO.sub.2]).[40,41] Thus, increased exercise capacity appears to be influenced more by the peripheral adaptation of skeletal muscle than by improvement in cardiac output.[42]

Surgical alternatives to heart transplantation are being used. Aside from heart transplantation, recent interventions include: high-risk coronary artery bypass surgery (CABG), transmyocardial revascularization (TMR), dynamic cardiomyoplasty (DCM), partial left ventriculectomy (PLV), and the use of a left ventricular assist device (LVAD). Patients undergoing these procedures are potentially candidates for exercise rehabilitation. This update is not intended to review exercise treatment approaches for individuals with CHF, as these approaches have been described previously.[43,44] The purposes of this update are to describe recent surgical and technological procedures in the treatment of people with CHF and to suggest exercise rehabilitation strategies.

Heart Transplantation

Heart transplantation remains the primary intervention for people with end-stage CHF. Although heterotopic transplants (the recipient's heart is not removed, and the donor heart is anastomosed in parallel) may be done in selected patients, orthotopic transplantation (removal of the recipient's heart and replacement with the donor heart) is associated with better survival and is most widely used.[45] Approximately 50% of people who received heart transplants from 1980 through 1985 were alive at 60 months postoperatively.[46] The survival rate improved to about 76% for people who received heart transplants from 1986 through 1990 and to about 78% for people who received heart transplants from 1991 through 1997.[46] The 2 major complications and leading causes of death postoperatively are infection and rejection of the transplanted heart.[45]

Physical therapists have traditionally played an important role in the assessment and management of this population. Sadowsky[47] has provided a relevant description of heart transplantation and review for physical therapy assessment and intervention. Postsurgical acute care for patients who have received heart transplants is similar to that for patients who have undergone a median sternotomy. Patients with heart transplantation frequently have a complex drug regimen due to immunosuppression. The major difference with respect to exercise remains the altered response of the heart to exercise. That is, in the denervated heart, the increase in heart rate to exercise is in response to the parallel increase in circulating catecholamines, and thus the initial rise in cardiac output is dependent on augmented preload and the Frank-Starling mechanism. As a result, abrupt increases in exercise demand are unusually fatiguing due to an increased need to meet the energy demand through anaerobic pathways. Given a more gradual warm-up and a lengthened cool-down period postexercise, patients who are stable following a heart transplant respond well to exercise therapy.[47]

Heart transplantation, however, has slowed in recent years due primarily to a lack of suitable donors, despite the use of older donors.[46] A total of 3,471 heart transplants were performed in 1997, reflecting a progressive decline from a peak of 4,117 heart transplants in 1995.[46] Given the estimated CHF prevalence of nearly 5 million and the rising numbers, alternatives to transplantation are crucial.

High-Risk Coronary Artery Bypass Surgery

Selected patients with poor left ventricular function, although at higher mortality risk, may benefit from coronary revascularization. The large magnitude of coronary artery disease and associated myocardial damage for many patients with CHF due to ischemia limits widespread use of CABG in this population. Historically, surgery was deferred for patients with severe CHF due to the poor benefit-to-risk ratio. Of those individuals who are appropriate candidates for coronary revascularization, 20% of patients with an ejection fraction of less than 30% experience operative mortality.[48] Survivors are reported to have a 5-year survival rate of 80%.[48] Shapira et al[49] demonstrated a survival rate of 83.3% 7 years post-CABG, an improvement in CHF classification, and a 12.2% increase in left ventricular ejection fraction in a group of patients with left ventricular dysfunction. Hausmann and colleagues[50] reported a 2-year survival rate of 87.8%, a 14.2% increase in ejection fraction, a 4.1-mm Hg decrease in left ventricular end-diastolic pressure, and a 5.4-mm Hg decrease in pulmonary wedge pressure.

Although the outcomes of patients with CHF undergoing CABG appear to be positive, there are indications that this group continues to be at increased risk of mortality postsurgery. Herlitz et al[51] found that preoperative ejection fraction was an independent predictor of mortality 2 years after CABG. In another study by Herlitz and colleagues,[52] a history of CHF prior to surgery was one of the factors that independently predicted mortality. Brandrup-Wognsen et al[53] also found that a history of CHF independently predicted mortality after CABG. As data continue to emerge that better clarify the risks and benefits of bypass surgery for patients with poor left ventricular dysfunction, more patients with advanced CHF may be reconsidered for coronary revascularization.

Although physical therapists have been treating patients with coronary revascularization for years, it is unclear whether these patients present new challenges. These patients remain at higher postoperative risk, given their preoperative clinical status, and special attention to sternal healing and stability may be warranted in cases where there have been multiple sternotomies. Regardless, the proportion of patients who are at higher risk undergoing coronary revascularization and who are referred for exercise training can be expected.

Transmyocardial Revascularization

Transmyocardial revascularization is a procedure intended to improve chronic angina not amenable to bypass grafting or angioplasty.[54] The TMR procedure is illustrated in Figure 1. A surgical laser creates a transmural channel in the area of the myocardium that has been identified as ischemic. The epicardial origin seals over once the laser has been removed, and oxygenated blood fills the newly created channel. The perfused channel supplies oxygenated blood to the surrounding myocardium.

[Figure 1 ILLUSTRATION OMITTED]

The theory is that symptoms are reduced due to an increased supply of oxygenated blood shunted directly to the myocardium via the transmural channels created by TMR.[55] Angiogenesis is another proposed benefit of this procedure.[56] Pelletier et al[56] using a rat model, reported an increase in vascular density following TMR. Mack et al[55] also found evidence of neovascularization in 6 sheep undergoing TMR. Literature to date reveals that the procedure is safe and, although reported outcomes vary, that anginal symptoms are decreased and exercise tolerance is improved. Paradoxically, measurable improvements in left ventricular function or evidence of improved myocardial perfusion has not been found.[54,56-58] Although data continue to emerge on the effectiveness of TMR, physical therapists may anticipate improved exercise performance with decreased angina but should be aware that risk status relative to left ventricular function or myocardial perfusion defects has not changed.

Dynamic Cardiomyoplasty

Dynamic cardiomyoplasty was first performed in 1985, and about 700 procedures have been performed to date.[59] In this procedure, the latissimus dorsi muscle is typically detached distally (with preservation of the neurovascular supply), then brought forward through a resected second rib space, where it is surgically wrapped about the left ventricle. The DCM procedure is illustrated in Figure 2. The intent is to provide a muscular assist during ventricular systole. To do so, the latissimus dorsi muscle is paced by a cardiomyostimulator to gradually transform the muscle's contractile behavior from type II to type 1 characteristics. The stimulator is paced to myocardial contraction to provide an assist in conjunction with native left ventricular contraction. Due to the nature of the procedure and subsequent latissimus dorsi muscle transformation, estimated as a 12-week process, patients do not begin to receive hemodynamic or functional benefit for 2 to 3 months. Additionally, the repositioning of the latissimus dorsi muscle may promote atelectasis due to its restrictive presence in the thorax.

[Figure 2 ILLUSTRATION OMITTED]

Improvements in functional capacity and quality of life, as measured by change in New York Heart Association (NYHA) functional class (Tab. 2), have been documented.[60] Lee et al[61] found that cardiomyoplasty improved cardiac output and decreased myocardial oxygen demands in patients with dilated cardiomyopathy. Other research[62,63] suggests that cardiomyoplasty reverses the deleterious myocardial remodeling process often seen in individuals with heart failure.

Survival rates seem to depend on presurgical characteristics. Moreira et al[64] found a 1-year survival rate of approximately 84% and a 5-year survival rate of approximately 45%. The severity of clinical status prior to surgery and the degree of cardiac impairment were both associated with survival rate. Patients who had NYHA class III functional status the majority of the time and lower pulmonary wedge pressures were found to have a 5-year survival rate of 64%. This survival rate is comparable to 5-year survival rates seen with heart transplantation.[64] Furnary and colleagues[65] found 1-year through 5-year survival rates to be 73%, 57%, 49%, 44%, and 40%. Predictors for poor survival rate were NYHA class IV functional status, high pulmonary wedge pressure, atrial fibrillation, and balloon pump use postsurgery.[65] In another study by Moreira et al,[66] survival rates in patients undergoing cardiomyoplasty were 86.6%, 78.7%, and 65.6% at 6 months, 1 year, and 2 years, as compared with survival rates of 58.8%, 41.1%, and 27.4% over the same time period in a group of patients receiving medical management for heart failure. Patients in both groups had either NYHA class III or IV functional status.[66]

Documented changes in [VO.sub.2] are mixed in patients undergoing cardiomyoplasty. Furnary et al[67] found no improvement in peak [VO.sub.2] 6 months postcardiomyoplasty. Moriera and colleagues,[64] however, found an improvement of 3.6 mL [O.sub.2]/[kg.sup.-1]/[min.sup.-1] in peak [VO.sub.2] postcardiomyoplasty. Bocchi et al[68] divided a group of patients undergoing cardiomyoplasty using a presurgery peak [VO.sub.2] of 14 mL [O.sub.2]/[kg.sup.-1]/[min.sup.-1] as a cutoff point. After cardiomyoplasty, the subgroup with a presurgery peak [VO.sub.2] of less than 14 mL [O.sub.2]/[kg.sup.-1]/[min.sup.-1] improved by 5.3 mL [O.sub.2]/[kg.sup.-1]/[min.sup.-1] at the 6-month follow-up. The subgroup with presurgery peak [VO.sub.2] values greater than 14 mL [O.sub.2]/[kg.sup.-1]/[min.sup.-1], however, had only a 0.9-mL [O.sub.2]/[kg.sup.-1]/[min.sup.-1] increase in peak [VO.sub.2] over the same time period. Peak [VO.sub.2] prior to cardiomyoplasty seems to have an influence on postsurgical peak [VO.sub.2] improvements. Changes in peak [VO.sub.2] past 6 months postcardiomyoplasty do not appear to be as thoroughly investigated.

Cardiomyoplasty appears to improve impairments in patients with chronic heart failure. The ability for certain presurgical variables to predict postsurgical survival rates, however, indicates that appropriate patient selection is important. This procedure is reserved for patients with end-stage heart failure whose treatment alternatives are limited. Malignant arrhythmia and sudden death with mortality rates as high as 33% have been reported postoperatively.[69,70] Dynamic cardiomyoplasty, although promising, remains a limited viable option for patients with CHF.

Partial Left Ventriculectomy

Partial left ventriculectomy, also known as the Batista procedure, is a volume reduction procedure for improving left ventricular function.[71] The rationale for the PLV is that a reduction in the left ventricular chamber radius, through surgical resection of a region of the myocardium, decreases wall tension and improves cardiac efficiency. The PLV procedure is illustrated in Figure 3. To minimize the dilatory effects of mitral regurgitation, the mitral valve is replaced or repaired. Coronary revascularization may be performed concomitantly in patients with ischemia. Although this procedure is fairly new, reported outcomes are promising. Suma et al[72] studied 10 patients who underwent PLV. Eight of the patients had NYHA class IV functional status, and 6 patients required support with inotropic medications to maintain acceptable cardiac function. Eight of the subjects survived the procedure. Mean NYHA classification improved from 3.8 to 1.8, left ventricular end-diastolic volume decreased 18 mL, and ejection fraction increased 14.8%. Batista et al[71] studied 120 patients who received a PLV. Most patients had NYHA class IV functional status at the time of surgery. The 30-day mortality rate was 22%, and the 2-year survival rate was 55%. Postsurgery, 57% of the patients improved to NYHA class I, and 33% improved to class II. Ten percent had no improvement in NYHA classification. McCarthy et al[73] reported survival rates as high as 87% at 11 months.

[Figure 3 ILLUSTRATION OMITTED]

Patients are generally discharged within 7 to 10 days, and although low-level activity may be initiated as soon as the patient is hemodynamically stable and cardiac rehabilitation can be initiated, vigorous exercise is deferred for 6 to 8 weeks, presumably to be consistent with other cardiac postoperative guidelines for vigorous exercise.[59] Although PLV is another surgical option that holds promise for selected patients with CHF, experience with the PLV procedure and subsequent outcomes data are needed and will likely emerge over the next several years.

Endoventricular circular patch plasty is a variation of left ventricular reduction in which a patch, typically Dacron(*) or human tissue, is sewn into the left ventricle to connect viable myocardial tissue while excluding nonfunctional scar tissue. With time, the patch reshapes the left ventricle for optimized function. Dor and colleagues[74] described their experience with over 750 patients, noting that 90% of the patients demonstrated improved left ventricular function, with mortality rates similar to those for patients with elective bypass surgery (~2%-3%).

Left Ventricular Assist Device

The best available surgical bridge to heart transplantation for patients with CHF who are unable to maintain essential cardiac function despite maximized inotropic therapy is an LVAD.[75] Although the devices differ in design, the essential concept of the LVAD is illustrated in Figure 4. An implanted LVAD, with outflow at the cannulated left ventricular apex and aortic inflow, assists left ventricular cardiac output by diverting normal cardiac blood flow through a pump to augment blood flow exiting the heart. The blood chamber empties when full, triggered by an internal volume sensor. By operating in a "fill-to-empty" mode, the LVAD rate increases in proportion to venous return, allowing for a natural physiological response to varied physical effort. Because the chamber volume is fixed at 85 mL, the increased pumping rate during exercise provides for a normalized cardiac output with up to moderate workloads. The LVAD provides virtually all the resting cardiac output and the majority of cardiac output during exercise, upwards of 11 L/min, which is sufficient for most activities of daily living and moderate exercise. Depending on the degree of left ventricular dysfunction, the native left ventricle can augment the exercise cardiac output. As noted, there are variations of LVADs, depending on the manufacturer. Figure 4 illustrates one LVAD (HeartMate([dagger])). A pneumatic or vented electrical system is used to drive the pump. The pneumatic device requires the use of a mobile console, and the cart, although easily maneuvered, presents some mobility challenges. In the electrical device, the line that actuates the pump is connected to a small control unit worn in a shoulder harness The electrical version provides for greater mobility, an obvious advantage for exercise intervention. Although the native heart rate and LVAD rate do not match perfectly, there is a parallel increase in response to exercise, as the native left ventricle augments cardiac output. Likewise, diminished preload, as experienced with orthostatic intolerance, slows the LVAD rate to permit chamber filling.

[Figure 4 ILLUSTRATION OMITTED]

Left ventricular assist device implantation as a bridge to heart transplantation has provided an important benefit to patients with CHF who are critically ill and no longer responsive to maximized inotropic support. In addition, LVAD implantation may be used as a bridge to both the DCM and PLV procedures previously described, and the LVAD is undergoing investigation as a possible permanent device. Exercise testing and training for patients using an LVAD has proven to be safe, and available data indicate improved physiological and functional status.[76-78] Once the patient is stabilized, usually within a few days after LVAD implantation, progressive ambulation and subsequent exercise training are initiated. Because the LVAD provides for an enhanced cardiac output, the intensity for endurance exercise can be increased to facilitate skeletal muscle adaptation at higher workloads. Monitoring of any signs and symptoms of exertional intolerance, such as hypotension, is important, and exercises that might stress the physical insertion of the line that actuates the pump should be avoided. Although peak [Vo.sub.2] values increase only slightly with endurance exercise training, submaximal workload tolerance is significantly increased.[77-79] Given the increasing prevalence of LVAD use, positive exercise outcomes data, and the epidemiology of CHF, physical therapists should encounter greater numbers of patients with assist devices. Thus, an understanding of the exercise physiology and training guidelines is essential and available.[80,81]

Summary

The surgical alternatives to heart transplantation have expanded in recent years to include selected coronary revascularization,[51] TMR,[55] DCM,[64] PLV,[72] and LVAD implantation.[76] The use of LVADs is currently considered a bridge to the other surgical interventions. Given the largely positive exercise testing and outcomes results to date, the use of LVADs will likely be increasingly prevalent in cardiopulmonary intervention programs.

(*) EI du Pont de Nemours & Co Inc, 1007 Market St, Wilmington, DE 19898.

([dagger]) Thermo Cardiosystems Inc, 470 Wildwood St, Woburn, MA 01888-2697.

References

[1] 1998 Heart and Stroke Statistical Update. Dallas, Tex: American Heart Association; 1997.

[2] Michael KA, Parnell KJ. Innovations in the pharmacologic management of heart failure. AACN Clin Issues. 1998;9:172-191.

[3] Wielenga RP, Huisveld IA, Bol E, et al. Safety and effects of physical training in chronic heart failure: results of the Chronic Heart Failure and Graded Exercise Study (CHANGE). Eur Heart J. 1999;20:872-879.

[4] Wenger NK, Froelicher ES, Smith LK, et al. Clinical Practice Guideline No. 17: Cardiac Rehabilitation. Rockville, Md: US Dept of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, and the National Heart, Lung, and Blood Institute; October 1995. AHCPR publication 96-0672.

[5] Ries AL, Carlin BW, Carrieri-Kohlman V, et al. Pulmonary rehabilitation: joint ACCP/AACVPR evidence-based guidelines. Chest. 1997; 112:1363-1396.

[6] Kiilavuori K, Toivonen L, Naveri H, Leinonen H. Reversal of autonomic derangements by physical training in chronic heart failure assessed by heart rate variability. Eur Heart J. 1995;16:490-495.

[7] Adamopoulos S, Ponikowski P, Cerquetani E, et al. Circadian pattern of heart rate variability in chronic heart failure patients: effects of physical training. Eur Heart J. 1995;16:1380-1386.

[8] Radaelli A, Coats AJ, Leuzzi S, et al. Physical training enhances sympathetic and parasympathetic control of heart rate and peripheral vessels in chronic heart failure. Clin Sci (Colch). 1996;91 (suppl):92-94.

[9] Agostini D, Lecluse E, Belin A, et al. Impact of exercise rehabilitation on cardiac neuronal function in heart failure: an iodine-123 metaiodobenzylguanidine scintigraphy study. Eur J Nucl Med. 1998;25:235-241.

[10] Keteyian SJ, Brawner CA, Schairer JR, et al. Effects of exercise training on chronotropic incompetence in patients with heart failure. Am Heart J. 1999;138(2 pt 1):233-240.

[11] Tyni-Lenne R, Gordon A, Sylven C. Improved quality of life in chronic heart failure patients following local endurance training with leg muscles. J Card Fail. 1996;2:111-117.

[12] Keteyian SJ, Levine AB, Brawner CA, et al. Exercise training in patients with heart failure: a randomized, controlled trial. Ann Intern Med. 1996;124:1051-1057.

[13] Kavanagh T, Myers MG, Baigrie RS, et al. Quality of life and cardiorespiratory function in chronic heart failure: effects of 12 months' aerobic training. Heart. 1996;76:42-49.

[14] Willenheimer R, Erhardt L, Cline C, et al. Exercise training in heart failure improves quality of life and exercise capacity. Eur Heart J. 1998;19:774-781.

[15] Wielenga RP, Erdman RA, Huisveld IA, et al. Effect of exercise training on quality of life in patients with chronic heart failure. J Psychosom Res. 1998;45:459- 464.

[16] Wilson JR, Groves J, Rayos G. Circulatory status and response to cardiac rehabilitation in patients with heart failure. Circulation. 1996; 94:1567-1572.

[17] Kiilavuori K, Sovijarvi A, Naveri H, et al. Effect of physical training on exercise capacity and gas exchange in patients with chronic heart failure. Chest. 1996;110:985-991.

[18] Meyer K, Schwaibold M, Westbrook S, et al. Effects of short-term exercise training and activity restriction on functional capacity in patients with severe chronic congestive heart failure. Am J Cardiol. 1996;78:1017-1022.

[19] Demopoulos L, Bijou R, Fergus I, et al. Exercise training in patients with severe congestive heart failure: enhancing peak aerobic capacity while minimizing the increase in ventricular wall stress. J Am Coll Cardiol. 1997;29:597-603.

[20] Gordon A, Tyni-Lenne R, Jansson E, et al. Improved ventilation and decreased sympathetic stress in chronic heart failure patients following local endurance training with leg muscles. J Card Fail. 1997;3:3-12.

[21] Meyer K, Schwaibold M, Westbrook S, et al. Effects of exercise training and activity restriction on 6-minute walking test performance in patients with chronic heart failure. Am Heart J. 1997;133:447-453.

[22] Tyni-Lenne R, Gordon A, Jansson E, et al. Skeletal muscle endurance training improves peripheral oxidative capacity, exercise tolerance, and health-related quality of life in women with chronic congestive heart failure secondary to either ischemic cardiomyopathy or idiopathic dilated cardiomyopathy. Am J Cardiol. 1997;80:1025-1029.

[23] Ehsani AA, Miller TR, Miller TA, et al. Comparison of adaptations to a 12-month exercise program and late outcome in patients with healed myocardial infarction and ejection fraction [is less than] 45% and [is greater than] 50%. Am J Cardiol. 1997;79:1258-1260.

[24] Klainman E, Fink G, Zafrir N, et al. Effect of controlled exercise training in coronary artery disease patients with and without left ventricular dysfunction assessed by cardiopulmonary indices. Cardiology. 1997;88:595-600.

[25] Experience from controlled trials of physical training in chronic heart failure: protocol and patient factors in effectiveness in the improvement in exercise tolerance: European Heart Failure Training Group. Eur Heart J. 1998;19:466-475.

[26] Tyni-Lenne R, Gordon A, Europe E, et al. Exercise-based rehabilitation improves skeletal muscle capacity, exercise tolerance, and quality of life in both women and men with chronic heart failure. J Card Fail. 1998;4:9-17.

[27] Belardinelli R, Georgiou D, Cianci G, Purcaro A. Randomized, controlled trial of long-term moderate exercise training in chronic heart failure: effects on functional capacity, quality of life, and clinical outcome. Circulation. 1999;99:1173-1182.

[28] Foster C, Gal RA, Murphy P, et al. Left ventricular function during exercise testing and training. Med Sci Sports Exerc. 1997;29:297-305.

[29] Dubach P, Myers J, Dziekan G, et al. Effect of exercise training on myocardial remodeling in patients with reduced left ventricular function after myocardial infarction: application of magnetic resonance imaging. Circulation. 1997;95:2060-2067.

[30] Giannuzi P, Temporelli PL, Corra U, et al. Attenuation of unfavorable remodeling by exercise training in postinfarction patients with left ventricular dysfunction: results of the Exercise in Left Ventricular Dysfunction (ELVD) trial. Circulation. 1997;96:1790-1797.

[31] Goebbels U, Myers J, Dziekan G, et al. A randomized comparison of exercise training in patients with normal vs reduced ventricular function. Chest. 1998; 113:1387-1393.

[32] Ali A, Mehra MR, Malik FS, et al. Effects of aerobic exercise training on indices of ventricular repolarization in patients with chronic heart failure. Chest. 1999;116:83-87.

[33] Rinder MR, Miler TR, Ehsani AA. Effects of endurance exercise training on left ventricular systolic performance and ventriculoarterial coupling in patients with coronary artery disease. Am Heart J. 1999; 138(1 pt 1):169-174.

[34] Hambrecht R, Fiehn E, Yu J, et al. Effects of endurance training on mitochondrial ultrastructure and fiber type distribution in skeletal muscle of patients with stable chronic heart failure. J Am Coll Cardiol. 1997;29:1067-1073.

[35] Cider A, Tygesson H, Hedberg M, et al. Peripheral muscle training in patients with clinical signs of heart failure. Scand J Rehabil Med. 1997;29:121-127.

[36] Katz SD, Yuen J, Bijou R, LeJemtel TH. Training improves endothelium-dependent vasodilation in resistance vessels of patients with heart failure. J Appl Physiol. 1997;82:1488-1492.

[37] Hambrecht R, Fiehn E, Weigl C, et al. Regular physical exercise corrects endothelial dysfunction and improves exercise capacity in patients with chronic heart failure. Circulation. 1998;98:2709-2715.

[38] Callaerts-Vegh Z, Wenk M, Goebbels U, et al. Influence of intensive physical training on urinary nitrate elimination and plasma endothelin-1 levels in patients with congestive heart failure. J Cardiopulm Rehabil. 1998;18:450-457.

[39] Squires R. Exercise Prescription for the High-Risk Cardiac Patient. Champaign, Ill: Human Kinetics Inc; 1998.

[40] Cintron G, Johnson G, Francis G, et al. Prognostic significance of serial changes in left ventricular ejection fraction in patients with congestive heart failure: The V-HeFT VA Cooperative Studies Group. Circulation. 1993;87 (suppl 6): 17-23.

[41] Cohn JN, Johnson GR, Shabetai R, et al. Ejection fraction, peak exercise oxygen consumption, cardiothoracic ratio, ventricular arrhythmias, and plasma norepinephrine as determinants of prognosis in heart failure: The V-HeFT VA Cooperative Studies Group. Circulation. 1993;87(suppl 6):5-16.

[42] Balady GJ. Exercise training in the treatment of heart failure: what is achieved and how? Ann Med. 1998;30(suppl 1):61-65.

[43] Cahalin LP. Heart failure. Phys Ther. 1996;76:516-533.

[44] Cahalin LP. Exercise training in heart failure: inpatient and outpatient considerations. AACN Clin Issues. 1998;9:225-243.

[45] Squires RW. Cardiac rehabilitation issues for heart transplant patients. J Cardiopulm Rehabil. 1990;10:159-168.

[46] Hosenpud JD, Bennett LE, Keck BM, et al. The Registry of the International Society for Heart and Lung Transplantation: fifteenth official report--1998. J Heart Lung Transplant. 1998;17:656-668.

[47] Sadowsky HS. Cardiac transplantation: a review. Phys Ther. 1996;76: 498 -515.

[48] Luciani GB, Faggian G, Razzolini R, et al. Severe ischemic left ventricular failure: coronary operation or heart transplantation? Ann Thorac Surg. 1993;55:719-723.

[49] Shapira I, Isakov A, Yakirevich V, Topilsky M. Long-term results of coronary artery bypass surgery in patients with severely depressed left ventricular function. Chest. 1995;108:1546-1550.

[50] Hausmann H, Ennker J, Topp H, et al. Coronary artery bypass grafting and heart transplantation in end-stage coronary artery disease: a comparison of hemodynamic improvement and ventricular function. J Card Surg. 1994;9:77-84.

[51] Herlitz J, Brandrup G, Caidahl K, et al. Death, mode of death, morbidity, and requirement for rehospitalization during 2 years after coronary artery bypass grafting in relation to preoperative ejection fraction. Coron Artery Dis. 1996;7:807-812.

[52] Herlitz J, Brandrup-Wognsen G, Haglid M, et al. Predictors of death during 5 years after coronary artery bypass grafting. Int J Cardiol. 1998;64:15-23.

[53] Brandrup-Wognsen G, Haglid M, Karlsson T, et al. Preoperative risk indicators of death at an early and late stage after coronary artery bypass grafting. Thorac Cardiovasc Surg. 1995;43:77-82.

[54] Krabatsch T, Tambeur L, Lieback E, et al. Transmyocardial laser revascularization in the treatment of end-stage coronary artery disease. Ann Thorac Cardiovasc Surg. 1998;4:64-71.

[55] Mack CA, Magovern CJ, Hahn RT, et al. Channel patency and neovascularization after transmyocardial revascularization using an excimer laser: results and comparisons to nonlased channels. Circulation. 1997;96(suppl 9):II65-69.

[56] Pelletier MP, Giaid A, Sivaraman S, et al. Angiogenesis and growth factor expression in a model of transmyocardial revascularization. Ann Thorac Surg. 1998;66:12-18.

[57] Lutter G, Saurbier B, Nitzsche E, et al. Transmyocardial laser revascularization (TMLR) in patients with unstable angina and low ejection fraction. Eur J Cardiothorac Surg. 1998;13:21-26.

[58] Diegeler A, Schneider J, Lauer B, et al. Transmyocardial laser revascularization using the Holium-YAG laser for treatment of end stage coronary artery disease. Eur J Cardiothorac Surg. 1998;13:392-397.

[59] Dimengo JM. Surgical alternatives in the treatment of heart failure. AACN Clin Issues. 1998;9:192-207.

[60] Chachques JC, Grandjean PA, Carpentier A. Patient management and clinical follow-up after cardiomyoplasty. J Card Surg. 1991;6 (suppl 1) :89-99.

[61] Lee KF, Dignan RJ, Parmar JM, et al. Effects of dynamic cardiomyoplasty on left ventricular performance and myocardial mechanics in dilated cardiomyopathy. J Thorac Cardiovasc Surg. 1991;102:124-13].

[62] Kass DA, Baughman KL, Pak PH, et al. Reverse remodeling from cardiomyoplasty in human heart failure: external constraint versus active assist. Circulation. 1995 ;91:2314-2318.

[63] Patel HJ, Lankford EB, Polidori DJ, et al. Dynamic cardiomyoplasty: its chronic and acute effects on the failing heart. J Thorac Cardiovasc Surg. 1997;114:169-178.

[64] Moreira LF, Bocchi EA, Stolf NA, et al. Dynamic cardiomyoplasty in the treatment of dilated cardiomyopathy: current results and perspectives. J Card Surg. 1996;11:207-216.

[65] Furnary AP, Chachques JC, Moreira LF, et al. Long-term outcome, survival analysis, and risk stratification of dynamic cardiomyoplasty. J Thorac Cardiovasc Surg. 1996;112:1640-1649.

[66] Moreira LF, Seferian P Jr, Bocchi EA, et al. Survival improvement with dynamic cardiomyoplasty in patients with dilated cardiomyopathy. Circulation. 1991;84 (suppl 5) :III296 -III302.

[67] Furnary AP, Jessup FM, Moreira LP. Multicenter trial of dynamic cardiomyoplasty for chronic heart failure: The American Cardiomyoplasty Group. J Am Coll Cardiol. 1996;28:1175-1180.

[68] Bocchi EA, Guimaraes GV, Moreira LF, et al. Peak oxygen consumption and resting left ventricular ejection fraction changes after cardiomyoplasty at 6-month follow-up. Circulation. 1995;92(suppl 9): II216-II222.

[69] Moreira LF, Stolf NA, Bocchi EA, et al. Clinical and left ventricular function outcomes up to five years after dynamic cardiomyoplasty. J Thorac Cardiovasc Surg. 1995;109:353-363.

[70] Furnary AP, Magovern JA, Christlieb IY, et al. Clinical cardiomyoplasty: preoperative factors associated with outcome. Ann Thorac Surg. 1992;54:1139-1143.

[71] Batista RJ, Verde J, Nery P, et al. Partial left ventriculectomy to treat end-stage heart disease. Ann Thorac Surg. 1997;64:634-638.

[72] Suma H, Isomura T, Horii T, et al. Early result of volume reduction left ventriculoplasty (Batista operation) for dilated cardiomyopathy. J Cardiol. 1998;31:83-90.

[73] McCarthy PM, Starling RC, Wong J, et al. Early results with partial left ventriculectomy. J Thorac Cardiovasc Surg. 1997;114:755-765.

[74] Dor V, Saab M, Coste P, et al. Endoventricular patch plasties with septal exclusion for repair of ischemic left ventricle: technique, results, and indications from a series of 781 cases. Jpn J Thorac Cardiovasc Surg. 1998;46:389 -398.

[75] Frazier OH, Macris MP, Myers TJ, et al. Improved survival after extended bridge to cardiac transplantation. Ann Thorac Surg. 1994;57: 1416-1422.

[76] Jaski BE, Kim J, Maly RS, et al. Effects of exercise during long-term support with a left ventricular assist device: results of the experience with left ventricular assist device with exercise (EVADE) pilot trial. Circulation. 1997;95:2401-2406.

[77] Morrone TM, Buck LA, Catanese KA, et al. Early progressive mobilization of patients with left ventricular assist devices is safe and optimizes recovery before heart transplantation. J Heart Lung Transplant. 1996;15:423-429.

[78] Foray A, Williams D, Reemtsma K, et al. Assessment of submaximal exercise capacity in patients with left ventricular assist devices. Circulation. 1996;94(suppl 9);II222-II226.

[79] Humphrey R, Manetz C, Tolman DE, et al. Exercise training responses in a patient with a left ventricular assist device. J Cardiopulm Rehabil. 1996;16:310.

[80] Humphrey R. Exercise physiology in patients with left ventricular assist devices. J Cardiopulm Rehabil. 1997;17:73-75.

[81] Humphrey R, Buck L, Cahalin L, Morrone T. Physical therapy assessment and intervention for patients with left ventricular assist devices. Cardiopulmonary Physical Therapy. 1998;9(2):3-7.

R Humphrey, PT, PhD, FAACVPR, FACSM, is Assistant Professor, Department of Physical Therapy and Department of Physical Medicine and Rehabilitation, and Collateral Assistant Professor of Education, Virginia Commonwealth University, Medical College of Virginia Health Sciences Campus, 1200 E Broad St, PO Box 980224, Richmond, VA 23298 (USA) ([e-mail]). Address all correspondence to Dr Humphrey.

R Arena, PT, is a doctoral student in the combined physical therapy/physiology program, Virginia Commonwealth University.

Writing was provided by Humphrey and Arena. Concept and research design, project management, and consultation (including review of manuscript before submission) were provided by Humphrey.