Congestive Heart Failure: A Review and Case Report
From a Chiropractic Teaching ClinicThis section is compiled by Frank M. Painter, D.C.
Send all comments or additions to: Frankp@chiro.org
FROM: J Manipulative Physiol Ther 2005 (Jun); 28 (5): 356-364 ~ FULL TEXT
Osterhouse MD, Kettner NW, Boesch R
Department of Radiology,
Logan College of Chiropractic,
Chesterfield, MO 63006-1065, USA.
imaging@logan.eduOBJECTIVE: To discuss the case of a 62-year-old woman with congestive heart failure (CHF), precipitated by a previous arteriovenous malformation, and to review the clinical presentation, pathophysiology, and treatment options for patients with CHF.
CLINICAL FEATURES: The patient complained of pain, rapid weight gain, and shortness of breath. The index event for this patient was known to be an arteriovenous malformation. Biventricular cardiomegaly with pulmonary venous hypertension was evident on chest radiographs.
INTERVENTION AND OUTCOME: The patient received both medical care (drug therapy) and chiropractic care (manipulation and soft tissue techniques to alleviate symptoms and discomfort).
CONCLUSION: Patients with known and undiagnosed CHF may visit the chiropractic physician; thus, knowledge of comprehensive care, differential diagnosis, and continuity of care are important. Chiropractic management may be helpful in alleviating patient discomfort. Further clinical investigations may help to clarify the role of complementary and alternative care in the diagnosis and treatment of CHF.
From the FULL TEXT Article:
Background
Heart failure is a leading killer, affecting 1% of people aged 50 to 60 years and 10% of people in their 80s, for a total of 4.9 million Americans. In the United States, 40,0000 new cases are diagnosed each year. [1] In 1993, the cost of treating heart failure patients was approximately US$10 billion, with each individual case costing approximately US$20,000 per year. [2] African Americans have a 40% higher mortality rate from heart failure than Caucasians, and men have a 25% higher mortality rate than women. [2] Heart failure accounts for approximately 25,0000 deaths per year and is the most frequent cause of hospitalization in the elderly. [1] The median survival after the diagnosis of heart failure is 1.37 years for men and 2.48 years for women. [2] Only 50% of cases are initially diagnosed correctly. [1] Due to the clinical magnitude of heart failure and the low rate of accurate diagnosis, it is our intent to offer chiropractic physicians a review of the diagnosis, pathophysiology, and range of treatment options for the patient with heart failure. We present a patient with chronic heart failure seen at a chiropractic teaching clinic.
Discussion
Pathophysiology
Heart failure exists when cellular respiration becomes impaired because the heart cannot pump enough blood to support the metabolic demands of the body. The initial signs and symptoms of heart failure include dyspnea, cough, nocturia, mental disturbances, anxiety, and generalized fatigue. Peripheral edema of cardiac origin may be present which is symmetric and worse in the evening. [3] Edema is detected when the extracellular volume exceeds 5 L. With time, gastrointestinal symptoms emerge, such as abdominal bloating, anorexia, and fullness in the right upper quadrant. Eventually, cardiac cachexia may arise secondary to protein loss from enteropathy and increased cytokine levels. [1]
Pathophysiological theories of heart failure include the hemodynamic theory and the neurohumoral theory. In recent years, the hemodynamic theory has been replaced by the neurohumoral theory. The hemodynamic theory states that impaired hemodynamics, as characterized by low cardiac output, compensatory vasoconstriction, and compensatory sodium and water retention, create a vicious cycle eventually leading to the patient's demise. These altered hemodynamics result in the symptoms of cardiac failure but do not represent the whole story, as evidenced by the long-term failure of the pharmacological regimens seeking to normalize hemodynamic status. These drugs include positive inotropes, peripheral vasodilators, and diuretics. [4]
The neurohumoral theory states that heart failure is initiated and perpetuated by the activation of endogenous neurohormones and cytokines as a consequence of an “index event.” This “index event” may represent an acute injury to the heart or genetic mutation. The process of heart failure is now defined as the development and progression of left ventricle myocardial remodeling. [5] The neurohumoral theory evolved from the introduction of angiotensin-converting enzyme inhibitors (ACEIs) in the 1980s. This drug was the only intervention that improved symptoms while prolonging life. Not only did ACEIs affect hemodynamics by acting both as a diuretic and vasodilator, but it also protected against endothelial dysfunction and suppressed the adverse remodeling of the cardiac and vascular walls. Coronary endothelial dysfunction is known to stimulate vasoconstriction, smooth muscle proliferation, increased lipid deposition, and thrombosis, thus explaining in part the exercise intolerance seen in heart failure. [4]
Heart failure is also known to activate myocardial collagenases or matrix metalloproteinases by the alteration of myocardial tissue oxidation-reduction states. The result is loss of the interstitial supporting structure. The increase in cardiac mass is a result of reactive fibrosis, myocyte hypertrophy, and altered cytoskeletal structure within the cardiomyocyte. [5]
More recently, excessive cytokine activity has been noted in chronic heart failure. Cytokines act at short distances in a paracrine or autocrine manner. The 2 cytokines associated with heart failure are endothelin, which is a vasoconstrictor, and the proinflammatory vasosuppressor cytokine, tumor necrosis factor (TNF). [4] TNF produces myocyte hypertrophy and apoptosis. [5] The major source of cytokines may be the heart itself. TNF mRNA and protein have been found in the failing heart but not in normal hearts. Cytokines most likely perpetuate heart failure but do not initiate the condition.
Elevated neurohormone production possibly evolves for the short-term stabilization of dehydration or other causes of reduced cardiac output. Prolonged states of neurohormonal activation, however, result in progression of left ventricle remodeling. [5] There is overlapping of neurohumoral imbalance, endothelial dysfunction, and elevated cytokine expression resulting in the initiation and progression of chronic heart failure. [4] The chronic heart failure starts with an “index event” causing structural remodeling and leading to the clinical syndrome of heart failure. [5]
The “index event” can be any disease that leads to heart failure (Fig 4). The indexing event seen in this case report was an AVM. Myocardial infarction leads to the loss of contractile tissue that is replaced by fibrosis. [5]
Hypertension is the most common risk factor for heart failure. Stage 2 hypertension doubles the risk of developing heart failure in patients aged 60 to 70 years. [2] Risk factors include increased heart rate, advanced age, [2] insulin resistance, glucose intolerance, elevated blood lipids, left ventricle hypertrophy, obesity, and cigarette smoking. [6] Diabetes is found in 1 of 4 to 1 of 3 of patients with CHF, and diabetes increases the risk of CHF in post–myocardial infarction patients. [7] With increasing age, vascular stiffness results from thickening of the media and adventitia. The stiffness is due to myocyte loss, delayed relaxation, and calcium-uptake abnormalities. This thickening causes increased afterload culminating in left ventricle hypertrophy. [2]
The clinical syndrome of heart failure may include myocardial energy starvation and salt and water retention. Arterial remodeling diminishes coronary vessel size and contributes to the energy starvation of heart failure. With decreases in cardiac output, arterial blood volume is reduced, which stimulates the sympathetic nervous system and the renin-angiotensin-aldosterone cycle. The result is reduced renal blood flow. Thus, the kidneys retain salt and water to restore perfusion, resulting in congestion and edema. [5]
The transition from this compensated hypertrophy to heart failure occurs when myocytes lose the ability to normally maintain calcium ion homeostasis. Heart failure is accompanied by a decreased amount of calcium ion release from the sarcoplasmic reticulum. Houser et al8 propose that the sarcoplasmic reticulum calcium ion release does not offset the frequency-dependent excitation-contraction (EC) coupling refractoriness. These abnormal levels of sarcoplasmic reticulum calcium thus produce the EC coupling defects of the failing myocyte. Therefore, abnormal EC coupling contributes to the dysfunctional calcium handling in heart failure. Treatment approaches that improve calcium ion homeostasis may prevent heart failure onset.
Clinical Diagnosis
Physical findings associated with congestive failure may include a weak thready pulse and pulsus alterans that suggests diminished left ventricle function. Cheyne-Stokes respiration and tachycardia are common. Tachycardia is the body's attempt at maintaining adequate cardiac output. [1] Beyond these vital signs, findings of congestion include jugular veins that show central venous pressure elevation or paradoxic inspiratory venous pressure rise, known as the Kussmaul sign. [3] This test for jugular venous distention is 90% specific but only 30% sensitive for elevated left ventricular filling. Valsalva maneuver is 91% specific and 69% sensitive for detecting left ventricle dysfunction.
The New York Heart Association (NYHA) functional classification of dyspnea is graded I to IV for left ventricular heart failure (Fig 5). On cardiac examination, the point of maximal impulse may be displaced laterally and downward, indicating cardiomegaly. [1] This patient showed cardiomegaly. Gallop rhythm is a reliable sign of a failing ventricle, especially the quadruple rhythm or summation gallop. [3] A third heart sound is 99% sensitive but only 24% specific for heart failure. Electrocardiography (ECG) may reveal atrial and ventricular arrhythmias that are not specific for heart failure, nonetheless a common finding. Pulmonary examination may show evidence of rales and pleural effusion. Right-sided heart failure may be manifested by the presence of hepatojugular reflux indicating congestive hepatomegaly. [1]
Diagnostic Imaging
After a physical examination suggestive of congestive failure, chest radiography should be obtained. Radiographic findings of heart failure may include cardiomegaly, cephalization of vessels, hilar haze, and interstitial edema. Cardiomegaly is determined by a cardiothoracic ratio greater than 0.50 on the posteroanterior projection. However, the finding of an elevated diaphragm, apical fat pad, and even anteroposterior expiratory films may mimic cardiomegaly.
Cardiomegaly is sensitive for determining the setting of decreased ejection fraction. Patients with diastolic failure may have a normal heart size, thus differentiating diastolic from systolic failure. [1] The normal heart size in diastolic failure is due to the inability of the ventricles to dilate normally during diastole. The heart is often imaged in diastole because it is the longest phase of the cardiac cycle. Therefore, the heart size appears normal. These patients have little, if any, systolic impairment to create cardiomegaly. Forty to 50% of the elderly with heart failure have the diastolic variety. [9] The radiographic findings of cephalization and hilar haze are more sensitive than cardiomegaly at determining increased preload. Cephalization occurs when the pulmonary venous pressure rises as a result of elevated left ventricular preload. Dilated upper lobe pulmonary veins and constricted lower lobe veins are then noted. Cephalization is also known as vascular redistribution, flow shift, flow inversion, or pulmonary venous hypertension. [10]
Interstitial edema is radiographically represented by linear densities known as Kerley lines or by hilar haze known as the butterfly pattern. Lastly, the plain film is helpful in identifying pleural effusion resulting from heart failure. [1] Badgett determined that the chest radiograph is only reliable when excluding or confirming increased preload or systolic dysfunction in patients with high or low prevalence of heart disease. The chest radiograph should be used then in conjunction with a comprehensive history, targeted physical examination, and confirmatory tests for an accurate diagnosis. [10]
CHF testing frequently includes use of ECG. It is not specific, however, for heart failure. Atrial and ventricular arrhythmia is common to heart failure and can be detected by ECG. Prolonged QRS duration has been correlated with decreased ejection fraction. [11] Echocardiography is more useful, and an ECG is simultaneously performed. The transthoracic 2-dimensional echocardiograph with Doppler flow assesses the left ventricle size, mass, and function. [1]
Echocardiography is currently the method of choice for anatomic cardiac characterization in most clinics and hospitals. [12] M-mode and 2-dimensional echocardiography are used to evaluate left ventricular functional impairment. The echocardiograph will display left ventricular enlargement, increased end-diastolic and systolic volumes, and reduced myocardial fractional shortening and calculate ventricular ejection fraction. Due to the diminished left ventricular compliance and elevated left ventricular end-diastolic pressure, mitral valve motion may be abnormal. [13] Stress echocardiography performed using low-dose dobutamine, as well as positron emission tomography (PET) and thallium 201 radionuclide scanning can identify hibernation. Hibernation is cardiac dysfunction that is reversible and occurs during ischemia. Identification of hibernation helps to determine suitable candidates for surgery that can provide improved ejection fraction and other measures of left ventricular function. [8] Echocardiography is portable, making it convenient. However, echocardiography is operator-dependent, and its acoustic window limitations constrain the field of view. Precise cardiac chamber size cannot be determined due to the arbitrary scan planes that result from contour variation of the chest wall. [12] Emerging cardiac imaging techniques include magnetic resonance imaging (MRI) and CT. They provide exquisite detail of the cardiac chambers and pericardium and a look at integrated cardiorespiratory systems. [12]
Cardiac MRI evaluates cardiac function by cine gradient-echo imaging of the ventricles. Cardiac wall motion, ventricular volumes, and flow analysis can be assessed. The flow analysis assesses cardiac function by measuring velocity and flow during the cardiac cycle. Ventricular volumes are obtained using Simpson's rule. The ventricular area is measured for each slice and then multiplied by the combined slice and gap thickness that represents each slice volume. Ventricular volume is the sum of the slice volumes. End-diastole and end-systole volumes can be used to calculate stroke volume, ejection fraction, regurgitant fractions, and shunts. Data points acquired throughout the cardiac cycle can be used to generate volume-time curves to detect diastolic filling or systolic ejection dysfunction. [14] Dilated cardiomyopathy has been shown with MRI to display heterogeneity in the wall thickness with thinning of the apical myocardium and posterior septum. Change in myocardial thickness for dilated cardiomyopathy is reversed from normal, with thickness decreasing through the anterolateral wall from base to apex. [13] More advanced tools allow for real-time MR fluoroscopy, myocardial perfusion, myocardial tagging, and myocardial viability. [15]
Cardiac MRI also has relevant limitations. MRI has many contraindications, including pacemaker, implanted defibrillator, Swan-Ganz catheter, recent coronary artery stenting, and cardiac arrhythmias that significantly impair cardiac imaging. A high-performance MRI system is costly but necessary to enable cine gradient-echo imaging and 3-dimensional contrast-enhanced MRA with acquisition times of less than 25 seconds (1 breath-hold).15 MRI sequences are also time-intensive, highly motion-sensitive, and subject to artifacts that degrade image quality. [12]
Ultrafast electron beam CT (EBCT) shows structural abnormalities and areas of decreased cardiac contractility. Ventricular volume measurements provide accurate calculations for stroke volume and ejection fraction of both right and left ventricles. Ultrafast EBCT is performed by magnetically focusing and deflecting an electron beam. It replaces tube rotation used in conventional CT scanning. The electron beam hits fixed tungsten target rings resulting in a collimated fan beam of radiation which allows extremely short imaging times of 50 milliseconds. This imaging time is fast enough to study ventricular function. However, unlike MRI, EBCT produces individual images rather than composite images. Multiple factors inhibit the widespread use of ultrafast EBCT imaging. Ultrafast EBCT scanners are not readily available. In addition, an examination results in a relatively large radiation dose of approximately 0.05 Gy (5 rad). Lastly, intravenous contrast may exclude patients with allergies or renal disease. [14]
The state-of-the-art CT is the multidetector row computed tomographic scanner. This 16-section scanner emerged in 2001 and has the advantage over its imaging counterparts by being faster with improved temporal resolution and better spatial resolution in the transverse plane. The image is isotropic, meaning that the resolution is equally adequate in the sagittal, coronal, and axial planes; therefore, there is no preferred plane for image reconstruction. The 16-section scanner even has an advantage over MRI. MRI requires the examiner to choose the plane of imaging before data acquisition, whereas this type of CT scanner allows for the optimal plane to be chosen after the examination. This new generation of scanner works by allowing simultaneous acquisition of up to 16-submillimeter sections with gantry rotation times of less than 0.5 seconds. Currently, the technology is being used for visualization of plaqued coronary artery branches or coronary stents (Fig 6). This technique may become the preferred modality for cardiac imaging. [16, 17]
With the continued development of new agents and instrumentation, nuclear medicine has its role in the analysis of heart disease. [18] Nuclear cardiology is used for heart disease screening, prognosis evaluation, and myocardial viability. [19] Patients with significant myocardial viability may benefit from revascularization rather than medical therapy. [20] Those patients with predominantly scar tissue may require heart transplantation and are not candidates for revascularization. [21] The most sensitive nuclear modalities for assessment of viability are thallium 201 and 18-fluorodeoxyglucose (FDG)–PET. [20] FDG-PET identifies patients who will show improvement of left ventricle function, relief from heart failure symptoms, and improved long-term prognosis when revascularization is used. However, PET is not readily available; therefore, a less expensive nuclear imaging technology, single photon emission CT is often used for FDG imaging. PET and single photon emission CT have been shown to demonstrate good agreement. [21] Cavitary tomoscintigraphy directly evaluates ejection fraction and volumes in both ventricles and will most likely replace traditional isotopic angiography. [20]
Catheter angiography is rarely indicated for ventricular assessment. However, this imaging technique does evaluate systolic function if noninvasive studies are inadequate. [22] Radionuclide angiography provides quantitative measurement of the left ventricle ejection fraction and regional wall motion. [1] Coronary arteriography is required if revascularization is contemplated for treatment. Arteriography determines the severity and extent of coronary artery disease. The most invasive procedure that may be indicated is the endomyocardial biopsy. It may determine the cause of cardiomyopathy. [22]
Clinical Laboratory
Laboratory evaluation is valuable in the diagnosis of heart failure. Patients already diagnosed with heart failure should undergo a thyroid panel to rule out hypothyroidism or hyperthyroidism as a cause. Severe anemia may also cause heart failure. More importantly, anemia should be ruled out because it worsens existing heart failure. [1] Plasma atrial natriuretic peptide levels are elevated in response to increased intra-atrial pressure, and the failing ventricle will secrete brain natriuretic peptide (BNP).
B-type natriuretic peptide, brain natriuretic peptide, or BNP, is a cardiac neurohormone secreted in response to increased ventricular volume and pressure. This peptide is known to increase in proportion to the severity of heart failure. BNP levels correlate with the following: left ventricle end-diastolic pressure, pulmonary artery wedge pressure and atrial pressure, ventricular systolic and diastolic dysfunction, and left ventricle hypertrophy. This test is a fluorescent immunoassay that quantitatively measures BNP levels in whole blood or plasma specimens. Sensitivity ranges from 85% to 97% and specificity from 84% to 92%. The negative predictive value is greater than 95%; therefore, a normal BNP level can help to rule out heart failure. The range of values is from 0 to 3500 pg/mL, with the most accepted upper limit of normal at 100 pg/mL. Values higher than 100 pg/mL suggest a diagnosis of heart failure. Depending on the severity of heart failure, BNP values can be elevated 25 times higher than in normal individuals. Right ventricular dysfunction will also have elevated BNP values but not to the same extent as left ventricular dysfunction.23 Multiple applications of natriuretic peptide are reported, ranging from screening to monitoring treatment (Fig 7).
Treatment
Growth hormone is 1 therapy that helps maintain normal cardiac structure and function. Growth hormone deficiency reduces the growth rate of the heart muscle, impairs cardiac performance, and negatively impacts myocardial contractility. Studies have shown that administering growth hormone may improve contractility, induce myocyte hypertrophy, and improve the metabolic efficiency of the heart. Other studies have disputed these results. The difference may be the result of acquired growth hormone resistance that occurs in heart failure patients, especially those with cardiac cachexia. After testing the patient for resistance, growth hormone may be a suitable treatment option for heart failure. [24]
Other pharmacological treatments include the use of ACEIs in conjunction with diuretics and digitalis. As previously discussed, the neurohormone blockers prevent progression of heart failure, whereas diuretics control the signs and symptoms of congestion. [5] However, ACEIs act on the renin-angiotensin-aldosterone system but are less effective in the elderly and obese who carry low levels of renin. Calcium antagonists are more effective for patients with low levels of renin. Autonomic responses are pharmacological targets. a1-Adrenoceptor blockers decrease peripheral resistance and reduce afterload, helping to reduce left ventricle hypertrophy. ß-Adrenoceptor antagonists reduce heart rate and cardiac output that improves exercise tolerance and reduces the recurrence rate of myocardial infarctions. [17] The future of drug therapy will likely focus on adrenergic ß-blockers, angiotensin II receptor blockers, ACEIs, endothelin inhibitors, TNF-a blockers, and drugs designed to increase plasma concentrations of counterregulaory atrial natriuretic peptides. [15]
New surgical techniques are on the horizon for heart failure treatment. Dr Randas J. Batista introduced surgical ventriculoplasty, where segments of still viable but abnormally functioning myocardium of the left ventricle are resected. This procedure has been shown to increase the cardiac ejection fraction. [4, 24] Several hundred cases of end-stage dilated cardiomyopathy have been successfully treated with the Batista procedure. [4] Alas, the only effective proven treatment to date for end-stage heart failure is heart transplantation. [24] Heart transplantation has a long-term survival rate of 92.7%, 81.3%, 79.3%, 80%, and 23% at 30 days, 1 year, 4 years, 10 years, and 19 years, respectively. [25-28]
Nonpharmacological therapies are also disease modifying and could be administered by chiropractic physicians in conjunction and as a complement to drugs and surgery in patients with CHF. A comprehensive holistic approach is patient-centered and beneficial. The congestive failure patient should be coached on dietary changes. The renal response to reduced cardiac output is the retention of sodium; therefore, sodium intake should be restricted to 3 g/dL. This level of sodium restriction can be obtained by reducing foods with high sodium content, such as canned foods and packaged luncheon meats. For severe volume overload, sodium intake should be reduced to less than 2 g to improve the effectiveness of diuretics. The patient should be advised of the potential harm in using salt substitutes high in potassium while using drugs that elevate potassium levels such as potassium-sparing diuretics, ACEIs, or renal insufficiency. Another necessary dietary change is to limit fluid intake in sodium-restricted patients. Fluid should be limited to less than 2 L/d in hyponatremic patients and those with severe volume overload. [29]
The patient's lifestyle must also be monitored. Alcohol is a cardiotoxin; its consumption is ill-advised. Alcohol should also be discouraged because of its myocardial depressant effect. Weight control is also necessary. The cardiac workload is increased in obesity even in the absence of hypertension. Nearly half of obese patients with sudden cardiac death have severe dilated cardiomyopathy. Clinicians should moderately restrict caloric intake and encourage exercise training to ensure a gradual weight loss. [29] Not only can an exercise regimen help with weight control, it can also have positive effects on cardiac functional capacity by improving endothelial function. However, the cardiac improvement is only maintained with a continuous exercise program, and all values are lost after 3 weeks of inactivity. Previous studies have shown that exercise decreases mortality by 25% (at a 3-year follow-up), increases the return-to-work rate, and may reduce patient cost due to reduced hospitalization.30 Lastly, nearly half of patients with heart failure die of ischemic events; thus, lifestyle changes to reduce coronary artery disease are essential. For example, adjust fat intake to control lipid levels and recommend cessation programs for smokers. [29]
Supplements may also be helpful for heart failure. Thiamine is often deficient in patients on high doses of diuretics. Coenzyme Q is important in mitochondrial energy transfer and has been shown to reduce hospitalizations in the heart failure patient. [29] Vitamin E (400-800 IU) and purple grape juice are antioxidants which may reduce lipid peroxidation that leads to atherosclerosis. Vitamin C potentiates the antioxidant effect of vitamin E. Magnesium may be needed in those on diuretics that induce magnesium loss. [29] A recent study revealed that Crataegus extract WS 1442 may be a safe and effective alternative to the conventional treatment of mild heart failure (NYHA class II). This extract is made from hawthorn leaves with flowers standardized to a constant content of oligomeric procyanidines. The pharmacological outcome is to produce a positive inotropic effect on the left ventricular muscle of terminally failing hearts, also acting as an antioxidant and demonstrating damage-preventing properties. The cardiac muscle underwent increased force of contraction with Crataegus allowing for improvements in physical exercise tolerance. [31]
Acupuncture may help to improve the prognosis of advanced heart failure patients. In heart failure, the sympathetic nerve activity of muscle is increased. There is an indirect relationship between the amount of sympathetic nerve activity and prognosis with higher activation resulting in the worst prognosis. Acupuncture has been found to create a sympathomodulatory effect with greater effects being found in diseased subjects compared with healthy subjects. The mechanism of this response is presumed to result from endogenous opioids in the central nervous system. Myocardial ischemia can be reduced in as little as 30 minutes after electroacupuncture. [32]
Spinal manipulation, in addition to its somatic benefits, may favorably modulate the autonomic and neuroendocrine imbalance of CHF and improve stress coping in this chronic illness. Validation of its role awaits scientific scrutiny.
Conclusion
Comprehensive care, differential diagnosis, and continuity of care are important aspects of primary care. These principles are emphasized in the chiropractic clinical curricula and delivered through chiropractic patient management. This case report also typifies the application of primary care principles in a chiropractic teaching clinic. Holistic care delivered with compassion but guided by rigorous science is in the best interest of the patient. A clinical trial using a multidisciplinary team could further clarify the role of complementary and alternative care in the diagnosis and treatment of CHF. It is our hope that this report stimulates research in this critically important area of patient care.
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