Diastolic Congestive Heart Failure

Michael J. Koren, M.D., F.A.C.C., Director/CEO, Jacksonville
Center for Clinical Research, Medical Director, Non-Invasive
 Cardiology, Memorial Hospital Jacksonville, FL

 

Diastolic Congestive Heart Failure

Diastolic left ventricular dysfunction is now increasingly recognized as a condition leading to morbidity, hospitalizations and death. Recent studies suggest that isolated diastolic heart failure occurs in 30-60% of all patients presenting to hospitals with evidence of congestive heart failure (CHF). This review examines the features that make diastolic heart failure a unique clinical entity.

Pathophysiology

In its broadest sense, heart failure is a condition during which heart function fails to meet the metabolic needs of the rest of the body. Although there are well recognized circumstances of "high output" cardiac failure caused by, for example, hyperthyroidism or severe anemia, until recently it had been thought that most cases of heart failure were caused by impaired left ventricular (LV) systolic function. Now clinicians have recognized that many cases of congestive heart failure occur in patients with normal or near normal left ventricular systolic function as assessed by imaging modalities such as echocardiography or gated nuclear cardiac studies. These patients, while symptomatic, are found to have characteristic clinical signs and symptoms of congestive heart failure (CHF), such as dyspnea, orthopnea, and pulmonary rales associated with a hemodynamic profile of elevated filling pressures of the right heart, left atrium and left ventricle at end diastole.

The underlying pathophysiological abnormality in diastolic dysfunction is impaired relaxation of the left ventricle resulting in reduced left ventricular compliance. This reduced compliance causes inadequate filling of the left ventricule at normal diastolic pressures. Therefore, to maintain left ventricular filling and cardiac output, left atrial pressure must increase to a level that creates a pressure gradient great enough to provide adequate ventricular filling. Not uncommonly, this elevation of left atrial pressure will be transmitted into the pulmonary vascular system leading to pulmonary congestion and shortness of breath.

Several factors have been shown to be predisposing conditions associated with the development of diastolic congestive heart failure. The most common of these conditions is hypertension. Studies show that 60% of patients with diastolic congestive heart failure are hypertensive. Elevations of blood pressure alter left ventricular diastolic function via several mechanisms, some of which are not well understood. One of these mechanisms is the development of left ventricular hypertrophy. Left ventricular hypertrophy is a short-term adaptive response which reduces local LV wall stress. Longterm, left ventricular hypertrophy is maladaptive and known to be associated with poor prognosis in patients with hypertension and other medical conditions. Left ventricular hypertrophy often leads to poor left ventricular compliance and a vicious cycle of ever greater left ventricular filling pressures and cardiac hypertrophy.

Coronary artery disease, even in the absence of infarction, is also associated with the development of left ventricular diastolic dysfunction. Animal models have shown that intermittent short-term coronary occlusions lead to left ventricular stiffness and cardiac hypertrophy. Recent data suggest that coronary artery disease is a contributing factor to left ventricular diastolic dysfunction in approximately one-third of patients with the condition.

Less common conditions associated with diastolic congestive heart failure are hypertrophic cardiomyopathy, infiltrative cardiomyopathy such as amelydosis, and rarely restrictive cardiomyopathies.

Valvular heart disease (most commonly aortic stenosis and mitral regurgitation) is also known to cause left ventricular diastolic dysfunction. Advanced age may also be a factor. It is well known that echocardiographic evidence of diastolic dysfunction is extremely common in the elderly even in the absence of overt clinical diastolic heart failure. It is unclear as to whether the normal aging process involves progressive myocardial stiffening and reduced left ventricular compliance or whether these common findings reflect the effects of other underlying pathologies such as hypertension and coronary artery disease.

Prevalence and Prognosis

Congestive heart failure is the most common diagnosis for hospitalization of Medicare patients. CHF is the second-most common reason for outpatient cardiovascular visits. Nearly 3.5 million Americans receive care for congestive heart failure each year generating eleven million outpatient visits.

Several studies have assessed the prevalence of isolated diastolic dysfunction among patients with congestive heart failure. These studies have produced highly variable results, largely due to the absence of standard diagnostic criteria for diastolic dysfunction. Recent reports of patients undergoing assessment of left ventricular function by echo proximate to the time of diagnosis of clinical congestive heart failure have shown that approximately half of all CHF patients have primary diastolic dysfunction. For example, Framingham investigators reported that 51% of CHF patients in their community-based study had normal left ventricular systolic function. A Mayo Clinic sponsored study in Olmsted County, Minnesota showed similar findings — 43% of CHF patients demonstrated intact systolic function. These and other studies have also shown that left ventricular diastolic dysfunction is a disease of the elderly. The V-HEFT investigators of pharmacological intervention for heart failure found that 15% of a middle-aged population (less than 60 years of age) of patients with CHF had isolated diastolic dysfunction. In contrast, for patients with the onset of heart failure after 80 years of age, most studies show at least half of patients have primary diastolic dysfunction as the etiology for heart failure.

Other data show that diastolic heart failure is more common in blacks, particularly in African-American populations with a high prevalence of hypertension and diabetes. Female patients are also more likely to have primary diastolic dysfunction. Prognosis in patients with diastolic dysfunction is similar to that for patients with CHF due to systolic dysfunction. Five-year survival rates of 36% were reported in one series of diastolic heart failure.

Diagnosis

The diagnosis of diastolic heart failure is currently based on three criteria: 1) the presence of signs or symptoms of congestive heart failure such as dyspnea, orthopnea and activity intolerance in association with clinical signs of pulmonary vascular congestion such as pulmonary rales, jugular venous distension, and a cardiac gallop; 2) documentation of normal or only minimally reduced left ventricular systolic function by a cardiac imaging technique; and 3) evidence of abnormalities of left ventricular relaxation. This last criterion is the most difficult to document since the analysis of diastolic function can be complex. Unlike systolic dysfunction, there is no single physiological parameter such as ejection fraction that reliably describes the presence and severity of diastolic problems.

Normal diastole has three components: early rapid diastolic filling, mid diastole or diastases and atrial contraction. In diastolic dysfunction, myocardial changes occur that result in exaggerated filling during the early rapid filling stage of diastole or an increased atrial contribution to LV filling. These hallmarks of diastolic dysfunction form the basis for some of the diagnostic techniques detailed below.

Echocardiography is the most commonly used tool to assess left ventricular diastolic function. Unfortunately, no echocardiographic measurement is universally reliable. Instead, certain Doppler patterns have been useful at defining diastolic dysfunction. The echocardiographic assessments that are most commonly used to evaluate diastolic dysfunction involve the Doppler patterns of mitral inflow. For example, the most common way of evaluating left ventricular filling involves a comparison of the peak velocity of the Doppler E-wave as compared to the peak velocity of the Doppler A-wave (See Figure 1).

A normal ratio of these velocities is considered to be between 0.7 and 1.5. A ratio below 0.7 usually reflects an abnormally high atrial contribution to filling of the left ventricle _ one of the hallmarks of poor left ventricular compliance and a pattern often seen in patients with a history of clinical diastolic CHF. This pattern is also common in elderly patients greater than 75 years of age without any known history of congestive heart failure.

Another Doppler pattern of left ventricular diastolic dysfunction is called a restrictive filling pattern. This pattern results in an E-to-A ratio of greater than 1.5. This abnormally increased ratio is a reflection of rapid, early diastolic filling of the left ventricle which is abruptly slowed due to ventricular noncompliance. This pattern is often seen in patients with acute heart failure signs and symptoms and may be seen in patients with ongoing myocardial ischemia. Because patterns of diastolic filling can change over a short period of time with changing myocardial conditions (such as the degree of myocardial ischemia), abnormal Doppler patterns can rapidly change from an increased E-to-A ratio to a decreased E-to-A ratio and vice versa. Thus, it is recognized that a patient can demonstrate "pseudonormalization" of the left ventricular filling pattern on transmitral Doppler. This phenomenon is one of many recognized pitfalls in the evaluation of left ventricular diastolic function. Other factors which can confound the value of Doppler measurements are inappropriate location of sampling of the mitral inflow Doppler velocities, the effects of heart rate and changes related to the respiratory cycle. The coexistence of valvular heart disease can further complicate Doppler analysis. Patients not in sinus rhythm or those with a pacemaker are particularly difficult to assess and may make Doppler analysis of primary diastolic dysfunction impossible. In light of these challenges, it is recommended that exams evaluating parameters of diastolic function be performed by an experienced echocardiography laboratory.

Other echocardiographic parameters of diastolic dysfunction that can be useful are the isovolemic relaxation time, the E-wave deceleration time (time from peak E-wave velocity to the onset of the A-wave or zero velocity), and assessment of pulmonary venous flow reversal during atrial contraction. The isovolemic relaxation time is another echocardiographic parameter in which either low or high values indicate problems with diastolic function. In most labs, normal isovolemic relaxation time by echocardiography is between 30 and 90 milliseconds.

Many other techniques are available for evaluation of diastolic dysfunction that are not routinely used clinically. These methods include detailed pressure volume loops using invasive hemodynamic monitoring in the catheterization lab, nuclear medicine radionuclide techniques, and newer techniques using magnetic resonance imaging and ultra-fast CT. New echocardiographic techniques are also being developed. One technique that holds promise to enhance echocardiographic evaluation of diastolic function involves tissue Doppler imaging. The technique allows for the measurement of the velocity of the movement of the heart tissue. Recent studies show that simultaneous consideration of the peak E-mitral inflow velocity divided by the peak velocity of the tissue in the mitral annulus can provide a more accurate assessment of left ventricular diastolic function and pulmonary capillary wedge pressures. It remains to be seen if this ratio, called the E/E' ratio, becomes the diastolic equivalent to ejection fraction in the echocardiographic assessment of left ventricular function. Other novel assessments of left ventricular systolic and diastolic function such as midwall LV mechanics may help distinguish diastolic dysfunction from occult systolic dysfunction. Details of these echocardiographic techniques are beyond the scope of this review but are referenced in the bibliography.

Treatment

There are no specific published guidelines for the treatment of left ventricular diastolic dysfunction. The absence of these guidelines stems largely from the exclusion of patients with isolated diastolic heart failure from large clinical trials of heart failure treatments. Therapeutic trials of patients with heart failure signs and symptoms and normal ejection fractions are just beginning.

Even in the absence of evidence-based data, most clinicians agree that certain measures appear effective in the treatment of isolated diastolic heart failure. As is the case for systolic heart failure, the use of diuretics plays an important role in reducing pulmonary congestion and heart failure symptoms. Beta blockers and calcium channel blockers which slow heart rate (verapamil and diltiazem) also appear to have a role. These calcium channel blockers, generally not recommended for systolic heart failure, may help diastolic performance by slowing the heart rate and prolonging left ventricular filling time. They may also work through direct myocardial relaxation effects. Angiotensin converting enzyme inhibitors (ACE-i) and angiotensin receptor blockers (ARBs) which are mainstays for the treatment of systolic LV dysfunction are of uncertain benefit in isolated diastolic heart failure. Although empiric clinical trial evidence for the benefit of these classes of drugs is limited to some small studies showing improved exercise tolerance, many heart failure experts believe that there is a great benefit of these drugs in diastolic heart failure due to blood pressure lowering and neuro-hormonal blocking effects. Ongoing trials assessing treatment of diastolic CHF are listed in Table 1.


For patients with acute heart failure exacerbations due to diastolic dysfunction, aggressive diuresis is the cornerstone of therapy. Recent data with nesiritide (Natrecor®), a brain natriuretic peptide, show that this new agent appears equally effective in systolic and diastolic left ventricular heart failure. Although not studied systematically, nitrates appear quite useful for the acute treatment of congestive heart failure due to diastolic dysfunction and may also be useful for long-term maintenance therapy. Digoxin has not shown benefit in isolated diastolic heart failure and should not be used unless required for treatment of coexisting atrial arrhythmias.

Conclusions

Diastolic heart failure is a distinct clinical entity which may be the etiology for nearly half of all patients admitted to the hospital with signs and symptoms of pulmonary edema. The diagnosis is made based on clinical features and the demonstration of normal or near-normal systolic function. Abnormal echocardiographic parameters of left ventricular filling are important supporting evidence for the diagnosis. Clinical trial data for treatment of isolated diastolic heart failure are sparse. Diuretic treatment is the cornerstone of therapy. Other classes of medication which appear to be beneficial include beta blockers, certain calcium channel blockers, nitrates, intravenous natriuretic peptides acutely, and perhaps ACE inhibitors and angiotensin receptors blockers. Control of underlying predisposing factors such as hypertension and coronary artery disease is important.

References And Suggested Follow-Up Reading

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  2. Baker DW, Chin MH, Cinquegrani MP, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult. ACC/AHA Practice Guidelines 2001:1-56. http://www.acc.org/clinical/guidelines/failure/hf_index.htm.
  3. Banerjee P, Banerjee T, Khand A, et al. Diastolic heart failure: neglected or misdiagnosed? J Am Coll Cardiol 2002;39(1)138-141.
  4. deSimone G, Devereux RB, Koren MJ, et al. Midwall left ventricular mechanics. An independent predictor of cardiovascular risk in arterial hypertension. Circulation 1996;93:259-65.
  5. Florea VG, Henein MY, Cicoira M, et al. Echocardiographic determinants of mortality in patients >67 years of age with chronic heart failure. Am J Cardiol 2000;86(2):158-61.
  6. Gardin JM, Arnold AM, Bild DE, et al. Left ventricular diastolic filling in the elderly: the cardiovascular health study. Am J of Cardiol 1998;82(3):345-51.
  7. Hart CYT, Redfield, MM. Diastolic heart failure in the community. Curr Cardiol Reports 2000;2:461-469.
  8. Lainchbury JG, Redfield MM. Doppler echocardiographic-guided diagnosis and therapy of heart failure. Curr Cardiol Reports 1999;1:55-66.
  9. Levy D, Larson MG, Vasan RS, et al. The progression from hypertension to congestive heart failure. JAMA 1996;275(20):1557-1562.
  10. Parthenakis FI, Kanoupakis EM, Kochiadakis GE, et al. Left ventricular diastolic filling pattern predicts cardiopulmonary determinants of functional capacity in patients with congestive heart failure. Am Heart J 2000;140(2):338-44.
  11. Senni M, Tribouilloy CM, Rodcheffer RI, et al. Congestive heart failure in the community: a study of all incident cases in Olmsted County Minnesota in 1991. Circulation 1998;98:2282-2289.
  12. Vasan RS, Larson MC, Benjamin EJ, et al. Congestive heart failure in subjects with normal versus reduced left ventricular ejection fraction: prevalence and mortality in a population-based cohort. J Am Coll Cardiol 1999;39:1948-1955.
  13. Warner JG, Metzger DC, Kitzman DW, et al. Losartan improves exercise tolerance in patients with diastolic dysfunction and a hypertensive response to exercise. J Am Coll Cardiol 1999;33:1567-1572.
Jacksonville Medicine / February, 2002

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