Editorials - April 15, 2001 - American Family Physician

Editorials

Heart Failure, Diastolic Dysfunction and the Role of the Family Physician

KEN GRAUER, M.D.
University of Florida College of Medicine
Gainesville, Florida

See article on page 1593.

The message conveyed in the article by Hoyt and Bowling¹ in this issue of American Family Physician is clear: heart failure is increasingly becoming a major reason older adults are admitted to hospitals. The morbidity and mortality associated with heart failure is alarmingly high. Despite exciting advances in treatment over the past few years, optimal therapy is frequently not used. The result is frequent recurrences of heart failure episodes that necessitate readmission after hospital discharge and ultimately lead to progressive deterioration of health status in a majority of cases.

Fortunately, as emphasized by Hoyt and Bowling,¹ much can be done now for patients with heart failure. Important interventions for physicians to consider include careful assessment and monitoring of patients to include regular follow-up visits; initiation and regulation of nonpharmacologic measures such as regular exercise, reduction of salt intake, recording daily weights; adjustment of standard medication regimens with early introduction of potentially life-prolonging agents (e.g., angiotensin-converting enzyme [ACE] inhibitors, beta blockers and spironolactone) when possible; and planning programs for continued home-based care with increased patient initiative and adjunctive use of physician extenders when appropriate. Family physicians can and should be at the forefront of implementing and overseeing the optimal use of these interventions in the care of patients with heart failure.

The optimal management of heart failure begins with an accurate diagnosis. Echocardiography is an indispensable component of the diagnostic work-up. The purpose of echocardiography is twofold: (1) noninvasive assessment for an underlying precipitating cause of symptoms, and (2) evaluation of left ventricular function. Clinical detection of flow-dependent valvular disorders is often more difficult in the presence of low-output states. For example, the murmur associated with aortic stenosis may not be appreciated or its severity may be underestimated in a patient with heart failure.

The treatment of choice for new-onset heart failure when the cause is critical aortic stenosis is valve replacement rather than medication (use of ACE inhibitors is ill- advised in this situation). Severe mitral or aortic regurgitation, hypertrophic cardiomyopathy and pulmonary hypertension are other potential precipitating causes of heart failure that might be detected by echocardiography and that mandate a different approach to treatment.

The second reason to routinely obtain echocardiograms on virtually all patients with new-onset heart failure is to determine whether heart failure is primarily the result of systolic dysfunction or diastolic dysfunction, or some combination. Although Hoyt and Bowling¹ intentionally limit the scope of their discussion to the management of patients with systolic dysfunction, family physicians must be equally skilled in the evaluation and treatment of patients with diastolic dysfunction.

Primary diastolic dysfunction accounts for the symptoms of heart failure in at least one third of cases.² Left ventricular contractility is normal or increased in these patients. The problem is that a physical examination cannot reliably distinguish between systolic and diastolic dysfunction because there is overlap of almost all signs and symptoms in these two forms of heart failure.³ Echocardiographic confirmation of diastolic dysfunction as the cause of heart failure is made not only on the basis of finding normal or increased contractility, but also on the basis of the presence of normal ventricular function that occurs in association with concentric hypertrophy and reduced ventricular compliance, as determined by Doppler examination. Mild or moderate left-atrial enlargement is also often found to be a consequence of the increased atrial pressure needed for filling the noncompliant ventricle. Failure to recognize that heart failure episodes are caused by diastolic rather than systolic dysfunction is an important cause of improper treatments and frequent readmission to hospitals.

Diastolic dysfunction should be strongly suspected as the possible cause of heart failure symptoms in older patients with longstanding hypertension. The principal problem in heart failure caused by pure diastolic dysfunction is inadequate ventricular filling during diastole because of increased contractility, ventricular hypertrophy and reduced ventricular compliance (ventricular thickening leads to stiffening and the inability to adequately relax during the diastolic filling phase), as opposed to generalized chamber dilatation with global reduction in contractility that is found in systolic dysfunction.

Treatment of heart failure caused by diastolic dysfunction remains controversial because no prospective, randomized clinical trials have been undertaken to study long-term management and outcome of this disorder. Definitive recommendations are therefore lacking, and the therapeutic approach is largely empiric.⁴ Nevertheless, certain treatment principles seem prudent. These include avoiding the use of digoxin (which would be expected to aggravate the problem of ventricular filling by further enhancing ventricular contractility); cautious use of diuretics (over-diuresis is likely to further impair ventricular filling); and consideration of negative inotropic agents such as verapamil, diltiazem and beta blockers in moderate to full doses as primary therapy. In contrast, verapamil and diltiazem should not be used in patients with systolic-dysfunction heart failure.

Although the use of beta blockers is now advocated as a life-prolonging measure for the treatment of systolic-dysfunction heart failure, therapy must be initiated at a very low dose, and only gradually (over a period of weeks to months) titrated upward to a moderate dose. This approach differs from the much more rapid upward titration of beta blocker dose when treating pure diastolic dysfunction, for which negative inotropy may be beneficial by improving compliance and facilitating ventricular filling. ACE inhibitors (and possibly angiotensin-receptor blocking agents) are indicated as primary therapy for both systolic- and diastolic-dysfunction heart failure; however, excessive afterload reduction must especially be avoided when diastolic dysfunction is present because of the adverse effect this can have on ventricular filling. Finally, vigorous control of hypertension is imperative in patients with heart failure caused by diastolic dysfunction, because control of hypertension may prevent progression or even reversal of the disorder by addressing the primary cause of most cases.

In summary, Hoyt and Bowling¹ suggest that management of heart failure will often involve a joint effort between family physicians and cardiologists. Attention given to the factors discussed in their article, active collaboration with cardiology colleagues and a keen awareness of when to refer patients should allow major assumption of the ambulatory care of these patients by family physicians in the majority of cases.⁵

Ken Grauer, M.D., is professor and assistant director of the Family Practice Residency Program in the Department of Community Health and Family Medicine at the University of Florida, Gainesville, Florida.

Address correspondence to Ken Grauer, M.D., University of Florida College of Medicine, Gainesville, 625 SW 4th Ave., P.O. Box 147001, Gainesville, FL 32614 (e-mail: grauer@fpmg.health.ufl.edu).

REFERENCES

Hoyt RE, Bowling LS. Reducing readmissions for congestive heart failure. Am Fam Physician 2001; 63:1593-8.

Kessler KM. Heart failure with normal systolic function: update of prevalence, differential diagnosis, prognosis, and therapy. Arch Intern Med 1988; 148:2109-11.

Vasan RS, Benjamin EJ, Levy D. Congestive heart failure with normal left ventricular systolic function: clinical approaches to the diagnosis and treatment of diastolic heart failure. Arch Intern Med 1996; 156:146-57.

Packer M, Cohn JN. Consensus recommendations for the management of chronic heart failure. On behalf of the membership of the advisory council to improve outcomes nationwide in heart failure. Am J Cardiol 1999;83:1A-38A.

Grauer K. Treating heart failure in primary care [Editorial]. J Fam Pract 1999;48:759-60.

Group A Beta-Hemolytic Streptococcal Pharyngitis

KENNETH BROMBERG, M.D.
State University of New York Health Science Center at Brooklyn College of Medicine
Brooklyn, New York

See article on page 1557.

In a review of group A beta-hemolytic streptococcal pharyngitis in this issue of American Family Physician, Hayes and Williamson¹ provide readers with some controversy. After discussing the uncontroversial epidemiology, diagnosis and therapy, the authors end with a prediction that penicillin might not be the drug of choice for the treatment of strep throat in the future.

Citing two important sources, the 2000 Red Book² and the practice guideline developed by the Infectious Diseases Society of America³ (now available on the Internet at http://www. journals.uchicago.edu/CID/home.html), Hayes and Williamson¹ stress the diagnosis of streptococcal pharyngitis. Because the rate of streptococcal carriage can be high, the way to avoid detection of carriers and unnecessary use of antibiotics is to perform cultures with discrimination. The authors support the use of prediction rules. Logically, cultures should not be obtained in patients who are unlikely to have group A beta-hemolytic streptococcal pharyngitis, such as those with upper respiratory tract infection, nor should cultures be repeated. By reducing the likelihood of treating carriers, this approach goes a long way toward eliminating some of the controversy related to the diagnosis and treatment of strep throat.

Hayes and Williamson¹ do not address the difference between treating pharyngitis in the general population and treating it in patients with a personal or family history of rheumatic fever. Like immunocompromised patients with fever, patients with rheumatic fever must be aggressively treated. On initial presentation with rheumatic fever, patients are given penicillin G benzathine without waiting for the results of the initial culture. With subsequent episodes of pharyngitis in these patients, post-treatment cultures should be performed to ensure that group A beta-hemolytic streptococci have been eradicated. This treatment approach is also appropriate during outbreaks of rheumatic fever in closed populations, but it is not appropriate for the general population.³

Many infectious disease experts strongly disagree with the notion that there is an ever-increasing rate of penicillin failure in the treatment of group A beta-hemolytic streptococcal pharyngitis.⁴ Although cephalosporins may result in a higher eradication rate for group A beta-hemolytic streptococci, the decision to replace treatment with penicillin or amoxicillin with the more expensive cephalosporins would be based on a resurgence of rheumatic fever from lower rates of streptococcal elimination, which has not been shown to be a problem to date. It is the majority opinion that most penicillin failures occur in carriers in whom the carrier state is not eradicated.

Erythromycin is the drug of choice in penicillin-allergic patients. Cephalosporins may be indicated in some situations, such as when erythromycin cannot be tolerated. Under these circumstances, it might be appropriate to use a beta-lactamasestable medication such as amoxicillin-clavulanate potassium (Augmentin) or an orally administered cephalosporin. However, only first-generation cephalosporins such as cephalexin (Keflex, Keftab) or cefadroxil (Duricef), taken twice daily, would be indicated. These agents have a narrower spectrum and are less expensive than second- or third-generation cephalosporins. These broader spectrum cephalosporins should not be used.

Physicians likely have access to the broader spectrum agents because they are currently being heavily marketed. Physicians should avoid the temptation to dispense samples of these agents to patients with streptococcal pharyngitis.

In their review, Hayes and Williamson¹ do not discuss the use of clindamycin (Cleocin). Because of its activity against resistant pneumococci as well as group A beta-hemolytic streptococci, clindamycin now has a role in the treatment of ear, nose and throat infections.

Unlike Streptococcus pneumoniae, group A beta-hemolytic streptococci have not developed resistance to penicillins. Penicillin will probably continue to be effective treatment for streptococcal pharyngitis and part of the effort against rheumatic fever.

Kenneth Bromberg, M.D., is associate professor of pediatrics, medicine (infectious diseases) and microbiology/immunology at the State University of New York Health Science Center at Brooklyn College of Medicine, Brooklyn.

Address correspondence to Kenneth Bromberg, M.D., Department of Pediatrics, SUNY at Downstate Medical Center, 450 Clarkson Ave., P.O. Box 49, Brooklyn, NY 11203.

REFERENCES

Hayes CS, Williams H Jr. Management of group A beta-hemolytic streptococcal pharyngitis. Am Fam Physician 2001;63:1557-64.

Pickering LK, ed. 2000 Red book: report of the Committee on Infectious Diseases. 25th ed. Elk Grove Village, Ill.: American Academy of Pediatrics, 2000.

Bisno AL, Gerber MA, Gwaltney JM, Kaplan EL, Schwartz RH. Diagnosis and management of group A streptococcal pharyngitis: a practice guideline. Infectious Diseases Society of America. Clin Infect Dis 1997;25:574-83.

Pichichero ME. Eradication of group A streptococci [Letter]. Pediatrics 2000;106(2 pt 1):380-2.

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