Diastolic Heart Failure in the Older Patient

Authors:
Ramona Gelzer-Bell, MD, and Paul A. Gurbel, MD
Johns Hopkins University

Citation:
Gelzer-Bell R, Gurbel PA. Diastolic heart failure in the older patient. Clin Geriatr. 2005;13(1):18-21.

CASE PRESENTATION

ER is a 76-year-old African-American woman with a history of coronary artery disease (CAD), myocardial infarction, stroke, hypertension, diabetes, and chronic renal insufficiency, who had a pacemaker placed for symptomatic bradycardia. The patient was transferred from a nursing home for evaluation of acute shortness of breath and chest tightness that was different from her typical anginal chest pain. She denied fever, chills, cough, nausea, vomiting, palpitations, and near syncope or syncope. The patient had at least two hospital admissions in the past year for decompensated congestive heart failure (CHF).

On her second hospital admission for CHF she underwent a cardiac catheterization that revealed a chronically occluded right coronary artery with left to right collaterals to the distal right coronary artery and hyperdynamic left ventricular (LV) systolic function. She then underwent DDDR pacemaker permanent placement for symptomatic bradycardia. In addition, on a prior admission, a magnetic resonance imaging (MRI) showed moderate bilateral renal artery stenosis. Medications included rabeprazole sodium, glipizide, NPH insulin, isosorbide mononitrate, furosemide, hydralazine, carvedilol, senna laxative, pravastatin, aspirin, and clopidogrel.

On presentation to the emergency room, the patient had a blood pressure of 190/84 mm Hg, and arterial oxygen saturation was 88% on a 100% nonrebreather mask. The heart rate was regular at 90 beats per minute. The lungs had rales at the bases, and cardiac exam revealed a normal S1 and S2 with an early peaking systolic ejection murmur, but no S3. The abdomen had no bruits or palpable masses, and extremities showed 1+ edema. The 12-lead electrocardiogram showed normal sinus rhythm with low voltage in the limb leads and nonspecific ST-T changes. The chest x-ray showed cardiomegaly, interstitial infiltrates, and pulmonary venous congestion. The pro-brain natriuretic peptide (BNP) was elevated. The troponin I, creatine phosphokinase, and myoglobin were normal. Blood urea nitrogen was 27 mg/dL and creatinine was 2.2 mg/dL.

The echocardiogram showed normal LV size with an ejection fraction of 65-70%, and concentric LV hypertrophy, inferior hypokinesis, aortic sclerosis without stenosis, and a pacing lead in the right ventricle. E-wave and A-wave reversal was noted of mitral diastolic flow and was consistent with impaired early diastolic filling. The E-wave corresponds to early ventricular filling when the mitral valve opens, and the later A-wave corresponds to further filling due to atrial contraction.

DISCUSSION

This is a case of diastolic heart failure in the older patient that illustrates many important issues. The incidence of heart failure increases dramatically with age, and 20-40% of these patients will have normal LV function or diastolic heart failure. In addition, there is a remarkable female predominance.^1-4 Approximately 6-10% of patients over the age of 65 have heart failure,⁵ and 80% of hospital admissions with a primary diagnosis of heart failure are persons over 65 years of age.⁶ The cost to care for these patients in 1991 was $38 billion.⁷

Heart failure is a major public health problem. It is important to understand the pathophysiology of diastolic heart failure in order to treat the disease. Diastolic heart failure reflects the effects of normal aging-related changes of impaired relaxation of the ventricle as well as vascular stiffness. As a result of the decreased elastic properties of the heart and the great vessels, there is increased sensitivity to volume and vasoconstriction, labile hypertension, and load-dependent diastolic dysfunction.⁸ Thus, hypertensive episodes due to labile hypertension, medical and dietary noncompliance, renal artery stenosis, nonsteroidal anti-inflammatory drugs, atrial fibrillation, ischemia, or iatrogenic volume overload can precipitate acute heart failure.

In addition, age-related changes in other organs or comorbidities may impair the patient’s ability to compensate for heart failure. The history and physical exam findings are not reliable and can be the same in systolic and diastolic heart failure. The BNP assay is particularly helpful when the diagnosis is more challenging and assesses disease severity and evaluates response to therapy. The BNP also cannot discriminate systolic from diastolic heart failure. Its negative predictive valve is greater than 95%. However, false-negative levels have been seen in flash pulmonary edema, and false-positive levels are seen with aging alone and in patients with renal insufficiency.

Doppler echocardiography is the noninvasive and reliable imaging method of choice to diagnose diastolic heart failure by assessing the E-wave to A-wave ratio of flow across the mitral valve. Normally, the E-wave is larger, but with impaired relaxation, the down slope of the E-wave is prolonged and the A-wave is larger.⁹ The outlook for patients with heart failure and preserved LV systolic function is better than for those patients with systolic dysfunction, but worse than for patients with no CHF at all.

The Framingham Heart Study showed an annual mortality of 8.9% in elderly patients with diastolic heart failure, and a two-fold increase when compared to age-matched controls. However, the mortality was only half that of patients with systolic heart failure.^10,11 The goal of therapy is the relief of symptoms, improvement in quality of life (improved exercise tolerance and reduced hospital admissions), and prolongation of survival. In the elderly, relief of symptoms and improvement of quality of life are crucial.

Treatment is directed toward determining the primary etiology and finding a reversible cause or precipitating factor. Nonpharmacologic treatment includes patient and caregiver education about the disease process, medications, and diet, including reduced salt intake, and in some cases, fluid restriction in volume-sensitive patients. In addition, teaching self-management skills and allowing for frequent follow-ups as well as implementing a multidisciplinary approach to care have been shown to be effective in heart failure clinics.¹²

The American College of Cardiology (ACC)/American Heart Association (AHA) Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult¹³ are supported by numerous clinical trials involving thousands of patients. Unfortunately, there are no specific treatment guidelines yet established for heart failure with preserved LV systolic function. This fact is primarily due to the lack of large, multicentered clinical trials investigating this entity. This fact is very disappointing given the high prevalence, substantial morbidity, and high mortality of diastolic dysfunction. However, there are numerous antihypertension trials showing that treatment with diuretics, beta blockers, or calcium-channel blockers, and angiotensin-converting enzyme (ACE) inhibitors reduce the incidence of heart failure and improve cardiovascular mortality.^14-18

The recent Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7)¹⁹ guidelines also supports these findings. Thus, while awaiting the very much needed trials, the incidence of heart failure can be reduced simply by utilizing these proven therapies.

The Candesartan in Heart failure Assessment of Reduction in Mortality and morbidity (CHARM) trial was a study that looked at the use of an angiotensin II receptor blocker (ARB) in the treatment of systolic and diastolic heart failure when added to an ACE inhibitor.^20-23 This was the first large-scale study, involving 3023 patients, specifically designed to address diastolic heart failure. The study did show an overall 9% decrease in mortality and a 21% decrease in heart failure admissions. However, the survival benefit was in the systolic dysfunction arms (those who are ACE inhibitor intolerant and those taking an ACE inhibitor); it failed to show this benefit in the patients with preserved LV systolic function, although the total number of heart failure admissions were slightly decreased.²²

If no precipitating factor is found, the ACC/AHA consensus guidelines are as follows:¹³

• Controlling blood pressure is the single most important treatment (diuretics as first line). The Systolic Hypertension in the Elderly Program (SHEP)¹⁷ and the Swedish Trial in Old Patients with Hypertension (STOP-Hypertension)¹⁸ have shown that diuretics and beta blockers are effective in reducing the incidence of heart failure and improving cardiovascular survival.
• Control the tachycardia. Sinus rhythm should be maintained. When this is not possible, rate control is important (and anticoagulation is indicated if atrial fibrillation is present and there are no contraindications). Tachycardia can decrease the time for ventricular filling and coronary perfusion. Beta blockers or calcium-channel blockers can allow more time for ventricular filling.
• Reduce central blood volume. Watch out for a small LV cavity and LV outflow tract obstruction due to a sigmoid hypertrophied septum.
• Alleviate myocardial ischemia. Ischemia can impair myocardial relaxation.

OUTCOME OF THE CASE PATIENT

The patient was diagnosed with flash pulmonary edema for the third time in one year. Systolic hypertension was present every time she presented with acute pulmonary edema. She has had an exhaustive work-up for causes of acute pulmonary edema and uncontrolled hypertension. A coronary angiogram is usually recommended in patients who present with flash pulmonary edema to rule out multivessel CAD. Renal artery stenosis also must be ruled out. A renal angiogram did not show significant renal artery stenosis. A pharmacologic stress test showed a small area of inferior ischemia. The patient was treated with intravenous furosemide and nesiritide. No other reversible causes were found. She has labile hypertension, and her antihypertensive regimen was again optimized to the highest tolerable doses.

CONCLUSION

Heart failure is the only cardiovascular disorder with an increasing incidence due to our aging population and improved treatment of CAD. Overall prognosis is poor, and studies are limited. The incidence of heart failure and recurrent hospital admissions in the older patient can be reduced by intense patient education, as well as the utilization and optimization of already proven therapies. Finally, other large, multicentered outcome trials are needed.