Diastolic Heart Failure in the Older Patient
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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.
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