Case Report of a 78-Year-Old Woman
Jeremy Mikolai, ND
Atrial fibrillation (AF) is the most common sustained heart arrhythmia encountered in clinical practice. Prevalence of AF increases with age. Approximately 1% of Americans have AF; more than 75% of those are older than 65 years.1 More than 9% of people older than 80 years have AF.2 The lifetime risk for developing AF by age 80 years is about 25%.3 New-onset AF requires considerations for urgent cardioversion, hospitalization, rate control, and antithrombotic (AT) therapy alongside the search for correctable etiologies.4
Prevention of venous thromboembolic events, especially stroke, is an important aspect of AF management. Stroke risk begins to rise 5 hours into an AF episode and reaches maximum within 72 hours.5,6 The risk of stroke in AF rises substantially with age, so its management has increased importance in our geriatric set.7,8 Atrial fibrillation can also cause hemodynamic instability, often manifesting as heart failure (HF). Frequently, AF and HF travel together, and either one can cause the other.9 The danger of HF can be more immediate than stroke, but it can be corrected through control of the heart rate.
A 78-year-old woman, “Helen,” was referred to our clinic for a resting electrocardiogram (ECG) and second opinion. Helen had presented the previous day to her ND with 3 days of nonproductive cough of sudden onset, exacerbated by reclining or bending over forward; she had to sleep in an upright position. Helen’s medical, family, and social histories were noncontributory. Her heart rate was irregular at 72 beats/min, and her blood pressure was 152/88 mm Hg, with 16 respirations/min; she was afebrile. There were no murmurs, rubs, or gallops appreciated on auscultation, but wheezes and rhonchi were present throughout all lung fields. Examination findings were normal for her lymphatic, vascular, neurologic, and ears, nose, and throat systems. Helen’s ND recommended she be evaluated in a local emergency department, but Helen had refused based on religious reasons.
We evaluated Helen the following day. Her heart rate was 100 beats/min and irregularly irregular by cardiac auscultation. Her blood pressure was 152/90 mm Hg, and her respiration was 20 breaths/min, with 99% resting oxygen saturation. Helen’s lungs demonstrated vesicular breath sounds without wheezes, rales, or rhonchi in all fields. Her thyroid, peripheral vascular, and neurological examinations were all within normal limits. The resting 12-lead ECG revealed an irregularly irregular rhythm with absent
P waves and an average ventricular rate of 123 beats/min, all consistent with AF with rapid ventricular response (AF-RVR).
We explained to Helen and her family that she was likely in HF resulting from the uncontrolled heart rate. We discussed options for referral, for immediate or future cardioversion, and the standard of care for new-onset AF-RVR. Helen and her family initially refused all standards of care and were reticent to consider any treatment due to Helen’s religious beliefs and their understanding of her advanced directive. We counseled the family and Helen at length about these concerns and explained that her condition did not need to be life-threatening; the minimum intervention required was to slow Helen’s heart rate and manage her stroke risk.
We consulted with the referring physician, who asked us to assume management of the patient. Helen agreed to complete minimal laboratory testing and a chest radiograph. She agreed to initiate oral diltiazem (30 mg) 4 times daily and return in 2 days for reevaluation. Due to her CHADS index (congestive heart failure, hypertension, age greater than 75, diabetic, and history of stroke) of 3, she was advised to initiate oral warfarin sodium, which she refused. She agreed to initiate oral aspirin (325 mg) twice a day. We advised her to report to the emergency department if she experienced worsening of symptoms, chest pain, syncope, swelling, or signs of stroke, including weakness, paralysis, facial droop, trouble speaking, confusion, or changes in vision or sensation.
Helen completed testing and imaging before returning to the clinic 2 days later. Her metabolic panel and magnesium level were normal. Her brain-type natriuretic peptide level was 541 pg/mL, and her chest radiograph revealed mild cardiomegaly, bilateral pleural effusions, perihilar pulmonary edema, and prominent pulmonary veins, all consistent with congestive HF. In the office, she reported that the diltiazem was helping and that she was able to lie reclined on 2 pillows without coughing; she was still short of breath on exertion and on bending forward. Her heartbeat was irregular at 92 beats/min, and her blood pressure was 107/80 mm Hg, with 16 respirations/min. Her pulmonary examination was clear, and the rest of her examination was normal across 8 systems. We counseled her again regarding the standards of care, but she declined further intervention or referral. She was instructed to follow up 1 week later for reassessment and “natural treatment options” for rhythm conversion and stroke prophylaxis.
The following week, Helen reported that she was “feeling much better than last week.” Her heart rate was controlled at 76 beats/min but still irregular. Her shortness of breath had almost completely resolved. Helen’s bleeding time (BT) was measured to be 8 minutes, and nattokinase (2000 fibrinolytic units per capsule, 1 capsule by mouth twice daily on an empty stomach) was initiated. She was instructed to follow up 1 month later for a repeat BT test and ECG and to return sooner as needed.
When she returned the following month, she reported having improved significantly since initiating treatment. She no longer had shortness of breath or cough. She had noticed palpitations once or twice daily lasting for 5 minutes. Her ECG revealed AF-RVR of 108 beats/min. Diltiazem was increased to 180 mg/d to improve rate control and was switched to extended-release form for once-daily dosing. Her BT had dropped to 5.5 minutes, so nattokinase was increased to 2 capsules (4000 fibrinolytic units) twice daily.
Over subsequent visits, Helen’s heart rate remained well controlled. Her BT reached target and was maintained in the therapeutic range. With these goals met, we discussed the next steps for management. She agreed to repeat laboratory testing and imaging.
Her chemistries were normal, and her brain-
type natriuretic peptide level had fallen to
240 pg/mL. Her chest radiograph documented that the pleural effusions and enlargement of her pulmonary veins had cleared and that active HF was no longer present, although her mild cardiomegaly persisted.
Helen eventually reached and maintained a BT target of greater than 10 minutes. Three capsules of nattokinase twice daily, 2 tablets of aspirin daily
(325 mg each), and essential fatty acids (4000 mg/d) were necessary to achieve this initially. Within 4 months of treatment, we were able to decrease her aspirin to 1 tablet daily (325 mg) and her nattokinase to 2 capsules twice daily.
Helen’s BT became inappropriately elevated at 21 minutes approximately 10 months into therapy. She experienced some spontaneous bruising, mostly on the dorsum of the left hand. Her BT was brought back under control and remained at target for several months. Approximately 16 months into the treatment period, Helen’s BT dropped below 8 minutes for the first time in
over a year. We added 150 mg/d of sustained-release grape seed extract to her regimen, which brought the BT immediately back into range. Helen persists in stable, permanent AF. She is asymptomatic and in good health.
AF—Perpetual Training Opportunity
Atrial fibrillation is a complex management scenario. Management strategies are highly dependent on several factors and are compounded by a patient’s ability to understand the risks and consequences of the various scenarios. Atrial fibrillation is a perpetual teaching opportunity for the physician and one that requires constant reassessment of the understanding and capacity of the patient. In the geriatric population, this can become especially challenging. Helen’s capacity is complete, and her understanding is excellent. However, her religious beliefs present a similar obstacle to management; they limit her ability to give full consideration to her options for diagnosis and management.
We initiated pharmacologic rate control in Helen’s case to resolve the AF-RVR and resultant HF. After acute resolution, there was a decision to be made, albeit a hypothetical decision in this case. We could have maintained Helen on long-term rate control, or we could have decided to control her heart rhythm instead. In this case, Helen was not interested in antiarrhythmic therapy, so she chose to remain in permanent AF. Permanent AF is a manageable condition that requires rate control, AT treatment, and monitoring. It is worth noting that, when a rhythm control strategy is utilized, tandem rate control is typically still necessary.1
Rate control has been repeatedly validated as a long-term strategy in persistent and permanent AF.10,11 Rate control is achieved using either
beta-blockade or calcium channel blockade. Beta-blockers other than labetalol hydrochloride are considered appropriate therapy; appropriate calcium channel blockers are limited to diltiazem or verapamil. Considerations regarding concomitant illnesses and cardiac diagnoses must be made when selecting the appropriate agent. The necessity for urgent control dictates whether the initial route of administration is intravenous; oral dosing is used long term or nonemergently.1 Unfortunately, no existing natural medications are reliable as rate control agents in AF-RVR.
BT Test is Preferred
We have mentioned the BT test throughout because it is our preferred method for monitoring natural AT therapies. The BT is a test of primary hemostasis and is clinically useful as a test of platelet responsiveness.12-14 Any agent that affects an aspect of blood clotting affects BT. This lack of specificity is an advantage because natural agents affect different aspects of blood clotting. Therefore, we can measure the combined effects of several agents on thrombogenesis in a single test.
The first duty of the primary care physician in acute AF and HF is recognition. Immediate referral is typically the best course in acute cases. In permanent AF, our general goals remain the same: to maintain heart rate control, prevent thromboembolic events, and monitor. Atrial fibrillation is becoming more common as our population ages. Mastering the management of chronic cases is imperative.
Jeremy Mikolai, ND is a 2010 alumnus of National College of Natural Medicine (NCNM), Portland, Oregon. He is a lead faculty member at the Naturopathic Institute of Cardiovascular and Pulmonary Medicine, in Portland, which provides training to practicing NDs in integrative cardiovascular and pulmonary medicine. Dr Mikolai is actively working toward the launch of an American Association of Naturopathic Physicians affiliate organization focused on cardiovascular medicine and board certification. He is the chief resident physician and a research faculty member at NCNM.
Fuster V, Rydén LE, Cannom DS, et al; American College of Cardiology Foundation/American Heart Association Task Force. 2011 ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2011;123(10):e269-e367.
Go AS, Hylek EM, Phillips KA, et al. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA. 2001;285(18):2370-2375.
Lloyd-Jones DM, Wang TJ, Leip EP, et al. Lifetime risk for development of atrial fibrillation: the Framingham Heart Study. Circulation. 2004;110(9):1042-1046.
Phang R, Olshansky B. Management of new onset atrial fibrillation. In: Basow DS, ed. UpToDate. Waltham, MA: UpToDate; 2012.
Hart RG, Pearce LA, Rothbart RM, et al. Stroke Prevention in Atrial Fibrillation Investigators. Stroke with intermittent atrial fibrillation: incidence and predictors during aspirin therapy. J Am Coll Cardiol. 2000;35(1):183-187.
Glotzer TV, Daoud EG, Wyse DG, et al. The relationship between daily atrial tachyarrhythmia burden from implantable device diagnostics and stroke risk: the TRENDS study. Circ Arrhythm Electrophysiol. 2009;2(5):474-480.
Frost L, Engholm G, Johnsen S, et al. Incident stroke after discharge from the hospital with a diagnosis of atrial fibrillation. Am J Med. 2000;108(1):36-40.
van Walraven C, Hart RG, Connolly S, et al. Effect of age on stroke prevention therapy in patients with atrial fibrillation: the Atrial Fibrillation Investigators. Stroke. 2009;40(4):1410-1416.
Wang TJ, Larson MG, Levy D, et al. Temporal relations of atrial fibrillation and congestive heart failure and their joint influence on mortality: the Framingham Heart Study. Circulation. 2003;107(23):2920-2925.
Wyse DG, Waldo AL, DiMarco JP, et al. Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med. 2002;347(23):1825-1833.
Van Gelder IC, Hagens VE, Bosker HA, et al. Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation Study Group. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med. 2002;347(23):1834-1840.
Del Vecchio A. Use of the bleeding time in the neonatal intensive care unit. Acta Paediatr Suppl. 2002;91(438):82-86.
Schwartz L, Brister SJ, Bourassa MG, et al. Interobserver reproducibility and biological variability of the Surgicutt II bleeding time. J Thromb Thrombolysis. 1998;6(2):155-158.
Buchanan GR, Holtkamp CA. A comparative study of variables affecting the bleeding time using two disposable devices. Am J Clin Pathol. 1989;91(1):45-51.