Internal Medicine Atrial Fibrillation/Mitral Stenosis Case File

Internal Medicine Atrial Fibrillation/Mitral Stenosis Case File

Eugene C. Toy, MD, Gabriel M. Aisenberg, MD

Case 8

A 26-year-old Nigerian woman presents to the emergency center complaining of the sudden onset of palpitations, severe shortness of breath, and coughing. She reports that she has experienced several episodes of palpitations in the past, often lasting 1 or 2 days, but never with dyspnea. She has a history of rheumatic fever at the age of 14. She is now pregnant at 20 weeks’ gestation with her first child and takes prenatal vitamins. She denies the use of any other medications, tobacco, alcohol, or illicit drugs.

On examination, her heart rate ranges from 110 to 130 beats per minute (bpm), blood pressure is 92/65 mm Hg, respiratory rate is 24 breaths/min, and oxygen saturation is 94% on room air. She appears uncomfortable, with labored respirations. She is coughing and producing scant amounts of frothy sputum with a pink tint. She has ruddy cheeks and normal jugular venous pressure. She has bilateral inspiratory crackles in the lower lung fields. On cardiac examination, her heart rhythm is irregularly irregular with a loud S1 and low-pitched diastolic murmur best heard at the apex with a nondisplaced apical impulse. Her uterine fundus is palpable at the umbilicus, and she has no peripheral edema. An electrocardiogram (ECG) is obtained (Figure 8–1).

Figure 8–1. Electrocardiogram. (Reproduced with permission, from Braunwald E, Fauci AS, Kasper KL,

et al. Harrison’s Principles of Internal Medicine. 16th ed. 2005. Copyright © McGraw Hill LLC. All rights

reserved.)

▶ What is the most likely diagnosis?

▶ What is your next step in management?

ANSWERS TO CASE 8:

Atrial Fibrillation/Mitral Stenosis

Summary: A 26-year-old woman presents with

• History of rheumatic fever during adolescence
• Pregnancy in the second trimester currently
• Acute onset of palpitations
• Atrial fibrillation (AF) with a rapid ventricular response
• Diastolic rumble suggestive of mitral stenosis leading to left atrial enlargement, which is the likely cause of her AF
• Increased blood volume from pregnancy, tachycardia, and loss of atrial contraction, which have likely led to pulmonary edema

Most likely diagnosis: AF caused by mitral stenosis.

Next step in management: Heart rate control with intravenous beta-blockers.

ANALYSIS

Objectives

1. Enumerate the causes of AF. (EPA 12)
2. Understand the management of AF with rapid ventricular response. (EPA 4, 10)
3. Understand the rationale for anticoagulation in chronic AF. (EPA 4, 12)
4. Describe the typical cardiac lesions of rheumatic heart disease and the physical findings in mitral stenosis. (EPA 1, 3)
5. Understand the physiologic basis of Wolff-Parkinson-White (WPW) syndrome and the special considerations in AF. (EPA 4, 12)

APPROACH TO:

Health Maintenance

DEFINITIONS

ATRIAL FIBRILLATION: Irregular heart rhythm with chaotic generation of electrical signals in the atria of the heart.

DIRECT CURRENT (DC) CARDIOVERSION: Converting an abnormal rhythm of the heart to normal sinus rhythm by applying DC electrical shock.

CLINICAL APPROACH

Background and Epidemiology

Atrial fibrillation is the most common arrhythmia for which patients seek treatment; it occurs in acute, paroxysmal, and chronic forms. With AF, there is disordered atrial depolarization from multiple irritable foci, often at rates exceeding 300 to 400 bpm; these atrial impulses produce an irregular ventricular response, depending on the number of impulses that are conducted through the atrioventricular (AV) node. The ECG is characterized by the absence of discrete P waves and an RR interval without a repetitive pattern, commonly referred to as an irregularly irregular rhythm. The incidence of AF increases with age, affecting 5% to 10% of patients older than 75 years. Although many patients can maintain a normal activity level and remain essentially asymptomatic with chronic AF, there are several causes of morbidity from this arrhythmia: It may trigger a rapid ventricular rate, leading to myocardial ischemia, exacerbation of heart failure in patients with heart disease, and thrombus formation in the noncontractile atrial appendage, which can lead to systemic embolization (AF is a common cause of ischemic stroke).

Pathophysiology

Anything that causes atrial dilation or excessive sympathetic tone can lead to AF, but the two most common causes of AF are hypertension and coronary atherosclerosis. The common causes of AF are listed in Table 8–1.

Treatment

Acute AF. Acute AF with rapid ventricular response must be addressed quickly. The four major goals are (1) hemodynamic stabilization, (2) rate control, (3) anticoagulation, and (4) possible conversion to sinus rhythm. If a patient is hemodynamically unstable (hypotensive, angina pectoris, pulmonary edema), urgent DC cardioversion is indicated. If the patient is hemodynamically stable, ventricular rate control can generally be achieved with intravenous beta-blockers, calcium channel blockers, or digoxin, which slow conduction through the AV node. Once the ventricular rate has been controlled, the underlying cause (eg, thyrotoxicosis, use of adrenergic stimulants, or worsening heart failure) should be reversed so that patients can undergo cardioversion to sinus rhythm. This may occur spontaneously or after correction of underlying abnormalities, or it may require pharmacologic or electrical

cardioversion. If the duration of AF exceeds 48 hours, the risk of intra-atrial thrombus formation increases.

Rate control alone (ie, the use of agents to maintain a slow ventricular response rate) is often effective in managing the symptoms of AF, and it has been shown to be as effective as rhythm control for long-term outcomes.

However, if patients are unstable or persistently symptomatic, they may require efforts to terminate the AF and restore sinus rhythm. The most effective method of terminating AF is electrical cardioversion. After cardioversion, the return of coordinated atrial contraction in the presence of an atrial thrombus may result in clot embolization, leading to a cerebral infarction or other ischemic event. Therefore, after 24 to 48 hours of AF, patients should receive 3 to 4 weeks of anticoagulant therapy prior to and after cardioversion to reduce the risk of thromboembolic phenomena. Alternatively, low-risk patients can undergo transesophageal echocardiography to exclude the presence of an atrial appendage thrombus prior to cardioversion. Postcardioversion anticoagulation is still required for 4 additional weeks, because though the rhythm returns to sinus, the atria do not contract normally for some time. Pharmacologic antiarrhythmic agents, such as propafenone, sotalol, and amiodarone, may be used to try to maintain sinus rhythm.

Many patients with AF even after cardioversion do not remain in sinus rhythm. Two important prognostic factors are left atrial dilation (atrial diameter > 4.5 cm predicts failure of cardioversion) and duration of AF. The longer the patient is in AF, the more likely the patient is to stay in that rhythm as a consequence of electrical remodeling of the heart.

Chronic AF. In patients with chronic AF, the management goals are rate control, using drugs to reduce AV nodal conduction (such as digoxin or beta-blockers) as described previously, and anticoagulation. Patients with chronic AF who are not anticoagulated have a 1% to 5% per year incidence of clinically evident embolization such as stroke. Risk assessment tools such as the CHA2DS2-VASc (see Table 8–2 for definition) score can be used to estimate stroke risk and need for anticoagulation. The CHA2DS2-VASc score correlates an increasing event rate with an increasing score (Tables 8–2 and 8–3).

Abbreviations: MI, myocardial infarction; PAD, peripheral artery disease; TIA, transient ischemic attack.

For chronic AF caused by valvular disease such as mitral stenosis, the annual risk of stroke is substantially higher. AF that develops in patients younger than 60 years without evidence of structural heart disease, hypertension, or other factors for stroke is termed lone AF, and the risk of stroke is very low, so anticoagulation with warfarin is not used. Instead, aspirin may be used.

Anticoagulation reduces the risk of stroke by two-thirds in patients with chronic AF. New oral anticoagulants such as dabigatran and rivaroxaban have been developed for use in AF, but the oral vitamin K antagonist warfarin remains the most widely used medication for this purpose. Warfarin does not produce a predictable dose-related response; therefore, the level of anticoagulation needs to be monitored by regular laboratory testing using the international normalized ratio (INR). In AF not caused by valvular disease, the target INR is 2 to 3.

The most common complication of warfarin therapy is bleeding resulting from excessive anticoagulation. The risk of bleeding increases with the INR. If the INR is markedly elevated (eg, INR 6–9) but there is no apparent bleeding, the values will return to normal over several days if the warfarin is held. For higher levels of INR (> 9) without bleeding, vitamin K can be administered. If clinically significant bleeding is present, warfarin toxicity can be rapidly reversed with administration of vitamin K, fresh frozen plasma (FFP), and prothrombin complex concentrate to replace clotting factors and provide intravascular volume replacement.

Rheumatic Heart Disease

In this case, the cause of this patient’s AF appears to be rheumatic mitral stenosis. Rheumatic heart disease is a late sequela of acute rheumatic fever, usually becoming symptomatic many years after the original illness. Valvular thickening, fibrosis, and calcifications lead to valvular stenosis. The mitral valve is most frequently involved. The aortic valve may also develop stenosis in combination with the mitral valve. The right side of the heart is rarely involved. Most cases of mitral stenosis in adults are secondary to rheumatic heart disease, especially in the developing world. Congenital mitral stenosis is also commonly seen.

The physical signs of mitral stenosis are a loud S1 and an opening snap following S2. The S2-OS (mitral valve opening snap) interval narrows as the severity of the stenosis increases. There is a low-pitched diastolic rumble after the opening snap, heard best at the apex with the bell of the stethoscope. Because of the stenotic

AV conduction is occurring through the accessory pathway rather than through the AV node, the ventricular rate may be very rapid, and the usual AV nodal–blocking drugs given for ventricular rate control will not affect the accessory pathway. In fact, beta-blockers, verapamil, and other AV nodal–blocking agents can, paradoxically, increase the ventricular rate and should be avoided in WPW patients with AF. If hemodynamically unstable, DC cardioversion should be performed. If hemodynamically stable, the agent of choice is procainamide or ibutilide to slow conduction and convert the rhythm to sinus.

CASE CORRELATION

• See also Case 4 (Heart Failure due to Critical Aortic Stenosis), Case 6 (Hypertension, Outpatient), and Case 36 (Transient Ischemic Attack).

COMPREHENSION QUESTIONS

8.1 A 28-year-old woman has been told she has rheumatic heart disease, specifically mitral stenosis. Which of the following murmurs is most likely present?

A. Diastolic rumble at apex of the heart

B. Early diastolic decrescendo at right upper sternal border

C. Holosystolic murmur at apex

D. Late-peaking systolic murmur at right upper sternal border

8.2 A 48-year-old woman is noted to have AF with a ventricular rate of 140 bpm. She is feeling dizzy and dyspneic, with a systolic blood pressure of 75/48 mm Hg. Which of the following is the most appropriate next step?

A. Intravenous digoxin

B. DC cardioversion

C. Vagal maneuvers

D. Intravenous diltiazem

8.3 A third-year medical student has been reading about the dangers of excessive anticoagulation and bleeding potential. He reviews the charts of several patients with AF currently taking warfarin. Which of the following patients is best suited to discontinue anticoagulation?

A. A 45-year-old man who has normal echocardiographic findings and no history of heart disease or hypertension, but a family history of hyperlipidemia

B. A 62-year-old man with mild chronic hypertension and dilated left atrium, but normal ejection fraction

C. A 75-year-old woman who is in good health except for a prior stroke, from which she has recovered nearly all function

D. A 52-year-old man with orthopnea and paroxysmal nocturnal dyspnea

8.4 A 59-year-old woman has been placed on warfarin after being found to have chronic AF. She is noted to have an INR of 5.8, is asymptomatic, and has no overt bleeding. Which of the following is the best management for this patient?

A. Transfuse with erythrocytes.

B. Give vitamin K.

C. Give fresh frozen plasma

D. Hold warfarin.

8.5 A 45-year-old woman is noted to have dizziness, a pounding feeling in her chest, and fatigue of 3 hours’ duration. On examination, she is noted to have a blood pressure of 110/70 mm Hg and a heart rate of 180 bpm. On ECG, she has AF, and a prior baseline ECG showed delta waves. The emergency department provider counsels the patient regarding cardioversion, but the patient declines. Which of the following is the best therapy for her condition?

A. Digoxin

B. Angiotensin-converting enzyme inhibitor

C. Calcium channel blocker

D. Procainamide

ANSWERS

8.1 A. A diastolic rumble at the cardiac apex suggests mitral stenosis. The early diastolic decrescendo murmur (answer B) is typical of aortic regurgitation; holosystolic murmur at the apex (answer C) is typical of mitral regurgitation; and late-peaking systolic murmur at the upper sternal border (answer D) is typical of aortic stenosis.

8.2 B. This individual has significant symptoms and hypotension caused by the AF and rapid ventricular rate; this is an unstable patient, and thus DC cardioversion is the treatment of choice. The other answer choices (answer A, digoxin, and answer D, diltiazem) would take time to work, and additionally answer C (vagal maneuvers) could potentially compromise cerebral blood flow if carotid massage is used.

8.3 A. Clinical factors associated with a higher risk for embolic stroke include congestive heart failure, hypertension, age > 65, diabetes, or prior stroke. Echocardiographic factors include dilated left atrium or the presence of an atrial thrombus. The man in answer A has “lone AF” with a CHADS2 score < 2 and has a low risk for stroke; thus, he would not benefit from anticoagulation. The other answer choices have high CHADS2 scores based on age and other comorbidities.

8.4 D. The target INR with warfarin is 2 to 3; thus, 5.8 is markedly elevated. However, because this patient has no overt bleeding and is asymptomatic, holding the warfarin until the INR reaches the acceptable range is a reasonable approach. Answer A (transfusion) is not indicated since the patient did not have bleeding. Patients with overt bleeding require more urgent intervention, such as administration of vitamin K (answer B), FFP (answer C), or prothrombin complex concentrate to replenish clotting factors.

8.5 D. This patient has AF with WPW, as indicated by the delta wave. In this setting, the typical agents (answer A, digoxin; answer B, angiotensin-converting enzyme inhibitor; and answer C, calcium channel blocker) used to treat AF that slow the AV node are contraindicated since the conduction through the accessory pathway could accelerate, leading to ventricular tachycardia. DC cardioversion is an option; however, in a hemodynamically stable patient, procainamide may be used since it will slow propagation through the accessory pathway. Because this patient declines cardioversion, procainamide is the best choice.

    CLINICAL PEARLS    

▶ The most common causes of AF are hypertension, atherosclerotic heart disease, pericardial or pulmonary disease, and hyperthyroidism.

▶ Acute AF is treated with direct current cardioversion if the patient is unstable. If the patient is stable, initial management is ventricular rate control with an AV nodal–blocking agent, such as beta-blockers, diltia-zem, or verapamil.

▶ Patients with chronic AF generally require long-term anticoagulation to prevent embolic strokes. An exception is “lone AF.”

▶ CHA2DS2-VASc score can help with risk stratification for both thrombo-embolic events and need for long-term anticoagulation.

▶WPW syndrome is a ventricular pre-excitation syndrome with a delta wave, short PR interval (< 0.12 seconds), and prolonged QRS interval (> 0.12 seconds).

▶WPW syndrome is associated with paroxysmal tachycardias, including AF. AF in WPW syndrome is treated with DC cardioversion or with procain-amide. AV nodal–blocking agents can, paradoxically, increase the ven-tricular rate.

▶Auscultatory findings in mitral stenosis include a loud S1 and an opening snap following the second heart sound (S2). The interval between S2 and the opening snap varies inversely with the severity of the stenosis.

REFERENCES

Centers for Disease Control and Prevention. Atrial Fibrillation Fact Sheet, 2017. Atlanta, GA: Centers for Disease Control and Prevention, US Department of Health and Human Services; 2017. 

Feldman T. Rheumatic mitral stenosis. On the rise again. Postgrad Med. 1993;93:93-104. 

Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach. Chest. 2010;137(2):263-272. 

Michaud GF, Stevenson WG. Atrial fibrillation. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 20th ed. New York, NY: McGraw Hill; 2018. 

O’Gara PT, Loscalzo J. Mitral stenosis. In: Jameson J, Fauci AS, Kasper DL, eds. Harrison’s Principles of Internal Medicine. 20th ed. New York, NY: McGraw Hill; 2018. 

Snow V, Weiss KB, LeFevre M, et al. Management of newly detected atrial fibrillation: a clinical practice guideline from the American Academy of Family Physicians and the American College of Physicians. Ann Intern Med. 2003;139:1009-1017. 

Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med. 2002;347:1834-1840.

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