Electrophysiology
A 68-year-old man is referred to your clinic for evaluation of new-onset atrial fibrillation (AF). Physical examination is remarkable only for an irregular pulse. An electrocardiogram demonstrates AF with a ventricular response of approximately 90 bpm. In addition to ordering an echocardiogram and discussing rate- versus rhythm-control strategies, you recommend anticoagulation with the novel oral anticoagulant rivaroxaban. He expresses concern about anticoagulation because his spouse uses warfarin and has had to make dietary and medication changes to avoid interactions that led to excess bleeding risk.
Which of the following drugs would be most likely to cause bleeding if combined with rivaroxaban?
A)Atorvastatin
B)Sotalol
C)Phenytoin
D)Clarithromycin
E)Trimethoprim-Sulfamethoxazole
D
Rivaroxaban is a novel oral anticoagulant with a similar efficacy to warfarin for preventing stroke in nonvalvular AF and is associated with a similar bleeding risk, although with fewer drug-drug and dietary interactions than warfarin. However, as a substrate of the cytochrome P450 (CYP3A4) and P-glycoprotein systems in the liver, there are clinically relevant drug-drug interactions that can affect the safe use of the drug.
Strong inhibitors of CYP3A4 can increase rivaroxaban levels, leading to bleeding: 1) azole-antimycotics, including ketoconazole, itraconazole, and voriconazole; 2) human immunodeficiency virus protease inhibitors, such as ritonavir; and 3) clarithromycin. Most antibiotics increase warfarin activity by changing gut flora and production of vitamin K. Sulfamethoxazole is also a CYP2C9 inhibitor that increases warfarin levels, but does not increase rivaroxaban levels. Phenytoin is an inducer of CYP3A4 and so would be expected to decrease rivaroxaban levels, and although this may be clinically significant (decreased anticoagulation efficacy), there would not be increased bleeding risk. Sotalol and atorvastatin do not have any significant interaction with rivaroxaban.
A 63-year-old man presents with chief complaints of chest heaviness. He tells you about an episode in the morning that subsided spontaneously after 10 minutes, and a new episode 2 hours before presentation that lasted about 30 minutes. Now he is asymptomatic, but his wife insisted on bringing him to the emergency department. He has been diabetic for the last 15 years and treated with metformin and glimepiride. He has also been prescribed amlodipine to control his blood pressure.
His blood pressure is now 145/90 mm Hg, his heart rate is 62 bpm, and creatinine is 1.12 mg/dl. The physical exam is unremarkable. He smokes about 10 cigarettes per day. His electrocardiogram is normal and on the first set, his troponin T is 0.06 ng/ml (99th percentile, 0.01 ng/ml). You calculate a GRACE score of 106 and TIMI score of 3.
Which of the following is the optimal management for this patient?
A)Coronary CT angiography.
B)Coronary angiography within 24 hours.
C)No further diagnostic testing.
D)Stress test.
E)Emergent coronary angiography.
B
The risk profile of this patient does not warrant an emergent catheterization. The 2011 focused update of the Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction (NSTEMI) considers an early invasive management strategy within 24 hours reasonable in the case of high-risk criteria or clinical instability. This patient is diabetic and has positive troponin, both of which favor an invasive approach within 24 hours.
This patient has a confirmed NSTEMI, and a stress test to provoke ischemia in this setting is not diagnostically useful and is unsafe. Coronary computed tomography angiography is predominantly useful when there is diagnostic uncertainty and the pretest probability is either low or intermediate.
A 25-year-old college student was playing with his young nephew, who had a fever and an erythematous rash. Subsequent to that visit, he develops dyspnea, rash, and fever. An echocardiogram revealed his ejection fraction to be 25%.
Which of the following is the most likely cause of myocarditis in this patient?
A)Alcohol
B)Chagas disease
C)Parvovirus B19
D)Adenovirus
E)Mumps
C
The most common viral etiology of myocarditis at present is parvovirus. Rashes are common with all types of viruses, and are suggestive of a virus-related myocarditis in this scenario. Adenovirus and mumps may cause myocarditis, but are rare etiologies. There is no reduviid-organism exposure to suggest Chagas, which is endemic to Central and South America.
A 20-year-old woman with a history of mitral valve repair 3 years prior (for mitral regurgitation [MR] due to mitral prolapse) is admitted with fever of unknown cause for one week. In retrospect, she has been feeling poorly for at least 2 months and notes her temperature tends to increase in the evening. She generally can get the temperature reduced with acetaminophen and has been able to continue to go to school. She has lost a few pounds, but has no other specific complaints.
She recently went to an urgent care facility, where she was prescribed azithromycin. She has taken this over for the last 3 days. On examination, she is mildly febrile (37.8°C) and tachycardic at 105 bpm. Her blood pressure is 100/75 mm Hg. Her lungs are clear. Cardiac exam reveals no jugular venous distention, no CV wave, and no hepatojugular reflux. Her carotid is normal. Apex is hyperdynamic with no thrills. On auscultation, there is a grade 3/6 MR murmur radiating to the axilla and to the back with an associated S3. The remainder of her exam is normal, with no peripheral stigmata for endocarditis.
An echocardiogram is obtained, and it reveals moderate to severe MR with a bright target observed on the anterior leaflet that is officially read as either calcium or a possible vegetation. Left ventricular (LV) function is normal as is the LV size, and there are no other abnormalities observed. You order two sets of blood cultures and admit her to the hospital. After 24 hours, neither set of cultures is positive for any growth of bacteria.
Which of the following is the best next step?
A)Repeat blood cultures.
B)Begin vancomycin and rifampin.
C)Begin ceftriaxone.
D)Begin ampicillin and gentamycin.
A
The correct answer is to wait until blood cultures can be obtained off antibiotics before starting empiric therapy. The patient has evidence for fever and a clinical scenario in which endocarditis is certainly possible. You are given no prior exams to know if the MR is new or worse from previous exams.
The target on the mitral valve is not definitive and a transesophageal echocardiogram would now be indicated to better define the lesion. She received antibiotics from the urgent care visit. Thus, the lack of positivity of the initial blood cultures may simply be due to the antibiotic therapy she has received. She remains stable, so antibiotics should not be initiated until cultures have been obtained that have not been potentially influenced by the prior antibiotic therapy. At this stage, she does not meet the modified Duke criteria for endocarditis, and a second set of cultures should be obtained and no therapy initiated until these results are back. If the cultures then become positive, the appropriate antibiotics can be administered or the patient can be empirically treated for culture-negative endocarditis.
A 33-year-old woman with a history of hypertension presents with sharp chest pain at rest, associated with dyspnea. She is 10 days postoperative from a hysterectomy. Her resting oxygen saturation is 91%. Her examination is otherwise normal. Her only medication is birth control pills. Her electrocardiogram shows sinus tachycardia and T-wave inversion in the anterior leads. Troponin I is elevated at 0.8 ng/L. She is given aspirin in the emergency room, but continues to complain of dyspnea and chest pain.
Which of the following should be the next step?
A)Schedule cardiac cath.
B)Refer for urgent cardiac cath.
C)Schedule exercise stress test.
D)Obtain computed tomography pulmonary angiogram.
D
The nonspecific electrocardiogram findings in a young patient with a low pretest probability for coronary artery disease should prompt consideration of alternative diagnoses. While troponin elevation is specific for myocardial injury, it is not specific for the etiology, and pulmonary embolism (PE) is a known cause of troponin elevation. In patients with PE, the presence of troponin elevation is an adverse prognostic indicator and should prompt an aggressive diagnostic and therapeutic course.
A 57-year-old man presents to your clinic with complaints of shortness of breath while walking less than a block. He has a past medical history significant for coronary artery disease, with an anterior ST elevation myocardial infarction treated with drug-eluting stent 6 months ago, hypertension, and hypercholesterolemia.
On physical examination, blood pressure is 118/72 mm Hg and heart rate is 38 bpm. Recent studies in the past 6 months include an echocardiogram with a left ventricular ejection fraction of 50%, and Holter monitoring with sinus bradycardia with an average heart rate of 40 bpm and minimum heart rate of 30 bpm while sleeping. His medications include aspirin 81 mg daily, clopidogrel 75 mg daily, metoprolol 25 mg twice daily, atorvastatin 40 mg daily, and lisinopril 10 mg daily.
Which of the following is the most appropriate recommendation for the patient’s symptoms?
A)Perform an exercise treadmill test.
B)Perform an electrophysiologic study.
C)Implant an dual chamber pacemaker.
D)Stop metoprolol.
E)Continue current medications.
C
Based on current guidelines, this patient meets a Class I indication for permanent pacemaker. Permanent pacemaker implantation is indicated for symptomatic sinus bradycardia that results from required drug therapy for medical conditions. This patient is presenting with symptomatic sinus bradycardia that is limiting his activity. Although metoprolol could be the potential cause for his symptoms due to the history of an anterior myocardial infarction and hypertension, this medication is an essential component of his treatment. Because the patient is experiencing sinus bradycardia, treatment intervention is required, and not doing anything is incorrect. No further studies are necessary to evaluate the patient’s condition.
A 47-year-old woman presents to the emergency department with 2 days of substernal chest pressure radiating to the jaw with minimal exertion relieved with rest. The last episode was 1 hour prior to presentation and lasted 15 minutes. She has no medical history and takes no medication. Her resting electrocardiogram is normal.
Which of the following is the most accurate biomarker strategy for diagnosing myocardial infarction (MI) in this patient?
A)CK-MB at time 0 and 6 hours.
B)BNP after 6 hours of observation.
C)Myoglobin at the time of presentation.
D)Cardiac specific troponin at time 0 and 6 hours.
E)High sensitivity troponin at presentation.
D
Cardiac biomarkers are part of the universal definition of MI. Although the specificity of cardiac-specific and high-sensitivity troponin assays are of concern, they are the biomarker of choice in patients with suspected acute coronary syndrome (ACS). The current American Heart Association/American College of Cardiology guideline recommends that cardiac-specific troponin (troponin I or T when a contemporary assay is used) levels should be measured at presentation and 3-6 hours after symptom onset in all patients who present with symptoms consistent with ACS to identify a rising and/or falling pattern (Class I).
Although high-sensitivity troponin may be positive earlier, a single measure at presentation is not sufficient to exclude MI. With contemporary troponin assays, creatine kinase myocardial isoenzyme (CK-MB) and myoglobin are not useful for diagnosis of ACS (Class III). Use of selected newer biomarkers, especially BNP, may be reasonable to provide additional prognostic information (Class IIb), but are not used for the initial diagnosis.
A 74-year-old woman with nonischemic dilated cardiomyopathy is seen 1 week after her third hospitalization in 6 months for progressive weight gain, peripheral edema, and reduced urine output, each time rapidly responsive to intravenous furosemide. Discharge medications were lisinopril 20 mg daily, carvedilol 25 mg twice daily, spironolactone 25 mg daily, and furosemide 120 mg twice daily.
Since discharge, she has gained 10 pounds. Her daughter confirms she is compliant with all of her medications and sodium restriction.
Which of the following interventions is most likely to be successful in restoring fluid balance with the minimum adverse potential?
A)Add metolazone
B)Substitute torsemide for furosemide
C)increase furosemide
D)increase lisinopril dose
E)increase spironolactone dose
B
The correct answer is to change to torsemide. The greater oral bioavailability of torsemide (e.g., approaching its intravenous action) provides benefits over furosemide, which has significant variable oral absorption. All of the other choices are more likely to produce untoward adverse effects, such as hypokalemia (e.g., metolazone), without significant clinical benefit, particularly since the patient’s baseline medications are already at the target doses used in the clinical trials.
A 57-year-old woman with a long smoking history presents with fever, malaise, and dyspnea. On examination, her vitals include temperature 37.9°C, heart rate 110 bpm, and blood pressure 98/64 mm Hg. Scattered wheezes are noted on lung auscultation. Heart sounds are distant but regular and tachycardic with no murmurs, rubs, or gallops. An electrocardiogram demonstrates sinus tachycardia and low voltages. The pulsus paradoxus is measured at 17 mm Hg. A stat echocardiogram is performed and shows no significant pericardial effusion and normal left ventricular function.
Which of the following is the most likely explanation for her pulsus paradoxus?
A)Thyrotoxicosis
B)COPD exacerbation
C)Restrictive lung disease
D)Anorexia nervosa
E)Pneumomediastinum
B
In patients with suspected pericardial tamponade, documentation of an elevated pulsus paradoxus is a key examination finding. Pulsus paradoxus is measured using slow deflation of a manual blood pressure cuff and calculating the pressure difference between the first auscultated Korotkoff sounds that occur only in expiration and the pressure at which Korotkoff sounds are audible for all heart beats. Normally, the pulsus paradoxus is <10 mm Hg. In pericardial tamponade, constraints on ventricular filling lead to respirophasic interventricular dependence that enhances fluctuations in left ventricular stroke volume. However, an elevated pulsus paradoxus is not limited to pericardial tamponade, but can also be observed in patients with obstructive lung disease, obesity, obstructive sleep apnea, and tension pneumothorax. In this patient, the air trapping and increased work of breathing lead to wide swings in intrathoracic pressure and create the elevated pulsus paradoxus.
A 36-year-old woman, 35 weeks pregnant, is seen in the emergency department with shortness of breath. Her blood pressure (BP) has been labile during her pregnancy, and she is maintained on hydralazine 50 mg 3 times daily. Her BP is 180/110 mm Hg, heart rate is 110 bpm and regular, and lungs with bibasilar rales. Her cardiac examination is regular, with a flow murmur and lower extremities with 2+ edema. She is given intravenous labetalol and furosemide with the resulting BP of 140/95 mm Hg and heart rate of 95 bpm. A urinalysis reveals 3+ proteinuria.
Which of the following is the next most appropriate step in her management?
A)Induction of labor
B)IV magnesium sulfate
C)Renal ultrafiltration
D)IV digoxin
E)Oral lisinopril
A
Urgent delivery/induction is recommended in women with gestational hypertension (HTN) and proteinuria in the setting of other adverse conditions such as pulmonary edema, coagulopathy, or fetal distress. Preeclampsia is defined as both HTN (140/90 mm Hg) and proteinuria or in face of new HTN without proteinuria: platelet count <100,000, serum creatinine >1.1, pulmonary edema, liver function tests more than two times normal, and cerebral or visual symptoms. This usually occurs in the third trimester of pregnancy. Eclampsia is differentiated from preeclampsia by the addition of seizures.
A 60-year-old man presents to the emergency department for increased swelling around his pacemaker site. He has a history of sick sinus syndrome, hypertension, and paroxysmal atrial fibrillation. A dual-chamber pacemaker was implanted 10 years ago, and the pacemaker generator was replaced 4 months ago. His last pacemaker check was 3 months ago when he was told everything was working normally. His medications include warfarin, metoprolol, and lisinopril. Last week he noticed some tenderness around his pacemaker, with redness developing at the lower edge of the pocket 2 days ago. He denies any fevers or chills.
On examination of the pacemaker site, there is a small to moderate amount of swelling and an area of erythema with induration that is about 2 cm in size at the inferior/lateral aspect of the pacemaker site. The remainder of his physical examination is normal, with normal vital signs. An echocardiogram is performed with normal findings. Blood cultures have been ordered.
Which of the following is the next step in management?
A)Extract pacemaker generator and leads.
B)Perform needle aspiration of the pacemaker pocket.
C)Initiate Vancomycin 1g q12hrs and reassess in 3 days.
D)Initiate Cephalexin 500mg QID and reassess in 7 days.
E)Revise pacemaker pocket and replace generator.
A
This patient has a pacemaker pocket infection with evidence of abscess formation. With infection in the pocket, both the generator and pacing leads are involved, and extraction of the entire system is needed to eradicate the infection (Class I). As this patient is otherwise in good health, this is the best course of action. Antibiotics alone will not eradicate the infection. Aspiration of the pocket should not be performed (Class III).
A 67-year-old woman with history of diabetes and asthma is admitted to the cardiac intensive care unit after percutaneous intervention with drug-eluting stent placement for an ST-elevation myocardial infarction (STEMI) involving the right coronary artery. She has not had any recurrent chest discomfort since her procedure. Her vital signs are temperature 37.5°C, heart rate 116 bpm, blood pressure 153/73 mm Hg, respiratory rate 24 breaths/minute, and oxygen saturation 96%. Physical examination is notable for an irregularly irregular heart rhythm, no jugular venous pressure, and moderate expiratory wheezing. Electrocardiogram demonstrates atrial fibrillation with a rapid ventricular response, but isoelectric ST segments and no Q waves. Her medications include aspirin, clopidogrel, and atorvastatin.
Which of the following would be the next best medication to consider?
A)Nitroglycerin
B)Amiodarone
C)Spironolactone
D)Diltiazem
E)Metoprolol.
D
Certain calcium channel blockers may be useful for the treatment of angina, hypertension, and atrial tachyarrhythmias in select patients after STEMI when beta-blockers (or nitrates) are ineffective, not tolerated, or contraindicated and in patients who have no signs of congestive heart failure, left ventricular dysfunction, or atrioventricular block. In this patient with recent STEMI, atrial fibrillation with rapid ventricular response, and elevated blood pressure, diltiazem would be a good choice to slow her ventricular rate and help control blood pressure. There is no evidence of active ischemia, and thus immediate electrical cardioversion is not necessary.
Metoprolol is contraindicated given the history of asthma and evidence of active bronchospasm. The duration of atrial fibrillation is unknown, thus amiodarone would not be a good choice at this point, as it also can cause cardioversion and other attempts at rate control have not been made. Nitroglycerin is not ideal in the setting of tachycardia and would not help to control heart rate. Aldosterone antagonists are recommended for patients with STEMI who are already receiving an angiotensin-converting enzyme inhibitor and beta-blocker and who have a left ventricular ejection fraction ≤40% and either symptomatic heart failure or diabetes. This patient would not qualify for an aldosterone antagonist at this time.
A 58-year-old woman presents with acute shortness of breath and chest pain. She had just left home after receiving a call that her husband died suddenly at work. She has never been hospitalized and has no cardiovascular history or risk factors. She looks anxious on exam and diaphoretic.
Her blood pressure is 170/80 mm Hg, her heart rate is 110 bpm, and her respiratory rate is 18 breaths/minute. Venous pressures are not elevated; lungs are clear; S4 on cardiac exam. Abdomen and extremities are unremarkable. Troponin I is 1.0 ng/dl; B-type natriuretic peptide (BNP) is 500 pg/ml. Her electrocardiogram shows deep anterior T-wave inversions. Her echocardiogram demonstrates left ventricular (LV) dysfunction with an ejection fraction (EF) of 30%. Cardiac catheterization shows normal coronaries and LV apical aneurysm. The patient is started on metoprolol.
Which of the following therapies is most appropriate in this patient?
A)ICD
B)Sacubitril/valsartan
C)Colchicine
D)Lisinopril
E)Apixiban
D
This patient most likely has Takotsubo cardiomyopathy, which is classically seen in middle-aged women who experience severe emotional distress, although any situation that could result in a massive catecholamine release can result in this type of myocardial insult. The ventricular wall motion abnormality is distinctive with preservation of the base and a large segment of apical ballooning. Other types of wall motion abnormalities have been described, but are generally not in coronary vascular distributions. Characteristically, the BNP elevation is greatly out of proportion to the troponin release, which is generally modest. Despite the severity of the wall motion abnormality, myocardial scarring is difficult to document by cardiac magnetic resonance. Commonly, complete normalization of LV function is expected.
Although there are no specific guidelines to direct therapy, medications that target the neurohormonal axis and cardiac remodeling are appropriate in this patient population. Therefore, angiotensin-converting enzyme (ACE) inhibitors would be indicated here. Anticoagulation with novel anticoagulants, such as apixiban in patients with apical aneurysms, has not been studied. There is no evidence of pericarditis; therefore, treatment with colchicine is not indicated. Sacubitril/valsartan has not been studied in patients with acute heart failure or in those who have not previously tolerated ACE inhibitors. ICD implantation is not indicated here since this is the first demonstration of low EF in this patient and myocardial recovery is common.
A 30-year-old man is referred for evaluation of a murmur. He reports no symptoms, and has no significant medical history. On physical examination, his height is 69 inches and weight is 185 lbs. The blood pressure is 135/70 mm Hg with a regular heart rate of 78 bpm. His lungs are clear. Prominent carotid pulsations are present. The jugular venous pulse is at the level of the sternal notch. The apical impulse is slightly enlarged and laterally displaced to the anterior axillary line. The S1 and S2 are normal, and an S3 is present. There is an early systolic click that does not change with inspiration. Both a soft (grade 2/6) crescendo-decrescendo systolic murmur and a soft (grade 2/4) decrescendo diastolic murmur are present along the left sternal border.
Which of the following is the most likely valvular abnormality?
A)Patent ductus arteriosus
B)Degenerative aortic valve stenosis with regurgitation
C)Rheumatic mitral stenosis and regurgitation
D)Bicuspid aortic valve with regurgitation
E)Pulmonic valve stenosis
D
Pulmonic valve stenosis is unlikely because the murmur does not change with respiration and the jugular venous pulse is normal. The intensity of the pulmonic ejection click decreases with inspiration. Degenerative aortic stenosis is not associated with a systolic click, and he is only 30 years old. Rheumatic mitral stenosis may be associated with a diastolic click, but not one that occurs during systole. Patent ductus arteriosus produces a continuous machine-like murmur and is not associated with a click or wide pulse pressure. BAV can be associated with sudden cessation of valve opening, leading to an ejection systolic click, and often is associated with significant AV regurgitation. Findings of chronic aortic regurgitation with left ventricular volume overload include an enlarged and laterally displaced apical pulse, wide aortic pulse pressure, and an S3.
A 55-year-old obese man with symptomatic paroxysmal atrial fibrillation presents to clinic for chronic fatigue. He feels tired all the time, and falls asleep whenever he is watching TV or reading a book. He is fearful because he fell asleep recently while driving in traffic, which resulted in a minor motor vehicle accident. His wife says that he snores loudly and has episodes when he stops breathing at night.
For which of the following is the patient at increased risk, if left untreated?
A)Sudden cardiac death during wakeful hours.
B)Altered testosterone levels.
C)Symptomatic bradycardia.
D)Atrial fibrillation.
E)Valvular heart disease.
D
The correct answer is increased risk of atrial fibrillation related to untreated obstructive sleep apnea (OSA). It has been shown that untreated OSA is associated with recurrent atrial fibrillation, including after cardioversion. However, when treated, the incidence of recurrent atrial fibrillation decreases. Increased risk of sudden cardiac death is true in patients with OSA, but has been found to occur during sleep hours, not during wakefulness. Valvular heart disease is not associated with the presence of OSA. Longstanding OSA can lead to pulmonary hypertension and resultant tricuspid regurgitation, but there is no direct correlation. There is either no change or a decrease in testosterone level associated with the presence of sleep apnea. While apneic episodes can result in arrhythmias such as bradycardia, these occur while sleeping, therefore are not considered symptomatic. When OSA is treated, or while the patient is awake, these apneic-associated arrhythmias resolve.
A 30-year-old woman presents for evaluation of episodes of recurrent syncope. Over the past 20 years she has fainted 10 times, but in the past 6 months she has had three episodes. Typical spells occur when she sings in the church choir and are preceded by about 30 seconds of nausea and sweating. She has not injured herself, but is embarrassed, as the last time she fainted the paramedics were called. She has no other past medical history and takes no medications. On physical examination, her blood pressure (BP) is 110/60 mm Hg and heart rate is 90 bpm. Her jugular venous pulse is 5 cm. There is a single S1 and physiologically split S2 without murmur. The remainder of her examination is unremarkable. An electrocardiogram in the office shows normal sinus rhythm at a rate of 93 bpm. The following day, she undergoes a tilt table study showing a supine BP of 120/70 mm Hg and a heart rate of 80 bpm. With passive tilt, the BP over the first 5 minutes is 110-120/55-65 mm Hg and heart rates are 80-100 bpm. At 8 minutes into the tilt, she complains of nausea just like she feels before her usual faints, and then 30 seconds after that she loses consciousness. Her BP reading obtained about 20 seconds before fainting is 65/40 mm Hg and heart rate is 40 bpm. At the moment when she faints, her heart rate is 30 bpm. She is immediately laid supine, with prompt return of her BP and heart rate to baseline levels.
Which of the following is the next best step in her management?
A)Avoid triggers for syncope
B)Initiate midodrine
C)Initiate metoprolol
D)Implant a dual chamber pacemaker
A
This patient has vasovagal syncope with a well-defined trigger: standing in the choir at church. Her tilt table study suggests a mixed vasodepressor and cardioinhibitory response, and it reproduced her symptoms. While a clinical syncopal spell may show a different physiologic response, the first step in management should be conservative, stressing hydration, salt, and avoidance of triggers. While other diagnostic tests such as echocardiogram and stress testing are commonly used, the diagnosis in this patient is clear, without the need for further diagnostic testing. Likewise, electrophysiologic study can be useful for patients with syncope suspected to be due to a ventricular arrhythmia, but does not play a role for the workup of vasovagal syncope. If conservative measures fail, then an implantable loop recorder can be considered to determine if clinical episodes show a marked cardio-inhibitory response (despite the tilt table findings), as there can be a role for pacing for patients with prolonged periods of asystole.
A 50-year-old man presents to the emergency department with an acute inferior myocardial infarction. A drug-eluting stent is placed in the mid right coronary artery, and he recovers well. The patient remarks, "I just had a stress test last week and passed with flying colors. How can I have had a heart attack?" You explain that atherosclerotic plaques may be too small to induce ischemia on stress testing, but may be vulnerable to rupture and result in acute thrombotic arterial occlusion.
Which of the following features is such vulnerable plaques most likely to have?
A)Thick overlying fibrous caps.
B)Reduced inflammatory markers.
C)Low macrophage content.
D)Large lipid-filled cores.
E)Increased smooth muscle proliferation.
D
Vulnerable plaques are most often plaques with lipid-rich cores, evidence of inflammation, and thin fibrous caps. Therefore, an exercise stress test may not predict the presence of such a plaque, because they are not necessarily flow limiting. These plaques typically have a high macrophage content relative to smooth muscle cells.
You are admitting a 65-year-old woman to the hospital because of dyspnea, orthopnea, and edema. She is well-known to your practice because of long-standing heart failure with ejection fraction (EF) of 45% and hypertension. Her medications include lisinopril 2.5 mg daily, carvedilol 12.5 mg bid, and furosemide 40 mg daily. Vital signs are temperature 36.9°C, heart rate 110 bpm, blood pressure 160/100 mm Hg, and oxygen saturation is 88% on room air.
Her physical exam is remarkable for elevated jugular venous pressure and an S3 gallop. She has 3+ edema to her knees and over the sacrum. Extremities are warm. Laboratory evaluation is significant for sodium 134 mEq/L, creatinine 2.0 mg/dl (baseline 1.2 mg/dl), and B-type natriuretic peptide 3400 pg/ml.
Which of the following findings in this patient is the most likely etiology of her renal failure?
A)ACE inhibitor use.
B)Venous congestion.
C)Low cardiac output.
D)LVEF
E)Hypoxemia.
B
Cardiorenal syndrome, especially type 1 (acute) cardiorenal syndrome, complicates 25-30% of hospitalizations for acute decompensated heart failure. Changes as small as 0.3 mg/dl in serum creatinine have been associated with prolonged hospitalization and increased mortality.
Multiple factors have been postulated to contribute to this syndrome, including venous congestion, low renal perfusion, and dysfunctional autoregulation of the kidney. In this patient, there is clear evidence of venous congestion and volume overload. Her physical exam does not suggest low cardiac output. Further, in the ESCAPE (Endovascular Treatment for Small Core and Proximal Occlusion Ischemic Stroke) trial, there was no correlation between renal function and cardiac index.
LVEF is not considered a risk factor for cardiorenal syndrome, and cardiorenal syndrome is seen in cases of heart failure with preserved or reduced EF. While ACE inhibitors can decrease glomerular filtration rate, they do not decrease renal blood flow and are therefore not responsible for renal failure in this patient. Hypoxemia in isolation is not a cause of renal failure.
A 26-year-old man presents with chest pain. He experienced an upper respiratory infection 2 weeks ago. For the past week, he has had chest pain that gets worse with inspiration and supine position. There is no exertional quality to the pain; otherwise, onset is unpredictable. He has had no fevers, chills, or sweats. He has no cough. On examination, he looks well. His blood pressure is 118/70 mm Hg, his heart rate is 70 bpm, and he is afebrile. Lungs are clear. An intermittent pericardial rub is noted. Chest X-ray is normal. His electrocardiogram in the office shows sinus rhythm, but is otherwise normal.
Which of the following is the most appropriate therapeutic strategy at this time?
A)Ibuprofen for 1-2 weeks, colchicine for 8-12 weeks.
B)Oxycodone for 1-2 weeks, Prednisone for 8-12 weeks.
C)Prednisone for 1-2 weeks, Oxycodone for 8-12 weeks.
D)Ibuprofen for 8-12 weeks, Colchicine for 1-2 weeks.
E)Prednisone for 8-12 weeks, Colchicine for 1-2 weeks.
A
This young man has pericarditis. It is most likely idiopathic or viral in light of his recent upper respiratory infection. The predominant therapeutic concerns are relief of symptoms and preventing recurrence. Nonsteroidal anti-inflammatory drugs (NSAIDs) are very effective at immediate pain relief and should be considered first line. The addition of colchicine has been shown to prevent recurrences in several prospective randomized trials. Prednisone has little role in the primary contemporary management of pericarditis and may be difficult to wean over extended periods of time, notwithstanding the significant side effects of chronic steroids. Narcotics have no specific anti-inflammatory actions and are inferior to anti-inflammatory approaches. NSAIDs should be used for symptom severity, generally about 2 weeks. Colchicine should be continued for 2-3 months to prevent recurrence.
A 65-year-old patient presents to your cardiology clinic for a routine follow-up visit. He has a history of coronary artery disease with a drug-eluting stent to his left anterior descending 3 years ago, hyperlipidemia, and borderline hypertension (HTN), which he has controlled with diet for the past few years. He reports that he has recently been diagnosed with metastatic renal cell carcinoma and is about to start therapy with bevacizumab. He denies any recent cardiovascular symptoms or changes in exercise tolerance. He is currently taking aspirin 81 mg daily, clopidogrel 75 mg daily, and simvastatin 40 mg daily. On examination, his heart rate is 58 bpm and blood pressure is 138/88 mm Hg. His cardiovascular examination is otherwise unremarkable. You discuss the cardiovascular risks of therapy with vascular endothelial growth factor (VEGF) inhibitors with him.
In addition to thromboembolism, which of the following other cardiovascular complications of the bevacizumab therapy is most likely to be seen in this patient?
A)HTN
B)Coronary vasospasm
C)LV dysfunction
D)A Fib
E)QT prolongation
A
Multiple investigative and clinical observations have demonstrated HTN to be a common class effect resulting from treatment with VEGF inhibitors, occurring in 10-30% of patients treated with bevacizumab. The rates of substantial HTN appear to depend on the antiangiogenic agent used, the tumor type, and patient-related factors, including age and comorbidity. Angiogenesis inhibitor-related HTN is typically manageable with early initiation of pharmacologic therapy to reach accepted blood pressure targets. Preferred antihypertensive agents for angiogenesis inhibitor-associated HTN include angiotensin-converting enzyme inhibitors and dihydropyridine calcium channel blockers, although there are minimal data to suggest superiority of a single class of agents. Early and aggressive initiation of antihypertensive therapy appears to help maintain treatment schedule and reduce the risk of substantial complications, including malignant HTN and reversible posterior leukoencephalopathy. Bevacizumab is not known to have any significant risk of QT prolongation or arrhythmias. There is a small increase in cardiac ischemia in trials of bevacizumab, which is likely due to thromboembolic complications rather than direct effect on the coronary arteries or vasospasm. There is an approximate 20% incidence of venous thromboembolism and an approximate 5-6% incidence of arterial thrombosis in patients treated with bevacizumab.
A 45-year-old woman with nonvalvular atrial fibrillation presents after a mechanical fall. She slipped and hit her head on the curb and has changes in her mental status. Computed tomography of the head reveals a small subdural bleed. Her current medications are metoprolol succinate and dabigatran.
Which of the following best describes the mechanism by which dabigatran causes anticoagulation?
A)Factor Xa inhibition.
B)Direct thrombin inhibition.
C)Vitamin K antagonism.
D)Antithrombin III inhibition.
E)ADP receptor antagonism.
B
Dabigatran is a direct thrombin inhibitor. Warfarin is a vitamin K antagonist. Low molecular weight heparin, as well as rivoroxaban, edoxaban, and apixaban inhibit factor Xa. Clopidogrel inhibits ADP receptors on the platelet surface. Heparin inhibits antithrombin III.
Effective dose-reduction strategies include appropriate patient selection.
For which of the following patients is coronary computed tomography angiography (CCTA) appropriate?
A)A 68 year old man with high risk for coronary disease with acute chest pain.
B)An asymptomatic 59 year old man with history of CABG 2 years ago.
C)A 45 year old male executive with intermediate risk for coronary disease and worsening chest pain with activity.
D)A 50 year old man unable to undergo risk assessment.
E)A 51 year old woman with low risk for coronary disease and typical angina.
E
Appropriate patient selection is an important first step in dose reduction. In general, due to its high sensitivity and negative predictive value, CCTA performs well in ruling out coronary artery disease in low-to-intermediate risk individuals. In patients with a high likelihood of coronary disease needing triage to invasive assessment, CCTA results in unnecessary radiation exposure with little added value. In such patients, CCTA is considered inappropriate.
A 45-year-old man with a history of ischemic cardiomyopathy and a left ventricular ejection fraction (LVEF) of 25% presents for routine follow-up. He denies orthopnea, edema, paroxysmal nocturnal dyspnea, or angina. He has dyspnea when walking two blocks or up one flight of stairs.
On examination, his blood pressure is 145/90 mm Hg and his heart rate is 80 bpm. His jugular venous pressure is 7 cm without hepato-jugular reflux. He has a laterally displaced point of maximum impulse (PMI), no S3, clear lungs, and no lower extremity edema.
His current medications include carvedilol 25 mg twice daily, lisinopril 40 mg daily, furosemide 40 mg twice daily, aspirin 81 mg daily, and simvastatin 40 mg daily. His laboratory data reveal an N-terminal-pro brain natriuretic peptide (NT-proBNP) level of 1232 pg/ml, sodium of 134 mmol/L, potassium of 4.2 mEq/L, and creatinine of 1.4 mg/dl.
Which of the following would be the most appropriate for his care?
A)Add losartan 25mg/d
B)Add isosorbide dinitrate 10 mg plus hydralazine 12.5 mg TID
C)Add amlodipine 10 mg daily
D)Add spironolactone 12.5 mg daily
E)Increase furosemide to 60mg bid
D
This patient has New York Heart Association (NYHA) class III symptoms and a reduced LVEF. Aldosterone-receptor antagonists are recommended in patients with NYHA class II-IV heart failure with an LVEF of 35% or less, unless contraindicated, to reduce morbidity and mortality. This patient’s creatinine and potassium levels are well below the recommended thresholds for initiating an aldosterone antagonist. Creatinine should be <2.5 mg/dl in men and <2.0 mg/dl in women, and potassium <5 mEq/L.
Although he has dyspnea with exertion and an elevated NT-proBNP, he appears euvolemic on examination. Thus, increasing furosemide would be not be appropriate. Calcium channel blocking drugs are not recommended as routine treatment for patients with heart failure and reduced EF.
A combination of isosorbide dinitrate and hydralazine is recommended for self-reported African-American patients with NYHA class III-IV heart failure and reduced EF on optimal therapy with an angiotensin-converting enzyme inhibitor (ACEI) and beta-blocker, or for any patient with symptomatic heart failure with reduced EF who cannot be given an ACEI or angiotensin-receptor blocker (ARB). However, this patient is Caucasian and is taking an ACEI, making this choice less appropriate.
The addition of an ARB to an ACEI and beta-blocker for a persistently symptomatic patient with heart failure and reduced EF should only be considered when an aldosterone receptor antagonist is not indicated or tolerated.
A 75-year-old man presents with 3 days of chest pain and worsening dyspnea on exertion. On examination, his blood pressure is 125/60 mm Hg, heart rate is 95 bpm, and jugular venous pressure is 12 cm. There is a harsh systolic murmur heard throughout the precordium without inspiratory augmentation. At the apex, it is noted that following a premature ventricular contraction, the murmur becomes transiently louder. An electrocardiogram shows Q waves in the inferior leads.
If the patient underwent a hemodynamic cardiac catheterization, which of the following would be found?
A)Large V wave on right atrial pressure tracing.
B)Increased pulmonary artery oxygen saturation.
C)large V wave on pulmonary capillary wedge pressure tracing.
D)Large right ventricular outflow to PA pressure gradient.
E)Large left ventricle to aorta gradient.
E
The patient has degenerative or age-related AS, the most common etiology of AS. On physical examination, he demonstrates Gallavardin phenomenon—a harsh AS murmur heard best at the apex. This is due to the high-frequency components of the AS murmur radiating to the left ventricular apex. It also can be differentiated from MR by noting a gap between S1, the murmur, and then S2. The MR murmur starts with S1 and continues through S2 until the mitral valve opens. The murmur of AS also increases with bradycardia or after a pause, such as after a premature ventricular contraction; an MR murmur would not change. This is not tricuspid regurgitation, which would be holosystolic and best heard at the left lower sternal border. Nor is this pulmonic stenosis, which would typically best be heard at the left upper sternal border.
Both of these right-sided murmurs would become louder with inspiration. If a hemodynamic cardiac catheterization were performed, it would demonstrate a large left ventricle to aorta pressure gradient, consistent with AS. A large V wave on pulmonary capillary wedge pressure is consistent with significant MR. A large V wave on the right atrium is consistent with significant tricuspid regurgitation. Increased PA oxygen saturation suggests the presence of a left-to-right shunt, such as a ventricular septal defect. A ventricular septal defect murmur is typically continuous and heard at the sternal border, not the apex. A large right ventricular outflow tract to PA pressure gradient is consistent with pulmonic stenosis.
A 63-year-old man is seen in the office for consultation. He has a history of coronary artery disease (CAD) with prior bypass surgery. Cardiac catheterization within the past year revealed patent bypass grafts. His medical history also includes hypertension that has been well controlled with medication, and a 25 pack-year history of cigarette use. His medications include low-dose aspirin, metoprolol, benazepril, and atorvastatin. His primary care physician had noted an enlarged pulsatile abdominal mass on his last physical exam and subsequently referred him for abdominal ultrasound. This confirmed the presence of a 6.1 cm infrarenal abdominal aortic aneurysm (AAA). The patient denies any abdominal pain or cardiac symptoms.
Which of the following is the estimated lifetime risk of rupture in this patient?
A)80%
B)40%
C)20%
D)60%
B
The correct answer is 40%. The lifetime risk of AAA rupture has been estimated at 20% for aneurysms >5.0 cm in diameter and 40% for aneurysms ≥6.0 cm in diameter. Patients with an infrarenal or juxtarenal AAA ≥5.5 cm in diameter should undergo surgical repair (Class I indication). CAD is an important comorbidity that must be managed in the perioperative period. This patient is already on beta-blocker therapy, which should be continued. Patients with infrarenal or juxtarenal AAAs that are 4.0-5.4 cm in diameter should be followed by serial computed tomography or abdominal ultrasound exams every 6-12 months to monitor for aneurysm expansion.