Simulación

1.  All of the following are contraindications to
the use of ACE inhibitors except
 Choices
 A
• bilateral renal artery stenosis
 B
• pregnancy
 C
• Angioedema
 D cough
Answer
D
Cough is a common side effect of ACE inhibitors. It is not a
contraindication to initiate patients on ACE inhibitors if they
have preexisting cough

2.  By which of the following mechanisms do diltiazem and
verapamil slow ventricular rate in patients with AFib?
 Choices
 A
• They decrease the conduction velocity within the AV node.
 B
• They decrease the refractory period of nodal tissue.
 C
• They stimulate vagal tone.
 D
• They prolong the refractory period of atrial tissue.
A
Diltiazem and verapamil decrease conduction velocity within the
AV node and increase RP of nodal tissue. This then causes
slowing of ventricular rate.

3.  Short-acting dihydropyridine calcium channel
blockers (CCBs) possess all of the following
properties except
 Choices
 A
• They cause peripheral edema.
 B
• They cause reflex tachycardia.
 C
• They cause flushing.
 D
• They slow ventricular response in patients with AFib.
D
Dihydropyridines are more selective for vascular smooth-muscle calcium
channels than for myocardial calcium channels. Dihydropyridine CCBs do not
slow AV-nodal conduction. Unlike verapamil and diltiazem, dihydropyridine CCBs
cause a reflex tachycardia and do not increase AV-nodal RP. Pedal edema is one
of the most common side effects of dihydropyridine-type CCBs and is associated
with short half-life, short-acting agents. Because of their ability to produce such
profound vasodilation, these agents can produce flushing as well.

4.  Which of the following CCBs is indicated in
patients presenting with a subarachnoid
hemorrhage?
 Choices
 A
• verapamil
 B
• diltiazem
 C
• isradipine
 D
• nimodipine
D. Nimodipine.
Nimodipine is the only agent indicated for patients with
subarachnoid hemorrhage. Nimodipine decreases the influx of
extracellular calcium, thus preventing vasospasm.

5.  All of the following are suggested
mechanisms of nitrate tolerance except
 Choices
 A
• sulfhydryl-group depletion
 B
• plasma volume expansion
 C
• free radical depletion
 D
• neurohormonal stimulation
C
Free radical depletion is not a suggested mechanism. Long-
term administration of nitroglycerin without a nitrate-free
interval may lead to nitrate tolerance

6.  A patient with CHF on lisinopril was experiencing a dry
cough and hyperkalemia. What would be the most
appropriate therapy to replace the ACE inhibitor?
 Choices
 Choices
 A
• losartan
 B
• metoprolol
 C
• digoxin
 D
• hydralazine and ISDN
D. Hydralazine and ISDN.

7.  A 35-year-old man, who is a smoker and has a family history of
CAD (father had MI at 40 years of age), has the following lipid
profile:
 Total cholesterol = 193 mg per dL
 LDL = 150 mg per dL
 HDL = 43 mg per dL
 Triglyceride (TG) = 175 mg per dL
 What, if any, medication is indicated?
 Choices
 A
• HMG-CoA reductase inhibitors.
 B
• Bile acid sequestrants.
 C
• Fibric acid derivative.
 D
• No medication is indicated at this time.
D. No medication is indicated at this time.
Because this patient is a smoker with a significant family history of CAD, he has
two risk factors for CHD. The therapeutic aim is reduction of LDL cholesterol
(goal, <=130 mg/dL) which should be attempted with the therapeutic
lifestyle changes diet. If after 3 months of therapeutic lifestyle changes alone
the LDL is less than 160 mg per dL, it should be continued. Drug therapy is not
indicated because the patient is not at high short-term risk. Drug therapy
should be initiated if the LDL is greater than or equal to 160 mg per dL.

8.  A 55-year-old patient with HF and a past medical history of
DM and CAD presents to the outpatient clinic for a follow-up
visit. Today's lipids are as follows: total cholesterol, 249 mg
per dL; TG, 561 mg per dL; HDL, 40 mg per dL; LDL, 97
mg per dL. Which agent would be most appropriate to
initiate in this patient?
 Choices
 A
• fenofibrate
 B
• atorvastatin
 C
• cholestyramine
 D
• no drug therapy at this time
A. Fenofibrate.
Because the patient's TG is in the category of very high (greater than or
equal to 500 mg/dL), the initial aim is to reduce the risk of pancreatitis by
using a TG-lowering agent. Fibrates or nicotinic acid would be indicated due
to their potential to reduce TGs 20% to 50%

9.  All of the following side effects occurring with
ARBs will occur with ACE inhibitors except
 Choices
 A
• cough
 B
• renal dysfunction
 C
• hyperkalemia
 D
• hypotension
A
ARBs have a very similar side-effect profile to ACE inhibitors.
They are both contraindicated in patients with bilateral renal
artery stenosis, and both can cause hyperkalemia and
hypotension. Cough is a major difference with these two agents.
ARBs do not increase the levels of bradykinin, whereas ACE
inhibitors will decrease the breakdown of bradykinins, thus
leading to accumulation and, thus, to cough.

10.  Which beta-blocker should not be used in
patients with CHF?
 Choices
 A
• carvedilol
 B
• metoprolol
 C
• pindolol
 D
• bisoprolol
C
Pindolol exhibits ISA and should, therefore, not be used on
patients with HF.

11.  A 57-year-old man who is status post MI has a
BP of 150/88 mm Hg. Which agent would be the
most appropriate for treatment of his HTN?
• Choices
 A
• hydrochlorothiazide
 B
• metoprolol
 C
• clonidine
 D
• losartan
B. Metoprolol.
The American College of Cardiology and the American Heart Association
recommend the use of beta-blockers in patients after surviving an MI to
decrease mortality, sudden death, and reinfarction

12.  All of the following medications used to treat HF
have been shown to improve survival except
 Choices
 A
• captopril
 B
• prazosin
 C
• hydralazine and isosorbide dinitrate (ISDN)
 D
• metoprolol
B
Prazosin has not been shown to improve survival. Multiple trials have
shown that ACE inhibitors, beta-blockers, and the combination of
hydralazine and ISDN improve survival in patients who have HF. In
the V-HeFT-I trial, prazosin was compared to placebo. in those
patients who received prazosin, there was no significant difference in
mortality when compared to placebo.

13.  B. J. is a 56-year-old woman with long-standing HTN that is
difficult to control. She is currently being treated with amlodipine,
10 mg q.d.; lisinopril, 40 mg q.d.; hydrochlorothiazide, 25 mg
q.d.; and clonidine, 0.4 mg three times per day. She presented to
the ER, and her initial BP was 200/110 mm Hg. She states she
had run out of one of her medications. Which one of her
medications would most likely be implicated in causing
hypertensive urgency?
 Choices
 A
• amlodipine
 B
• lisinopril
 C
• hydrochlorothiazide
 D
• clonidine
D. Clonidine.
Abrupt withdrawal of an alpha2 agonist is the most likely cause
of severe rebound HTN. Typically, this is seen within 24 to 48
hours of discontinuation of clonidine and typically occurs in
patients taking large doses for longer than 3 months. The best
treatment for this is to restart clonidine. Beta-blockers could
make the situation worse due to causing unopposed alpha1
stimulation

14.  76-year-old white man with a past medical history significant for DM type
2, HTN, and chronic AFib was recently diagnosed with CAD and
hypercholesterolemia and was initiated on gemfibrozil,, and atorvastatin,.
His other medications include glyburide, metoprolol, furosemide,
levothyroxine, insulin, and aspirin. Two weeks later, he began to
experience pain in his right calf, with pain and stiffness throughout his
back, buttocks, and thigh. On admission, his BUN was elevated, and the
urinalysis showed orange, cloudy urine; and myoglobin, 1,367. Which of
the following statements is true?
 Choices
 A
• The patient is experiencing rhabdomyolysis secondary to the drug interaction of
atorvastatin and glyburide.
 B
• Forced diuresis with urine alkalinization and discontinuation of gemfibrozil and
atorvastatin are indicated for this patient.
 C
• Atorvastatin is contraindicated in a patient with DM type 2 and HTN.
 D
• If nicotinic acid, rather than gemfibrozil, had been used for
hypercholesterolemia, this reaction would have been prevented.
B.
Rhabdomyolysis secondary to the interaction of atorvastatin and gemfibrozil is responsible for
this clinical picture. Rhabdomyolysis is defined as the disintegration of muscle, associated with
the excretion of myoglobin in the urine. Clinical signs and symptoms include myalgias,
elevated creatine kinase, elevated urine and serum myoglobin, and dark urine.. In addition,
renal failure due to products of tissue degradation must be combatted with urinary
alkalinization and maintenance of a high urine volume.

15.  All of the following drugs produce changes
in lipid profiles except
 Choices
 A
• thiazide diuretics
 B
• beta-blockers
 C
• protease inhibitors
 D
• ACE inhibitors
D
ACE inhibitors have no effect on the lipid profile. Beta-blockers and
thiazide diuretics typically have the most effect on raising TG levels.
Beta-blockers may decrease HDL levels, whereas thiazide diuretics
may increase LDL and total cholesterol. Protease inhibitors have the
most effect on TGs and total cholesterol and cause adipose tissue
redistribution.

16.  A. F. is a 52-year-old man with a history of AFib, TIAs,
HTN, and rheumatic heart disease. The recommendations
from the Sixth American College of Chest Physicians (ACCP)
Consensus Conference on Antithrombotic Therapy suggest
that this patient be initiated on __________ for
antithrombotic therapy because of AFib.
 Choices
 A
• aspirin, 81 mg q.d.
 B
• aspirin, 325 mg q.d.
 C
• warfarin, with a target-goal INR of 2.5
 D
• warfarin, with a target-goal INR of 3.5
C
Warfarin, with a target goal INR of 2.5. This patient is at high risk for a
thromboembolic event. Recommendations for antithrombotic therapy
include risk stratification. Risks are stratified into high, moderate, and
low. High-risk patients include patients with prior stroke or TIA or
systemic embolus, history of HTN, poor LV systolic function, age older
than 75 years, rheumatic mitral valve disease, and a prosthetic heart
valve.. Low-risk patients are those younger than 65 years old with no
clinical or TTE evidence of cardiovascular disease.

17.  The patient above is going to be electively cardioverted.
What is the timing of PO anticoagulant therapy?
 Choices
 A
• warfarin with a target INR of 3.5 for 4 weeks before
cardioversion and continued for 6 weeks after cardioversion
 B
• warfarin with a target INR of 3.5 for 3 weeks before
cardioversion and continued for 6 weeks after cardioversion
 C
• warfarin with a target INR of 2.5 for 3 weeks before
cardioversion and continued for 4 weeks after cardioversion
 D
• warfarin with a target INR of 2.5 for 6 weeks before
cardioversion and continued for 6 weeks after cardioversion
C
Warfarin with a target INR of 2.5 for 3 weeks before cardioversion and
continued for 4 weeks after cardioversion. Also, an alternative approach
would to be initiate anticoagulation, have the patients undergo a TEE, and
have the cardioversion performed if no thrombi are seen. Warfarin should
be continued for at least 4 weeks, as long as the patient maintains NSR.

18.  Which of the following side effects
differentiate ticlopidine from clopidogrel?
 Choices
 A
• diarrhea
 B
• rash
 C
• neutropenia
 D
• thrombotic thrombocytopenic purpura
C. Neutropenia.
Ticlopidine causes neutropenia in 2.4% of patients who are initiated
on therapy. Nearly 1% of patients develop severe neutropenia.
Therefore, a complete blood count is required every 2 weeks during
initiation of therapy for the first 3 months of therapy. Both agents
can cause diarrhea and rash. Structurally, these two drugs are so
similar that allergic cross-reactivity is expected. Thrombotic
thrombocytopenic purpura has been reported with both agents

19.  By which of the following mechanisms do
clopidogrel and ticlopidine exert their antiplatelet
effects?
 Choices
 A
• cyclooxygenase inhibitor
 B
• glycoprotein IIb/IIIa inhibitor
 C
• adenosine diphosphate (ADP) inhibitor
 D
• direct thrombin inhibitor
C
ADP inhibitor.

20.  All of the following are considered
contraindications to abciximab administration
except
 Choices
 A
• readministration of abciximab
 B
• thrombocytopenia with a platelet count of less than
100,000 cells per µL
 C
• active internal bleeding
 D
• intracranial tumor, arteriovenous malformation, or
aneurysm
A
Readministration of abciximab is not a
contraindication (estreptokinasa)

21.  Which of the following glycoprotein IIb/IIIa
inhibitors has the highest incidence of severe
thrombocytopenia?
 Choices
 A
• tirofiban
 B
• abciximab
 C
• eptifibatide
 D
• The incidence is not different between the different
agents.
B. Abciximab.
All glycoprotein IIb/IIIa inhibitors may cause
thrombocytopenia. However, abciximab has the
highest rate of all, based on the clinical trials.

22.  Which of the following glycoprotein IIb/IIIa
inhibitors has the shortest half-life but the
longest duration of therapy?
 Choices
 A
• tirofiban
 B
• eptifibatide
 C
• abciximab
 D
• lamifiban
C. Abciximab.
Abciximab has a serum half-life of 10 to 30 min; however,
because of its high binding affinity to the glycoprotein IIb/IIIa
receptor, it maintains its activity for many hours after
discontinuation of therapy, and abciximab can be detected in the
serum for longer than 2 weeks.

23.  Heparin must first bind to __________ to exert
its anticoagulant activity.
 Choices
 Choices
 A
• antithrombin
 B
• thrombin
 C
• factor X
 D
• protein C
A. Antithrombin.
Heparin must first bind to antithrombin to exert is anticoagulant
effect. This complex accelerates antithrombin effect. Heparin
potentiates antithrombin's effect by binding to a glucosamine unit
within a pentasaccharide sequence.

24.  J. M. was initiated on heparin and was given a 5,000-unit
bolus. Five min after the loading dose of heparin, she began
to have bloody emesis, and her systolic pressure dropped
to 80 mm Hg. How much protamine will she require?
 Choices
 A
• 25 mg
 B
• 50 mg
 C
• 75 mg
 D
• 100 mg
B. 50 mg.
Every 1 mg of protamine will antagonize approximately
100 units of heparin

25.  Each LMWH has varying degrees of IIa:Xa
activity. Which of the following agents has the
highest IIa:Xa ratio?
 Choices
 A
• tinzaparin
 B
• dalteparin
 C
• enoxaparin
 D
• danaparoid
C. Enoxaparin.

26.  Patients who develop heparin-induced
thrombocytopenia have an in vitro cross
reactivity with LMWH by what percent?
 Choices
 A
• 90% to 100%
 B
• 60% to 70%
 C
• 25% to 45%
 D
• 5% to 10%
A. 90% to 100%.
There have been several reports of patients who have heparin-
induced thrombocytopenia being treated with LMWH. However, the
cross reactivity in vitro approaches 100%. The use of LMWH should
be considered a contraindication unless there is a documented
negative test for antibodies against LMWH.

27.  All of the following are potential advantages of
LMWHs except
 Choices
 A
• There is little need for monitoring.
 B
• SC bioavailability is predictable in most patients.
 C
• There is convenient q.d. or b.i.d. dosing for most
indications.
 D
• There is no need to adjust the dose in patients with
severe renal dysfunction.
D
LMWHs are approximately one-third the size of unfractionated heparin.
Because of their predictable ability to bind to factor Xa and consistent
bioavailability, there is little need for laboratory monitoring for efficacy.
However, there are limitations in pharmacokinetic data for
administration of these agents in patients with renal dysfunction and in
the very obese patient. Another limitation is the fact that the factor Xa
activity is only partially neutralized by protamine.

28.  Which of the following is not a
contraindication to thrombolytic therapy?
 Choices
 A
• acute pericarditis
 B
• aortic dissection
 C
• intracranial neoplasm
 D
• diabetic retinopathy
D
Diabetic retinopathy is not a contraindication to thrombolytic therapy.
A review of large clinical trials did not show an increase in the rates of
intraocular hemorrhage in patients with diabetic proliferative
retinopathy. Other absolute contraindications include previous
hemorrhagic stroke, other strokes or cerebrovascular events within 1
year, and active bleeding

29.  Which of the following is not a risk factor for
intracranial hemorrhage in patients receiving
fibrinolytic therapy in the treatment of ST
segment-elevation MI?
 Choices
 A
• HTN
 B
• body weight
 C
• age
 D
• time to presentation
D
Time to presentation is not a risk factor for intracranial hemorrhage in
patients receiving thrombolytic therapy. In clinical trials, the risks for
intracranial hemorrhage included age older than 65 years, low body
weight (less than 70 kg), HTN on hospital admission, and the use of
alteplase. Also, the levels of concomitant anticoagulation can also
increase the risk of intracranial hemorrhage.

30.  R. M. is a 65-year-old man presenting to the emergency
department with an ST segment-elevation MI. It is decided
to initiate thrombolytic therapy to induce reperfusion. The
patient weighs 72 kg. What is the most effective dose of
alteplase for this patient?
 Choices
 A
• 0.9 mg per kg, with a maximum of 90 mg
 B
• 15 mg bolus; then 54 mg over 30 min; then 36 mg over 60
min
 C
• 15 mg bolus; then 50 mg over 30 min; then 35 mg over 60
min
 D
• 60 mg over 1 hour; then 20 mg per hour for 2 hours
C
15-mg bolus; then 50 mg over 30 min; then 35 mg over 60 min.
Based on the first GUSTO trial, the most effective dosing for acute
ST segment-elevation MI is front-loaded t-PA. The maximum dose
should be 100 mg and, therefore, answer B may increase the risk of
major bleeding, specifically intracranial hemorrhage. Finally, answer
A is the recommended dosing for acute ischemic stroke.

31.  P. is a 48-year-old woman with a history of an anterior wall MI 3 months
ago. Her most recent TTE revealed an EF of 25%. She was discharged on
lisinopril, 10 mg q.d.; digoxin, 0.125 mg q.d.; metoprolol succinate
(Toprol XL), 100 mg q.d.; aspirin, 81 mg q.d.; simvastatin, 20 mg q.d.;
and furosemide, 80 mg b.i.d. She is being seen today with a report of mild
dizziness and fatigue and notes that she is making less urine over the past
few days. Laboratory values are as follows: sodium, 148 mEq per L;
potassium, 3.2 mmol L; chloride, 88; bicarbonate, 41; BUN, 76; SrCr, 2.8
mg per dL; glucose, 87 mg per dL. Which of the medications is most likely
responsible for the above laboratory findings?
 Choices
 A
• lisinopril
 B
• metoprolol
 C
• digoxin
 D
• furosemide
D. Furosemide.
Loop diuretics can cause hypokalemic metabolic alkalosis with a
coexisting chloride deficit. Loop diuretics enhance the renal secretion of
K+ and H+, causing hypokalemic metabolic alkalosis. This is a function
of the magnitude of the diuretic effect and can typically be reversed by
K+ replacement and correction of hypovolemia. Potassium chloride is the
preferred potassium salt for replacement in this setting.

32.  All of the following metabolic or electrolyte
abnormalities occur with thiazide diuretics except
 Choices
 A
• hypokalemia
 B
• hypocalcemia
 C
• hyperuricemia
 D
• hypomagnesemia
B. Hypocalcemia.
Thiamine diuretics retain calcium by increasing reabsorption in the
proximal tubule. Therefore, these agents need to be avoided in patients
with hypercalcemia, in contrast to loop diuretics, which are used to treat
hypercalcemia. Like loop diuretics, thiazide diuretics cause hypokalemia,
hyperuricemia, and hypomagnesemia. Hyperuricemia is not typically
problematic; however, it can produce gout attacks.

33.  Which of the following agents is effective for
converting AFib to sinus rhythm and for
maintaining sinus rhythm after it is restored?
 Choices
 A
• digoxin
 B
• amiodarone
 C
• diltiazem
 D
• propranolol
B. Amiodarone.
Although amiodarone does not carry an FDA indication for the
treatment of AFib, it can convert to and maintain NSR. The other
agents listed are only used for rate control when used for AFib.

34.  R. is a 65-year-old man with a history of AFib, MI, status post
CABG 5 years ago, HTN, deep venous thrombosis, and
hypercholesterolemia, who presented to the emergency
department with AFib and a rapid ventricular rate. After initiation
of beta-blockers, his rate was well controlled (heart rate, 80
bpm). A. R. has been on warfarin for a deep venous thrombosis
that developed after a fall. He has not been on antiarrhythmic
therapy. All of the following are appropriate choices except
 Choices
 A
• amiodarone
 B
• sotalol
 C
• procainamide
 D
• flecainide
D
Flecainide is not an appropriate choice. In general, antiarrhythmic agents are proarrhythmic
and possess myocardial-depressant effects. Flecainide, encainide, and moricizine were
evaluated in the Cardiac Arrhythmia Suppression Trial I or II. These agents were evaluated in
patients with multiple PVCs after MI. By suppressing ventricular ectopy, it was felt that there
would be a decrease in mortality. However, there was an increase in mortality in all groups
despite suppression of initial arrhythmia. At this time, class IC antiarrhythmics are indicated
for life-threatening sustained VT and paroxysmal SVT, including Wolff-Parkinson-White
syndrome and AFib or flutter in patients without structural heart disease.

35.  All of the following side effects may occur
during amiodarone therapy except
 Choices
 A
• pulmonary toxicity
 B
• hyperthyroidism
 C
• peripheral neuropathy
 D
• diarrhea
D
Diarrhea is not a side effect. Pulmonary toxicity in the form of pulmonary fibrosis and
hypersensitivity pneumonitis occurs in approximately 3% to 17% of patients on amiodarone
therapy. Pulmonary toxicity occurs primarily with doses greater than 400 mg q.d. and after
several months to years. Pulmonary toxicity is very difficult to diagnose, because symptoms and
signs are similar to HF and pneumonia. Patient self-reporting is the most effective way to identify
pulmonary toxicity early. Thyroid dysfunction occurs in approximately 10% of patients on
amiodarone. Patients can present with either hyper- or hypothyroidism and should be evaluated
at baseline and every 6 months thereafter. Neuropathy and other neurologic side effects can
occur in up to 20% of patients on chronic amiodarone therapy. Most frequently, amiodarone
causes constipation in long-term administration.

36.  How does digoxin improve myocardial
contractility?
 Choices
 A
• inhibition of the Na+/K+-adenosine triphosphatase
 B
• inhibition of the breakdown of cyclic adenosine
monophosphate (cAMP)
 C
• increases intracellular K+, leading to the opening of
calcium channels
 D
• directly stimulates calcium release from the
sarcoplasmic reticulum
A. Inhibition of the Na+/K+-adenosine triphosphatase.
Digoxin inhibits the Na+/K+-adenosine triphosphatase pump on the
myocardial cell surface. This inhibits the ability of the cell to exchange
potassium for sodium and thus leads to an increase in intracellular
sodium. This increase in intracellular sodium leads to exchange of
sodium for calcium, increasing intracellular calcium concentrations.
Increased intracellular calcium enhances contraction coupling.

37.  A 75-year-old man with a history of HF and AFib was initiated on
amiodarone and warfarin. He has been treated for many years with
captopril, furosemide, potassium, amlodipine, and digoxin. After 3 days in
the hospital, the patient was sent home. One week after discharge, he
developed nausea, vomiting, confusion, and symptomatic VT. His serum
digoxin concentration was 3.9 ng per mL, and his serum potassium level
was 5.8 mmol per L. The rhythm was treated with lidocaine, and the
patient is now having episodes of nonsustained VT with a BP of 80/40 mm
Hg during each episode. What should be your next course of action?
 Choices
 A
• discontinue the amiodarone and digoxin and observe
 B
• discontinue the digoxin and administer digoxin-specific antibodies
 C
• decrease the dose of digoxin
 D
• discontinue digoxin and observe
B. Discontinue the digoxin and administer digoxin-specific antibodies.
Digoxin-immune Fab is indicated for patients with life-threatening
ventricular arrhythmias relating to digoxin toxicity. It is also indicated
in patients with progressive bradyarrhythmias, such as severe sinus
bradycardia or second- or third-degree heart block not responsive to
atropine. It should not be used for milder forms of digoxin toxicity.

38.  Which of the following statements is true?
 Choices
 A
• Serum levels are used to guide the selection of the dose of
digoxin.
 B
• Because spironolactone was found to have mortality benefit in
the Randomized Aldactone Evaluation Study (RALES), the
addition of spironolactone should be considered for all CHF
patients.
 C
• The benefit of long-term IV inotropic therapy may outweigh
the increased mortality risk in refractory patients unable to be
weaned from IV inotropic support.
 D
• Digoxin exhibits both symptomatic and mortality benefit in
patients with CHF.
C. The benefit of long-term IV inotropic therapy may outweigh the increased mortality risk in
refractory patients unable to be weaned from IV inotropic support.
Little evidence supports the practice of dosing digoxin according to serum levels.
In the RALES trial, spironolactone was shown to be associated with reduced mortality and
morbidity. However, the patients who were included in this trial were patients with class IV HF.
Efficacy and safety of spironolactone's use in patients with mild to moderate HF is yet to be
determined.
. The DIG (Digitalis Investigation Group) trial showed that digoxin's benefit in HF was the
alleviation of symptoms and improvement in clinical status. These findings were associated with a
decreased morbidity (fewer hospitalizations) but not mortality.

39.  A 56-year-old white man who is status post CABG 3 years
ago is in need of a dental root canal. The patient has a
history of hives due to cephalexin. What prophylactic
regimen for endocarditis is indicated for this patient?
 Choices
 A
• amoxicillin, 2 g PO 1 hour before the procedure
 B
• clindamycin, 600 mg PO 1 hour before the procedure
 C
• amoxicillin, 2 g PO 1 hour before the procedure, then 500 mg
PO every 4 hours for two doses
 D
• azithromycin, 500 mg 1 hour before the procedure
 E
• No prophylaxis is recommended in this patient.
E. No prophylaxis is recommended in this patient.
This patient has only a negligible risk for endocarditis post-CABG. In
individuals with innocent heart murmurs or structurally normal hearts,
prophylaxis is not required.