ABIM Cardiovascular Disease Certification: Clinical Decisions and Interpretation Study Guide

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A patient with intermittent AF, hypertension and a previous ischemic stroke returns in sinus rhythm. Explain that restored rhythm does not remove the underlying stroke risk, and assess oral anticoagulation alongside renal function, bleeding history and preferences.

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A patient with AF and rheumatic mitral stenosis asks to replace warfarin with apixaban. Retain warfarin under the disease-specific recommendation; do not make this recommendation conditional on first demonstrating moderate or severe stenosis or on reaching a CHA2DS2-VASc threshold.

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A young adult has an irregular wide-complex tachycardia at approximately 240 beats/min and a previous ECG showing a delta wave. With preserved perfusion, select a pathway-appropriate antiarrhythmic while preparing for cardioversion if instability develops.

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A stable patient reports five days of continuous AF and has not received anticoagulation. Plan either anticoagulation before delayed cardioversion or a thrombus-excluding imaging strategy, and explicitly arrange post-cardioversion anticoagulation rather than stopping after rhythm restoration.

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A stable patient with EF 45% may meet the EF criterion for diltiazem, provided the overall clinical state permits it. A patient with EF 25% and pulmonary congestion should not receive intravenous diltiazem. Assess perfusion, decompensation and whether AF is causing instability before selecting an alternative; AF-related instability requires electrical cardioversion.

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A patient with HCM survives a documented ventricular tachyarrhythmic arrest and has an LVEF of 65%. Assess for secondary-prevention ICD treatment rather than rejecting the device because the EF is above the usual HFrEF primary-prevention threshold.

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An ambulatory monitor records marked sinus bradycardia during sleep, but dizziness occurs during normal daytime rates. Review medications and sleep-apnea symptoms, and seek symptom–rhythm correlation before attributing the dizziness to sinus node disease or recommending pacing.

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A stable patient has regular sinus P waves at constant P–P intervals. Several consecutive P waves conduct with PR intervals of 180 ms, one on-time P wave fails to conduct, and subsequent conducted beats retain PR intervals of 180 ms. There is no sinus slowing around the block, and premature atrial beats are excluded. This pattern supports Mobitz II. After excluding reversible causes such as medication toxicity, ischemia and electrolyte abnormalities, arrange permanent pacing evaluation even if the patient denies syncope.

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A patient taking a QT-prolonging antiarrhythmic develops renal impairment, potassium depletion and sustained polymorphic VT with hypotension. Deliver an immediate unsynchronized shock; do not wait for magnesium administration or synchronization markers. Subsequently give magnesium for recurrent long-QT torsades, replace depleted electrolytes and discontinue the accumulating culprit drug. Review the preceding sinus-rhythm ECG to establish whether QT prolongation supports torsades.

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A patient undergoes PCI for ACS and has no major bleeding risk or indication for oral anticoagulation. Plan the default DAPT course, explain adherence, and reassess if bleeding, surgery or a new anticoagulation indication changes the balance.

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After uncomplicated PCI, a patient with AF requires ongoing anticoagulation and has a previous gastrointestinal bleed. Plan a short aspirin exposure followed by anticoagulation plus an appropriate P2Y12 inhibitor, with explicit review of coronary and bleeding risks.

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A patient with an occluded right coronary artery, hypotension and cool extremities also has severe stable LAD disease. Prioritize emergency treatment of the infarct-related artery and reassess the nonculprit lesion once the shock state has been addressed.

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A stable patient has successful culprit-lesion PCI and another important proximal coronary stenosis. Develop a complete revascularization plan that considers lesion complexity, surgical suitability and clinical recovery instead of automatically leaving the residual lesion untreated.

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A patient with ACS requires PCI and has suitable radial anatomy. Select radial access when feasible, particularly because antithrombotic treatment increases bleeding exposure, while preserving an alternative access plan if the procedure requires it.

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Ongoing ischemic chest pain with diagnostic ST elevation requires emergency reperfusion assessment without waiting for troponin elevation. In sepsis, rising troponin without ischemic evidence supports acute myocardial injury. Add profound hypotension and new ischemic ST depression, and historical type 2 MI becomes supportable after evaluating competing coronary causes. Under the Fifth Universal Definition, those findings support consideration of secondary MI; they do not alone confirm it when appropriate imaging can be obtained. A new ischemic regional wall-motion abnormality supplies a qualifying confirmation finding. If imaging is inappropriate, explain the clinical evidence supporting a presumed secondary MI and the limits of that assessment.

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A patient recovering from atherosclerotic ACS has LDL cholesterol of 86 mg/dL while consistently taking maximally tolerated high-intensity statin therapy. Add a nonstatin agent while continuing the tolerated statin. The LDL remains above the guideline's intensification threshold even if the laboratory does not flag it as abnormal. If the patient has instead been missing doses, address adherence so the LDL result can be interpreted against the treatment actually received.

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A patient had an MI four years ago, has an LVEF of 60%, and reports fatigue without angina, arrhythmia or uncontrolled hypertension. Review whether beta blockade still has an indication and discuss a supervised medication adjustment.

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A patient with stable exertional angina has a resting pulse of 48/min, blood pressure of 142/78 mm Hg and LVEF of 60%. Amlodipine is a reasonable antianginal choice because blood pressure permits vasodilation and the drug does not ordinarily slow nodal conduction. Avoid automatically adding a beta blocker or substituting diltiazem or verapamil, which could worsen the bradycardia. Continue indicated preventive treatment because symptom relief and prevention of cardiovascular events require separate treatment decisions.

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A patient remains unable to walk to work because of angina despite tolerated antianginal therapy. Angiography shows a significant treatable stenosis corresponding to the ischemic territory. Discuss revascularization for symptom improvement using shared decision-making.

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A patient two years after PCI exercises regularly, has no angina and has unchanged functional capacity. Continue clinical follow-up and preventive care rather than ordering an annual stress study solely because another year has passed.

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A patient recovering from ACS cannot attend a center because of travel distance and caregiving duties. Arrange an appropriate home-based rehabilitation option and address medication access instead of allowing the attendance barrier to end the rehabilitation discussion.

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Several days after an inferior MI, a patient suddenly develops pulmonary edema and hypotension despite no clear recurrent ST elevation. Obtain emergency echocardiography for acute MR and other mechanical complications rather than assuming that congestion simply reflects the original infarct size.

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A stable patient with LVEF 30% takes furosemide and lisinopril. Review all four foundational classes. If switching to sacubitril/valsartan is appropriate, first exclude a history of angioedema, stop lisinopril and allow at least 36 hours before the first ARNI dose; select one of the three beta blockers with demonstrated HFrEF benefit.

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A patient with symptomatic HFrEF has an eGFR of 42 mL/min/1.73 m² and potassium of 4.6 mEq/L. Consider an MRA and arrange follow-up chemistry testing, especially because concurrent renin–angiotensin therapy can also increase potassium.

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A patient with established HFpEF has recurrent congestion, normal glycated hemoglobin and no diabetes. Consider an SGLT2 inhibitor as heart failure treatment rather than rejecting it because glucose-lowering therapy appears unnecessary in this individual.

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A patient whose LVEF increased from 25% to 52% feels well and asks to stop every heart failure medication. Explain the risk of recurrent dysfunction and continue disease-modifying therapy while reviewing whether the diuretic requirement has changed.

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A patient with HFrEF has orthopnea, elevated jugular venous pressure and leg edema despite foundational therapy. Adjust diuretic treatment and monitor response rather than assuming disease-modifying medications alone will promptly correct substantial fluid retention.

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A patient is 150 days after MI and culprit-vessel PCI, has received maximally tolerated GDMT for 120 days, and has repeat LVEF 28%, NYHA I status and expected meaningful survival beyond one year. The reassessment intervals have elapsed, and the separate post-MI NYHA I pathway supports primary-prevention ICD treatment. By contrast, a patient only 60 days after MI and PCI with 60 days of GDMT still requires later EF reassessment after the applicable treatment and revascularization intervals, even though the minimum post-MI interval has passed.

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A patient in sinus rhythm has LVEF of 30%, persistent NYHA III symptoms despite guideline-directed therapy, and LBBB with a 164-millisecond QRS. This combination establishes a strong indication for CRT. During device assessment, also determine whether defibrillator capability is appropriate for the patient's sudden-death risk and overall prognosis.

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A patient with HCM and exertional presyncope has a resting gradient of 20 mm Hg and a Valsalva gradient of 32 mm Hg. Exercise Doppler echocardiography can determine whether physiological exertion produces a gradient of at least 50 mm Hg that helps explain the symptoms.

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A newly diagnosed patient with HCM asks whether an asymptomatic adult sibling needs evaluation. Recommend family assessment and discuss genetic counseling, explaining that absence of symptoms does not exclude a phenotype or eliminate future surveillance needs.

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A patient with thick ventricular walls, low ECG voltage and carpal tunnel history has positive cardiac tracer uptake. Check the complete monoclonal-protein screen before labeling ATTR; an abnormal result changes the diagnostic pathway and can require tissue typing.

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A patient with exertional syncope has a calcified aortic valve, peak velocity of 4.6 m/s and mean gradient of 49 mm Hg. Recognize symptomatic severe high-gradient stenosis and refer for valve-intervention assessment rather than treating the murmur alone.

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Consider LVEF of 25%, resting valve area of 0.8 cm² and mean gradient of 24 mm Hg. If flow increases during dobutamine and valve area remains 0.8 cm² while peak velocity reaches 4.2 m/s, the result supports true severe obstruction. If increased flow instead enlarges valve area to 1.3 cm² while peak velocity remains 3.2 m/s, the result supports pseudo-severe disease: incomplete opening at low flow had exaggerated resting severity.

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For a 60-year-old with long expected survival and an ascending aneurysm requiring repair, favor surgical planning. For an 84-year-old with feasible transfemoral access, no concomitant surgical need and a reasonable prospect of meaningful recovery, favor TAVR. A suitable symptomatic 72-year-old should discuss both approaches.

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An asymptomatic patient with confirmed severe chronic AR has LVEF 60%, LVESD 52 mm, and body surface area 2.0 m². Indexed LVESD is 26 mm/m². Surgery is reasonable because both dimensional thresholds are exceeded despite preserved EF. By comparison, an asymptomatic patient with severe AR and LVEF 53%, without another explanation for dysfunction, meets the indication for surgery based on systolic dysfunction.

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A patient with severe degenerative MR feels well but has LVEF of 58% and LV end-systolic dimension of 42 mm. Refer for valve-team assessment rather than waiting for the EF to fall to conventional HFrEF levels.

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A patient remains symptomatic with severe secondary MR despite optimized HFrEF therapy. Review ventricular dimensions, EF, pulmonary pressure and transesophageal valve anatomy before proposing edge-to-edge repair, rather than assuming that regurgitation severity alone establishes candidacy.

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A patient with symptomatic rheumatic mitral stenosis has pliable commissural fusion and mild MR. Arrange transesophageal assessment for atrial thrombus; if absent and anatomy remains favorable, balloon commissurotomy may offer an appropriate intervention without valve replacement.

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A patient with a mechanical mitral valve asks to switch from warfarin to a direct oral anticoagulant to avoid monitoring. Explain the device-specific thrombotic risk and retain vitamin K antagonist therapy while addressing practical barriers to safe INR follow-up.

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A patient with a prosthetic aortic valve is scheduled for a dental extraction. Recognize the high-risk cardiac condition and qualifying procedure, arrange appropriate prophylaxis, and reinforce ongoing dental hygiene rather than limiting prevention to the procedure day.

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A patient with a pericardial effusion develops hypotension, tachycardia and elevated neck veins; echocardiography shows right ventricular diastolic collapse. Recognize impaired filling and arrange urgent drainage instead of waiting for the effusion to become larger.

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A stable, afebrile patient has pleuritic pain relieved by leaning forward, diffuse ST elevation and elevated C-reactive protein. The compatible presentation plus ECG changes and inflammatory-marker elevation supplies more than one additional criterion, supporting definite pericarditis. Echocardiography shows no large effusion or tamponade. After evaluating the cause and medication contraindications, prescribe aspirin or an NSAID with colchicine and arrange follow-up of symptoms and inflammatory activity.

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An adult with Fontan palliation feels well and has preserved ventricular function but has not received liver assessment. Arrange comprehensive congenital follow-up that includes hepatic and rhythm surveillance rather than limiting review to an annual ventricular EF.

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An adult has unexplained right ventricular enlargement and an interatrial communication. Assess shunt magnitude, pulmonary pressures, resistance and anatomy before choosing closure. Cyanosis or evidence of bidirectional or right-to-left flow should prompt evaluation for advanced pulmonary vascular disease rather than reflex closure.

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An adult with repaired tetralogy has declining endurance, a pulmonary diastolic murmur and RV enlargement. Evaluate pulmonary regurgitation and quantify RV consequences rather than focusing only on LV EF or attributing reduced activity to deconditioning.

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A patient with abrupt chest pain has CT evidence of a dissection extending into the ascending aorta. Initiate monitored anti-impulse treatment and emergency surgical coordination rather than treating the improved blood pressure as evidence that medical therapy is sufficient.

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A patient with descending aortic dissection develops worsening abdominal pain and evidence of mesenteric malperfusion despite blood pressure control. Recognize a complicated type B dissection and arrange urgent aortic-team assessment for intervention rather than continuing observation alone.

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A patient with ascending aortic dissection has no Marfan features and no identified mutation. Recommend screening imaging for first-degree relatives rather than reassuring the family that the absence of a recognizable syndrome excludes inherited susceptibility.

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A patient with a left internal mammary graft develops angina while carrying groceries with the left arm and has a weaker left radial pulse. Assess bilateral arm pressures and image the subclavian inflow and bypass circulation rather than assuming the only possible explanation is a new coronary stenosis.

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A patient's office readings are repeatedly elevated, but carefully obtained home readings are lower. Review cuff validation, positioning and the measurement record before escalating medication, and assess whether a white-coat pattern explains the discrepancy in this clinical context.

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A patient with established coronary disease and a confirmed average pressure of 134/84 mm Hg should begin medication alongside lifestyle treatment under this guideline. A second patient with the same pressure, no cardiovascular disease, previous stroke, diabetes or chronic kidney disease, and PREVENT risk of 4% can initially receive lifestyle treatment. If the second patient's average pressure remains 134/84 mm Hg after four months, medication should be started while lifestyle measures continue. The pressure is identical, but the higher-risk patient's indication for medication is present at the initial treatment decision.

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A patient starting antihypertensive therapy frequently eats high-sodium prepared meals because of work hours. Develop a feasible lower-sodium food strategy and home-monitoring plan while prescribing medication, rather than treating the prescription as a replacement for risk-factor modification.

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Two patients have similarly severe pressures: one is asymptomatic, while the other has acute pulmonary edema. Identify acute organ injury in the second patient and choose monitored emergency treatment rather than applying the same immediate pressure-lowering strategy to both.

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Catheterization shows mean pulmonary pressure 34 mm Hg, wedge pressure 12 mm Hg and cardiac output 4 L/min. Calculate PVR as 5.5 Wood units and recognize precapillary physiology, then investigate its cause before assigning disease-specific treatment.

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A patient has unexplained pulmonary hypertension and persistent exertional dyspnea after a previous pulmonary embolism. Obtain V/Q imaging to assess chronic thromboembolic obstruction and arrange expert evaluation if mismatched defects are found rather than assuming idiopathic pulmonary arterial hypertension.

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A patient with CKD taking an MRA develops repeated potassium values of 5.8 mEq/L after a decline in renal function. Assess urgency, confirm the result when appropriate, review contributing drugs and correct the abnormality; do not continue the MRA unchanged if potassium cannot be maintained below 5.5.

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During anthracycline treatment, an asymptomatic patient's LVEF remains 58%, but GLS changes from −20% to −16%. Recognize a 20% relative deterioration and assess for mild asymptomatic dysfunction, including biomarkers and treatment planning, rather than waiting for reduced EF or edema.

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A patient recently started on an ICI develops weakness, elevated troponin and new high-grade AV block with LVEF 60%. Interrupt treatment, hospitalize with continuous ECG monitoring and urgent cardiac assessment, evaluate competing diagnoses, and promptly begin high-dose corticosteroids when myocarditis is likely. Do not delay treatment solely to obtain CMR or biopsy.

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An outflow diameter of 2.0 cm and VTI of 20 cm yield approximately 63 mL per beat. RV areas of 25 cm² in diastole and 15 cm² in systole yield FAC of 40%; keep the two measurements conceptually separate.