The scenario describes a patient with a history of hypertension and dyslipidemia presenting with exertional chest pain, suggestive of stable angina. The electrocardiogram (ECG) shows ST-segment depression in the anterior leads, a hallmark of myocardial ischemia. The echocardiogram reveals moderate hypokinesis of the anterior wall, correlating with the ECG findings and indicating impaired contractility in that region. The question asks about the most appropriate next step in management, considering the diagnostic findings and the need for definitive risk stratification and potential intervention. The patient’s symptoms, ECG findings, and echocardiographic abnormalities strongly suggest significant coronary artery disease (CAD). While medical management with antiplatelets, statins, and beta-blockers is crucial for secondary prevention, the presence of exertional symptoms and objective evidence of ischemia necessitates further investigation to assess the extent and severity of CAD. Coronary angiography is the gold standard for visualizing the coronary arteries and identifying obstructive lesions. This procedure allows for precise localization and quantification of stenoses, guiding decisions regarding revascularization (percutaneous coronary intervention or coronary artery bypass grafting) versus continued medical therapy. Considering the patient’s presentation and the diagnostic workup, proceeding directly to coronary angiography is the most logical and evidence-based next step. This will provide the necessary anatomical information to tailor the long-term management strategy and improve prognosis. While further medical optimization is always important, it should not delay the definitive assessment of the coronary anatomy in this context. Stress testing could be considered if the initial diagnosis was less certain or if the patient was unable to undergo angiography, but given the clear signs of ischemia, angiography offers more direct and actionable information.

The question assesses the understanding of the physiological mechanisms underlying the development of pulmonary edema in a patient with severe mitral regurgitation and left ventricular dysfunction. In this scenario, the primary issue is the backward transmission of pressure from the failing left ventricle to the left atrium and then to the pulmonary circulation. Severe mitral regurgitation means that a significant portion of the left ventricular stroke volume is ejected backward into the left atrium during systole, rather than forward into the aorta. This leads to an elevated left atrial pressure. Because the mitral valve is incompetent, this elevated left atrial pressure is directly transmitted to the pulmonary veins and capillaries. The Starling forces governing fluid movement across the pulmonary capillary membrane are crucial here. Pulmonary capillary hydrostatic pressure increases significantly due to the elevated left atrial pressure. Normally, pulmonary capillary hydrostatic pressure is balanced by plasma oncotic pressure and interstitial hydrostatic pressure, with a small net filtration driving fluid into the interstitium. However, when pulmonary capillary hydrostatic pressure rises substantially, it overwhelms the opposing forces, leading to increased net filtration of fluid from the capillaries into the interstitial space of the lungs. If this filtration rate exceeds the lymphatic drainage capacity of the lungs, interstitial edema develops. In severe cases, fluid can then flood the alveolar spaces, causing alveolar edema, which impairs gas exchange. The left ventricular dysfunction exacerbates this by reducing the forward cardiac output, leading to a compensatory increase in sympathetic tone and potentially further increases in systemic vascular resistance, which can increase afterload on the left ventricle and worsen regurgitation. However, the direct cause of the pulmonary edema in this specific context is the elevated pulmonary venous pressure secondary to the mitral regurgitation and left ventricular failure. Therefore, the most direct and immediate physiological consequence leading to pulmonary edema is the increased pulmonary capillary hydrostatic pressure.

The scenario describes a patient with a history of hypertension and type 2 diabetes mellitus presenting with symptoms suggestive of acute coronary syndrome. The electrocardiogram (ECG) shows ST-segment elevation in leads II, III, and aVF, indicating an inferior wall myocardial infarction. The patient’s blood pressure is 160/95 mmHg, heart rate is 88 bpm, and oxygen saturation is 96% on room air. The primary goal in managing an ST-elevation myocardial infarction (STEMI) is rapid reperfusion. Given the patient’s presentation within the recommended timeframe for primary percutaneous coronary intervention (PCI), this is the preferred reperfusion strategy. The explanation should focus on the rationale for choosing primary PCI over fibrinolysis, considering the patient’s comorbidities and the availability of timely intervention. The presence of hypertension and diabetes are significant risk factors for cardiovascular disease and can influence management decisions, but they do not contraindicate primary PCI. Fibrinolysis is typically reserved for situations where primary PCI is not available within the recommended timeframes. Therefore, the most appropriate initial management strategy, assuming timely access to a cardiac catheterization laboratory, is immediate primary PCI. This approach aims to restore blood flow to the ischemic myocardium as quickly as possible, thereby minimizing infarct size and improving patient outcomes. The explanation should also touch upon the importance of dual antiplatelet therapy and anticoagulation as adjuncts to reperfusion therapy, as well as beta-blockers and statins for secondary prevention, but the immediate priority is reperfusion.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain radiating to the left arm, accompanied by diaphoresis and dyspnea. An electrocardiogram (ECG) reveals ST-segment elevation in leads II, III, and aVF. This pattern is indicative of an inferior myocardial infarction. The management of an ST-elevation myocardial infarction (STEMI) prioritizes rapid reperfusion. In the absence of contraindications, primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy if it can be performed within a timely manner (typically within 90 minutes of first medical contact). If primary PCI is not feasible within the recommended timeframe, fibrinolytic therapy should be administered as soon as possible (ideally within 30 minutes of arrival). Given the information provided, the most critical immediate step, assuming timely access to PCI, is to initiate the process for this intervention. This involves activating the cardiac catheterization lab and preparing the patient for angioplasty and stenting. While aspirin and a P2Y12 inhibitor are crucial antiplatelet agents, and beta-blockers and statins are important for long-term management, the immediate priority in STEMI is restoring blood flow to the ischemic myocardium. Therefore, arranging for primary PCI is the most appropriate next step.

The scenario describes a patient with a history of hypertension and dyslipidemia presenting with acute chest pain suggestive of an acute coronary syndrome. The initial management involves assessing hemodynamic stability, administering oxygen if hypoxic, and providing antiplatelet therapy (aspirin and a P2Y12 inhibitor), nitroglycerin for pain relief, and potentially a beta-blocker. Given the ST-segment elevation on the ECG, immediate reperfusion therapy is indicated. The choice between primary percutaneous coronary intervention (PCI) and fibrinolysis depends on the availability and timeliness of PCI. If PCI can be performed within guideline-recommended timeframes (typically 90 minutes from first medical contact), it is the preferred strategy. If not, fibrinolysis is considered, followed by transfer for angiography and potential PCI. The question asks about the *most appropriate next step* in management. While all listed interventions are part of ACS management, the immediate priority in STEMI is reperfusion. Therefore, initiating antiplatelet therapy with aspirin and a P2Y12 inhibitor, alongside considering reperfusion strategy, is paramount. The explanation focuses on the rationale for immediate antiplatelet therapy in the context of STEMI, emphasizing its role in stabilizing the thrombus and preventing further propagation, which is a critical early step before definitive reperfusion. The calculation is conceptual, highlighting the importance of dual antiplatelet therapy (DAPT) in reducing ischemic events.

The scenario describes a patient with a history of well-controlled hypertension and hyperlipidemia presenting with acute onset of severe, crushing substernal chest pain radiating to the left arm, accompanied by diaphoresis and nausea. An electrocardiogram (ECG) reveals ST-segment elevation in leads II, III, and aVF. This pattern is indicative of an inferior myocardial infarction. The initial management of an ST-elevation myocardial infarction (STEMI) prioritizes reperfusion therapy. Given the patient’s presentation within the recommended time window for primary percutaneous coronary intervention (PCI), this is the preferred reperfusion strategy. If PCI is not readily available or feasible within the recommended timeframe, fibrinolytic therapy becomes the alternative. The question asks about the most appropriate next step in management. Considering the ECG findings and the goal of restoring blood flow to the ischemic myocardium, initiating antiplatelet therapy (e.g., aspirin and a P2Y12 inhibitor) and anticoagulation (e.g., heparin) are crucial components of initial STEMI management, regardless of the reperfusion strategy chosen. However, the immediate priority after recognizing STEMI is to facilitate reperfusion. Therefore, arranging for emergent PCI is the most critical next step. The explanation focuses on the pathophysiology of STEMI, the diagnostic significance of the ECG findings, and the evidence-based management principles for STEMI, emphasizing the importance of timely reperfusion. The rationale for antiplatelet and anticoagulant therapy is also discussed as adjunctive measures. The explanation highlights that while supportive care and other medications are important, the definitive management of STEMI revolves around restoring coronary blood flow.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain radiating to the left arm, accompanied by diaphoresis and dyspnea. An electrocardiogram (ECG) reveals ST-segment elevation in the anterior leads (V2-V4) and reciprocal ST-segment depression in the inferior leads (II, III, aVF). Cardiac biomarkers show an elevated troponin I level. This constellation of symptoms, ECG findings, and biomarker elevation is diagnostic of an ST-elevation myocardial infarction (STEMI) affecting the anterior wall of the left ventricle, most commonly due to occlusion of the left anterior descending (LAD) artery. The management of STEMI requires prompt reperfusion therapy to restore blood flow to the ischemic myocardium and limit infarct size. The most effective reperfusion strategy, when available within guideline-recommended timeframes, is primary percutaneous coronary intervention (PCI). This involves cardiac catheterization with balloon angioplasty and stent placement to open the occluded coronary artery. If primary PCI is not feasible within the recommended time, fibrinolytic therapy (thrombolysis) is an alternative, though generally less effective and associated with a higher risk of bleeding complications. Given the prompt presentation and the availability of PCI at the Fellowship of the Royal College of Physicians of Canada (FRCPC) University’s affiliated teaching hospital, primary PCI is the preferred initial management strategy. This approach offers superior outcomes in terms of myocardial salvage, reduction in major adverse cardiac events, and improved long-term survival compared to fibrinolysis. The explanation focuses on the rationale for choosing primary PCI based on the clinical presentation and established evidence-based guidelines for STEMI management, aligning with the rigorous standards of care expected within the Fellowship of the Royal College of Physicians of Canada (FRCPC) curriculum. The other options represent less optimal or inappropriate management strategies for this specific clinical scenario.

The core of this question lies in understanding the interplay between cardiac electrophysiology, pharmacodynamics, and the interpretation of electrocardiographic findings in the context of a specific medication. The scenario describes a patient experiencing new-onset atrial fibrillation with rapid ventricular response (AFib RVR) while on flecainide. Flecainide is a Class Ic antiarrhythmic agent that primarily blocks sodium channels, slowing conduction in the atria and ventricles. A critical adverse effect of flecainide, particularly in patients with underlying structural heart disease or impaired left ventricular function (which is often the case in patients requiring antiarrhythmics), is its proarrhythmic potential. This can manifest as a worsening of existing arrhythmias or the induction of new ones. In the context of AFib, flecainide’s mechanism of action can paradoxically prolong the refractory period of the atrioventricular (AV) node more than the atrial tissue itself. This differential effect can lead to a situation where the atrial fibrillation continues, but the ventricular response becomes slower and more organized, potentially mimicking a different rhythm. However, a more dangerous proarrhythmic effect of flecainide, especially in the presence of AFib, is the potential for it to convert AFib into atrial flutter with 2:1 conduction, or even ventricular tachycardia, by slowing conduction without adequately increasing refractoriness in all atrial pathways. The ECG findings described – a regular narrow complex tachycardia at 150 bpm with evidence of AV dissociation – are highly suggestive of a supraventricular tachycardia (SVT) with aberrant conduction or a ventricular tachycardia. Given the patient was on flecainide and had pre-existing AFib, the most concerning proarrhythmic manifestation would be the induction of a rapid, regular ventricular rhythm originating from a reentrant circuit that is not responsive to the flecainide’s atrial effects, or a conversion to a more organized but still problematic atrial flutter with rapid ventricular response. The question asks for the most appropriate next step. Discontinuing flecainide is paramount due to its proarrhythmic potential. However, the patient is currently hemodynamically stable but has a concerning ECG. The options presented test the understanding of managing iatrogenic arrhythmias. Let’s analyze the options: 1. **Immediate cardioversion:** While AFib RVR can sometimes warrant cardioversion, the new regular narrow complex tachycardia at 150 bpm with AV dissociation is not typical AFib RVR. It suggests a different, potentially more dangerous, rhythm induced by flecainide. Cardioversion might be considered if the patient were unstable, but the prompt states stability. 2. **Administering intravenous beta-blockers or calcium channel blockers:** These agents are used to slow ventricular rate in AFib RVR. However, in the context of flecainide-induced proarrhythmia, particularly if a ventricular tachycardia is suspected, these agents might not be effective and could even be detrimental if the underlying rhythm is a VT dependent on a slow ventricular rate. 3. **Discontinuing flecainide and initiating intravenous amiodarone:** Amiodarone is a Class III antiarrhythmic that prolongs repolarization and slows conduction. It is effective for both atrial and ventricular arrhythmias and is often used when proarrhythmic effects from other agents are suspected. Discontinuing the offending agent (flecainide) is the first step. Amiodarone is a reasonable choice for managing a potentially life-threatening iatrogenic arrhythmia like a flecainide-induced VT or a rapid atrial flutter with aberrant conduction, especially in a patient with potential underlying cardiac disease. 4. **Increasing the dose of flecainide:** This is contraindicated as flecainide is the suspected cause of the new arrhythmia. Therefore, the most appropriate management is to discontinue the offending agent and initiate a broad-spectrum antiarrhythmic that can address both atrial and ventricular dysrhythmias, such as amiodarone, while monitoring the patient closely. The calculation is conceptual, focusing on the sequence of clinical decision-making and drug management rather than numerical computation. The correct approach involves recognizing the proarrhythmic potential of flecainide in this context and choosing an agent that can effectively and safely manage the resulting complex arrhythmia.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain radiating to the left arm, accompanied by diaphoresis and nausea. An electrocardiogram (ECG) reveals ST-segment elevation in leads II, III, and aVF, indicative of an inferior wall myocardial infarction. The patient’s initial management includes aspirin, a P2Y12 inhibitor, and anticoagulation, consistent with current guidelines for ST-elevation myocardial infarction (STEMI). The critical decision point is the choice of reperfusion strategy. Given the symptom onset within the last 2 hours and the availability of percutaneous coronary intervention (PCI) within a recommended timeframe at the Fellowship of the Royal College of Physicians of Canada (FRCPC) University-affiliated hospital, primary PCI is the preferred reperfusion strategy. This approach offers superior outcomes compared to fibrinolysis in eligible patients, including reduced rates of reinfarction, stroke, and mortality. Fibrinolysis is typically reserved for situations where timely PCI is not feasible. The explanation for this choice rests on the established evidence supporting the efficacy of primary PCI in restoring coronary blood flow and salvaging myocardium in STEMI. The promptness of intervention is paramount in minimizing infarct size and preserving left ventricular function, which are key determinants of long-term prognosis. Therefore, the most appropriate next step in management, following initial medical therapy, is to proceed with primary PCI.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain radiating to the left arm, accompanied by diaphoresis and shortness of breath. An electrocardiogram (ECG) reveals ST-segment elevation in leads II, III, and aVF, indicative of an inferior myocardial infarction. The patient’s troponin I levels are elevated at 5.2 ng/mL, confirming myocardial injury. Given the ST-elevation myocardial infarction (STEMI) diagnosis and the patient’s presentation within the recommended timeframe for reperfusion therapy, the most appropriate initial management strategy is primary percutaneous coronary intervention (PCI). This intervention aims to restore blood flow to the affected myocardium by opening the occluded coronary artery, typically the right coronary artery in inferior STEMI. The success of PCI is often assessed by achieving a TIMI (Thrombolysis In Myocardial Infarction) flow grade of 3 in the culprit vessel, signifying complete restoration of antegrade flow. While thrombolytic therapy is an alternative if PCI is not readily available, primary PCI is generally preferred due to its higher efficacy and lower risk of reocclusion. Aspirin and a P2Y12 inhibitor (like clopidogrel or ticagrelor) are crucial antiplatelet agents to prevent further thrombus formation. Beta-blockers are indicated to reduce myocardial oxygen demand and prevent arrhythmias. High-intensity statin therapy is initiated to stabilize atherosclerotic plaques and reduce future cardiovascular events. Nitroglycerin may be used for symptom relief, but caution is advised in inferior STEMI due to potential right ventricular involvement and hypotension. Therefore, the comprehensive management involves immediate reperfusion, dual antiplatelet therapy, beta-blockade, and statin therapy.

No calculation is required for this question as it assesses conceptual understanding of diagnostic reasoning and ethical considerations in a clinical context. The scenario presented requires the candidate to integrate knowledge of cardiovascular physiology, diagnostic test interpretation, and the ethical principles governing patient care, particularly concerning informed consent and shared decision-making, as emphasized in the Fellowship of the Royal College of Physicians of Canada (FRCPC) curriculum. The patient’s history of exertional dyspnea and atypical chest discomfort, coupled with a non-diagnostic resting ECG, necessitates a more advanced assessment. The choice of a stress echocardiogram is a well-established method for evaluating inducible ischemia in patients with suspected coronary artery disease, especially when resting ECG findings are inconclusive. This diagnostic modality allows for the assessment of myocardial function and wall motion abnormalities during induced physiological stress, providing crucial information about the presence and severity of coronary artery disease. Furthermore, the explanation must highlight the importance of discussing the risks, benefits, and alternatives of this procedure with the patient, aligning with the FRCPC’s commitment to patient autonomy and ethical practice. The rationale for selecting this particular diagnostic pathway over others, such as a purely pharmacological stress test or immediate invasive angiography without further non-invasive assessment, hinges on balancing diagnostic yield with patient invasiveness and risk stratification. The explanation should underscore that the decision-making process should be collaborative, ensuring the patient understands the rationale behind the proposed investigation and is comfortable proceeding. This approach reflects the FRCPC’s emphasis on evidence-based medicine and patient-centered care, where diagnostic strategies are tailored to individual patient circumstances and preferences.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain radiating to the left arm, accompanied by diaphoresis and dyspnea. An electrocardiogram (ECG) reveals ST-segment elevation in leads II, III, and aVF. This pattern is indicative of an inferior myocardial infarction. The initial management of ST-elevation myocardial infarction (STEMI) prioritizes reperfusion therapy. Given the patient’s presentation within the recommended timeframe for primary percutaneous coronary intervention (PCI), this is the preferred reperfusion strategy. If PCI is not readily available or feasible within the recommended time window, fibrinolytic therapy would be considered. However, the question asks for the most appropriate *initial* management step focused on restoring myocardial blood flow. Therefore, initiating dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor, along with anticoagulation (e.g., heparin), is crucial to prevent further thrombus formation and propagation. Beta-blockers are indicated to reduce myocardial oxygen demand and improve outcomes, but their administration should be cautious in the presence of signs of heart failure or cardiogenic shock. ACE inhibitors are beneficial in the subacute and chronic phases to prevent ventricular remodeling. While all these interventions are important in the overall management of STEMI, the immediate priority for reperfusion and antithrombotic therapy is paramount. The calculation is conceptual, focusing on the sequence of critical interventions.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute chest pain suggestive of unstable angina. The initial management involves antiplatelet therapy, anticoagulation, and beta-blockade. The question probes the understanding of the underlying pathophysiology and the rationale for specific diagnostic and therapeutic interventions in the context of acute coronary syndromes, a core competency for internal medicine specialists trained at Fellowship of the Royal College of Physicians of Canada (FRCPC) University. The patient’s symptoms, ECG findings (ST-segment depression), and elevated troponin levels confirm an NSTEMI (Non-ST Elevation Myocardial Infarction). The management of NSTEMI, as per current guidelines emphasized in FRCPC University’s curriculum, involves risk stratification and early invasive strategy for high-risk patients. The TIMI (Thrombolysis In Myocardial Infarction) risk score is a validated tool for this purpose. To calculate the TIMI risk score for this patient: 1. Age \(\geq\) 65 years: 1 point 2. \(\geq\) 3 risk factors for CAD (hypertension, hyperlipidemia, diabetes, smoking, family history): The patient has hypertension and hyperlipidemia, so 2 risk factors. This contributes 0 points. 3. Prior aspirin use in the last 7 days: Not mentioned, assume 0 points. 4. Recent (<24 hours) coronary artery disease: Not mentioned, assume 0 points. 5. \(\geq\) 2 episodes of angina in the last 24 hours: The patient presents with acute chest pain, but the frequency in the last 24 hours is not specified. Assuming this is the initial presentation of significant angina, this would contribute 1 point. 6. Coronary artery stenosis \(\geq\) 50% on prior angiography: Not mentioned, assume 0 points. 7. Elevated cardiac marker (troponin or CK-MB): Elevated troponin is present, contributing 1 point. Total TIMI Risk Score = 1 (age) + 0 (risk factors) + 0 (aspirin) + 0 (prior CAD) + 1 (angina episodes) + 0 (stenosis) + 1 (cardiac marker) = 3. A TIMI risk score of 3 places the patient in an intermediate-to-high risk category, indicating a significant risk of adverse cardiovascular events. For such patients, an early invasive strategy, typically involving coronary angiography and potential percutaneous coronary intervention (PCI), is recommended. This approach aims to restore blood flow to the ischemic myocardium, reduce infarct size, and improve outcomes, aligning with the evidence-based medicine principles taught at Fellowship of the Royal College of Physicians of Canada (FRCPC) University. The explanation emphasizes the integration of clinical presentation, diagnostic findings, risk stratification tools, and guideline-directed management, which are crucial for successful practice as a Fellow of the Royal College of Physicians of Canada.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with new-onset exertional chest pain, suggestive of stable angina. The physician is considering initiating therapy to manage this condition. The question asks for the most appropriate initial pharmacologic intervention for stable angina in a patient with these comorbidities. For a patient with stable angina, the primary goals of pharmacologic management are to relieve symptoms and prevent adverse cardiovascular events, particularly myocardial infarction and death. Beta-blockers are considered first-line therapy for symptom relief in stable angina due to their ability to reduce myocardial oxygen demand by decreasing heart rate, contractility, and blood pressure. They also have proven mortality benefits in patients with coronary artery disease. Given the patient’s history of hypertension, a beta-blocker would also contribute to blood pressure control. While calcium channel blockers and nitrates can also be used for symptom relief, beta-blockers are generally preferred as initial therapy due to their combined benefits on symptoms and prognosis. Statins are crucial for managing hyperlipidemia and secondary prevention of cardiovascular events, but they do not directly address the acute symptoms of angina. Aspirin is also important for secondary prevention, but again, it is not the primary agent for immediate symptom relief in stable angina. Therefore, initiating a beta-blocker addresses both the symptomatic management of angina and the patient’s underlying cardiovascular risk factors.

The scenario describes a patient with a history of hypertension and hyperlipidemia, presenting with exertional chest pain suggestive of stable angina. The physician is considering diagnostic strategies. The question asks to identify the most appropriate initial non-invasive investigation to assess for inducible myocardial ischemia. The patient’s symptoms and risk factors strongly point towards coronary artery disease (CAD). While a coronary angiogram is the gold standard for diagnosing CAD, it is invasive and typically reserved for patients with high suspicion or those who have failed less invasive testing. Electrocardiography (ECG) is a fundamental diagnostic tool, but a resting ECG may be normal in patients with stable angina. Echocardiography provides structural and functional information about the heart but does not directly assess for inducible ischemia without stress. Stress testing, particularly stress echocardiography or myocardial perfusion imaging (MPI) with SPECT or PET, is the cornerstone of non-invasive assessment for inducible ischemia in patients with suspected CAD. These modalities combine physiological stress (pharmacological or exercise) with imaging to detect areas of the myocardium that are underperfused during stress, indicating significant coronary stenoses. Given the need for a non-invasive approach to evaluate for inducible ischemia, stress testing is the most appropriate initial step. Among the stress testing modalities, stress echocardiography is often preferred due to its availability, ability to assess regional wall motion abnormalities, and lack of radiation exposure compared to MPI. However, the question asks for the most appropriate *initial* non-invasive investigation to assess for *inducible myocardial ischemia*. Both stress echocardiography and myocardial perfusion imaging are valid options for this purpose. Without further clinical details or specific local availability considerations, the principle of assessing for inducible ischemia through a stress modality is paramount. Let’s consider the options in terms of their directness in assessing inducible ischemia: – Resting ECG: Primarily assesses electrical activity at rest, may show signs of prior infarction or strain, but not inducible ischemia. – Echocardiography (resting): Assesses structure and function at rest, not inducible ischemia. – Stress Echocardiography: Combines stress with echocardiography to assess for inducible ischemia via wall motion abnormalities. – Myocardial Perfusion Imaging (SPECT/PET): Combines stress with radionuclide imaging to assess for inducible ischemia via perfusion defects. Both stress echocardiography and myocardial perfusion imaging directly address the question of inducible ischemia. However, the question asks for the *most appropriate initial non-invasive investigation*. In many clinical pathways, stress echocardiography is a highly effective initial choice for assessing inducible ischemia due to its comprehensive assessment of both ischemia and valvular/structural heart disease. Calculation: Not applicable as this is a conceptual question. The correct approach involves identifying the diagnostic modality that directly assesses for the presence of myocardial ischemia induced by stress. This requires understanding the limitations of resting investigations and the specific capabilities of stress-based diagnostic tools. The chosen investigation should provide functional information about myocardial perfusion or contractility under stress, thereby revealing the presence and extent of coronary artery disease that may not be apparent at rest. This aligns with the principles of evidence-based medicine and the systematic approach to diagnosing cardiovascular conditions, prioritizing non-invasive methods when appropriate. The ability to differentiate between ischemic and non-ischemic segments of the myocardium during a stress challenge is key.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute chest pain suggestive of myocardial infarction. The initial ECG shows ST-segment elevation in the inferior leads, indicating an ST-elevation myocardial infarction (STEMI). The management of STEMI hinges on rapid reperfusion therapy. In the absence of contraindications, primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy if it can be performed within a timely manner (typically within 90 minutes of first medical contact). Fibrinolysis is an alternative if PCI is not readily available or feasible within the recommended timeframe. Given the patient’s presentation and the ECG findings, immediate administration of aspirin and a P2Y12 inhibitor is crucial to prevent further platelet aggregation and thrombus formation. Intravenous nitroglycerin is indicated for symptom relief and to reduce preload, provided there are no contraindications like hypotension or right ventricular infarction. Beta-blockers are generally beneficial in STEMI management to reduce myocardial oxygen demand and improve outcomes, but their administration should be cautious in the acute phase, especially if there are signs of heart failure or bradycardia. Morphine can be used for pain relief if nitroglycerin is insufficient. The core principle is to restore blood flow to the ischemic myocardium as quickly as possible. Therefore, the most critical immediate intervention, after initial assessment and stabilization, is to facilitate reperfusion.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain radiating to the left arm, accompanied by diaphoresis and shortness of breath. An electrocardiogram (ECG) reveals ST-segment elevation in leads II, III, and aVF. This pattern is indicative of an inferior myocardial infarction. The patient’s vital signs are stable, but their blood pressure is elevated at \(160/95\) mmHg. The management of an ST-elevation myocardial infarction (STEMI) prioritizes reperfusion therapy. Given the patient’s presentation within the recommended timeframe for primary percutaneous coronary intervention (PCI), this is the preferred reperfusion strategy. However, if PCI is not readily available or feasible within the target timeframes, fibrinolytic therapy becomes a crucial alternative. The question asks for the most appropriate next step in management. Considering the available information: 1. **Reperfusion Therapy:** The primary goal is to restore blood flow to the ischemic myocardium. 2. **Antiplatelet Therapy:** Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor is essential to prevent further thrombus formation and stent thrombosis if PCI is performed. 3. **Anticoagulation:** Anticoagulation (e.g., heparin) is necessary to prevent thrombus propagation and embolization. 4. **Beta-blockers:** Beta-blockers are indicated to reduce myocardial oxygen demand, decrease the risk of arrhythmias, and improve long-term outcomes, provided there are no contraindications. 5. **ACE Inhibitors/ARBs:** These are beneficial in reducing ventricular remodeling and improving long-term survival, especially in patients with anterior MI or impaired left ventricular function, but are not the immediate priority over reperfusion and initial antiplatelet/anticoagulant therapy. 6. **Statins:** High-intensity statin therapy should be initiated early to stabilize atherosclerotic plaques and reduce cardiovascular events. The patient has an inferior STEMI. While PCI is ideal, if it’s not immediately available, fibrinolysis is indicated. Regardless of the reperfusion strategy, immediate administration of aspirin and a P2Y12 inhibitor is paramount. The elevated blood pressure, while needing management, does not preclude initial antiplatelet therapy. Therefore, initiating dual antiplatelet therapy alongside preparations for reperfusion is the most critical immediate step. The question implies a need for a definitive immediate action. Administering aspirin and a P2Y12 inhibitor addresses the underlying thrombotic process and is a cornerstone of STEMI management, irrespective of the chosen reperfusion modality. The correct approach is to initiate dual antiplatelet therapy with aspirin and a P2Y12 inhibitor. This addresses the acute thrombotic event and is a prerequisite for successful reperfusion, whether via PCI or fibrinolysis.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain radiating to the left arm, accompanied by diaphoresis and dyspnea. An electrocardiogram (ECG) reveals ST-segment elevation in leads V2-V4, indicative of an anterior ST-elevation myocardial infarction (STEMI). The immediate management of STEMI, as per Fellowship of the Royal College of Physicians of Canada (FRCPC) guidelines, prioritizes reperfusion therapy. This involves either primary percutaneous coronary intervention (PCI) or fibrinolysis if PCI is not readily available. Given the prompt presentation and the availability of PCI, this is the preferred strategy. Following reperfusion, dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor is crucial to prevent stent thrombosis and recurrent ischemic events. Beta-blockers are indicated to reduce myocardial oxygen demand and improve long-term outcomes by decreasing heart rate and contractility. Angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) are recommended to prevent left ventricular remodeling and reduce the risk of heart failure. High-intensity statin therapy is essential for lipid-lowering and plaque stabilization. Therefore, the comprehensive management strategy includes reperfusion, DAPT, beta-blockers, ACE inhibitors/ARBs, and high-intensity statins.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain radiating to the left arm, accompanied by diaphoresis and shortness of breath. An electrocardiogram (ECG) reveals ST-segment elevation in leads II, III, and aVF. This pattern is indicative of an inferior ST-elevation myocardial infarction (STEMI). The immediate management of STEMI involves reperfusion therapy. Given the patient’s presentation within the recommended timeframe for percutaneous coronary intervention (PCI) and the availability of such services at Fellowship of the Royal College of Physicians of Canada (FRCPC) University’s affiliated teaching hospital, primary PCI is the preferred reperfusion strategy. This approach offers superior outcomes compared to fibrinolysis in eligible patients, including reduced rates of reinfarction, stroke, and mortality. The explanation of the correct answer focuses on the rapid restoration of blood flow to the ischemic myocardium, which is paramount in limiting infarct size and preserving left ventricular function. The rationale for choosing primary PCI over fibrinolysis is based on established clinical guidelines and evidence demonstrating its efficacy in improving patient outcomes. The promptness of intervention is critical, and the question tests the understanding of the most effective reperfusion strategy in a common and time-sensitive cardiovascular emergency, aligning with the advanced clinical knowledge expected of FRCPC candidates.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain radiating to the left arm, accompanied by diaphoresis and shortness of breath. An electrocardiogram (ECG) reveals ST-segment elevation in the anterior leads (V1-V4). This pattern is highly suggestive of an acute ST-elevation myocardial infarction (STEMI) affecting the anterior wall of the left ventricle, typically due to occlusion of the left anterior descending (LAD) artery. The immediate management of suspected STEMI, as per Fellowship of the Royal College of Physicians of Canada (FRCPC) guidelines, prioritizes reperfusion therapy. The most effective and timely reperfusion strategy for STEMI is primary percutaneous coronary intervention (PCI). This involves mechanically opening the occluded coronary artery with angioplasty and stenting. If primary PCI is not available within the recommended timeframe (typically 90 minutes from first medical contact), fibrinolytic therapy (thrombolysis) is considered as an alternative, although PCI is generally preferred due to its higher efficacy and lower rates of re-occlusion and bleeding complications. In this specific case, the prompt implies a hospital setting where advanced cardiac interventions are available. Therefore, the most appropriate next step, after initial stabilization (e.g., aspirin, P2Y12 inhibitor, anticoagulation, beta-blocker, statin, and pain relief), is to proceed with emergent cardiac catheterization for primary PCI. This intervention directly addresses the underlying cause of the STEMI – the coronary artery occlusion – and is crucial for salvaging myocardial tissue and improving long-term outcomes. Other options, such as initiating a beta-blocker alone, would be adjunctive therapy and not the definitive immediate management for reperfusion. Echocardiography, while useful for assessing ventricular function, is not the primary reperfusion strategy. Administering a diuretic without addressing the coronary occlusion would be inappropriate in the acute STEMI phase.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain, radiating to the left arm, and diaphoresis. An electrocardiogram (ECG) shows ST-segment elevation in leads II, III, and aVF. This pattern is indicative of an inferior ST-elevation myocardial infarction (STEMI). The immediate management of STEMI involves reperfusion therapy. Given the patient’s presentation within the recommended timeframe for primary percutaneous coronary intervention (PCI) and the availability of such facilities at Fellowship of the Royal College of Physicians of Canada (FRCPC) University’s affiliated teaching hospitals, primary PCI is the preferred reperfusion strategy. This involves mechanical revascularization of the occluded coronary artery. If PCI is not readily available or feasible within the recommended time window, fibrinolytic therapy would be considered. However, the question implies a setting where advanced cardiac care is accessible. Therefore, the most appropriate next step in management, after initial stabilization (e.g., aspirin, nitroglycerin, oxygen, morphine if needed), is to proceed with primary PCI. The explanation focuses on the rationale for choosing primary PCI over other reperfusion strategies or diagnostic tests, emphasizing the time-sensitive nature of STEMI and the goal of restoring myocardial blood flow as quickly as possible to minimize infarct size and preserve left ventricular function. This aligns with current evidence-based guidelines for STEMI management, which are central to the advanced clinical training at Fellowship of the Royal College of Physicians of Canada (FRCPC) University.

The scenario describes a patient with a history of hypertension and dyslipidemia presenting with acute chest pain. The electrocardiogram (ECG) shows ST-segment elevation in the anterior leads (V2-V4), indicative of an acute ST-elevation myocardial infarction (STEMI). The immediate management of STEMI involves reperfusion therapy. Given the patient’s presentation within the recommended timeframe for primary percutaneous coronary intervention (PCI), this is the preferred reperfusion strategy. The calculation of the door-to-balloon time is a critical quality metric in STEMI management. If the patient arrived at 08:00 and the PCI procedure commenced at 08:45, the door-to-balloon time is 45 minutes. The target door-to-balloon time for primary PCI is typically less than 90 minutes. Therefore, the calculated time of 45 minutes meets this benchmark. The explanation should focus on the rationale for primary PCI in STEMI, the importance of timely reperfusion, and the quality metrics associated with this process, such as door-to-balloon time. It should also touch upon the underlying pathophysiology of STEMI, where a complete occlusion of a coronary artery leads to myocardial ischemia and necrosis, necessitating prompt restoration of blood flow. The management of underlying risk factors like hypertension and dyslipidemia is also crucial for long-term prognosis and secondary prevention, aligning with the comprehensive care expected at Fellowship of the Royal College of Physicians of Canada (FRCPC) University. The explanation will highlight the critical role of interdisciplinary collaboration in achieving these time-sensitive goals.

The scenario describes a patient with a history of poorly controlled hypertension and type 2 diabetes mellitus presenting with acute onset dyspnea and chest pain. Initial investigations reveal ST-segment elevation in leads V2-V4 on the electrocardiogram, indicative of an anterior ST-elevation myocardial infarction (STEMI). The patient’s elevated troponin levels confirm myocardial injury. Given the diagnosis of STEMI, the immediate management goal is to restore coronary blood flow as quickly as possible. The most effective strategy for this is primary percutaneous coronary intervention (PCI). This involves cardiac catheterization to identify the occluded artery and then balloon angioplasty and stenting to open the blockage. The explanation for why this is the correct approach lies in the pathophysiology of STEMI: a complete blockage of a coronary artery leads to irreversible myocardial damage if blood flow is not restored promptly. Primary PCI has been shown to significantly reduce infarct size, improve left ventricular function, and decrease mortality compared to fibrinolysis, especially when performed within a suitable timeframe. The patient’s comorbidities, while important for long-term management, do not contraindicate primary PCI in the acute setting; rather, they underscore the need for aggressive management of cardiovascular risk factors. The question tests the understanding of acute coronary syndrome management, specifically the preferred reperfusion strategy for STEMI, which is a cornerstone of cardiovascular medicine and a critical skill for physicians in training at Fellowship of the Royal College of Physicians of Canada (FRCPC) University.

The scenario describes a patient with a history of well-controlled hypertension and hyperlipidemia presenting with new-onset exertional angina. The initial ECG shows ST-segment depression in the inferior leads, suggestive of myocardial ischemia. The echocardiogram reveals moderate hypokinesis of the inferior wall, consistent with previous or ongoing ischemic damage. The crucial element for diagnosis and management planning in this context, especially for a Fellow of the Royal College of Physicians of Canada (FRCPC) candidate, is to identify the extent and significance of coronary artery disease. Coronary angiography remains the gold standard for visualizing the coronary arteries and quantifying the severity of stenoses. While stress testing can provide functional information about ischemia, it is less definitive than angiography for anatomical detail. Cardiac MRI can offer insights into myocardial viability and scar burden, but it does not directly visualize the coronary arteries. A chest X-ray is primarily for evaluating pulmonary and cardiac silhouette, not for diagnosing coronary artery disease. Therefore, coronary angiography is the most appropriate next step to guide definitive management, such as percutaneous coronary intervention or surgical revascularization, aligning with the FRCPC’s emphasis on evidence-based, diagnostic precision in cardiovascular medicine.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with acute onset chest pain radiating to the left arm, accompanied by diaphoresis and shortness of breath. An electrocardiogram (ECG) reveals ST-segment elevation in leads II, III, and aVF, indicative of an inferior ST-elevation myocardial infarction (STEMI). The patient’s blood pressure is 160/95 mmHg, heart rate is 90 bpm, and oxygen saturation is 96% on room air. The immediate management of an inferior STEMI involves reperfusion therapy, typically primary percutaneous coronary intervention (PCI) or fibrinolysis if PCI is not readily available. Given the patient’s presentation and ECG findings, the priority is to restore blood flow to the affected myocardium. In addition to reperfusion, antiplatelet therapy (aspirin and a P2Y12 inhibitor like clopidogrel or ticagrelor) and anticoagulation (e.g., heparin) are crucial to prevent further thrombus formation and propagation. Beta-blockers are generally indicated to reduce myocardial oxygen demand, unless contraindicated (e.g., signs of heart failure, bradycardia, hypotension). ACE inhibitors or ARBs are beneficial in the long term for ventricular remodeling and reducing mortality. Statins are essential for lipid management and plaque stabilization. Considering the options, the most appropriate initial management strategy, after confirming the STEMI diagnosis and initiating reperfusion, involves a combination of therapies aimed at reducing myocardial oxygen demand, preventing further clot formation, and initiating long-term cardiovascular risk reduction. Specifically, the administration of a beta-blocker addresses the increased sympathetic tone and reduces myocardial oxygen consumption, which is vital in the acute phase of myocardial infarction. Aspirin and a P2Y12 inhibitor are standard dual antiplatelet therapy for STEMI. An ACE inhibitor is important for long-term management and preventing adverse ventricular remodeling. A high-intensity statin is also crucial for secondary prevention. Therefore, a comprehensive approach that includes these elements is the most appropriate. The calculation is conceptual, focusing on the synergistic benefits of multiple therapeutic classes in managing acute myocardial infarction. The question assesses the understanding of the foundational pharmacotherapy for STEMI, emphasizing the multi-faceted approach required for optimal patient outcomes. The correct approach integrates immediate interventions with long-term risk modification strategies, reflecting the comprehensive care expected in advanced internal medicine practice at Fellowship of the Royal College of Physicians of Canada (FRCPC) University.

The scenario describes a patient with a history of hypertension and dyslipidemia, presenting with new-onset exertional chest pain radiating to the left arm, accompanied by diaphoresis and nausea. An electrocardiogram (ECG) reveals ST-segment depression in leads V4-V6 and I, along with T-wave inversions in leads II, III, and aVF. These findings are indicative of myocardial ischemia, specifically affecting the anterolateral and inferior walls of the left ventricle. The elevated troponin I level confirms myocardial injury. Given the clinical presentation and diagnostic findings, the most appropriate initial management strategy focuses on reperfusion therapy and medical stabilization. The patient’s symptoms and ECG changes strongly suggest an acute ST-elevation myocardial infarction (STEMI) or, more likely given the ST depression and T-wave inversions, a non-ST-elevation myocardial infarction (NSTEMI) with significant ischemia. The goal is to restore myocardial blood flow and prevent further infarction. This involves administering antiplatelet agents (e.g., aspirin and a P2Y12 inhibitor) to prevent thrombus propagation, anticoagulation (e.g., heparin) to inhibit clot formation, and beta-blockers to reduce myocardial oxygen demand. Nitroglycerin can be used for symptom relief and vasodilation. In the context of NSTEMI, early invasive management with percutaneous coronary intervention (PCI) is often indicated, especially in patients with high-risk features, which this patient exhibits. Therefore, the immediate priority is to initiate these medical therapies while preparing for potential angiography and revascularization. The calculation is conceptual, not numerical. The diagnostic findings (ST depression, T-wave inversions, elevated troponin I) point towards myocardial ischemia and injury. The management principles for acute coronary syndromes (ACS) dictate the use of antiplatelet therapy, anticoagulation, beta-blockers, and potentially nitroglycerin. Early consideration of invasive angiography and PCI is crucial for patients with NSTEMI and high-risk features.

The scenario describes a patient with a history of well-controlled hypertension and hyperlipidemia presenting with new-onset exertional dyspnea and chest discomfort. An electrocardiogram (ECG) reveals ST-segment depression in the anterior leads, and an echocardiogram shows moderate anterior wall hypokinesis with a preserved ejection fraction of \(50\%\). Cardiac biomarkers are elevated. The most appropriate next step in management, considering the evidence of myocardial ischemia and the need for definitive assessment of coronary artery anatomy, is to proceed with a coronary angiogram. This invasive procedure allows for direct visualization of the coronary arteries, identification of stenotic lesions, and potential percutaneous coronary intervention (PCI) if indicated. While medical management with antiplatelets, statins, and beta-blockers is crucial, it does not provide the diagnostic certainty required for guiding revascularization decisions. Stress testing might be considered in a stable patient with equivocal symptoms, but in the presence of ECG changes and elevated biomarkers suggestive of acute coronary syndrome, a coronary angiogram is the preferred diagnostic and therapeutic pathway. The echocardiogram findings, while important, do not negate the need to assess the underlying coronary supply. Therefore, the direct visualization of the coronary vasculature is paramount.

The scenario describes a patient with a history of hypertension and dyslipidemia presenting with exertional chest pain. The initial ECG shows ST-segment depression in the inferior leads, indicative of myocardial ischemia. A subsequent echocardiogram reveals regional wall motion abnormalities in the inferior wall, consistent with prior ischemic damage. The patient’s symptoms and diagnostic findings strongly suggest stable angina secondary to coronary artery disease. The management of stable angina focuses on symptom relief, prevention of myocardial infarction, and improvement of prognosis. This involves lifestyle modifications, risk factor management, and pharmacotherapy. Beta-blockers are a cornerstone of treatment, reducing myocardial oxygen demand by decreasing heart rate and contractility. Calcium channel blockers can also be used, either as monotherapy or in combination with beta-blockers, to improve vasodilation and reduce afterload. Nitrates provide symptomatic relief through venodilation and coronary vasodilation. Antiplatelet therapy, typically aspirin, is crucial for preventing thrombus formation in atherosclerotic plaques. Statins are essential for lipid-lowering and plaque stabilization. Considering the patient’s ongoing symptoms despite initial medical management, and the need to definitively assess the extent of coronary artery disease and guide further treatment, coronary angiography is the next logical step. This invasive procedure allows for direct visualization of the coronary arteries, identification of stenotic lesions, and assessment of their severity. Based on the angiographic findings, revascularization strategies such as percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) can be considered if significant obstructive disease is present. Therefore, the most appropriate next step in the management of this patient, aiming to establish a definitive diagnosis and plan for revascularization if indicated, is coronary angiography.

The scenario describes a patient with newly diagnosed hypertension and hyperlipidemia, presenting a common clinical challenge in internal medicine. The question probes the understanding of evidence-based management principles for secondary prevention in cardiovascular disease, a core competency for FRCPC candidates. The patient’s age, blood pressure, and lipid profile necessitate a multi-faceted approach. First, consider the blood pressure. A reading of \(155/95\) mmHg in a patient with new hypertension warrants intervention. Guidelines from organizations like Hypertension Canada or the American Heart Association recommend a target blood pressure of less than \(130/80\) mmHg for most adults with hypertension, especially those with comorbid cardiovascular risk factors. Next, address the hyperlipidemia. The patient has an LDL cholesterol of \(4.5\) mmol/L. For individuals with established cardiovascular disease or high cardiovascular risk (as indicated by hypertension and hyperlipidemia), the goal is typically to lower LDL cholesterol significantly. While specific targets can vary based on risk stratification tools (e.g., ASCVD risk calculator), a common recommendation for secondary prevention is an LDL reduction of at least \(50\%\) from baseline or an absolute target of less than \(1.8\) mmol/L. Given these findings, a combination of lifestyle modifications and pharmacotherapy is indicated. Lifestyle changes, including dietary adjustments (e.g., DASH diet, reduced sodium intake), regular physical activity, weight management, and smoking cessation (if applicable), are foundational. Pharmacologically, for hypertension, a thiazide diuretic, an ACE inhibitor, an ARB, or a calcium channel blocker are typically first-line agents. For hyperlipidemia, statins are the cornerstone of therapy. A moderate-to-high intensity statin is usually recommended for secondary prevention to achieve the desired LDL reduction. Therefore, the most appropriate initial management strategy involves initiating a statin for hyperlipidemia and a thiazide diuretic for hypertension, alongside comprehensive lifestyle counseling. This approach targets both primary risk factors effectively and aligns with current evidence-based guidelines for cardiovascular risk reduction. The combination of a statin and a thiazide diuretic addresses both lipid and blood pressure management, providing a synergistic effect in reducing overall cardiovascular risk.

The scenario describes a patient with a history of hypertension and hyperlipidemia presenting with new-onset exertional chest pain, suggestive of stable angina. The electrocardiogram (ECG) shows ST-segment depression in the inferior leads, which, in the context of chest pain, indicates myocardial ischemia. Echocardiography reveals moderate hypokinesis of the inferior wall, further supporting regional myocardial dysfunction. The question asks about the most appropriate next step in management, considering the diagnostic findings and the need to establish a definitive diagnosis and guide therapy. The patient’s presentation strongly suggests coronary artery disease (CAD). While medical management with antiplatelets, statins, and beta-blockers is crucial for secondary prevention, the presence of exertional symptoms and ECG changes necessitates further investigation to assess the extent and severity of CAD. Coronary angiography is the gold standard for visualizing the coronary arteries, identifying stenotic lesions, and guiding revascularization decisions. It directly visualizes the anatomy and hemodynamics of the coronary circulation, providing critical information for treatment planning, such as percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Other diagnostic options have limitations in this context. A repeat ECG might show resolution of the ST depression but does not provide anatomical information. Stress echocardiography or nuclear stress testing could further assess inducible ischemia but would not definitively delineate the coronary anatomy as well as angiography. Cardiac MRI could provide functional and structural information but is not the primary modality for assessing coronary stenosis. Therefore, proceeding to coronary angiography is the most logical and evidence-based next step to confirm the diagnosis, quantify the disease burden, and inform subsequent therapeutic interventions, aligning with the principles of evidence-based medicine and patient-centered care emphasized at Fellowship of the Royal College of Physicians of Canada (FRCPC) University.