MKSAP 19 (ACS-Medical therapy for ACS)

What is the defining characteristic of stable angina pectoris?

Which demographic groups may present only with atypical symptoms of angina?

What is the first step in diagnostic testing for angina?

What is the characteristic feature of unstable angina?

What is the duration criterion for stable angina pectoris?

Which of the following is a characteristic used to evaluate angina?

What may some demographic groups, including women and patients with diabetes mellitus, present with as atypical symptoms of angina?

What is the first step in diagnostic testing for angina?

What type of angina is precipitated by a stable level of exertion or emotional stress and relieved with rest?

Which condition is associated with increased short-term risk for acute myocardial infarction?

What is an important component of guideline-directed medical therapy for stable angina pectoris?

What is the goal of blood pressure control in patients with stable angina?

What is the purpose of antianginal medications in the treatment of stable angina pectoris?

What is a key component of guideline-directed medical therapy for stable angina pectoris?

What is the goal of antianginal medications in the treatment of stable angina pectoris?

What is the primary purpose of cardioprotective medications in the treatment of stable angina pectoris?

Which of the following is a key component of guideline-directed medical therapy for stable angina pectoris?

What is the primary purpose of antianginal medications in the treatment of stable angina pectoris?

What is an important aspect of risk factor modification in the treatment of stable angina pectoris?

What is the recommended first-line therapy in patients with stable angina?

What is the recommended resting heart rate range to be achieved through B-Blocker dosage titration?

Which type of B-Blocker is preferred in patients with significant lung disease?

In patients with reduced left ventricular (LV) function, which B-Blockers are associated with reduced long-term mortality?

What should be used with caution in patients taking B-Blockers due to additive negative inotropic and chronotropic effects?

What are the side effects of B-Blockers?

Why should caution be exercised in using B-Blockers in the setting of significant conduction disease or LV dysfunction?

What is the recommended resting heart rate range to be achieved through B-Blocker dosage titration?

Which type of B-Blocker is preferred in patients with significant lung disease?

In patients with reduced left ventricular (LV) function, which B-Blockers are associated with reduced long-term mortality?

What side effects are associated with B-Blockers?

Why should caution be exercised in using B-Blockers in the setting of significant conduction disease or LV dysfunction?

What is a key consideration when choosing a B-Blocker for patients with stable angina?

What is the primary reason for caution when using B-Blockers in patients taking nondihydropyridine calcium channel blockers (verapamil, diltiazem)?

Which type of B-Blockers is preferred in patients with significant lung disease?

What is the recommended resting heart rate range to be achieved through B-Blocker dosage titration?

Which B-Blockers are associated with reduced long-term mortality in patients with reduced left ventricular (LV) function?

What are the side effects associated with B-Blockers?

Why should caution be exercised in using B-Blockers in the setting of significant conduction disease or LV dysfunction?

What demographic groups may present only with atypical symptoms of angina?

Which type of calcium channel blockers should be avoided in the treatment of angina due to the risk of paradoxically worsening angina?

What is the recommended interval needed with long-acting nitrates to avoid the development of nitrate tolerance and reduced efficacy?

Which medication can improve myocardial oxygen delivery through coronary vasodilation and reduce oxygen demand by reducing preload, thereby reducing ventricular wall stress?

Why should nondihydropyridine calcium channel blockers not be used in patients with left ventricular (LV) dysfunction?

What is the potential consequence of using short-acting sublingual nitrates for acute relief of angina without combining them with beta-blockers or calcium channel blockers?

What is the primary reason for prescribing short-acting sublingual nitrates for acute relief of angina?

What is a potential side effect associated with long-acting nitrates?

What is a contraindication for concurrent use of ranolazine and phosphodiesterase 5 inhibitors?

What effect does ranolazine have on the QT interval?

When should the QT interval be monitored in patients taking ranolazine?

What is the recommended action when patients are receiving moderate inhibitors of cytochrome P450 3A4 (CYP3A4)?

Why should ranolazine not be used in combination with strong CYP3A4 inhibitors?

What is the mechanism by which ranolazine reduces angina and increases exercise time?

What is the primary reason for caution when using ranolazine in combination with strong CYP3A4 inhibitors?

What is the mechanism of action by which ranolazine reduces angina?

When should the QT interval be monitored in patients taking ranolazine?

What is the effect of ranolazine on the QT interval?

In patients receiving moderate inhibitors of cytochrome P450 3A4 (CYP3A4), what is indicated regarding ranolazine dosage?

What is contraindicated due to the risk for hypotension when using ranolazine?

Which type of calcium channel blockers should be avoided in the treatment of angina due to the risk of paradoxically worsening angina?

What is the primary reason for prescribing short-acting sublingual nitrates for acute relief of angina?

Why should nondihydropyridine calcium channel blockers not be used in patients with left ventricular (LV) dysfunction?

What is the potential consequence of using short-acting sublingual nitrates for acute relief of angina without combining them with beta-blockers or calcium channel blockers?

What is the recommended interval needed with long-acting nitrates to avoid the development of nitrate tolerance and reduced efficacy?

What is the mechanism by which long-acting nitrates improve myocardial oxygen delivery?

What is a potential side effect associated with long-acting nitrates?

Which medication is indicated for stable angina with concomitant left ventricular dysfunction, heart failure, and chronic kidney disease?

What is the first-line therapy for stable angina?

What should all patients with coronary artery disease be counseled on?

Patients with coronary artery disease should not be counseled on lifestyle modification, blood pressure control, and management of diabetes mellitus.

First-line therapy for stable angina includes aspirin, statin therapy, and p-blocker therapy.

ACE inhibitor therapy is not indicated for stable angina with concomitant left ventricular dysfunction, heart failure, diabetes mellitus, chronic kidney disease, or history of myocardial infarction.

What is the primary goal of revascularization in stable syndromes?

In which patients is revascularization indicated for prevention of future events and improved survival?

When should patients with unstable or acute presentations undergo revascularization?

Revascularization is indicated for prevention of future events and improved survival in unstable or acute presentations as well as in stable patients with high-risk anatomic or clinical features.

The primary goals of revascularization in stable syndromes are to lessen angina and improve quality of life.

Revascularization is not indicated for patients with angina refractory to medical therapy or markedly abnormal stress testing or coronary CT angiography results.

What do techniques like fractional flow reserve and instantaneous wave free ratio provide information on?

What is the primary basis for identifying revascularization targets?

What is the purpose of revascularization in stable syndromes?

Fractional flow reserve and instantaneous wave free ratio provide information on the functional hemodynamic significance of indeterminate lesions identified on angiographic imaging.

Revascularization targets are identified based on anatomic and functional physiologic characteristics associated with myocardial ischemia.

Revascularization targets are identified based solely on anatomic characteristics associated with myocardial ischemia.

What is the primary indication for Percutaneous Coronary Intervention (PCI)?

What is the most common type of stent used in PCI procedures currently?

In patients with stable angina, how does PCI compare to guideline-directed medical therapy in reducing the risk for death or myocardial infarction (MI)?

PCI is indicated to relieve symptoms in patients with medically refractory angina, those unable to tolerate optimal medical therapy, and those with high risk features on non-invasive testing.

PCI has been shown to be superior to guideline directed medical therapy in reducing the risk for death or MI in patients with stable angina with or without diabetes.

Most PCI procedures currently involve second generation drug eluting stent placement, which reduces the risk for in stent restenosis compared with bare metal stenting.

What is the primary benefit of coronary artery bypass grafting (CABG) with optimal medical therapy for patients with multivessel coronary artery disease (CAD)?

In which patient population is CABG associated with improved survival?

What is the impact of myocardial viability on survival and ventricular recovery following revascularization in patients with LV dysfunction?

Coronary artery bypass grafting (CABG) is generally recommended for patients with multivessel CAD due to its association with improved survival and decreased recurrence of angina.

CABG results in lower rates of MI and fewer repeat revascularization procedures compared with PCI or medical therapy alone.

Myocardial viability testing before revascularization has been established as a predictor of outcome.

What is the minimum duration of dual antiplatelet therapy (DAPT) recommended for patients treated with bare metal stent placement?

For how long is dual antiplatelet therapy (DAPT) recommended for patients with stable angina after drug eluting stent placement, according to current guidelines?

In patients at high risk for bleeding, what duration of dual antiplatelet therapy (DAPT) followed by lifelong antiplatelet monotherapy is supported by current evidence?

For patients requiring oral anticoagulation for atrial fibrillation, when can warfarin or a direct oral anticoagulant (preferred) plus clopidogrel be considered without aspirin?

Revascularization is only indicated for a specific duration of time

Aspirin is recommended indefinitely after revascularization

DAPT duration depends on clinical considerations such as patient presentation and bleeding and ischemic risks

In patients requiring oral anticoagulation for atrial fibrillation, warfarin or a direct oral anticoagulant plus clopidogrel can be considered without aspirin, often after 2 to 4 weeks of triple therapy

What is the preferred revascularization method for stable angina patients with left main or three-vessel coronary artery disease?

How long should dual antiplatelet therapy be continued after drug eluting stent placement in patients with stable angina who undergo percutaneous coronary intervention?

What is the impact of percutaneous coronary intervention on mortality and risk for myocardial infarction in patients with stable angina?

In patients with coronary artery disease and severe left ventricular dysfunction, how does coronary artery bypass grafting compare with medical therapy in terms of survival?

Is percutaneous coronary intervention the preferred revascularization method for patients with left main or three-vessel coronary artery disease or multivessel coronary artery disease plus diabetes mellitus?

Is ten-year survival improved in patients with coronary artery disease and severe left ventricular dysfunction who undergo coronary artery bypass grafting compared with those who receive medical therapy?

Should dual antiplatelet therapy be continued for at least 6 months after drug eluting stent placement in patients with stable angina who undergo percutaneous coronary intervention?

Does percutaneous coronary intervention decrease mortality or risk for myocardial infarction in patients with stable angina?

What is the key differentiation between ST elevation MI (STEMI) and non ST elevation acute coronary syndrome (NSTE ACS)?

What ECG feature is characteristic of Posterior MI?

What is a potential equivalent of ST elevation MI (STEMI)?

How is NSTE-ACS categorized?

Acute Coronary Syndrome (ACS) can result from acute or subacute plaque rupture or erosion and coronary blood flow impairment.

ST elevation MI (STEMI) is differentiated from non ST elevation acute coronary syndrome (NSTE ACS) by findings on ECG.

Posterior MI typically manifests as ST segment elevation in the anterior leads (V1 through V4) with tall R waves.

New bundle branch block may be considered a STEMI equivalent and potentially reflects an acute left anterior descending artery occlusion or extensive injury.

Which ECG finding is commonly associated with patients presenting with accelerated hypertension, significant LV hypertrophy, and cardiomyopathies?

What ECG changes may look similar to ST segment elevation injury currents but are typically concave in appearance?

What ECG findings are associated with patients presenting with supraventricular tachycardias?

What is a distinguishing feature of acute pericarditis that helps differentiate it from ST-elevation myocardial infarction (STEMI)?

What is a diagnostic clue for acute aortic syndromes that can cause ST-segment elevation?

What is the manifestation of transmural myocardial ischemia in ST-elevation myocardial infarction (STEMI)?

What is the primary purpose of reperfusion therapy in the context of STEMI?

Severe hypercalcemia may result in ST segment depression that mimics ACS.

Supraventricular tachycardias may present with chest pain, ST-segment elevation, and elevated cardiac enzyme levels.

Comparison with previous ECG findings is not helpful in identifying acute changes.

ST-segment elevation in acute pericarditis is usually concave in shape and may be diffusely or locally distributed

Acute aortic syndromes can cause ST-segment elevation only if the dissection involves the left coronary artery

Reperfusion therapy for STEMI should be initiated rapidly to restore blood flow to the myocardium

Acute pericarditis and myopericarditis can cause confusion in diagnosis due to release of cardiac enzymes

What is the goal time from first medical contact until PPCI?

Why is PPCI preferred over thrombolysis for treating STEMI?

When is PPCI the preferred method of treating STEMI?

PPCI is the preferred method of treating STEMI when the patient can be transferred quickly to a PCI-capable center

The goal time from first medical contact until PPCI is 120 minutes or less

PPCI results in higher and more reliable vessel patency compared to thrombolysis

When is thrombolytic therapy recommended for patients with STEMI?

Which thrombolytic agents are associated with improved infarct artery patency and fewer allergic reactions compared to streptokinase?

When does fibrin cross linking render the clot relatively resistant to lysis in thrombolytic therapy for STEMI?

Thrombolytic therapy is recommended for patients with STEMI even if PPCI is available within 120 minutes of first medical contact

Thrombolytic therapy is most effective within the first 3 to 6 hours from symptom onset

Newer fibrin specific thrombolytic agents are associated with improved infarct artery patency and fewer allergic reactions compared to streptokinase

What is the recommended loading dose of aspirin for all patients without a specific contraindication?

What is the primary risk associated with thrombolytic therapy?

What ECG finding confirms reperfusion after thrombolytic therapy, reflected by at least 50% improvement in maximal ST segment elevation?

What is the recommended action when rescue PCI is available following thrombolytic therapy?

Thrombolytic therapy is without risk of bleeding.

All patients without a specific contraindication should receive a loading dose of aspirin.

Clopidogrel loading has been demonstrated to decrease rates of vessel patency.

Rescue PCI is associated with improved outcomes compared with conservative management in cases of failed reperfusion.

What is a potential consequence of untreated cardiogenic shock?

Which factor is associated with a higher rate of survival in patients with cardiogenic shock?

What is the primary purpose of weaning the patient from mechanical and inotropic support in cardiogenic shock treatment?

What is the recommended approach for managing atrial fibrillation in patients with STEMI?

What is the recommended action for postinfarction ventricular arrhythmias occurring beyond 48 hours?

What is the recommended approach for managing accelerated idioventricular rhythm that arises after reperfusion?

When does Mobitz type 2 second degree atrioventricular block require permanent pacing?

Ventricular tachycardia or fibrillation may occur during MI or after reperfusion.

Routine suppression of ventricular ectopy with antiarrhythmic agents is recommended and is associated with increased arrhythmias and adverse outcomes.

Cardiogenic shock is a common complication of STEMI.

Permanent pacing is often required for atrioventricular block, including Wenckebach and complete heart block, after inferior infarction.

Cardiogenic shock carries a mortality rate of 50% to 80%, and must be recognized early.

Untreated cardiogenic shock can progress rapidly to end organ failure.

Patients younger than 75 years have a higher rate of survival if they receive emergent revascularization.

What is the recommended duration of anticoagulation for LV apical thrombus in cases of anterior STEMI?

How is right ventricular (RV) infarction typically identified?

What may be revealed by transthoracic echocardiography in cases of RV infarction?

What is contraindicated in cases of LV free wall rupture to avoid worsening hypotension?

LV apical thrombus is generally not treated with anticoagulation in cases of anterior STEMI without other indications, such as atrial fibrillation.

Right ventricular (RV) infarction can be identified by ST segment elevation on right sided ECG leads V1 and V4R.

Nitrates are contraindicated in cases of RV infarction because they may worsen hypotension by reducing preload.

LV free wall rupture is more common in younger adults, men, and patients with delayed reperfusion.

What is the most common presentation of patients with acquired ventricular septal defect (VSD) from septal wall rupture following STEMI?

What is the approximate mortality rate in patients with medically treated postinfarct VSDs?

Why can percutaneous closure with a VSD occluder device be often unsuccessful in postinfarct VSDs?

What may result from interruption of the posteromedial papillary muscle blood supply during myocardial infarction?

Patients with postinfarct VSDs typically present with worsening heart failure and shock

The mortality rate in patients with medically treated postinfarct VSDs approaches 50%

Percutaneous closure with a VSD occluder device is often successful in postinfarct VSDs

Interrupted blood supply to the posteromedial papillary muscle may result in severe acute mitral regurgitation several days after STEMI

What is the primary purpose of risk stratification in suspected NSTE ACS?

Which risk score predicts 14-day death, recurrent MI, and urgent revascularization rates in patients with suspected NSTE ACS?

What do fractional flow reserve and instantaneous wave-free ratio provide information on in patients with stable angina?

What is the primary goal of revascularization in stable syndromes?

NSTEMI ACS involves complete coronary obstruction resulting in ST segment elevation.

The TIMI risk score predicts in-hospital and post-discharge death and MI risk.

The GRACE risk score incorporates only clinical features and ECG findings.

Prognostic assessment helps determine the most appropriate therapeutic strategy.

When is urgent invasive treatment recommended for patients with NSTE ACS?

What is the timing for cardiac catheterization in patients with an elevated clinical risk score, significant ST segment deviation, or elevated cardiac biomarkers?

When is the choice of revascularization procedure (PCI or CABG) based on the results of angiography?

When is the ischemia guided approach appropriate?

An early invasive strategy improves the composite clinical endpoint of death, recurrent MI, and repeat hospitalization compared with an ischemia-guided approach.

Cardiac catheterization is usually performed within 24 hours of presentation in patients with an elevated clinical risk score, significant ST segment deviation, or elevated cardiac biomarkers.

Patients with diabetes, stage 2 to 3 chronic kidney disease, LV dysfunction, and recent PCI without elevated risk scores may be safely evaluated with coronary angiography within 72 hours of presentation (delayed invasive strategy).

With an ischemia-guided strategy, patients undergo noninvasive stress testing with LV function assessment before hospital discharge.

When is cardiac catheterization usually performed for patients with an elevated clinical risk score, significant ST segment deviation, or elevated cardiac biomarkers?

For which patients is delayed invasive strategy with coronary angiography within 72 hours of presentation considered appropriate?

What determines the choice of revascularization procedure (PCI or CABG) for patients with NSTE ACS?

When is the ischemia guided approach considered appropriate for patients with NSTE ACS?