What defines dilated cardiomyopathy, and why is it not simply any enlarged heart with a low ejection fraction?

The 2023 ESC definition requires left ventricular dilation with global or regional systolic dysfunction that is not explained solely by abnormal loading conditions or coronary artery disease. Right ventricular involvement may occur but is not required. Genetic disease, myocarditis, alcohol, and cardiotoxic drugs are among the causes. Neither dilation of all four chambers nor an arbitrary EF below 40% is a universal diagnostic requirement.

How is the ankle–brachial index calculated and interpreted under the 2024 AHA/ACC PAD guideline?

For each leg, divide the higher dorsalis pedis or posterior tibial systolic pressure by the higher brachial systolic pressure from either arm. ABI ≤0.90 is abnormal, 0.91–0.99 borderline, 1.00–1.40 normal, and >1.40 noncompressible. A high value can reflect arterial calcification rather than normal perfusion and calls for toe-pressure assessment. Symptoms with normal or borderline resting ABI may require exercise testing.

How do US AAA screening recommendations differ from thresholds for aneurysm repair?

USPSTF recommends one-time ultrasound screening for men aged 65–75 who have ever smoked; other groups require their own risk-based recommendations. Screening is not a repair indication. Under the 2022 ACC/AHA guideline, unruptured AAA repair is recommended at ≥5.5 cm in men or ≥5.0 cm in women, or for attributable symptoms. Growth ≥0.5 cm in six months may justify repair. Anatomy, operative risk, and patient preferences also matter.

What vascular pattern and clinical clues suggest Takayasu arteritis?

Takayasu is a large-vessel inflammatory disease affecting the aorta and major branches, sometimes causing stenosis, occlusion, or aneurysms. It is more common in younger women, but sex and ancestry do not determine the diagnosis. Limb claudication, diminished pulses, bruits, or unequal arm pressures are clues and may be preceded by constitutional symptoms. Noninvasive vascular imaging evaluates the distribution and vessel-wall changes; absent pulses are not required in every case.

What are the major diagnostic domains in the 2023 Duke-ISCVID criteria for infective endocarditis?

They include qualifying microbiological evidence, qualifying cardiac imaging, and a new domain of direct surgical evidence when other definitive evidence is unavailable. Imaging extends beyond echocardiography to specified CT and FDG-PET/CT findings; selected molecular and serological tests also qualify. Clinical definite IE can meet two major criteria, one major plus three minor, or five minor. Apply the full definitions: a positive culture or an abnormal scan does not automatically count.

How does microscopic polyangiitis differ from granulomatosis with polyangiitis?

MPA is a predominantly small-vessel necrotizing vasculitis with few or no immune deposits. Glomerulonephritis and pulmonary capillaritis, including alveolar hemorrhage, are important manifestations. Granulomatous inflammation characteristic of GPA is absent. MPO-ANCA is common, but PR3-positive and ANCA-negative cases occur. The distinction requires the whole clinical and pathological pattern; ANCA subtype alone is insufficient.

What are Aschoff bodies and Anitschkow cells in rheumatic carditis?

Aschoff bodies are characteristic inflammatory foci containing fibrinoid injury surrounded by lymphocytes, occasional plasma cells, and activated macrophages. Anitschkow cells are the plump macrophages with a wavy, caterpillar-like pattern of nuclear chromatin; multinucleated forms may also occur. This is a pathology association, not a requirement to biopsy every patient: acute rheumatic fever is assessed clinically with the Jones framework and supporting investigations.

Why is serial cardiac troponin preferred to CK-MB for suspected myocardial infarction, including recurrent symptoms?

High-sensitivity cardiac troponin I or T is preferred; interpret serial changes using the assay's thresholds, including sex-specific upper reference limits. A raised result alone indicates myocardial injury, not necessarily infarction: ischemic evidence is also needed. New or recurrent symptoms require reassessment with serial troponin, ECG, and appropriate imaging. CK-MB is less sensitive and specific and does not become the preferred test merely because a recent infarction may leave troponin elevated.

Why is CT pulmonary angiography not the first test for every patient with possible pulmonary embolism?

Testing begins with clinical probability. Selected very-low-risk patients may meet PERC, while appropriate low- or intermediate-probability patients can avoid imaging after a negative D-dimer using a validated threshold or pathway. When imaging is required, CTPA is commonly used; ventilation–perfusion scanning is an alternative when appropriate. Unstable patients need an urgent adapted pathway. ECG findings such as S1Q3T3 neither confirm nor exclude PE.

Why can nitrates worsen hypotension in right ventricular infarction?

An injured right ventricle may depend on adequate filling to maintain pulmonary flow and left ventricular preload. Nitrate-induced venodilation can therefore reduce cardiac output and blood pressure. The 2025 AHA/ACC ACS guideline advises avoiding nitrates in suspected RV infarction. Hypotension with elevated jugular venous pressure and relatively clear lungs is a clue, not a required triad. Fluids and other treatments must be guided by perfusion and congestion, not given automatically.

What is the common genetic basis of hypertrophic cardiomyopathy, and what limits that generalization?

Many familial cases involve pathogenic sarcomere-gene variants, especially MYH7 or MYBPC3, often with autosomal dominant inheritance and variable penetrance. However, a causative variant is not identified in every patient, and other diseases can produce a hypertrophic phenotype. Myocyte hypertrophy and disarray are characteristic pathological findings, but neither a gene result nor disarray alone replaces the clinical and imaging assessment.

When should giant cell arteritis be suspected, and why must investigation not delay treatment?

In an adult usually aged 50 or older, new headache, scalp tenderness, jaw claudication, or visual symptoms can suggest GCA; large-vessel manifestations also occur. Threatened vision requires urgent assessment and treatment. EULAR's 2023 imaging recommendations favor expert temporal and axillary artery ultrasound when promptly available; biopsy or other imaging remains useful in appropriate settings. Treatment should not wait for imaging when clinical suspicion is strong, particularly with ischemic symptoms.

Why is the posteromedial papillary muscle more vulnerable to infarction-related rupture?

It usually has a single arterial supply from the RCA or circumflex system, depending on dominance, whereas the anterolateral muscle generally has dual supply. Rupture can cause abrupt severe mitral regurgitation, pulmonary edema, and shock, often within days of MI. The murmur may be faint or absent as ventricular and atrial pressures rapidly equalize. Urgent echocardiography is needed; transesophageal imaging may clarify an inconclusive transthoracic study.

How is cardiac amyloidosis confirmed and typed, and is myocardial biopsy always necessary?

Tissue amyloid typically stains with Congo red and shows apple-green birefringence under polarized light; deposits must also be typed. AL and ATTR are distinct causes. In a compatible clinical setting, grade 2–3 uptake on appropriate bone-tracer cardiac scintigraphy can establish ATTR without biopsy when a monoclonal protein screen is negative. That screen includes serum free light chains and serum/urine immunofixation. Abnormal screening or uncertain imaging requires further specialist evaluation, often biopsy.

Which findings should raise suspicion of acute aortic dissection, and what imaging is used?

Abrupt severe chest, back, or abdominal pain, pulse or blood-pressure differences, new aortic regurgitation, syncope, or organ ischemia are important clues; no single classic finding is obligatory. CT angiography is usually the initial test because it is fast and shows the extent and branches involved. TEE or MRI are alternatives selected according to stability, availability, and contraindications. A normal chest radiograph does not exclude dissection.

What distinguishes polyarteritis nodosa from small-vessel ANCA-associated vasculitis?

PAN causes necrotizing inflammation of medium and small muscular arteries. Renal arterial ischemia can cause hypertension, but glomerulonephritis and pulmonary capillaritis are not features of the defining disease. Neuropathy, livedo or nodules, and mesenteric ischemia may occur. PAN is not an ANCA-associated vasculitis. Hepatitis B causes a subset of cases and changes management; it should not be assumed to underlie every case.

What should suggest ventricular septal rupture after myocardial infarction, and how is it confirmed?

A new harsh systolic murmur, heart failure, or shock after MI should raise concern for a new left-to-right ventricular shunt. Rupture often develops during the first week, but timing varies. Urgent echocardiography with Doppler identifies the defect and shunt. A right-sided oxygen-saturation step-up supports the diagnosis if catheter measurements are obtained. Prompt specialist assessment is essential; the presentation can range from a murmur to circulatory collapse.

Which pattern suggests granulomatosis with polyangiitis, and how should PR3-ANCA be interpreted?

GPA often combines destructive upper-airway disease, pulmonary nodules or hemorrhage, and pauci-immune glomerulonephritis, but limited presentations occur. Necrotizing granulomatous inflammation is characteristic. PR3-ANCA is strongly associated, yet some patients have MPO-ANCA or no detectable ANCA. Neither a complete ENT–lung–kidney triad nor a positive PR3 result is compulsory; diagnosis integrates clinical findings, testing, imaging, and biopsy when appropriate.

How do STEMI, NSTEMI, and unstable angina differ, and how do they relate to the 2026 MI classification?

STEMI and NSTEMI describe the presenting ECG pattern, not the depth of necrosis. STEMI has persistent diagnostic ST elevation or an occlusion-equivalent pattern; NSTEMI lacks persistent diagnostic ST elevation but has acute myocardial injury with evidence of ischemia. Unstable angina has acute ischemic symptoms without MI on serial testing. New LBBB alone is insufficient. The 2026 universal definition separately classifies MI by mechanism: primary, secondary, or procedure-related.

Which features distinguish takotsubo syndrome from a single fixed pattern of coronary infarction?

Takotsubo causes usually reversible ventricular dysfunction, often extending beyond one coronary territory. Apical ballooning is familiar, but midventricular, basal, and focal patterns also occur. Physical or emotional stress may trigger it but is not required, and coronary artery disease can coexist. Adrenergic stress is important in its proposed mechanisms. Because its symptoms, ECG, and biomarkers can mimic ACS, urgent coronary and cardiac assessment is needed before assigning the diagnosis.

How are the revised Jones criteria used for an initial episode of acute rheumatic fever?

Usually, evidence of preceding group A streptococcal infection accompanies either two major manifestations or one major plus two minor. Major features include clinical or subclinical carditis, qualifying joint disease, chorea, erythema marginatum, and subcutaneous nodules. Joint criteria differ between low-risk and higher-risk populations. Do not count the same joint or cardiac manifestation twice. Chorea and indolent carditis can be exceptions; echocardiography is recommended even without a murmur.

How is Kawasaki disease recognized without requiring every feature or waiting unnecessarily for day five?

Classic KD combines persistent fever with at least four of five features: bilateral nonpurulent conjunctivitis, oral changes, rash, extremity changes, and cervical lymphadenopathy. Diagnosis is commonly made after five days of fever, but a clear complete presentation can be diagnosed earlier by experienced clinicians. Incomplete KD has fewer features and needs laboratory and echocardiographic assessment. Coronary aneurysms and thrombosis are major complications; suspected disease needs prompt pediatric evaluation.

How can late syphilitic aortitis produce an aneurysm or aortic regurgitation?

Inflammation and obliterative endarteritis of the vasa vasorum impair nourishment of the aortic wall, damaging elastic tissue and causing fibrosis. The ascending thoracic aorta is a typical site. Consequences can include aneurysm, aortic regurgitation, and coronary ostial narrowing. A wrinkled tree-bark appearance is a classic pathological clue, but diagnosis also requires clinical, laboratory, and pathological context; cardiovascular involvement is not inevitable in syphilis.

What do the six Ps of acute limb ischemia signal, and what determines urgency?

Pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia are warning signs, not a checklist that must be complete. Sensory and motor loss indicate threatened viability. Emergency assessment includes Doppler signals and limb viability; systemic unfractionated heparin is generally started unless contraindicated. Salvageable limbs need urgent or emergency revascularization according to severity. An irreversibly ischemic limb should not be revascularized because reperfusion can cause serious harm.

What pattern suggests eosinophilic granulomatosis with polyangiitis, and does ANCA negativity exclude it?

Think of EGPA when asthma and eosinophilia accompany features such as neuropathy, pulmonary infiltrates, sinus disease, or other organ involvement. Eosinophilic inflammation and small- to medium-vessel vasculitis are central. Only about 30% have detectable ANCA at diagnosis, usually MPO-ANCA, so a negative test does not exclude EGPA. Exclude mimics such as other eosinophilic disorders; classification scores are not stand-alone diagnostic tests.

Which ECG leads reflect inferior-wall infarction, and which coronary artery is usually responsible?

Leads II, III, and aVF view the inferior wall. The culprit is commonly the right coronary artery, but the left circumflex can also supply this territory, depending on coronary anatomy. ECG patterns help localize the injury and suggest the culprit; they do not prove the responsible artery. Coronary imaging establishes the anatomy, and right-sided leads help assess associated right ventricular involvement.

Which findings suggest coarctation of the aorta, and how does presentation vary with age?

Higher arm than leg blood pressure and weak or delayed femoral pulses suggest narrowing of the aorta. Severe neonatal disease can cause heart failure or shock as the ductus closes; milder disease may present later with hypertension. Intercostal collateral vessels can cause rib notching in older patients, but its absence does not exclude coarctation. Bicuspid aortic valve and Turner syndrome are important associations. Echocardiography, sometimes supplemented by CT or MRI, defines the anatomy.

How does early post-infarction pericarditis differ from Dressler syndrome?

Early pericarditis follows local inflammation extending from the infarct, usually within hours to the first few days. Dressler syndrome is a delayed, presumed immune-mediated post-cardiac injury syndrome, often beginning around 1–2 weeks later, with a variable interval. Pleuritic pain, fever, a rub, or effusion may occur. Timing alone does not establish either diagnosis, and new pain after MI also requires assessment for recurrent ischemia and mechanical complications.

How does the 2026 AHA/ACC PE framework identify patients who may need advanced reperfusion treatment?

It uses categories A–E rather than relying only on older labels such as massive or submassive. Category C denotes elevated clinical severity, with or without RV or biomarker abnormalities, D denotes incipient cardiopulmonary failure, and E denotes failure with persistent hypotension or worse. Advanced therapies may be appropriate for selected D or E patients after assessing bleeding risk and available expertise. Thrombolysis is not routine for every PE or every patient with RV strain.

How does Stanford classification guide the initial approach to aortic dissection?

Type A involves the ascending aorta and generally requires emergency surgical evaluation. Type B does not involve the ascending aorta; it can include the arch and descending aorta. Initial monitored care controls pain, heart rate, and blood pressure while preserving organ perfusion. Uncomplicated type B is usually managed medically, but rupture, malperfusion, progression, or other complications may require urgent intervention. Type B does not mean harmless.

How do Osler nodes, Janeway lesions, Roth spots, and splinter hemorrhages differ?

Osler nodes are typically tender nodules on fingers or toes; Janeway lesions are usually painless lesions on palms or soles. Roth spots are retinal hemorrhages with pale centers, while splinter hemorrhages are thin longitudinal streaks under nails. These can support suspicion of endocarditis but are often absent and are not individually diagnostic. Pain and presumed mechanism should not be treated as infallible distinctions.

What are the three components of Virchow's triad, and how do they help explain thrombosis?

They are abnormal blood flow, especially venous stasis; endothelial injury or dysfunction; and hypercoagulability. For example, immobility slows flow, surgery can injure vessels, and cancer or inherited thrombophilia can increase clotting tendency. These mechanisms often interact. The triad explains risk and pathogenesis; it is not a diagnostic test, and a patient does not need all three components identified to develop a thrombus.

Cardiology & Vascular Disease: Diagnostic Patterns and Emergencies

Review 32 focused clinical concepts across acute coronary syndromes, cardiomyopathies, endocarditis, vasculitis, aortic disease, and thromboembolism. Practice distinguishing useful diagnostic clues from required criteria, with named guideline versions where recommendations differ.

Level: intermediate
Languages: en → en
Cards: 32
Markdown: Cardiology & Vascular Disease: Diagnostic Patterns and Emergencies (.md)

Flashcards (32)

#	Front (Term / Question)	Back (Definition / Answer)
1	What defines dilated cardiomyopathy, and why is it not simply any enlarged heart with a low ejection fraction?	The 2023 ESC definition requires left ventricular dilation with global or regional systolic dysfunction that is not explained solely by abnormal loading conditions or coronary artery disease. Right ventricular involvement may occur but is not required. Genetic disease, myocarditis, alcohol, and cardiotoxic drugs are among the causes. Neither dilation of all four chambers nor an arbitrary EF below 40% is a universal diagnostic requirement.
2	How is the ankle–brachial index calculated and interpreted under the 2024 AHA/ACC PAD guideline?	For each leg, divide the higher dorsalis pedis or posterior tibial systolic pressure by the higher brachial systolic pressure from either arm. ABI ≤0.90 is abnormal, 0.91–0.99 borderline, 1.00–1.40 normal, and >1.40 noncompressible. A high value can reflect arterial calcification rather than normal perfusion and calls for toe-pressure assessment. Symptoms with normal or borderline resting ABI may require exercise testing.
3	How do US AAA screening recommendations differ from thresholds for aneurysm repair?	USPSTF recommends one-time ultrasound screening for men aged 65–75 who have ever smoked; other groups require their own risk-based recommendations. Screening is not a repair indication. Under the 2022 ACC/AHA guideline, unruptured AAA repair is recommended at ≥5.5 cm in men or ≥5.0 cm in women, or for attributable symptoms. Growth ≥0.5 cm in six months may justify repair. Anatomy, operative risk, and patient preferences also matter.
4	What vascular pattern and clinical clues suggest Takayasu arteritis?	Takayasu is a large-vessel inflammatory disease affecting the aorta and major branches, sometimes causing stenosis, occlusion, or aneurysms. It is more common in younger women, but sex and ancestry do not determine the diagnosis. Limb claudication, diminished pulses, bruits, or unequal arm pressures are clues and may be preceded by constitutional symptoms. Noninvasive vascular imaging evaluates the distribution and vessel-wall changes; absent pulses are not required in every case.
5	What are the major diagnostic domains in the 2023 Duke-ISCVID criteria for infective endocarditis?	They include qualifying microbiological evidence, qualifying cardiac imaging, and a new domain of direct surgical evidence when other definitive evidence is unavailable. Imaging extends beyond echocardiography to specified CT and FDG-PET/CT findings; selected molecular and serological tests also qualify. Clinical definite IE can meet two major criteria, one major plus three minor, or five minor. Apply the full definitions: a positive culture or an abnormal scan does not automatically count.
6	How does microscopic polyangiitis differ from granulomatosis with polyangiitis?	MPA is a predominantly small-vessel necrotizing vasculitis with few or no immune deposits. Glomerulonephritis and pulmonary capillaritis, including alveolar hemorrhage, are important manifestations. Granulomatous inflammation characteristic of GPA is absent. MPO-ANCA is common, but PR3-positive and ANCA-negative cases occur. The distinction requires the whole clinical and pathological pattern; ANCA subtype alone is insufficient.
7	What are Aschoff bodies and Anitschkow cells in rheumatic carditis?	Aschoff bodies are characteristic inflammatory foci containing fibrinoid injury surrounded by lymphocytes, occasional plasma cells, and activated macrophages. Anitschkow cells are the plump macrophages with a wavy, caterpillar-like pattern of nuclear chromatin; multinucleated forms may also occur. This is a pathology association, not a requirement to biopsy every patient: acute rheumatic fever is assessed clinically with the Jones framework and supporting investigations.
8	Why is serial cardiac troponin preferred to CK-MB for suspected myocardial infarction, including recurrent symptoms?	High-sensitivity cardiac troponin I or T is preferred; interpret serial changes using the assay's thresholds, including sex-specific upper reference limits. A raised result alone indicates myocardial injury, not necessarily infarction: ischemic evidence is also needed. New or recurrent symptoms require reassessment with serial troponin, ECG, and appropriate imaging. CK-MB is less sensitive and specific and does not become the preferred test merely because a recent infarction may leave troponin elevated.
9	Why is CT pulmonary angiography not the first test for every patient with possible pulmonary embolism?	Testing begins with clinical probability. Selected very-low-risk patients may meet PERC, while appropriate low- or intermediate-probability patients can avoid imaging after a negative D-dimer using a validated threshold or pathway. When imaging is required, CTPA is commonly used; ventilation–perfusion scanning is an alternative when appropriate. Unstable patients need an urgent adapted pathway. ECG findings such as S1Q3T3 neither confirm nor exclude PE.
10	Why can nitrates worsen hypotension in right ventricular infarction?	An injured right ventricle may depend on adequate filling to maintain pulmonary flow and left ventricular preload. Nitrate-induced venodilation can therefore reduce cardiac output and blood pressure. The 2025 AHA/ACC ACS guideline advises avoiding nitrates in suspected RV infarction. Hypotension with elevated jugular venous pressure and relatively clear lungs is a clue, not a required triad. Fluids and other treatments must be guided by perfusion and congestion, not given automatically.
11	What is the common genetic basis of hypertrophic cardiomyopathy, and what limits that generalization?	Many familial cases involve pathogenic sarcomere-gene variants, especially MYH7 or MYBPC3, often with autosomal dominant inheritance and variable penetrance. However, a causative variant is not identified in every patient, and other diseases can produce a hypertrophic phenotype. Myocyte hypertrophy and disarray are characteristic pathological findings, but neither a gene result nor disarray alone replaces the clinical and imaging assessment.
12	When should giant cell arteritis be suspected, and why must investigation not delay treatment?	In an adult usually aged 50 or older, new headache, scalp tenderness, jaw claudication, or visual symptoms can suggest GCA; large-vessel manifestations also occur. Threatened vision requires urgent assessment and treatment. EULAR's 2023 imaging recommendations favor expert temporal and axillary artery ultrasound when promptly available; biopsy or other imaging remains useful in appropriate settings. Treatment should not wait for imaging when clinical suspicion is strong, particularly with ischemic symptoms.
13	Why is the posteromedial papillary muscle more vulnerable to infarction-related rupture?	It usually has a single arterial supply from the RCA or circumflex system, depending on dominance, whereas the anterolateral muscle generally has dual supply. Rupture can cause abrupt severe mitral regurgitation, pulmonary edema, and shock, often within days of MI. The murmur may be faint or absent as ventricular and atrial pressures rapidly equalize. Urgent echocardiography is needed; transesophageal imaging may clarify an inconclusive transthoracic study.
14	How is cardiac amyloidosis confirmed and typed, and is myocardial biopsy always necessary?	Tissue amyloid typically stains with Congo red and shows apple-green birefringence under polarized light; deposits must also be typed. AL and ATTR are distinct causes. In a compatible clinical setting, grade 2–3 uptake on appropriate bone-tracer cardiac scintigraphy can establish ATTR without biopsy when a monoclonal protein screen is negative. That screen includes serum free light chains and serum/urine immunofixation. Abnormal screening or uncertain imaging requires further specialist evaluation, often biopsy.
15	Which findings should raise suspicion of acute aortic dissection, and what imaging is used?	Abrupt severe chest, back, or abdominal pain, pulse or blood-pressure differences, new aortic regurgitation, syncope, or organ ischemia are important clues; no single classic finding is obligatory. CT angiography is usually the initial test because it is fast and shows the extent and branches involved. TEE or MRI are alternatives selected according to stability, availability, and contraindications. A normal chest radiograph does not exclude dissection.
16	What distinguishes polyarteritis nodosa from small-vessel ANCA-associated vasculitis?	PAN causes necrotizing inflammation of medium and small muscular arteries. Renal arterial ischemia can cause hypertension, but glomerulonephritis and pulmonary capillaritis are not features of the defining disease. Neuropathy, livedo or nodules, and mesenteric ischemia may occur. PAN is not an ANCA-associated vasculitis. Hepatitis B causes a subset of cases and changes management; it should not be assumed to underlie every case.
17	What should suggest ventricular septal rupture after myocardial infarction, and how is it confirmed?	A new harsh systolic murmur, heart failure, or shock after MI should raise concern for a new left-to-right ventricular shunt. Rupture often develops during the first week, but timing varies. Urgent echocardiography with Doppler identifies the defect and shunt. A right-sided oxygen-saturation step-up supports the diagnosis if catheter measurements are obtained. Prompt specialist assessment is essential; the presentation can range from a murmur to circulatory collapse.
18	Which pattern suggests granulomatosis with polyangiitis, and how should PR3-ANCA be interpreted?	GPA often combines destructive upper-airway disease, pulmonary nodules or hemorrhage, and pauci-immune glomerulonephritis, but limited presentations occur. Necrotizing granulomatous inflammation is characteristic. PR3-ANCA is strongly associated, yet some patients have MPO-ANCA or no detectable ANCA. Neither a complete ENT–lung–kidney triad nor a positive PR3 result is compulsory; diagnosis integrates clinical findings, testing, imaging, and biopsy when appropriate.
19	How do STEMI, NSTEMI, and unstable angina differ, and how do they relate to the 2026 MI classification?	STEMI and NSTEMI describe the presenting ECG pattern, not the depth of necrosis. STEMI has persistent diagnostic ST elevation or an occlusion-equivalent pattern; NSTEMI lacks persistent diagnostic ST elevation but has acute myocardial injury with evidence of ischemia. Unstable angina has acute ischemic symptoms without MI on serial testing. New LBBB alone is insufficient. The 2026 universal definition separately classifies MI by mechanism: primary, secondary, or procedure-related.
20	Which features distinguish takotsubo syndrome from a single fixed pattern of coronary infarction?	Takotsubo causes usually reversible ventricular dysfunction, often extending beyond one coronary territory. Apical ballooning is familiar, but midventricular, basal, and focal patterns also occur. Physical or emotional stress may trigger it but is not required, and coronary artery disease can coexist. Adrenergic stress is important in its proposed mechanisms. Because its symptoms, ECG, and biomarkers can mimic ACS, urgent coronary and cardiac assessment is needed before assigning the diagnosis.
21	How are the revised Jones criteria used for an initial episode of acute rheumatic fever?	Usually, evidence of preceding group A streptococcal infection accompanies either two major manifestations or one major plus two minor. Major features include clinical or subclinical carditis, qualifying joint disease, chorea, erythema marginatum, and subcutaneous nodules. Joint criteria differ between low-risk and higher-risk populations. Do not count the same joint or cardiac manifestation twice. Chorea and indolent carditis can be exceptions; echocardiography is recommended even without a murmur.
22	How is Kawasaki disease recognized without requiring every feature or waiting unnecessarily for day five?	Classic KD combines persistent fever with at least four of five features: bilateral nonpurulent conjunctivitis, oral changes, rash, extremity changes, and cervical lymphadenopathy. Diagnosis is commonly made after five days of fever, but a clear complete presentation can be diagnosed earlier by experienced clinicians. Incomplete KD has fewer features and needs laboratory and echocardiographic assessment. Coronary aneurysms and thrombosis are major complications; suspected disease needs prompt pediatric evaluation.
23	How can late syphilitic aortitis produce an aneurysm or aortic regurgitation?	Inflammation and obliterative endarteritis of the vasa vasorum impair nourishment of the aortic wall, damaging elastic tissue and causing fibrosis. The ascending thoracic aorta is a typical site. Consequences can include aneurysm, aortic regurgitation, and coronary ostial narrowing. A wrinkled tree-bark appearance is a classic pathological clue, but diagnosis also requires clinical, laboratory, and pathological context; cardiovascular involvement is not inevitable in syphilis.
24	What do the six Ps of acute limb ischemia signal, and what determines urgency?	Pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia are warning signs, not a checklist that must be complete. Sensory and motor loss indicate threatened viability. Emergency assessment includes Doppler signals and limb viability; systemic unfractionated heparin is generally started unless contraindicated. Salvageable limbs need urgent or emergency revascularization according to severity. An irreversibly ischemic limb should not be revascularized because reperfusion can cause serious harm.
25	What pattern suggests eosinophilic granulomatosis with polyangiitis, and does ANCA negativity exclude it?	Think of EGPA when asthma and eosinophilia accompany features such as neuropathy, pulmonary infiltrates, sinus disease, or other organ involvement. Eosinophilic inflammation and small- to medium-vessel vasculitis are central. Only about 30% have detectable ANCA at diagnosis, usually MPO-ANCA, so a negative test does not exclude EGPA. Exclude mimics such as other eosinophilic disorders; classification scores are not stand-alone diagnostic tests.
26	Which ECG leads reflect inferior-wall infarction, and which coronary artery is usually responsible?	Leads II, III, and aVF view the inferior wall. The culprit is commonly the right coronary artery, but the left circumflex can also supply this territory, depending on coronary anatomy. ECG patterns help localize the injury and suggest the culprit; they do not prove the responsible artery. Coronary imaging establishes the anatomy, and right-sided leads help assess associated right ventricular involvement.
27	Which findings suggest coarctation of the aorta, and how does presentation vary with age?	Higher arm than leg blood pressure and weak or delayed femoral pulses suggest narrowing of the aorta. Severe neonatal disease can cause heart failure or shock as the ductus closes; milder disease may present later with hypertension. Intercostal collateral vessels can cause rib notching in older patients, but its absence does not exclude coarctation. Bicuspid aortic valve and Turner syndrome are important associations. Echocardiography, sometimes supplemented by CT or MRI, defines the anatomy.
28	How does early post-infarction pericarditis differ from Dressler syndrome?	Early pericarditis follows local inflammation extending from the infarct, usually within hours to the first few days. Dressler syndrome is a delayed, presumed immune-mediated post-cardiac injury syndrome, often beginning around 1–2 weeks later, with a variable interval. Pleuritic pain, fever, a rub, or effusion may occur. Timing alone does not establish either diagnosis, and new pain after MI also requires assessment for recurrent ischemia and mechanical complications.
29	How does the 2026 AHA/ACC PE framework identify patients who may need advanced reperfusion treatment?	It uses categories A–E rather than relying only on older labels such as massive or submassive. Category C denotes elevated clinical severity, with or without RV or biomarker abnormalities, D denotes incipient cardiopulmonary failure, and E denotes failure with persistent hypotension or worse. Advanced therapies may be appropriate for selected D or E patients after assessing bleeding risk and available expertise. Thrombolysis is not routine for every PE or every patient with RV strain.
30	How does Stanford classification guide the initial approach to aortic dissection?	Type A involves the ascending aorta and generally requires emergency surgical evaluation. Type B does not involve the ascending aorta; it can include the arch and descending aorta. Initial monitored care controls pain, heart rate, and blood pressure while preserving organ perfusion. Uncomplicated type B is usually managed medically, but rupture, malperfusion, progression, or other complications may require urgent intervention. Type B does not mean harmless.
31	How do Osler nodes, Janeway lesions, Roth spots, and splinter hemorrhages differ?	Osler nodes are typically tender nodules on fingers or toes; Janeway lesions are usually painless lesions on palms or soles. Roth spots are retinal hemorrhages with pale centers, while splinter hemorrhages are thin longitudinal streaks under nails. These can support suspicion of endocarditis but are often absent and are not individually diagnostic. Pain and presumed mechanism should not be treated as infallible distinctions.
32	What are the three components of Virchow's triad, and how do they help explain thrombosis?	They are abnormal blood flow, especially venous stasis; endothelial injury or dysfunction; and hypercoagulability. For example, immobility slows flow, surgery can injure vessels, and cancer or inherited thrombophilia can increase clotting tendency. These mechanisms often interact. The triad explains risk and pathogenesis; it is not a diagnostic test, and a patient does not need all three components identified to develop a thrombus.