Pathology
What is the first step in coronary artery plaque formation?
Lipid deposition/fatty streak formation
What are the three main anti-ischemic therapies to be used in NSTEMI/UA and provide one contraindication for each.
Beta blocker- Heart failure exacerbation, heart block, cardiogenic shock, ACTIVE bronchospasm or reactive airway disease
CCB- significant LV dysfunction, conduction disease, at risk for cardiogenic shock (mainly non-dihydropiridines)
Nitrates- Hypotension, recent PDE-5 inhibitory use
What defines an Acute Coronary Syndrome
Abrupt reduction in coronary blood flow or a myocardial supply/demand oxygen mismatch
A 57-year-old man comes to a rural hospital without percutaneous coronary intervention (PCI) capabilities with an acute anterior STEMI. Due to a thunderstorm, helicopter transport is not possible and the nearest PCI hospital is 250 miles away. He is given a thrombolytic agent with successful reperfusion with resolution of chest pain and normalization of ST segments. Two days later, he reports chest pain while ambulating to the bathroom.
What is the best next step in evaluation of this patient?
Coronary Angiogram
Recent STEMI and thrombolytic use with recurrent chest pain with minimal exertion is concerning for ischemia.
In addition to invasive ischemic evaluation, medical optimization is warranted
Which isoforms of troponin are specific for cardiac myocytes?
Troponin I
Troponin T
(Not troponin C)
A 54-year-old man presents to the office for the evaluation of chest discomfort. He reports substernal chest pressure over the prior 2 months that is triggered by walking up one flight of stairs. The chest pressure is associated with mild shortness of breath and is always relieved with 1-2 min of rest. His symptoms have not changed over the prior 4 months. His medical history includes hypertension and dyslipidemia. His daily medications include amlodipine 5 mg, atorvastatin 40 mg, and tamsulosin 0.4 mg. He smokes half a pack of cigarettes daily.
On examination, his heart rate is 78 bpm and blood pressure is 154/78 mm Hg. His jugular venous pressure is 6 cm H2O, lungs are clear, heart is regular with a grade 2/6 systolic ejection murmur at the left upper sternal border, abdomen is soft, and extremities are warm without edema. His laboratory test results include creatinine level 1.2 mg/dL and hemoglobin level 12.4 g/dL. An electrocardiogram (ECG) is performed showing 1mm STE in V2/V3
What is the most likely mechanism of Action?
Fiberous atherosclerotic plaque limiting blood low
- Patient in this case has STABLE angina given symptom description, chronicity and stability
A 57-year-old man with a medical history of hypertension and non–insulin-dependent type 2 diabetes mellitus presents to the emergency department with 2 hours of severe substernal chest discomfort.
On examination, he appears distressed and diaphoretic. His heart rate (HR) is 104 bpm and blood pressure is 90/62 mm Hg. He is breathing 16 times per minute with oxygen saturation 96% on room air. His cardiac examination reveals normal heart sounds. Lungs are clear. Jugular venous distension is present. An electrocardiogram is performed on arrival showing STE in II, III, aVF . He is administered aspirin 325 mg and intravenous (IV) heparin.
What is the best next step in management?
Hypotension + Inferior lead MI + JVD = RV infarct
First step is to give fluids and maximize preload
What is the major pathophysiological difference between STEMI and NSTEMI/UA
Complete versus subtotal occlusion of non-microvascular coronary flow
A 58-year-old woman with a history of hypertension, chronic kidney disease, asthma with twice yearly emergency room visits for severe exacerbation, hyperlipidemia, and a recent ankle fracture is seen in clinic for the evaluation of several weeks of substernal chest pressure that occurs with emotional stress. The chest pressure lasts 5 minutes before resolving. Medications include amlodipine 10 mg daily, atorvastatin 40 mg daily, and albuterol inhaler as needed. Her blood pressure is 134/84 mm Hg, heart rate is 62 bpm, and oxygen saturation is 94% on room air. Her lung examination reveals scattered wheezes. Her cardiovascular examination reveals a regular rhythm with no murmurs. There is trace lower extremity edema. Her electrocardiogram (ECG) shows sinus rhythm without ST segment changes. Her laboratory values include a hemoglobin of 10 g/dl, potassium of 4.3 mEq/L, blood urea nitrogen of 46 mg/dl, and creatinine of 2.2 mg/dl.
What is the best diagnostic test for this patient
Dobutamine stress echo
- Avoid treadmill due to recent ankle fracture
- Avoid regadenoson and adenosine due to active wheezing and recurrent admission for asthma exacerbation
- Avoid contrast exposure due to renal dysfunction
A 55-year-old man is brought to the emergency department with chest pain and ST segment elevation in leads II, III and aVF.
What finding on electrocardiogram (ECG) would be associated with the highest mortality risk?
1mm STE in V1 or right precordial lead V4R
- Most sensitive marker of RV injury
Aside from vasoconstriction, what additional effect can cocaine use have which may contribute to ACS?
Cocaine may induce platelet activation which can result in thrombosis.
Achieved by cocaine induced increase in platelet factor 4 and thromboglobulin resulting in increased platelet microaggregate formation
A 65-year-old man presents to the office to establish cardiovascular (CV) care. He says he feels well except for occasional angina, which is reliably relieved by one dose of nitroglycerin. His medical history is remarkable for a myocardial infarction (MI) treated with thrombolytics 8 years prior, asthma, hypertension (HTN), and dyslipidemia. His current medications are rosuvastatin 40 mg daily, losartan 50 mg daily, carvedilol 6.25 mg twice daily, and sublingual nitroglycerin as needed. He has previously experienced bronchospasm with aspirin.
His vital signs include blood pressure 132/80 mm Hg, pulse rate 64 bpm, and respiratory rate 14 breaths/min. His CV examination reveals normal S1 and S2, as well as no murmurs. The lungs are clear. Peripheral pulses are 2+ throughout. An electrocardiogram shows inferior Q waves.
What is the most appropriate addition to his medical regimen?
Clopidogrel 75mg daily
ASA is class Ia recommendation for stable ischemic heart disease
CAPRIE (Clopidogrel vs. Aspirin in Patients at Risk of Ischemic Events) compared Clopidogrel to ASA 325 as secondary prevention and found clopidogrel superior for preventing atherosclerotic vascular events
What is MINOCA and provide one potential causative factor or example.
A clinical event that meets the universal definition of MI but is found to have non obstructive coronary arteries on angiography (<50%) and no alternative cause identified at presentation.
1. Coronary Spasm
2. Microvascular disruption
3. Plaque disruption without thrombus at time of angiography
A 56-year-old man presents to the clinic to establish care after moving to the area. He has a history of coronary artery disease and an anterior ST-segment elevation myocardial infarction (STEMI) with subsequent percutaneous coronary intervention to the left anterior descending artery 1 year earlier. He has occasional sharp pains in his left chest that are exacerbated by rotation of the thorax but no breathlessness.
His vital signs and cardiac examination findings are unremarkable. His electrocardiogram (ECG) obtained in clinic is significant for persistent mild STE in V1-V3 with associated Qwaves.
What is the best next step in management?
TTE, persistent STE after ischemic event may be indicative of LV aneurism.
A 54-year-old man is seen in the preventive cardiology clinic. He denies any cardiac symptoms. He is a prior cigarette smoker but quit 10 years previously. He has no known prior history of cardiac disease.
On examination, his heart rate is 75 bpm with blood pressure of 158/90 mm Hg. The remainder of the examination is benign. An electrocardiogram is normal. Laboratory evaluation reveals hemoglobin A1c 6.2%, C-reactive protein (CRP) 12 mg/dL, high-density lipoprotein 40 mg/dL, low-density lipoprotein 134 mg/dL, triglycerides 130 mg/dL, and total cholesterol 200 mg/dL. A coronary artery calcium (CAC) score is obtained and is 500 Agatston units.
What in the information provided about the patient is associated with highest risk for future cardiovascular events?
CAC score of 500
High CAC score (>400) has been shown to translate to higher risk for future events when compared to more traditional risk factors, even when compared to family history, ABI and high sensitivity CRP.
What are characteristics of an "unstable" or "Vulnerable" plaque?
1. Presence and thickness of Fibrous cap
2. Size of the Necrotic lipid core
3. Plaque Location (proximal or bifurcation plaques are highest risk for rupture)
A 62-year-old woman presents to the emergency department with 1 hour of chest pain. She has a history of hypertension and prior tobacco use. Her only medication is hydrochlorothiazide 25 mg daily. Her blood pressure is 152/84 mm Hg and heart rate is 92 bpm. Her physical examination is unremarkable. An electrocardiogram shows diffuse ST depressions. She is treated with aspirin, sublingual nitroglycerin, and metoprolol. Initial troponin I is 0.89 ng/mL. In anticipation of cardiac catheterization, she is given ticagrelor 180 mg.
Which part of the coagulation cascade is most directly affected by ticagrelor?
ADP- induced platelet aggregation
Ticagrelor reversibly inhibits the P2Y12 receptor distrupting platelet activation and aggregation induced by ADP
At which stage of the coagulation cascade do GPIIb/IIIa take effect (what step do they prevent)?
And give one example
Prevention of fibrin cross linking.
Abiciximab, Eptifibatide, Tirofiban
A 72-year-old woman with severe osteoarthritis of her left hip is referred for preoperative evaluation after an abnormal echocardiogram. She is asymptomatic and denies any history of heart disease. She lives independently in her single-story house but cannot walk more than 1 block due to hip pain. Her past medical history is significant for type 2 diabetes mellitus, hypertension, and hyperlipidemia. Her medications include lisinopril 40 mg daily, atorvastatin 40 mg daily, insulin glargine 20 units at bedtime. On examination she is well appearing and in no acute distress. Her blood pressure is 118/68 mm Hg, heart rate is 72 bpm, and body mass index is 21 kg/m2. Her lungs are clear, and heart has an early peaking 1/6 systolic ejection murmur heard best at the right upper sternal border. Extremities are without edema. Her echocardiogram shows hypokinesis of the inferior wall and her electrocardiogram (ECG) shows inferior Q waves.
What is the next best step in the care of this patient?
Pharmacologic MPI
Patient likely has a history of prior unrecognized MI and is high risk for silent MI, should undergo further workup.
Provide 3 factors which contribute to troponin elevation in patients with ESRD
1. Impaired troponin catabolism resulting in decreased renal clearance
2. Microvascular lesions due to ESRD
3. Direct myocyte damage due to stretching, toxicity or hypoxia
All three are components of cardiomyopathy of hemodialysis.
What are the stages of the platelet cascade in ACS?
Plaque rupture --> exposure of thrombogenic material (Tissue factor) --> Platelet adhesion --> Platelet activation --> platelet aggregation --> Clot formation
A 64-year-old man with a recent non−ST-segment elevation myocardial infarction presents to your office for a 4-week follow-up. He had been revascularized with a single drug-eluting stent to a 90% first obtuse marginal. Intravascular ultrasound was used to confirm good stent apposition without evidence of dissection. Additionally, he had a 40% stenosis in the distal left anterior descending artery (fractional flow reserve of 0.92) and moderate diffuse atherosclerosis in a nondominant right coronary artery. Echocardiography showed preserved ejection fraction (EF) without valvular abnormalities.
Since his hospital discharge, he has modified his previously-sedentary lifestyle and is now trying to walk more. He mentions several episodes of mild exertional chest pain while climbing two flights to his office. It is relieved with a few minutes of rest. Physical examination reveals heart rate 86 bpm, blood pressure 128/78 mm Hg, and pulse oximetry 99% on room air. There are normal S1 and S2 with no murmurs. Lungs are clear to auscultation bilaterally. There is no lower extremity edema. Electrocardiography in the office is notable for sinus rhythm with left anterior fascicular block. His medications include aspirin 81 mg daily, ticagrelor 90 mg twice daily, atorvastatin 80 mg daily, and metoprolol succinate 50 mg daily.
What is the best next step?
Patient now has stable angina with recent successful PCI, anti-anginal therapy should be maximized as tolerated given low risk presentation.
List all 5 components of acute myocardial infarction based on the 4th universal definition of myocardial infarction.
1. Rise and or fall of troponin with at least 1 value above the 99th percentile
2. Symptoms of ischemia
3. New ischemic ECG changes (including new Q waves)
4. Imaging evidence of loss of viable myocardium
5. Identification of coronary thrombus by angiography or autopsy.
A 55-year-old man presents to the clinic for evaluation of chest pain of 6 months' duration. He describes chest pressure and dyspnea associated with physical exertion, particularly when walking upstairs or uphill. The symptoms generally resolve within 5 minutes with rest. His medical history is notable for type I diabetes mellitus, hypertension, chronic kidney disease (stage III), active tobacco use (80 pack-year smoking history), and coronary artery disease (CAD). He had undergone stenting of the mid left anterior descending artery 10 years prior. His medications include aspirin 81 mg daily, amlodipine 10 mg daily, rosuvastatin 20 mg daily, metoprolol succinate 50 mg daily, lisinopril 20 mg daily, insulin glargine 40 units at bedtime, and an insulin sliding scale with meals.
His primary care clinician recently increased his doses of amlodipine and metoprolol succinate, with some improvement in symptoms. An exercise radionuclide myocardial perfusion imaging (rMPI) was performed the prior week. He exercised on a treadmill for 3 minutes, achieving 4 metabolic equivalents, stopping due to chest pain. There were diffuse 2 mm ST depressions noted on electrocardiography; these changes resolved 4 minutes into recovery. Perfusion imaging demonstrated normal perfusion without reversible perfusion defects.
What is the best next step in evaluation of this patient?
What is the reason for this patients MPI results?
Patient is high risk with significant ischemic symptoms, best next step is Coronary Angiography
The patient has high likelihood for balanced ischemic disease resulting in falsely normal MPI.
A 68-year-old man with hyperlipidemia and hypertension is brought to the catheterization laboratory with an anterior ST-segment elevation myocardial infarction (MI) and receives a drug-eluting stent to a culprit lesion in the left anterior descending artery with resulting Thrombolysis in Myocardial Infarction (TIMI) -3 flow. Angiography also demonstrates a 60% stenosis of the right coronary artery. His heart rate is 110 bpm and blood pressure is 80/60 mm Hg. A dopamine infusion is initiated in the catheterization laboratory and titrated to 8 mcg/kg/minute.
Post-stent deployment, his blood pressure and heart rate are unchanged. His oxygen saturation is 90% on 3 liters per minute O2. Dopamine is uptitrated to 15 mcg/kg/minute with minimal effect.
What is the next best step in the management of this patient?
- IABP placement
- Temporary mechanical support is indicated in persistent cardiogenic shock despite revascularization
- IABP is class IIa indication, Impella is class IIb