Coronary Artery Disease Flashcards
(53 cards)
What is stable angina, and how does it develop?
Stable angina results from fixed atherosclerotic plaques in coronary arteries causing a mismatch between oxygen supply and demand during exertion, where oxygen demand exceeds supply. This is caused by a gradual narrowing of heart blood vessels by atherosclerosis and becomes symptomatic after about 75% stenosis.
What is the most common underlying cause for coronary artery disease?
Atherosclerosis
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Put in context, Diabetes > smoking > HTN, are the most acceleratory (i.e., worst) risk factors for atherosclerosis. Patients with diabetes are managed as a cardiovascular disease equivalent.
What are the major and minor risk factors for coronary artery disease (CAD) collectively?
Most common:
- Atherosclerosis
Most severe:
- Diabetes
Other Major Risk Factors:
- Smoking
- Hypertension
- Hyperlipidemia
- Family history of premature of CAD (<45 men and <55 women)
- Family history of MI (men <55 and <65 in females)
Other Minor Risk Factors:
- Low HDL
- Obesity
- Sedentary lifestyle
- Stress
- Alcohol excess
- ESRD
- HIV
- mediastinal radiation
A 55-year-old woman comes to the office due to exertional dyspnea for 3 months. The patient has had no chest pain. Medical history is significant for hypertension and chronic kidney disease. Medications include furosemide, amlodipine, and lisinopril. The patient has never smoked cigarettes. Temperature is 37 C (98.6 F), blood pressure is 128/80 mm Hg, and pulse is 80/min. Oxygen saturation is 98% on room air. BMI is 27. There is no jugular venous distension. Cardiopulmonary examination is normal. Trace bilateral pedal edema is present. Laboratory studies are as follow:
Hemoglobin 10.8 g/dL, Blood urea nitrogen 38 mg/dL, Serum creatinine 2.2 mg/dL, Estimated glomerular filtration rate 28 mL/min/1.73. ECG is unremarkable. Chest x-ray reveals clear lung fields. Which of the following is the most appropriate next step in management of this patient?
Patients with chronic kidney disease (CKD) are at increased risk of coronary artery disease (CAD) and cardiovascular events. Physicians should have a low threshold for pursuing cardiac stress testing (eg, stress echocardiography) in CKD patients with atypical CAD symptoms (eg, exertional dyspnea). Chronic kidney disease (CKD) independently increases the risk for coronary artery disease (CAD) and cardiovascular events. This association may be due to altered calcium balance (eg, secondary hyperparathyroidism) leading to arterial calcium deposition and accelerated atherosclerosis, loss of protein in the urine facilitating an unfavorable lipid profile (ie, high LDL/HDL ratio), or increased systemic inflammation contributing to accelerated atherosclerosis and instability of atherosclerotic plaques. Although symptomatic CAD usually presents with typical symptoms (ie, anginal chest pain), patients with CKD, particularly women, are more likely to have atypical symptoms (eg, anginal equivalents such as dyspnea or nausea). Therefore, high suspicion should exist for stable angina in this patient with several months of exertional dyspnea (a possible “anginal equivalent” in the setting of CKD and other risk factors for CAD (eg, hypertension). Cardiac stress testing in the form of stress echocardiography or treadmill stress testing is most appropriate.
What is the number one modifiable risk factor for CAD?
Smoking. Smoking cessation results in the greatest immediate improvement in a patient for CAD. Within one year after stopping smoking the risk of CAD decreases by 50% and within two years after stopping smoking the risk is reduced by 90%. This means that of all risk factors for CAD, including diabetes mellitus, hypertension, hyperlipidemia, and weight loss management, smoking is the number one modifiable risk factor in patients with CAD.
What is the role of HDL and LDL in CAD risk?
High LDL increases plaque formation; low HDL reduces reverse cholesterol transport and worsens CAD risk.
How does diabetes mellitus impact CAD risk?
Diabetes accelerates atherosclerosis and is considered a CAD equivalent for the justifiable rationale of being the most severe risk factor for the development of CAD. Diabetes works as a synergistic component with considering other risk factors. When considering concomitant conditions such as hypertension (which is a stand alone risk factor for CAD), the need for blood pressure control amplifies in importance. Thus patients with diabetes should keep their blood pressure below 140/90 mmHg. Diabetics with nephropathy (proteinuria ≥500 mg/day) have a recommended blood pressure of <130/80 mmHg .
In diabetic patients, does tight glycemic control reduce the risk for developing coronary heart disease or stroke?
No. Tight glycemic control does mitigate this risk of developing microvascular disease (retinopathy, nephropathy, and neuropathy), however, does not lower the risk of macrovascular disease (stroke or coronary heart disease).
What makes diabetes the most significant risk factor in terms of CAD?
The risk of mortality is equivalent to patients with established coronary heart disease and prior MI.
How does smoking mitigate the development of coronary heart disease?
Smoking is an important modifiable CHD risk factor. Most studies have shown that the most significant increase in CHD risk is in patients smoking ≥1 packs daily. The risk of cardiovascular events declines rapidly after smoking cessation and approaches that of nonsmokers in 2-3 years.
What prognostic factors are associated with worse outcomes in CAD?
- Left ventricular EF <50%.
- Left main or multi-vessel disease.
- Higher Killip classes at presentation (e.g., heart failure, cardiogenic shock) are directly linked to increased short-term mortality.
- Extent of ischemia on stress testing: The larger the area of ischemia, the worse the prognosis.
- Age: Older age is a risk amplifier due to cumulative atherosclerotic burden and comorbidities but is less predictive than EF and Killip class.
What factors predict mortality in ACS patients?
- Older age.
- Higher Killip class.
- Reduced EF.
- Extent of myocardial damage on imaging.
What are the typical symptoms of stable angina pectoris?
Substernal pressure or tightness lasting 1-5 minutes, worsened by exertion or stress, and relieved by rest or nitroglycerin.
How does exertion trigger angina symptoms?
Exertion increases myocardial oxygen demand, unmasking ischemia due to fixed coronary stenosis.
What is the significance of angina that improves with rest or nitroglycerin?
Relief with rest or nitroglycerin suggests ischemia and helps differentiate from non-cardiac causes.
What are the key steps in clinically managing patients with CAD presenting with chest pain?
Patients with suspected ACS should be given aspirin 325 mg (if not already administered) and can be given sublingual nitroglycerin if experiencing active chest pain. Further evaluation should consist of troponin I levels and, in the setting of ongoing chest pain, serial ECGs approximately every 30 minutes. The general recommendation is the collection of at least 2 troponin levels 3 hours apart, keeping in mind that levels may require up to 6-12 hours from the onset of symptoms to become detectable. Patients with significantly elevated troponin levels are diagnosed with non-ST elevation myocardial infarction, and those with negative troponin levels but ongoing chest pain and/or evolving ischemic ECG changes may be diagnosed with unstable angina. Patients with negative troponin levels and no other clinical suggestion of ACS can be discharged with a diagnosis of noncardiac chest pain or undergo stress testing for further evaluation.
A 62-year-old man presents to the emergency department for evaluation of chest pain. The patient reports that he was lifting heavy boxes at work when he suddenly became nauseous, and sweaty, and developed substernal chest discomfort radiating down his left arm. The patient states that the pain has been persistent. Past medical history includes hypertension, hyperlipidemia, diabetes, and a 10-pack year smoking history. Temperature is 37°C (98.6°F), blood pressure is 100/71 mmHg, pulse is 89/min, respiratory rate is 14/min, and oxygen saturation is 99% on room air. The patient appears clammy and pale. Physical examination is otherwise unremarkable. Defibrillator pads are placed, and IV access is established. Initial laboratory results and electrocardiogram are shown below. A platelet P2Y 12 receptor blocker is administered. Laboratory values: Hemoglobin 13 g/dL, White blood cell count (WBC) 16,000/mm^3
and Troponin 120 ng/mL. What is next best step in management?
This patient has low blood pressure, therefore administration of nitroglycerin may worsen his clinical condition. Administration of aspirin and heparin is a more appropriate therapy. All patients with NSTEMI should receive aspirin, heparin, and a platelet P2Y12 receptor blocker unless there are contraindications, as well as cardiac catheterization for definitive management with revascularization. This patient presents with features of acute coronary syndrome (ACS). He has evidence of ischemic changes on his electrocardiogram (anterolateral ST-depressions) and an elevated troponin level, confirming a non-ST elevation myocardial infarction (NSTEMI). The next best step in management is administration of aspirin and heparin, in addition to a platelet P2Y12 receptor blocker and cardiac catheterization with revascularization if needed. Coronary artery disease (CAD), is caused by atherosclerosis of the coronary arteries, which occurs when plaque builds up in the vessels, eventually narrowing the lumen, and causing a mismatch between oxygen supply and demand of the heart. Over time, reduced oxygen supply can lead to myocardial ischemia or infarction. The acute management for all patients with suspected ACS involves assessment of stability including airway, breathing, and circulation. Patients should be placed on continuous cardiac telemetry, be given supplemental oxygen, and have cardiac defibrillator pads placed in the event the patient develops a shockable arrhythmia. All patients that have evidence of STEMI, NSTEMI, or unstable angina should receive aspirin therapy if there are no contraindications (e.g. recent gastrointestinal bleed), as early administration has been shown to decrease mortality. In addition, patients with NSTEMI should be given heparin, additional antiplatelet therapy, as well as cardiac catheterization with revascularization if needed.
What features help differentiate ischemic chest pain from other causes like musculoskeletal pain?
Ischemic pain is poorly localized, non-reproducible by palpation, and not positional or pleuritic.
What are the indications for performing a stress test in suspected CAD?
Stress testing is used to confirm CAD diagnosis, assess severity, and evaluate therapy response or risk stratification. Pretest probability may help guide management, particularly for the patients with nonspecific or no changes on ECG in an at risk age category, and with or without risk factors.
What would preclude a patient from being able to perform an ECG Stress Test?
Patients who have baseline ECG abnormalities such as left bundle branch block, pre-existing ST segment changes, or left ventricular hypertrophy. Stress testing is only performed on those who can actually perform the test and without ECG findings at presentation. Exercise stress ECGs has the highest sensitivity for those who are able to exercise and have a normal ECG at baseline, thus is the initial test for normal baseline ECG.
How is an exercise stress ECG performed, and what findings indicate ischemia?
Patients are stressed with exercise to increase their heart rate to 85% of maximum predicted for their age where the maximum heart rate is calculated by subtracting age from 220.
What would indicate a positive stress test?
ST-segment changes; >1 mm depression indicates ischemia.
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Sudden onset of heart failure.
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ventricular arrhythmia.
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Hypotension.
What are the advantages of stress echocardiography over an exercise ECG?
Stress echo detects wall motion abnormalities and is preferred in patients with baseline ECG changes.
How is a stress echo performed?
An echo is done before and after exercise.
