Medicine, via pristina

Medicine, via pristina

Coronary Artery Disease (CAD)

1. Knuuti J, Wijns W, Saraste A, Capodanno D, Barbato E, Funck-Brentano C, et al. 2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes. Eur Heart J. 2020;41(3):407-477.
PMID: 31504439
DOI: https://doi.org/10.1093/eurheartj/ehz425


2. Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas AP, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease. J Am Coll Cardiol. 2012;60(24):e44-e164.
PMID: 23182125
DOI: https://doi.org/10.1016/j.jacc.2012.07.013


3. Khan MA, Hashim MJ, Mustafa H, Baniyas MY, Al Suwaidi SKBM, AlKatheeri R, et al. Global epidemiology of ischemic heart disease: Results from the Global Burden of Disease Study. Cureus. 2020;12(7):e9349.
PMID: 32742886
DOI: 10.7759/cureus.9349


4. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39(2):119-177.
PMID: 28886621
DOI: https://doi.org/10.1093/eurheartj/ehx393


5. Amsterdam EA, Wenger NK, Brindis RG, Casey DE Jr, Ganiats TG, Holmes DR Jr, et al. 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2014;64(24):e139-e228.
PMID: 25260716
DOI: https://doi.org/10.1016/j.jacc.2014.09.017

Background 

Coronary Artery Disease (CAD) refers to the narrowing or blockage of coronary arteries due to atherosclerosis, resulting in reduced blood flow to the myocardium. This ischemia may lead to angina, myocardial infarction, heart failure, or sudden cardiac death.  

CAD is also known as ischemic heart disease (IHD) or atherosclerotic heart disease. 

 Classification/Types  

Coronary Artery Disease (CAD) is categorized into: 

  • Stable Angina (Angina Pectoris): Predictable chest pain with exertion, relieved by rest or nitroglycerin.  
  • Acute Coronary Syndromes (ACS):  

      I) Unstable Angina (UA): New  or worsening chest pain, 

          not relieved by rest. 

     II) Non-ST-Elevation Myocardial Infarction (NSTEMI): 

        Chest pain at rest with elevated cardiac enzymes and no ST  

        elevation.  

       III) ST-Elevation Myocardial Infarction (STEMI)

        Chest pain at rest with elevated cardiac enzymes and ST elevation. 

Epidemiology  

  • Sex: CAD is more common in men until women reach menopause, then risk equals  
  • Age: Typically >45 years in men, >55 years in women  
  • Race/Region: Higher in South Asians, African Americans; developed countries  
  • Socioeconomic status: Increased in low SES due to risk factor clustering 

Despite advances in prevention and treatment, CAD remains the leading cause of death globally and in the United States, accounting for approximately 1 in every 5 deaths. (ACC/AHA 2023 CCD Guideline)

Etiology 

Coronary Artery Disease is caused by atherosclerosis of the coronary arteries due to endothelial injury and lipid deposition leading to plaque formation and vascular narrowing.  

Risk Factors  

I)Modifiable:   

          -Hypertension   

          -Diabetes mellitus (DM)  

          -Hyperlipidemia  

          -Smoking  

          -Obesity  

          -Sedentary lifestyle, poor diet, stress  

II) Non-modifiable:

           -Age (men above age 45, women above age 55) 

           -Sex (males)  

           -Family history of premature CAD (men less than 55 years,  

            women more than 65 year of age)  

  • Others: Chronic inflammatory states (e.g., lupus), chronic kidney disease 

Clinical Presentation 

I) History (Symptoms)

  • Stable Angina (Angina Pectoris): Exertional chest pain (pressure-like), relieved by rest or nitroglycerin  
  • Acute Coronary Syndrome (ACS):  
  • Chest pain at rest or with minimal exertion  
  • Radiation to left arm, jaw, or back  
  • Associated symptoms: dyspnea, diaphoresis, nausea, dizziness, palpitations  

Note: Women, older adults, and patients with diabetes are more likely to present with atypical symptoms, including dyspnea, fatigue, nausea, or epigastric pain rather than classic chest pain.

II) Physical Exam (Signs)

Coronary artery disease (CAD) may not always have specific physical exam findings, especially in stable or early stages. However, certain signs can suggest CAD itself, its risk factors, or complications such as heart failure or prior myocardial infarction. 

  • General Appearance
  •   -Anxious, diaphoretic during angina 
  •   -Pale or cool skin in acute ischemia 
  • Vital Signs
  •   -Hypertension or hypotension (esp. in MI) 
  •   -Tachycardia or bradycardia 
  •   -Low-grade fever post-MI 
  •   -Narrow pulse pressure (LV dysfunction) 
  • Cardiac Exam
  •   -Inspection: Levine sign, JVD in heart failure 
  •   -Palpation: Displaced point of maximal impulse (PMI), heaves/thrills 
  •   -Auscultation
  • ∼S4: Stiff ventricle (eg, in chronic HTN, HFpEF) 
  • ∼S3: Volume overload (eg, in HFrEF) 
  • New murmur (e.g., MR) 
  • ∼Pericardial rub (pericarditis) 
  • Diminished heart sounds (pericardial effusion, severe LV failure) 
  • Pulmonary
  •   -Crackles/rales (pulmonary congestion) 
  •   -Wheezing (cardiac asthma) 
  •   -Dullness/decreased breath sounds (effusion) 
  • Peripheral Vascular
  •   -Diminished pulses, carotid/femoral bruits 
  •   -Peripheral edema 
  •   -Cool extremities 
  • Skin & Extremities
  •   -Xanthelasma/xanthomas (hyperlipidemia) 
  •   -Cyanosis, mottling (low cardiac output) 

Diagnostic Tests 

Initial Tests  

I) Electrocardiogram (ECG):  

Best initial test for chest pain (look for ST changes, arrhythmias).  

  • ECG in Different CAD Presentations:  

A) Stable Angina

  • Normal at rest  
  • May show:  
  • Non-specific ST-T changes  
  • LVH, prior MI evidence (Q waves)  
  • Exercise Stress Testing is used to detect ischemia  

B) Unstable Angina (UA) / NSTEMI 

  • ST-segment depression   
  • T-wave inversion  
  • No ST elevation  
     
  • Cardiac enzymes (CK-MB, troponins) help differentiate UA (normal CK-MB, troponins) from NSTEMI (elevated troponin)  

C) ST-Elevation Myocardial Infarction (STEMI)

  • Persistent ST-segment elevation in two or more contiguous leads  
  • Q waves (develop later) = transmural infarction  
  • Indicates complete coronary artery occlusion → emergent reperfusion needed  

  

Localizing MI with EKG  

MI Location  EKG Leads  Artery Involved  
Anterior  V1–V4  Left Anterior Descending (LAD)  
Lateral  I, aVL, V5, V6  Left Circumflex (LCx) or diagonal  
Inferior  II, III, aVF  Right Coronary Artery (RCA) or LCx  
Posterior  V7–V9 (optional leads)  RCA or LCx  
Right Ventricular  V4R (right-sided lead)  Proximal RCA  

   

II) Cardiac enzymes (Troponins, CK-MB):  

Cardiac enzymes (biomarkers) are primarily used to diagnose myocardial infarction (MI). When a patient presents with acute chest pain, the goal is to determine if myocardial injury has occurred — which is when cardiac enzymes become essential.  

Are gold standard for myocardial infarction evaluation after initial EKG.  

Key Cardiac Biomarkers  

Biomarker  Rise Time  Peak Time  Return to Normal  Source  
Troponin I/T  3–6 hrs  12–24 hrs  7–14 days  Cardiac myocytes (specific)  
CK-MB  3–6 hrs  12–24 hrs  2–3 days  Cardiac + skeletal muscle  
Myoglobin  1–2 hrs  6–9 hrs  24 hrs  Nonspecific (muscle)  

  

A) Troponins (I & T) 

Are gold standard for detecting myocardial injury. Highly sensitive and specific for cardiac muscle necrosis. Elevated in NSTEMI and STEMI, but not in unstable angina.  

Serial measurements (typically at 0, 3, and 6 hours) help confirm rising or falling levels → key to diagnosis of acute MI.  

B) CK-MB 

Less specific than troponin; elevated in skeletal muscle injury.  

Preferred to detect reinfarction (second MI within days), as it returns to baseline quicker than troponin.  

C) Myoglobin

Very early marker; rises before troponin.  

Not specific for cardiac tissue → mostly used to rule out MI early due to its rapid normalization. 

II) Stress Testing: 

Stress testing, in stable patients, identify who may benefit from further testing or revascularization. The types of stress testing are exercise stress testing (EST), stress echocardiography, and nuclear stress test.  

  

A) Exercise stress test is best for patients with normal resting ECG, low to intermediate   pretest probability, and ability to exercise. 

  

B) Stress Echocardiography combines exercise or pharmacologic stress with   echocardiography. It detects new wall motion abnormalities during stress (suggesting   ischemia), using dobutamine (increases HR and contractility). Stress echo is useful for patients unable to exercise or those with abnormal baseline ECG. 

   

C) Nuclear Stress Test (Myocardial Perfusion Imaging) uses radioactive tracers (e.g., technetium-99m, thallium-201) to assess blood flow at rest and stress. Perfusion defects suggest ischemia or infarction. Pharmacologic agents used are: adenosine, regadenoson, dipyridamole (vasodilators). It is useful in baseline ECG abnormalities (e.g., LBBB, LVH) or inability to exercise 

III) Coronary angiography:   

Provides definitive diagnostic evaluation for CAD. Also called cardiac catheterization, coronary angiography is an invasive diagnostic procedure used to visualize the coronary arteries, evaluate the degree of stenosis, and guide management of suspected or known CAD, when diagnosis is unclear after noninvasive testing (equivocal stress test) or when urgent revascularization is needed.  

Therapeutically, it provides Percutaneous Coronary Intervention (PCI) (eg, stenting), Ballon Angioplasty, and assessment for Coronary Artery Bypass Grafting (CABG).  

   

Additional Testing 

  • Complete blood count (CBC) 
  • Comprehensive metabolic panel (CMP)  
  • Lipid panel  
  • Chest X-ray (to rule out alternative causes of chest pain)  
  • ABG if hypoxic  
  • BNP (if heart failure suspected)  
  • Type and crossmatch (in case of cath/blood loss)  
  • Coagulation panel (PT, INR) [before anticoagulation or surgery] 
  • Urine drug screen (if young or unclear etiology) 

 

 Treatment 

I) Stabilize if Unstable (ACS):

  • ABC approach  
  • Oxygen (if hypoxic, O2 <90%), 2 large-bore IVs for shock states  
  • Telemetry and cardiac monitoring 
  • Aspirin 325 mg PO chewed  
  • Nitroglycerin (unless hypotensive or inferior MI)  
  • Morphine (if pain persists)  
  • Beta-blockers (if no contraindications)  
  • Heparin/enoxaparin  
  • P2Y12 inhibitors (clopidogrel/ticagrelor)  
  • High-intensity statin  
  • Move to ICU or cath lab  
  • Cardiology consults for possible PCI or CABG  

II) If Stable:

  • Lifestyle modification  
  • Daily aspirin + statin + beta-blocker + ACEi (if hypertensive or diabetic)  
  • Antianginals: nitrates, calcium channel blockers (for vasospasm or refractory angina)  
  • Risk factor control: glucose, lipids, smoking cessation  
  • Consider stress testing and elective angiography  

Consults 

  • Cardiologist: All ACS, refractory or high-risk stable angina  
  • Nutritionist: Heart-healthy diet planning (eg, DASH diet
  • Social Worker: For medication access, transportation, insurance, substance use support  

Patient Education  

Counseling:  

  • Smoking cessation  
  • Diet: low saturated fats, DASH or Mediterranean  
  • Exercise: 30 min/day, 5x/week  
  • Medication adherence  

Screening:  

  • Lipid panel, blood pressure, HbA1c (diabetics)  

Vaccines:  

  • Influenza, pneumococcal, Tdap

Follow-Up 

  • Cardiology and primary care follow-up in 1 week (post-discharge)  
  • Monitor BP, lipid panel, renal function, treatment adherence  
  • Cardiac rehab referral 

 

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