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 males 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

Pathophysiology

Coronary artery disease develops due to atherosclerosis, a chronic inflammatory process affecting the coronary arteries. It begins with endothelial injury—caused by risk factors such as hypertension, smoking, diabetes, and hyperlipidemia—which leads to increased vascular permeability and leukocyte adhesion.

Low-density lipoprotein (LDL) cholesterol infiltrates the intima, becomes oxidized, and triggers an inflammatory response. Macrophages engulf oxidized LDL, becoming foam cells, which accumulate and form fatty streaks. Over time, smooth muscle cells proliferate and deposit extracellular matrix, forming a fibrous cap over a lipid-rich core—this is the atheromatous plaque.

As plaques grow, they narrow the arterial lumen, reducing blood flow and causing myocardial ischemia during increased oxygen demand (e.g., exertion). If a plaque ruptures, it can trigger thrombus formation, leading to partial or complete occlusion of the coronary artery, resulting in acute coronary syndromes like unstable angina or myocardial infarction.

 

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 

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

  1.  

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 (before anticoagulation or surgery) 
    • Urine drug screen (if young or unclear etiology)
 

Treatment

I) Stabilize if Unstable (ACS):

      • ABC approach 
      • Oxygen (if hypoxic), 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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