PCI in a Patient with Triple Vessel Disease (TVD)

PCI in a Patient with Triple Vessel Disease (TVD)

2D Echocardiography (14-07-2025)

• EF: 50% – mildly reduced
• RWMA: Apical cap and apical anteroseptum mildly hypokinetic
• LVH: Mild concentric
• LV Diastolic Dysfunction: Grade I (E/e’ = 11.1)
• PASP: 10–15 mmHg (Normal)
• Valves: Trivial TR, no AR/MR
• IVC: Normal, >50% collapse

Conclusion:

• Mild LV systolic dysfunction with segmental wall motion abnormality suggestive of ischemia (especially LAD territory)

Pre-procedure ECG

Rhythm:

• Sinus tachycardia (HR ~103 bpm)

Findings:

• T wave inversion in V4–V6, I, aVL
• Poor R wave progression V1–V3
• Incomplete RBBB

Interpretation:

• Suggestive of ischemia in anterior and lateral wallEmergency Decision-Making

Based on:

• Persistent symptoms despite medication
• ECG + echo evidence of ischemia
• Suspected high-risk CAD

Patient shifted for emergency coronary angiography (CAG) via right radial artery.

Coronary Angiography Findings (CAG)

Vessel Lesion

• RCA 99% proximal stenosis, 80% mid stenosis (culprit)
• LAD Total chronic occlusion (non-culprit)
• OM1 60% plaque (non-culprit)

Diagnosis: Triple Vessel Disease (TVD)

Hemodynamics during procedure: Bradycardia, hypotension, hypoxia

PCI Procedure Details

• Indication: RCA was culprit (high-grade obstruction, unstable angina, ECG changes)

Procedure:

• Two Drug Eluting Stents (DES) deployed to RCA
• Access via right radial artery

Intra-Procedural Complications:

Complication	Likely Cause	Immediate Management
Bradycardia	AV nodal ischemia (RCA territory)	Inj. Atropine 2A IV
Hypotension	Vagal response / Ischemia	Norad infusion @ 2 mL/hr
Hypoxia	Transient perfusion deficit	Nasal oxygen

Mechanism of Atropine:

• Anticholinergic: Blocks vagal stimulation to heart
• Increases SA/AV nodal activity

Mechanism of Noradrenaline:

• α1-agonist: Peripheral vasoconstriction → ↑BP
• Mild β1-effect: ↑ myocardial contractility

Post-Procedure ICU Management

• Patient shifted with radial sheath in situ
• Vitals stable post 2 hours
• No further inotropic/O2 requirement
• Sheath removed uneventfully
• ECG

Post-PCI Medications with Justification

Drug	Dose	Mechanism	Purpose
Inj.Nikoran	48 mg @ 2 mL/hr	Nitrate donor & K+ channel opener	↓ Coronary spasm, ↑ perfusion
Inj.Agramed	70 mL @ 7 mL/hr	GPIIb/IIIa inhibitor	Prevent acute instent thrombosis
Inj.Monocef	1g IV BD	3rd-gen cephalosporin	Prophylaxis (ICU setting)
Inj.Pantoprazole	40 mg IV BD	PPI	Stress ulcer prophylaxis
Inj.Emset	4 mg IV BD	5HT3 antagonist	Antiemetic
Inj.NS	50ml/hr	Hydration	Maintain perfusion & renal flow
Tab Ecosprin	75 mg OD	COX-1 inhibition	Antiplatelet
Tab Brilinta	90 mg BD	P2Y12 inhibitor	DAPT maintenance
Tab Rosuvas	20 mg HS	HMG-CoA reductase inhibitor	Stabilize plaque, ↓LDL

Clinical Reasoning

1. Why RCA was the culprit: ECG changes + echo + anginal symptoms + RCA supplies AV
   node
2. Why PCI was needed: Unstable symptoms + critical stenosis + risk of infarction
3. Why no immediate CABG: LAD CTO + RCA culprit; staged revascularization strategy
   often preferred in elderly with high-risk lesions

Final Diagnosis

• Triple Vessel Disease (TVD) with culprit RCA lesion, causing ischemic bradycardia
  and hypotension. Successfully treated by PCI with DES.
  

Teaching Mnemonic – “RCA = RAVEN”

• R – Reflex Bradycardia
• A – AV Node Ischemia
• V – Vasovagal Reflex
• E – Ectopy
• N – Nodal Supply Compromised

Suggested Discharge Plan

• Continue DAPT for 12 months
• Lifestyle changes + BP & cholesterol control
• Stress/rest perfusion scan after recovery
• Consider CABG if LAD revascularization indicated

Conclusion

• This case illustrates the importance of rapid recognition and intervention in RCArelated ischemia, especially when conduction abnormalities and hemodynamic
  compromise occur. Timely PCI salvaged the myocardium and conduction system,
  restoring perfusion and preventing major infarction.
  

Fun Fact

• In 85% of individuals, the RCA supplies the AV node. Hence, RCA occlusion
  commonly causes bradycardia and heart blocks.