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Case Study: Coronary Artery Disease (CAD)

Patient Presentation

Patient: Mr. D.K., 58-year-old male Chief Complaint: Recurrent, pressure-like chest pain radiating to the left arm and jaw for the past 3 weeks, now occurring at rest for 45 minutes.

History of Present Illness: Mr. D.K. has had exertional chest pressure for the past 6 months, which he attributed to "stress." Over the past 3 weeks, episodes have increased in frequency, duration, and now occur at rest - a pattern shift suggesting progression from stable to unstable angina. Today's episode lasted 45 minutes and was accompanied by diaphoresis, nausea, and mild dyspnea. He denies syncope or palpitations.

Past Medical History:

Type 2 diabetes mellitus (12 years, on metformin)
Hypertension (8 years, on amlodipine)
Hyperlipidemia (diagnosed incidentally 3 years ago, untreated)
Current smoker - 30 pack-years

Family History: Father died of a heart attack at age 52. Maternal uncle with "heart problems."

Social History: Sedentary desk job, high-fat diet, BMI 29.4 (overweight), occasional alcohol use.

Review of Systems: Denies fever, weight loss, hemoptysis, cough, or leg swelling.

Physical Examination

Parameter	Finding
BP	158/96 mmHg
HR	94 bpm, regular
RR	18 breaths/min
SpO2	96% on room air
Temperature	37.1°C
BMI	29.4

Cardiovascular: Mild tachycardia; no murmurs, rubs, or gallops detected. No JVD. Peripheral pulses symmetric. Respiratory: Clear to auscultation bilaterally, no crackles. Abdomen: Soft, non-tender, no organomegaly. Extremities: No peripheral edema. No xanthomas noted.

Background: Disease Overview

Definition

Coronary artery disease (CAD), also called ischemic heart disease (IHD), is the most common cause of mortality worldwide. It results from atherosclerotic obstruction of coronary arteries, creating an imbalance between myocardial oxygen supply and demand. This presents across a clinical spectrum ranging from stable angina to acute coronary syndromes (ACS). - Lippincott Illustrated Reviews: Pharmacology, p. 412

Epidemiology

Atherosclerosis and IHD have been correlated with multiple risk factors in prospective analyses, including the landmark Framingham Heart Study. These risk factors are roughly multiplicative in effect: two risk factors increase MI risk approximately 4-fold, and three factors (hyperlipidemia, hypertension, smoking) increase the rate by a factor of 7. - Robbins & Kumar Basic Pathology, p. [Table 8.2]

Pathophysiology

Atherosclerotic Plaque Formation

The underlying lesion of CAD is the atherosclerotic plaque. The process begins with endothelial dysfunction (from hypertension, dyslipidemia, smoking, or hyperglycemia), followed by:

Lipid accumulation: LDL particles enter the subendothelial space and are oxidized. High LDL ("bad cholesterol") distributes cholesterol to peripheral tissues; HDL is protective by absorbing cholesterol from arterial walls. - Guyton & Hall Textbook of Medical Physiology
Inflammatory response: Monocytes migrate in and differentiate into macrophages, engulfing oxidized LDL to form foam cells. Growth of atheroma is fueled by leukocyte trafficking and plaque hemorrhage.
Fibrous cap formation: A fibrous cap overlies the lipid-rich necrotic core. Stable plaques have thick caps; vulnerable plaques have thin caps prone to rupture.
Plaque rupture: Erosion or rupture of a vulnerable plaque exposes subendothelial proteins. Circulating platelets adhere, change shape, release thromboxane/ADP/fibrinogen, and activate GPIIb/IIIa receptors. Fibrinogen cross-links adjacent platelets, forming a platelet plug. Thrombin is then generated, converts fibrinogen to fibrin, and creates a platelet-rich thrombus. - Goldman-Cecil Medicine, p. 641

Ischemia Cascade

Subtotal occlusion → transient ischemia without myonecrosis = Unstable Angina
Subtotal occlusion + elevated troponin = NSTEMI (non-Q wave MI predominantly)
Total occlusion → ST elevation on ECG → necrosis = STEMI (Q wave MI)

ACS diagnostic pathway showing coronary thrombus morphology and ECG/biomarker differentiation of UA, NSTEMI, and STEMI

Figure: Acute coronary syndrome (ACS) - Diagnostic pathways based on ECG findings and cardiac biomarkers. - Goldman-Cecil Medicine, Fig. 57-1

Risk Factors (This Patient)

Non-modifiable

Factor	Presence in Mr. D.K.
Male sex	Yes
Age >40 years	Yes (58)
Family history	Yes (father MI at 52)

Modifiable

Factor	Status	Notes
Hypertension	Active	Increases CAD risk ≥2-fold alone
Diabetes mellitus	Active	>2-fold increased risk; with HTN = 8-fold risk
Hyperlipidemia	Untreated	LDL-driven, sufficient to cause lesions independently
Cigarette smoking	Active (30 pk-yr)	Direct endothelial toxin
Physical inactivity + overweight	Present	BMI 29.4

When hypertension, diabetes, and hyperlipidemia are all present together, the risk for atherosclerotic coronary artery disease is increased almost 20-fold. - Guyton & Hall Textbook of Medical Physiology

Diagnostic Workup

Electrocardiogram (ECG)

Findings in Mr. D.K.: ST segment depression of 1.5 mm in leads V4-V6, T-wave inversions in leads I, aVL - consistent with lateral wall ischemia (NSTEMI pattern).

STEMI = ST elevation ≥1 mm in ≥2 contiguous leads, or new LBBB
NSTEMI/UA = ST depression, T-wave inversion, or non-diagnostic ECG with biomarker elevation
Myocardial ischemia is highly likely when anginal symptoms are accompanied by ECG abnormalities (Q waves, ST depression or elevation ≥1 mm, T-wave inversion in multiple precordial leads). - Goldman-Cecil Medicine, p. 641-642

Cardiac Biomarkers

Biomarker	Finding	Interpretation
Troponin I (hs-cTnI)	Elevated at 0h and 3h	Confirms myocardial necrosis
CK-MB	Mildly elevated	Supportive
BNP	Mildly elevated	Suggests early LV strain

The presence of elevated serum troponin distinguishes NSTEMI from unstable angina. - Goldman-Cecil Medicine

Additional Testing

The following diagnostic modalities are used in CAD evaluation per Sabiston Textbook of Surgery:

Test	Purpose
Chest radiograph	Exclude pulmonary edema, cardiomegaly, aortic dissection
Transthoracic echocardiography (TTE)	Assess wall motion abnormalities, LV function (EF), valvular disease
Coronary CT angiography (CCTA)	Non-invasive visualization of coronary stenoses; excellent negative predictive value
Stress testing (exercise/pharmacologic)	Functional ischemia assessment in stable patients
Diagnostic cardiac catheterization	Gold standard - defines anatomy, stenosis severity; allows FFR/iFR measurement
FFR / iFR / OCT / IVUS	Intracoronary hemodynamic and anatomic assessment
SYNTAX score	Guides PCI vs. CABG decision in multivessel disease

In Mr. D.K.: Given active NSTEMI presentation, urgent coronary angiography was performed, revealing:

85% stenosis in the proximal LAD (left anterior descending artery)
70% stenosis in the proximal RCA (right coronary artery)
LVEF 50% (mildly reduced)

ACS Classification (Fourth Universal Definition)

Type	Mechanism
Type 1	Spontaneous plaque rupture/erosion with thrombus
Type 2	Ischemic imbalance (e.g., demand ischemia from tachyarrhythmia, severe anemia)
Type 3	Sudden cardiac death before biomarker results available
Type 4	PCI-related MI
Type 5	CABG-related MI

Mr. D.K. = Type 1 NSTEMI. - Sabiston Textbook of Surgery

Risk Stratification

TIMI Score for UA/NSTEMI (Mr. D.K. scores 5/7 - High Risk):

Age ≥65: No (1 pt)
≥3 CAD risk factors: Yes (1 pt) - diabetes, HTN, hyperlipidemia, smoking, family history
Known CAD (stenosis ≥50%): Yes (1 pt)
ST deviation ≥0.5 mm: Yes (1 pt)
≥2 anginal events in 24h: Yes (1 pt)
Aspirin use in past 7 days: No
Elevated cardiac markers: Yes (1 pt)

GRACE Score: Also calculated (incorporates age, heart rate, systolic BP, Killip class, creatinine, cardiac arrest, ST deviation, biomarkers). GRACE available at outcomes-umassmed.org/grace. - Goldman-Cecil Medicine

Differential Diagnosis

Diagnosis	Key Distinguishing Features
NSTEMI (Working Dx)	Troponin rise, ST changes, typical pain, risk factors
Unstable Angina	Troponin negative
STEMI	ST elevation or new LBBB
Aortic Dissection	BP differential between arms, "tearing" pain to back
Pulmonary Embolism	Pleuritic pain, dyspnea, hypoxia, D-dimer elevation
Pericarditis	Friction rub, positional/pleuritic pain, diffuse ST elevation
Costochondritis	Reproducible tenderness on sternal palpation
GERD / esophageal spasm	Relief with antacids, no ECG changes

Management

Immediate (Emergency)

MONA-B Protocol:

Intervention	Rationale
Morphine (cautious use)	Analgesic, reduces anxiety/catecholamines
Oxygen	Maintain SpO2 ≥94%
Nitrates (sublingual/IV nitroglycerin)	Venodilation → reduces preload and myocardial O2 demand
Aspirin 325 mg (loading)	Irreversible COX-1 inhibition → reduces TXA2-mediated platelet aggregation
Beta-blocker	Reduces HR and myocardial O2 demand (IV metoprolol acutely, oral thereafter)

Antiplatelet and Antithrombotic Therapy

The goals of treatment of non-ST elevation ACS are to prevent recurrent ischemia, prevent thrombus propagation, and stabilize the vulnerable plaque. - Goldman-Cecil Medicine, p. [treatment section]

Agent	Mechanism	Notes
Aspirin	COX-1 inhibitor, reduces TXA2	Lifelong therapy
P2Y12 inhibitor (ticagrelor, prasugrel, or clopidogrel)	Blocks ADP-mediated platelet activation	Dual antiplatelet therapy (DAPT) for 12 months post-ACS
UFH / LMWH (enoxaparin)	Thrombin/factor Xa inhibition	Short-term peri-procedural anticoagulation
GPIIb/IIIa inhibitors (tirofiban, eptifibatide)	Block fibrinogen cross-linking of platelets	High-risk/PCI patients

A 2025 individual patient data meta-analysis in The Lancet (PMID: 40902613) found that clopidogrel may be comparable to aspirin for secondary prevention in some CAD patients - an important evolving evidence update.

Revascularization

PCI (Percutaneous Coronary Intervention):

Preferred for NSTEMI/STEMI when technically feasible
Recommended within 24-48 hours for high-risk NSTEMI
Stent placement (drug-eluting stents preferred) restores coronary flow

CABG (Coronary Artery Bypass Grafting):

Preferred over PCI in: left main disease, 3-vessel disease, diabetic patients with multivessel disease (FREEDOM trial)
CABG reduces symptoms, cardiovascular events, and mortality in diabetic patients with extensive multivessel CAD. - Goldman-Cecil Medicine

In Mr. D.K.: Given 2-vessel disease and diabetes, a Heart Team discussion was held. PCI to the proximal LAD with a drug-eluting stent was performed successfully (TIMI 3 flow restored). The RCA lesion will be staged.

Guideline-Directed Medical Therapy (GDMT)

Drug Class	Agent	Mechanism/Goal
Beta-blocker	Metoprolol succinate	Reduces HR, O2 demand, post-MI mortality
ACE inhibitor / ARB	Ramipril	Reduces afterload, prevents LV remodeling
Statin (high-intensity)	Rosuvastatin 40 mg	LDL lowering, plaque stabilization, anti-inflammatory
Antiplatelet (DAPT)	Aspirin + ticagrelor	Prevent stent thrombosis, recurrent ACS
Nitrate (as needed)	Sublingual nitroglycerin	Acute angina relief

All patients with IHD should receive guideline-directed medical therapy with emphasis on lifestyle modifications (smoking cessation, physical activity, weight management) and management of modifiable risk factors (hypertension, diabetes, dyslipidemia). - Lippincott Illustrated Reviews: Pharmacology, p. 412

Medications for stable angina:

Beta-blockers (metoprolol, bisoprolol, atenolol) - first-line; reduce HR and contractility
Calcium channel blockers - dihydropyridines (amlodipine) for vasodilation; non-DHP (diltiazem, verapamil) for rate control
Nitrates - nitroglycerin (sublingual, transdermal), isosorbide mono/dinitrate (long-acting)
Ranolazine - sodium channel blocker; late INa inhibition reduces diastolic tension and O2 demand; useful as add-on therapy
Lippincott Illustrated Reviews: Pharmacology

Complications

Complication	Notes
Left ventricular dysfunction/failure	Most common serious complication
Ventricular arrhythmias (VF/VT)	Leading cause of sudden cardiac death post-MI
Mechanical complications	LV pseudoaneurysm, ventricular septal defect (VSD), papillary muscle rupture with mitral regurgitation
Cardiogenic shock	~5-10% of STEMI; high mortality
Reinfarction / stent thrombosis	Reason for mandatory DAPT
Pericarditis (Dressler's syndrome)	Autoimmune; 1-8 weeks post-MI
Heart failure (chronic)	Long-term remodeling

Sabiston Textbook of Surgery enumerates these mechanical complications as specific surgical indications.

Cardiac Rehabilitation and Secondary Prevention

Component	Goal
Smoking cessation	Single most impactful modifiable intervention
Supervised exercise program	Improves functional capacity, reduces mortality
Dietary modification	Low saturated fat, Mediterranean-pattern diet
Weight management	BMI target <25
BP control	Target <130/80 mmHg
Diabetes management	HbA1c <7%; SGLT2 inhibitors/GLP-1 agonists for CV benefit
Lipid management	LDL target <55 mg/dL (very high risk); high-intensity statin +/- ezetimibe/PCSK9i
Psychosocial support	Depression screening and treatment; a 2025 systematic review in the European Heart Journal (PMID: 40878995) highlights that depression in CAD is under-addressed in guidelines

Hospital Course and Outcome

Mr. D.K. was admitted to the cardiac care unit, placed on DAPT (aspirin + ticagrelor), anticoagulated with enoxaparin, and underwent urgent PCI with drug-eluting stent placement to the proximal LAD within 24 hours. Post-procedure TIMI 3 flow was restored. Echo at discharge showed LVEF recovery to 55%. He was discharged on day 4 with:

Aspirin 81 mg daily (lifelong)
Ticagrelor 90 mg BD (12 months)
Metoprolol succinate 50 mg daily
Ramipril 5 mg daily
Rosuvastatin 40 mg nightly
Sublingual nitroglycerin (PRN)
Metformin continued; endocrinology referral placed
Cardiac rehab enrollment
Smoking cessation counseling + varenicline prescription

Key Learning Points

CAD is atherosclerosis-driven - endothelial injury, lipid deposition, inflammation, and plaque rupture lead to thrombus formation and ischemia.
Risk factors are multiplicative: The combination of hypertension + diabetes + hyperlipidemia increases CAD risk ~20-fold. - Guyton & Hall
ACS spectrum is defined by ECG (ST elevation vs. no ST elevation) and troponin (elevated vs. negative), distinguishing STEMI, NSTEMI, and UA.
High-risk NSTEMI requires early invasive strategy (PCI within 24-48h); STEMI requires primary PCI within 90 minutes (door-to-balloon time).
GDMT is mandatory post-ACS: DAPT, beta-blocker, ACE-inhibitor, high-intensity statin, with aggressive lifestyle modification.
CABG is preferred over PCI in diabetic patients with multivessel disease and in left main disease.
Secondary prevention must address all modifiable risk factors to prevent recurrence.

Sources:

Goldman-Cecil Medicine, International Edition (2 Volume Set) - Chapter 57
Robbins & Kumar Basic Pathology - Chapter 8
Guyton & Hall Textbook of Medical Physiology - Chapter on Coronary Physiology
Lippincott Illustrated Reviews: Pharmacology - Chapter 12 (IHD)
Sabiston Textbook of Surgery - Chapter on Coronary Artery Disease and CABG
Valgimigli M et al. Clopidogrel versus aspirin for secondary prevention of CAD. Lancet, 2025. PMID: 40902613
Blatch Armon D et al. Depression and cardiovascular disease. Eur Heart J, 2025. PMID: 40878995

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Case Study: Coronary Artery Disease - Triple Vessel Disease (CAD-TVD)

Geetanjali Medical College & Hospital, Udaipur (Rajasthan)

Department of Cardiology | Radial Lounge Primary Consultant: Dr. Ramesh Patel (DM Cardiology, PGIMER Chandigarh; FACC, FSCAI USA; Professor & HOD, Cardiology, GMCH)

1. Patient Identification

Parameter	Details
Name	Mr. Fakir Mohammad
Age / Sex	63 Years 6 Months / Male
Date of Birth	01/01/1963
Address	Gosi Mohella, Pani Ki Tanki, Abu Road, Sirohi, Rajasthan
UHID	6246620
IPD No.	1207687
Admission Date	13/07/2026 at 12:03 PM
Expected Discharge	23/07/2026
Ward / Bed	Radial Lounge / MDI003
Payer	AB Scheme - Maa Yojana

2. Chief Complaints

Shortness of Breath (SOB) - on exertion, NYHA Class II
Chest pain on exertion - for 1-2 months (progressive)

3. History of Present Illness

Mr. Fakir Mohammad, a 63-year-old male with a known history of Coronary Artery Disease, Type 2 Diabetes Mellitus (T2DM), and Hypertension (HTN), presented to the Cardiology OPD on 13/07/2026 with a 1-2 month history of progressively worsening exertional chest pain and dyspnea on exertion (DOE Class II). He was already on cardiac medications including anti-anginals, antiplatelets, statins, and antidiabetics.

Given the worsening symptom burden despite medical therapy, he was advised admission for coronary angiography (CAG) in the Radial Lounge to reassess coronary anatomy and plan further intervention.

4. Past History (Relevant and Significant)

Condition	Details
Hypertension (HTN)	Known, on treatment
Type 2 Diabetes Mellitus (T2DM)	Known, on antidiabetic therapy
CAD - Anterior Wall MI (AWMI)	Prior myocardial infarction - anterior wall
P/PCI to LM-LAD	Previous PCI to Left Main and LAD in 2016
P/PCI to LAD	Repeat PCI to LAD on 18/02/2025
EF ~35-40%	Chronically reduced ejection fraction
Antipsychotic medication	On medication for sleep disturbance/psychiatric co-morbidity
No H/o	Tuberculosis, Thyroid disease, Blood disorders (Bronchial Asthma)

Clinical note: This patient has had three PCI procedures (LM-LAD 2016, LAD Feb 2025, and now planned LAD + RCA). His progressive disease despite prior revascularization is consistent with in-stent restenosis and advancing native vessel atherosclerosis in the setting of inadequately controlled risk factors.

5. Personal History

Parameter	Details
Tobacco use	H/o chewing tobacco (significant risk factor)
Alcohol	No history
Smoking	No history
Sleep	Disturbed (on antipsychotic/sleep medication)
Appetite	Normal
Bladder / Bowel	Normal

Family History: Not significant (N/S)

6. General Physical Examination

Parameter	13/07/2026	14/07/2026 (AM)	15/07/2026 (AM)
BP	120/69 mmHg	135/70 mmHg	121/61 mmHg
Pulse	79 bpm	97 bpm	70/min
RR	20/min	20/min	20/min
SpO2	-	94% on RA	96%
Temperature	Afebrile	Afebrile	Afebrile

General: No anemia, no cyanosis, no jaundice, no pedal edema, no clubbing, no lymphadenopathy, thyroid normal.

7. Systemic Examination

System	Findings
CNS	Conscious and oriented
CVS	S1 S2 heard, no added sounds documented
Respiratory	Bilateral air entry present; bilateral lungs clear (no crackles)
Abdomen	Soft, non-tender

8. Investigations

8A. Echocardiography (13/07/2026)

Parameter	Value
LVIDd	5.2 cm (dilated)
LVIDs	4.0 cm
LV End-Diastolic Volume	133 mL
LV End-Systolic Volume	70 mL
IVSd	1.4 cm (thickened)
PWd	1.3 cm (thickened)
Left Atrium	3.3 cm
Aortic root	2.9 cm
LVEF (Visual)	40-45%

Echo Impression:

CAD with Regional Wall Motion Abnormality (RWMA+)
Hypokinesia involving apical septum and apex - consistent with prior anterior wall MI territory
Moderate LV systolic dysfunction; LVEF ~40-45%
Grade I LV diastolic dysfunction
Concentric LVH (IVSd 1.4 cm, PWd 1.3 cm - from chronic hypertension)
IAS/IVS intact; no vegetation or intra-cardiac masses

Clinical significance: LVEF 40-45% places this patient in the category of HFmrEF (Heart Failure with mildly reduced Ejection Fraction). The concentric LVH reflects long-standing hypertension, while the apical hypokinesia reflects the sequela of his prior anterior MI. This makes him high-risk for arrhythmias and worsening heart failure.

8B. Lab Investigations (Ordered)

Per progress notes, the following were ordered:

CBC (Complete Blood Count) - Hb 8.20 g/dL noted (significant anemia)
TLC - 6.88 × 10³/µL
KFT (Kidney Function Tests) - serum creatinine
LFT (Liver Function Tests)
HbA1c (glycemic control assessment)
CBT (Clotting / Bleeding Time)
Chest X-Ray (CXR)

Anemia (Hb 8.20 g/dL) is a significant co-morbidity in this patient. It increases myocardial oxygen demand (type 2 MI mechanism), worsens angina, and is a bleeding risk factor with antiplatelet therapy. The team noted: "Arrange 10 PRBC" (arrange 10 units packed red blood cells - or likely 1 unit PRBC transfusion was planned).

8C. Coronary Angiography Report (13/07/2026)

Institution: GMCH, Dept. of Cardiology
Access: Right Radial Artery
Catheter: 5 Fr Tiger
Dye: Omnipaque
Aortic pressure: 120/70 mmHg
Consultant team: Dr. Ramesh Patel, Dr. Dilip Jain, Dr. Gaurav Mittal, Dr. Rohin K. Saini

Vessel	Findings
Left Main (LM)	Patent stent (from 2016 PCI) with plaque+
Left Anterior Descending (LAD)	Type III; mid 80-90% disease; patent stent (from Feb 2025 PCI)
Left Circumflex (LCx)	Chronic Total Occlusion (CTO) with retrograde supply from RCA
Right Coronary Artery (RCA)	Dominant; proximal 70-80% stenosis

Impression: CAD - Triple Vessel Disease (CAD-TVD) Advice: PCI to LAD and RCA

Anatomy summary: This is complex, high-risk anatomy. The LCx CTO receiving collateral supply from RCA means the RCA is currently providing retrograde perfusion to an entire LCx territory on top of its own. Treating the RCA with PCI (removing the 70-80% obstruction) will restore antegrade flow and protect both the RCA and LCx territories.

9. Diagnosis (Final / Working)

#	Diagnosis
1	CAD - Triple Vessel Disease (CAD-TVD)
2	Prior AWMI (Anterior Wall Myocardial Infarction)
3	Post PCI to LM-LAD (2016)
4	Post PCI to LAD (18/02/2025)
5	Moderate LV Systolic Dysfunction (LVEF 40-45%)
6	Type 2 Diabetes Mellitus (T2DM)
7	Hypertension (HTN)
8	Symptomatic Anemia (Hb 8.2 g/dL)

10. Progress Notes Summary

Date	Vitals	Plan
13/07/2026 (Eve)	BP 135/70, P 97, RR 20, SpO2 94% RA	CAG done. Findings: CAD-TVD. Plan: PCI to LAD + RCA. CNS examination - normal
14/07/2026 (AM)	BP 130/68, HR 68, RR 16, Temp afebrile, SpO2 94% RA	Advise: CBC, KFT, LFT, HbA1c. Arrange PRBC. Plan: PCI to LAD + RCA
15/07/2026 (AM)	BP 121/61, HR 70, RR 20, SpO2 96%	CBT, CBC, KFT, LFT, HbA1c. Plan: PCI to LAD + RCA

11. Medications (Current - Prescribed 13/07/2026 by Dr. Ramesh Patel)

#	Drug (Brand)	Composition	Dose	Timing	Rationale
1	Rozucor Gold 20mg	Aspirin 75mg + Clopidogrel 75mg + Rosuvastatin 20mg	0-0-1	9 PM daily	DAPT (dual antiplatelet) + statin for CAD secondary prevention
2	Sitaxa DM 10/100/500mg	Dapagliflozin 10mg + Metformin 500mg + Sitagliptin 100mg	0-1-0	Before lunch	Triple antidiabetic; SGLT2i (dapagliflozin) adds cardiovascular mortality benefit in CAD + T2DM
3	Met XL R 25/2.5mg	Metoprolol 25mg + Ramipril 2.5mg	1-0-0	9 AM	Beta-blocker (reduces HR/O2 demand) + ACEi (reduces LV remodeling, controls BP)
4	Renuca 500mg	Ranolazine 500mg	1-0-1	After breakfast + dinner	Anti-anginal (late INa inhibitor); reduces diastolic tension, relieves chronic angina
5	Monit GTN 2.6mg	Nitroglycerin 2.6mg (sustained release)	1-1-0	8 AM + 4 PM	Nitrate for angina prophylaxis; reduces preload and O2 demand
6	Pantocid DSR	Pantoprazole 40mg + Domperidone 30mg	1-0-0	7 AM	Gastroprotection (PPI) given dual antiplatelet therapy

Pharmacology note: Dapagliflozin (SGLT2 inhibitor) in this patient is particularly important. In the DAPA-HF trial, dapagliflozin reduced cardiovascular death and worsening heart failure in patients with HFrEF/HFmrEF regardless of diabetes status. This patient's LVEF of 40-45% and T2DM make him a strong candidate. - Lippincott Illustrated Reviews: Pharmacology

12. Pathophysiology Applied to This Patient

Why Did the Disease Progress Despite Prior PCI?

In-stent restenosis / disease progression: The 2016 LM-LAD stent is patent but has plaque accumulation. The 2025 LAD stent is also patent but has developed mid-vessel 80-90% disease distal to it. This represents progressive native vessel disease.
Inadequately controlled risk factors: Ongoing T2DM, HTN, and tobacco chewing (a significant risk factor even without cigarette smoking - causes endothelial injury and platelet activation) drive continued atherosclerotic progression.
LCx CTO: Complete occlusion of the circumflex likely occurred gradually. Retrograde collateral supply from the dominant RCA is maintaining viability of the LCx territory - this is a protective mechanism (collateral circulation).
Reduced EF (35-45%): Result of the prior anterior wall MI (apical septum + apex hypokinesia on echo), representing permanent scar from the AWMI. The remaining viable but ischemic myocardium is at risk if the LAD disease and RCA stenosis are not treated.
Concentric LVH: Driven by long-standing hypertension. This reduces LV compliance (Grade I diastolic dysfunction), increases O2 demand, and worsens the supply-demand mismatch.

13. Planned Procedure: PCI to LAD and RCA

Indication: Symptomatic CAD (exertional chest pain + dyspnea) despite GDMT, with angiographically severe multivessel disease (LAD 80-90%, RCA 70-80%).

Approach: Right Radial Artery access (already used for diagnostic CAG - reduces bleeding risk vs. femoral access, allows early ambulation).

Procedural considerations:

LAD PCI: Mid-vessel 80-90% lesion (Type III vessel). Likely requires drug-eluting stent (DES). Prior stent is patent - this is a new lesion.
RCA PCI: Proximal 70-80% stenosis in a dominant RCA. Critical to treat - this vessel also supplies the LCx territory retrograde. Successful PCI will restore flow to two territories.
LCx CTO: Not planned for intervention in this admission (complex; CTO PCI carries higher risk and requires specialized retrograde approach techniques).

Pre-procedure preparation:

Ensure adequate antiplatelet loading (aspirin + clopidogrel already on board via Rozucor Gold)
Correct anemia (Hb 8.2 - arrange PRBC transfusion pre-procedure to reduce type 2 ischemia risk)
Optimize glycemic control (HbA1c pending)
KFT / creatinine clearance - for contrast dosing (dye load calculation, risk of contrast nephropathy)

14. Key Learning Points from This Case

#	Learning Point
1	CAD-TVD with prior AWMI represents an advanced, high-risk phenotype. Multiple prior PCIs do not prevent disease progression if underlying risk factors (DM, HTN, tobacco) are uncontrolled.
2	LCx CTO with retrograde collateral supply from RCA illustrates the importance of the dominant RCA in collateral circulation - treating the RCA stenosis protects two territories simultaneously.
3	LVEF 40-45% (HFmrEF) - Moderate LV dysfunction in this patient is irreversible (scar from AWMI) + potentially reversible (hibernating myocardium in ischemic zones). Successful revascularization may partially improve EF.
4	Concentric LVH + Grade I diastolic dysfunction from chronic hypertension co-exists with systolic dysfunction - a "double burden" on this heart.
5	Anemia (Hb 8.2 g/dL) is a type 2 MI trigger (increased demand, decreased supply) and must be corrected before intervention. It also increases bleeding risk on DAPT.
6	Tobacco chewing (without cigarette smoking) is a recognized independent cardiovascular risk factor - platelet activation, endothelial injury, and nicotine-mediated vasospasm.
7	Ranolazine is appropriately added for chronic angina refractory to nitrates and beta-blockers - late INa inhibition reduces diastolic wall tension and O2 consumption.
8	SGLT2 inhibitor (Dapagliflozin) in CAD + T2DM + reduced EF provides triple benefit: glycemic control, heart failure risk reduction, and renal protection.
9	Radial access for PCI reduces vascular complications vs. femoral access in a high-risk patient on DAPT.

Hospital: Geetanjali Medical College & Hospital, Udaipur, Rajasthan Consultant Team: Dr. Ramesh Patel (HOD Cardiology), Dr. Dilip Jain, Dr. Gaurav Mittal, Dr. Rohin K. Saini, Dr. Manisha Sir, Dr. Megha

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