Ischemic Heart Disease (IHD) for NEET SS: Complete Study Guide

At two in the morning, a 52-year-old man with diabetes enters your emergency room. diaphoretic. holding onto his chest. claims to have experienced "heaviness" for four hours. You take an ECG. Just a few T-wave inversions in V1–V4, no ST elevation. Troponin returns at 0.8 ng/mL.

Your senior gives you a look. "NSTEMI or unstable angina? What's his GRACE score? Cath in 2 hours or 24 hours?"

You pause.

NEET SS questions are specifically made to take advantage of this hesitancy. It doesn't matter if you are aware that IHD exists—of course, you are—but rather if you are aware of its gradations. On the spectrum, where does this patient fall? What is required of him in his position?

For thirty years, I've seen stable angina, unstable angina, NSTEMI, STEMI, cardiogenic shock, mechanical consequences, and secondary prevention are likely the six or seven subjects covered in trench coats. From this category, NEET SS presents you with four to six questions, each of which tests a different concept.

Since 2019, I have observed that examiners have shifted from asking "what is the ECG finding in anterior MI" (which is too simple) to asking decision-point questions. When will you take this patient to the catheter? Which P2Y12 inhibitor and under what circumstances? Papers are reflecting the many revisions made to the 2023 ESC ACS guidelines. Residents struggle with this. Let's make that right.

IHD is not a single concept.

Pathophysiology of Coronary Artery Disease: Understanding Plaque Morphology

The behavior of coronary artery disease is solely dependent on the appearance of the plaque, not how much it is blocking. This is something that most textbooks hide in chapter three, but ought to be on page one.

A thick fibrous cap and a 70% stenosis? That is your patient, who has had stable exertional angina for eight years. He uses GTN spray, gets out of breath while going uphill, and is likely to die from something else.

A 40% stenosis with a large lipid core, a thin cap, and fibrous tissue being chewed by macrophages? That's your time bomb. It could rupture at rest on Tuesday of next week, resulting in a massive anterior STEMI.

The degree of stenosis doesn't predict acute episodes. The morphology of plaques does.

The lipid core strikes the bloodstream when a weak plaque bursts. The clotting cascade is triggered by tissue factor. Platelets accumulate. A thrombus is now present in a coronary artery.

You acquire unstable angina or non-ST elevation myocardial infarction (NSTEMI) if that thrombus is partial. You get STEMI if it's complete (no flow).

We treat them differently because of this. STEMI indicates that the artery is currently totally stopped. Your heart kills every minute you wait. NSTEMI indicates that there is still a small amount of flow; you have hours rather than minutes to take action. Different tempo, same illness.

IHD Spectrum: Stable Angina vs Unstable Angina vs NSTEMI vs STEMI

I'll give you the table, but don't just memorize it. Understand what each column means:

How to Differentiate Unstable Angina from NSTEMI

Troponin is the only test used to distinguish between unstable angina and NSTEMI. same pathophysiology. The same ECG options. Same management at first. Whether or not cardiac cells have died (troponin leak) is the only distinction.

I've observed intelligent locals overanalyzing this. Avoid doing so. NSTEMI is defined as troponin positive with ACS presentation. Angina that is unstable is troponin negative. That's all.

Chronic Coronary Syndromes: Diagnosis and Management

Clinical Features of Angina Pectoris

Angina pectoris was first reported by William Heberden in 1768, and his description is still valid today. Three characteristics:

• Substernal discomfort (heaviness, pressure, and infrequently "pain")
• Caused by physical strain or psychological stress
• Relieved in a matter of minutes by nitrates or rest

Typical angina is all three. Atypical = two. Non-anginal = one or none.

This is significant since your entire diagnostic strategy is based on pre-test likelihood. A stress test adds very little to the pre-test probability (>90%) of a 62-year-old male smoker with classic angina. You suspect CAD even if the test is negative. Angiography is probably necessary for him.

A woman in her 32s who has unusual chest pain but no risk factors? Perhaps 3% is her pre-test probability. Here, a negative stress test is quite comforting.

Diagnostic Tests for Stable Angina: Which Test for Which Patient?

This is immediately questioned. Understand the reasoning:

Exercise ECG Testing: Inexpensive, accessible, but only beneficial if the patient is able to exercise sufficiently, the pre-test probability is intermediate, and the baseline ECG is interpretable. 70% sensitivity and 80% specificity. Not very good, but not worthless.

Stress Imaging (CMR, Nuclear, Echo): Use when it is impossible to interpret the baseline ECG. Digoxin, timed rhythm, left bundle branch block, LVH with strain pattern, and pre-excitation can all render ST segments useless during exercise. Instead of just reading squiggles, you must look at the heart.

CT Coronary Angiography (CTCA): Excellent for excluding CAD in patients with low to intermediate likelihood. The patient does not have obstructive coronary disease if the CTCA is clean. Forget about it. Low heart rate is necessary and is restricted by excessive calcification (blooming artifact).

NEET SS Exam Trap: A patient is referred for stress testing because their baseline ECG shows LBBB. Exercise ECG by itself is never the solution. LBBB cannot be used to interpret ST changes. Imaging is necessary.

Medical Management of Chronic Coronary Syndrome

Two objectives. distinct medications for each.

Objective 1: Anti-Anginal Drugs for Symptom Control

Beta-blockers (First Line): They lessen the need for oxygen by lowering cardiac rate and contractility.

Calcium Channel Blockers: Dihydropyridines, such as amlodipine, are effective if you detect a vasospastic component since they produce vasodilation. If beta-blockers are intolerable, non-dihydropyridines like verapamil and diltiazem can help lower the heart rate. However, due to the possibility of severe bradycardia, avoid using them alongside beta-blockers.

Nitrates: Can be used preventively before identified triggers and alleviate acute episodes. To avoid tolerance, long-acting nitrates require a nitrate-free gap of 10–12 hours each day. This is questioned.

Objective 2: Disease-Modifying Therapy for Prognosis

Aspirin: 75–100 mg every day. Not negotiable.

High-Intensity Statin: Rosuvastatin 20–40 mg or Atorvastatin 40–80 mg. According to the 2019 ESC guidelines, very high-risk patients should aim for LDL levels below 55 mg/dL. Keep that amount in mind if you don't remember anything else regarding lipids in CAD. less than 55.

ACE Inhibitors: Particularly in cases of CKD, diabetes, hypertension, or LV failure.

SGLT2 Inhibitors: Here's the most recent addition. Even in non-diabetics with preexisting atherosclerotic disease, empagliflozin and dapagliflozin lower cardiovascular death and heart failure hospitalization (EMPA-REG OUTCOME, DECLARE-TIMI 58). These medications are now used to treat cardiovascular disease as well as diabetes. Be prepared for inquiries.

Revascularization in Stable CAD: ISCHEMIA Trial Findings

The ISCHEMIA trial (2020) provided an answer to the question we have been debating for decades: would early invasive management (angiography ± revascularization) outperform effective medical therapy in stable CAD with moderate-to-severe ischemia on stress testing?

In response, no. It has no bearing on survival. Revascularization reduces symptoms, especially the frequency and quality of life of angina. However, as compared to vigorous medical care in stable individuals, it does not lower death or MI.

Revascularize for anatomical high-risk traits, such as left main disease, significant proximal LAD stenosis, or three-vessel disease with LV dysfunction, or for symptoms that restrict life despite therapy.

Just because you discovered a blockage doesn't mean you should revascularize.

Acute Coronary Syndrome (ACS): Emergency Management

Initial Assessment in First 10 Minutes

A patient arrives complaining of chest pain. Obtain an ECG before proceeding. in ten minutes. Since this is the only method of identifying STEMI, which completely alters your strategy, it cannot be negotiated.

Examine hemodynamics while the ECG is printing. Does this patient fall into Killip class IV (cardiogenic shock) or Killip class I (no indications of heart failure)? This determines urgency and stratifies mortality.

Treatment should begin without waiting for troponin results. Aspirin is administered right away. Based on what the ECG indicates, everything else is determined.

STEMI Diagnosis: ECG Patterns Including STEMI Equivalents

The textbook STEMI is simple: ≥2 mm in V1-V3 or ≥1 mm ST elevation in two consecutive limb leads. Examiners, however, don't inquire about textbook presentations. They inquire about the people who deceive you.

Posterior STEMI ECG Findings

There are no conventional ECG leads on the posterior wall. Instead, you detect tall R waves with ST depression in V1-V3 (mirror picture). It is simple to mistake posterior infarction for anterior ischemia. If you observe ST elevation on V7-V9 (posterior leads), that is your diagnosis.

Right Ventricular Infarction: Diagnosis and Management

30–40% of inferior STEMIs are accompanied by this. Signs include clear lung fields, increased JVP, hypotension, and inferior ST elevation (II, III, aVF). Verify that ST elevation tightens it with V4R.

RV infarction is important for the following reasons: These individuals rely on preload. Without sufficient filling pressure, the injured right ventricle is unable to force blood forward. They crash if you give them diuretics or nitrates, which lower preload. The remedy is fluids. One of my favorite exam scenarios is this one. "Inferior STEMI, hypotensive, what do you give?" Initially, the solution is IV fluids rather than vasopressors.

De Winter T-Waves: A STEMI Equivalent

There is absolutely no ST elevation. Rather, the precordial leads have tall, symmetric, peaked T-waves with an upsloping ST depression at the J-point. Acute LAD blockage is indicated by this pattern. It is comparable to STEMI. If you ignore it because "there's no ST elevation," your heart is dying.

Wellens Syndrome: Warning Sign of Critical LAD Stenosis

This is a warning sign rather than an acute occlusion. The patient's chest pain has finally subsided. Deeply inverted or biphasic T-waves are seen in V2-V3 of the ECG. This suggests that the artery is on the verge of occlusion due to critical proximal LAD stenosis. This patient should not be sent for a stress test because doing so could cause an infarction. Angiography is required.

New LBBB in ACS: Sgarbossa Criteria

Taught as a STEMI equivalent in the past. The truth is more complex: a new LBBB should be catheterized if there is a significant clinical suspicion of ACS. Though not ideal, the Sgarbossa criteria (concordant ST elevation >1mm, ST depression >1mm in V1-V3, discordant ST elevation >5mm) are helpful.

NSTEMI Management: GRACE Score and Timing of Invasive Strategy

The treatment of STEMI is simple: open the artery as soon as you can. Because not everyone requires urgent catheterization, NSTEMI care is stratified.

GRACE Score for Risk Stratification in NSTEMI

Make use of the GRACE score. Not your intuition, not TIMI (less predictive). Age, heart rate, systolic blood pressure, creatinine, Killip class, cardiac arrest at presentation, ST deviation, and high troponin are all included in GRACE.

• GRACE <109 (Low Risk): In-hospital mortality is less than 1%. Invasive approach in less than 72 hours, if at all.
• GRACE 109-140 (Intermediate Risk): Early invasive procedure within 24 hours is necessary.
• GRACE >140 (High Risk): Significant risk, necessitates action within a day.

Very High-Risk Features Requiring Immediate Catheterization (<2 Hours)

However, some individuals are unable to wait even a day. High-risk characteristics require catheterization right away (within two hours): hemodynamic instability, cardiogenic shock, persistent or repeated chest discomfort in spite of the most effective medical treatment, and potentially fatal arrhythmias.

Hemodynamic instability, cardiogenic shock, persistent or recurrent chest pain despite maximal medical therapy, life-threatening arrhythmias (sustained VT, VF), mechanical complications (new murmur of MR or VSD), or recurrent dynamic ST changes are extremely high-risk features that require immediate catheterization (less than two hours).

NEET SS Exam Scenario: NSTEMI patient, no longer in pain, steady blood pressure, GRACE score of 90, T-wave inversions on the ECG. When should I take a cath? 72 hours from now. This patient poses little risk. Avoid hurrying.

Pharmacotherapy in Acute Coronary Syndrome

Antiplatelet Therapy in ACS

For everyone with ACS (unless contraindicated):

Aspirin: Chew a 300 mg loading dose for quick absorption, then take 75–100 mg every day for the rest of your life.

P2Y12 Inhibitor: This is the complex part.

Ticagrelor: Has a quick onset, direct action, and reversibility. Most guidelines recommend first-line treatment for both NSTEMI and STEMI. The twice-daily dosage, dyspnea (a true side effect, not worry), and the need to avoid it if there has previously been a cerebral hemorrhage are among its drawbacks.

High-Yield Point: The final point is put to the test. Tenecteplase is administered to STEMI patients when PCI is not accessible within 120 minutes. Which inhibitor of P2Y12? Clopidogrel.

Anticoagulation in ACS

During the acute phase, anticoagulation may involve bivalirudin, enoxaparin, or UFH. The choice is based on bleeding risk and technique (conservative vs. intrusive). After PCI, it is typically stopped unless there is another indication.

Statin: Regardless of baseline LDL, high-intensity (atorvastatin 80 mg) was initiated right away. Waiting for fasting lipids is not advised.

STEMI Treatment: Primary PCI vs Fibrinolysis

Primary PCI Timing

If possible, primary PCI should be accomplished within 120 minutes of the initial medical contact. The "system delay" aim is this. Door-to-balloon time should be less than ninety minutes in a hospital with PCI capability.

Fibrinolysis: When and How

Give fibrinolysis if PCI is not possible within 120 minutes. Tenecteplase is the simplest medication to deliver because it is weight-based and administered as a single bolus. It works best within three hours of the onset of symptoms and continues to be helpful for up to twelve hours.

The patient still needs angiography following fibrinolysis. The pharmaco-invasive approach is this. Two to twenty-four hours after a successful lysis is the ideal time.

Role of GP IIb/IIIa Inhibitors

The role of GP IIb/IIIa inhibitors, such as eptifibatide, tirofiban, and abciximab, is diminishing. They are no longer commonplace. When there is a significant thrombus burden or delayed flow during PCI, think of them as a bailout for thrombotic problems.

Secondary Prevention After ACS: DAPT Duration and Medications

Long-term results are decided here. The acute incident is only the start.

Dual Antiplatelet Therapy (DAPT) Duration After ACS

Standard: Aspirin plus a P2Y12 inhibitor for a full year following ACS.

However, nothing is truly typical these days. Individualized length based on ischemia vs. bleeding risk is currently encouraged by guidelines:

High Bleeding Risk (HAS-BLED, PRECISE-DAPT score): Reduce the duration to six months, or even three months, and then switch to P2Y12 monotherapy (keeping ticagrelor and stopping aspirin).

Low Bleeding Risk, High Ischemic Risk (diabetes, previous MI, diffuse CAD): Go beyond a year. Ticagrelor 60 mg BID was beneficial for PEGASUS-TIMI 54 up to three years after MI.

De-escalation Strategy: Another option involves starting with ticagrelor or prasugrel during the acute phase (when thrombotic risk is highest) and switching to clopidogrel after one to three months (when bleeding risk begins to dominate). This is supported in stable patients by studies such as TROPICAL-ACS and TOPIC.

Other Secondary Prevention Medications

Beta-blockers: If there is LV dysfunction (EF <40%), keep going forever. Recent trials have questioned the effect of preserved EF after MI (ABYSS, REDUCE-AMI revealed no mortality benefit). Although guidelines haven't completely changed yet, keep an eye out.

ACE Inhibitors: In the event of anterior MI, heart failure, EF <40%, diabetes, or hypertension, begin within 24 hours. Continue all your life.

Statins: Lifelong, intense. LDL <55 mg/dL is the target. Add ezetimibe if the goal is not met. PCSK9 inhibitors (evolocumab, alirocumab) if the goal is still not met.

MRA (Eplerenone): Include either diabetes or symptomatic heart failure if EF is less than 40%. This is evidence from the EPHESUS trial. Although it has higher anti-androgen effects, spironolactone is also effective.

Mechanical Complications of Myocardial Infarction

These usually occur three to seven days after myocardial infarction, when necrotic myocardium is at its weakest. Paradoxically, reperfusion has made them less common (reduced transmural necrosis), yet they still occur in real life and on examinations.

Free Wall Rupture

The patient abruptly worsens, experiencing tamponade and PEA arrest. Usually deadly before you can stop it. First MI, anterior site, female sex, and delayed presentation are risk factors. The only chance is if they manage to get to surgery by some miracle.

Post-MI Ventricular Septal Defect (VSD)

A thrilling new strident holosystolic murmur near the left sternal boundary. increase in oxygen saturation during a right heart catheterization from RA to RV. collapse of hemodynamics due to shunting from left to right.

Papillary Muscle Rupture Causing Acute Mitral Regurgitation

Severe mitral regurgitation that is acute. At the apex, a new holosystolic murmur radiates to the axilla. pulmonary edema that happens quickly.

How to Differentiate VSD from Papillary Muscle Rupture

On examination, VSD can be differentiated from papillary rupture because the left-to-right shunt overloads the right side, causing right ventricular failure (elevated JVP, clear lungs). Because blood regurgitates into the left atrium and pulmonary veins, papillary rupture manifests as pulmonary edema.

Classic NEET SS Question: Hypotension, increased JVP, clean lungs, new murmur, post-MI day 5. That's not MR; that's VSD.

Both require immediate surgery. When making arrangements, bridge with IABP and reduce afterload.

LV Aneurysm After MI

Develops after several weeks. heart failure symptoms, arrhythmias, mural thrombus with embolic risk, and persistent ST elevation that never goes away. anticoagulation to prevent thrombus. surgery in cases of arrhythmias or refractory heart failure.

Post-MI Pericarditis

Two varieties:

Early (Days 2-3): Inflammation of the pericardium following a transmural infarction. Friction rub, generalized ST elevation, and pleuritic chest discomfort (though this might be confused after MI). Because NSAIDs and steroids hinder cardiac repair, treat with high-dose aspirin.

Cardiogenic Shock: Definition and Management

5-8% of STEMI cases are complicated. 40–50% of deaths occur.

Definition of Cardiogenic Shock

In the context of sufficient filling pressures, sustained hypotension (SBP <90 for >30 minutes or requiring vasopressors) with signs of tissue hypoperfusion (altered mental status, chilly extremities, oliguria, high lactate). Hemodynamically: PCWP >15, CI <2.2.

Management of Cardiogenic Shock: Step-by-Step

Step 1 - Revascularization: The causative lesion's emergent PCI. In cardiogenic shock, culprit-only PCI is better than immediate multivessel PCI, according to the 2017 CULPRIT-SHOCK trial. In fact, complete revascularization raised mortality. Later, stage the remaining lesions.

Step 2 - Vasopressors: First-line norepinephrine (SOAP II study revealed fewer arrhythmias than dopamine). If inotropy is required, add dobutamine.

Step 3 - Mechanical Support: After IABP-SHOCK II failed to demonstrate a mortality advantage, IABP was demoted. However, stabilization is still a use for it. Impella and VA-ECMO for refractory patients, although there is no proof that they reduce mortality.

High-Yield Points for NEET SS Medicine: IHD Summary

The things that cannot be negotiated:

• Troponin = unstable angina vs. NSTEMI. That's all. A troponin positive indicates necrosis in the same illness.
• If primary PCI can be completed in less than 120 minutes, it is superior to thrombolysis.
• Prasugrel should not be used if you have had a previous stroke or transient ischemic attack. Completely stop.
• Give fluids and stay away from nitrates if you have a right ventricular infarction.
• Wellens syndrome and De Winter T-waves are comparable to STEMI. The lack of abrupt coronary occlusion does not imply the absence of ST elevation.
• In NSTEMI, invasive timing is determined by the GRACE score. Not everyone who is at high risk gets to the catheter in two hours.
• Cardiogenic shock with culprit-only PCI (CULPRIT-SHOCK).
• The use of colchicine after MI is currently supported by evidence (COLCOT).
• After ACS, the LDL goal is less than 55 mg/dL.
• VSD after MI: new murmur, clear lungs, increased JVP, and hypotension.
• Post-MI papillary rupture: new murmur, pulmonary edema, and hypotension.

Conclusion

Regurgitation is not rewarded by IHD inquiries. Understanding the gradient—where a patient falls on the continuum from stable angina to cardiogenic shock, and what that position requires—is rewarding. Clinical judgments, scheduling decisions, and revisions to guidelines have all altered practice in recent years.

The man with diabetes who was 52 years old at the beginning of this article? He received a GRACE score of 127. Within a day, he had catheterization, received a drug-eluting stent to a 90% mid-LAD lesion, and left five days later on metoprolol, aspirin, ticagrelor, atorvastatin 80, and ramipril.

Understand the purpose of each of those medications. Recognize when each might differ.

They are testing that.

Frequently Asked Questions (FAQs)

What is the difference between NSTEMI and unstable angina?

The only difference is troponin. Both have the same pathophysiology (ruptured plaque with partial thrombus) and similar ECG findings. NSTEMI is troponin-positive, indicating myocardial necrosis, while unstable angina is troponin-negative.

When should you give fluids instead of nitrates in MI?

In right ventricular infarction (accompanying 30-40% of inferior STEMIs). The RV depends on preload, so nitrates and diuretics that reduce preload will cause hemodynamic collapse. IV fluids are the correct initial treatment.

What is the GRACE score used for?

GRACE score stratifies risk in NSTEMI/unstable angina to determine timing of invasive strategy: <109 = low risk (72 hours), 109-140 = intermediate (24 hours), >140 = high risk (same day).

What are De Winter T-waves?

A STEMI equivalent showing tall, symmetric, peaked T-waves with upsloping ST depression at the J-point in precordial leads, indicating acute LAD occlusion despite the absence of ST elevation.

What is the LDL target after ACS?

Less than 55 mg/dL per the 2019 ESC guidelines. Achieve with high-intensity statin, add ezetimibe if needed, then PCSK9 inhibitors if still not at goal.

Hope you found this blog helpful for your E-learning for NEET SS Medicine. For more informative and interesting posts like these, keep reading PrepLadder’s blogs. 

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