Ischemic heart disease

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Ischemic Heart Disease (IHD)

Definition and Overview

Ischemic heart disease (IHD) is a broad term encompassing several closely related syndromes caused by an imbalance between cardiac blood supply (perfusion) and myocardial oxygen and nutritional demands. It is the leading cause of mortality in the United States and other high-income nations, accounting for approximately 7.5 million deaths worldwide each year.

In more than 90% of cases, IHD results from reduced coronary blood flow secondary to obstructive atherosclerotic vascular disease - making IHD largely synonymous with coronary artery disease (CAD). The remaining cases involve:

Increased demand (tachycardia, hypertension)
Diminished blood volume (hypotension, shock)
Diminished blood oxygenation (pneumonia, CHF)
Diminished oxygen-carrying capacity (anemia, carbon monoxide poisoning)

- Robbins & Kumar Basic Pathology, p. 351

Epidemiology

~800,000 Americans experience an MI each year; roughly half die
Since peaking in 1963, IHD mortality in the US has declined by 50%
This decline is attributed to: smoking cessation, hypertension/diabetes treatment, statins, aspirin prophylaxis, thrombolysis, angioplasty/stenting, coronary artery bypass grafting (CABG), and coronary care units
Remaining challenges: aging baby boomers and the global obesity epidemic

- Robbins & Kumar Basic Pathology, p. 352

Clinical Syndromes

IHD presents as four main clinical syndromes:

Syndrome	Mechanism
Angina pectoris	Ischemia sufficient to cause pain but not myocyte death
Myocardial infarction (MI)	Ischemia sufficient to cause cardiomyocyte death
Chronic IHD with CHF	Progressive pump failure after MI or cumulative ischemic insults
Sudden cardiac death (SCD)	Ischemia-induced lethal ventricular fibrillation

The term acute coronary syndrome (ACS) applies to the three catastrophic manifestations: unstable angina, MI, and SCD.

Pathogenesis

1. Chronic ("Fixed") Atherosclerotic Occlusion

<70% occlusion: typically asymptomatic even with exertion
>70% occlusion ("critical stenosis"): causes symptoms with increased demand → stable angina
>90% occlusion: may cause symptoms at rest → unstable angina
Clinically significant plaques occur: first few cm of LAD and LCX, and along the entire RCA
Gradual occlusion over years allows collateral vessel development, protecting against MI; acute blockage does not allow time for this

2. Acute Plaque Change

In most patients with ACS, the trigger is sudden plaque disruption (rupture or erosion) followed by thrombosis:

Plaque rupture/fissuring/ulceration exposes thrombogenic contents → rapid thrombosis
Hemorrhage into the plaque core expands volume, acutely worsening luminal occlusion
Partial thrombus → subendocardial infarct
Complete thrombotic occlusion → transmural MI (the typical STEMI)

3. Vasoconstriction / Vasospasm

Triggered by:

Circulating adrenergic agonists
Locally released platelet contents
Imbalance between endothelial relaxing factors (nitric oxide) and contracting factors (endothelin)
Mediators from perivascular inflammatory cells

- Robbins & Kumar Basic Pathology, pp. 352-354

Types of MI by Location

Patterns of transmural vs nontransmural myocardial infarctions based on coronary artery occlusion

FIG. 9.9: Transmural infarcts (left) result from permanent occlusion of major coronary arteries (LAD, LCX, RCA). Nontransmural infarcts (right) result from transient/partial obstruction, global hypotension, or small vessel occlusions. Reperfusion converts a transmural infarct into a nontransmural (subendocardial) pattern.

Transmural MI: Involves >50% of ventricular wall thickness; most commonly left ventricle and/or interventricular septum; 15-30% of posterior/posteroseptal MIs extend into RV
Subendocardial MI: Inner third to half of the ventricular wall; may be circumferential (from global hypotension) or regional (from transient/partial occlusion)
Microscopic infarcts: Small vessel occlusions from vasculitis, emboli, cocaine-induced vasospasm, or pheochromocytoma

Morphology: Time-Sequence of MI

The gross and microscopic appearance of an MI changes in a highly characteristic sequence:

Time	Gross Appearance	Microscopy
0-12 hrs	Usually not grossly visible; TTC stain shows pale (unstained) area after 3 hrs	Wavy fibers, coagulative necrosis beginning
12-24 hrs	Pale/mottled	Coagulative necrosis + edema, early neutrophilic infiltrate
1-3 days	Pale yellow, well-defined	Dense neutrophilic infiltrate
3-7 days	Hyperemic rim, yellow-tan center	Macrophage infiltration, early phagocytosis
7-10 days	Maximally yellow-tan, soft	Nearly complete macrophage removal of necrotic cells
2-8 weeks	Gray-white scar forming	Granulation tissue (loose connective tissue + capillaries)
>2 months	Dense white collagenous scar	Dense fibrous scar, few residual myocytes

Note: Myocardial necrosis proceeds invariably to scar formation without significant regeneration.

Gross Specimen: Acute MI

Acute myocardial infarct of the posterolateral left ventricle; pale area (arrow) indicates necrosis where TTC staining is absent; white scar (arrowhead) indicates remote infarction; asterisk shows ventricular rupture site

FIG. 9.10: Acute MI of the posterolateral LV. Arrow = pale necrotic area (no TTC staining due to enzyme leakage). Arrowhead = white scar from old remote infarction. Asterisk = ventricular rupture (cause of death).

Microscopic Progression

Microscopic sequence of myocardial infarction repair from coagulative necrosis through scar formation

FIG. 9.11: (A) 1-day-old infarct: coagulative necrosis and wavy fibers; (B) 2-3 days: dense neutrophilic infiltrate; (C) 7-10 days: macrophage-mediated phagocytic removal; (D) Granulation tissue with loose connective tissue and capillaries (Masson trichrome - collagen blue); (E) Healed scar: dense collagenous replacement (Masson trichrome).

Reperfusion Injury

When blood flow is restored after ischemia, reperfusion itself causes additional injury through:

Calcium overload - increased Ca²⁺ influx leads to cytoskeletal contraction, uncontrolled myofibril contraction, and cell death
Free radical production (O₂⁻, H₂O₂, •OH, peroxynitrite) - damages membrane proteins and phospholipids
"No-reflow" phenomenon - leukocyte aggregation occludes microvasculature; mediated by phospholipase A₂, prostaglandins, complement activation
Contraction band necrosis - irreversibly damaged myocytes develop intensely eosinophilic hypercontracted sarcomeres from calcium influx (pathognomonic of reperfused infarcts)

Angina Pectoris - Types

Type	Mechanism	Features
Stable (typical)	Fixed stenosis >70%; demand exceeds supply	Predictable with exertion; relieved by rest/nitroglycerin
Vasospastic (Prinzmetal)	Coronary artery spasm	Occurs at rest; ECG shows transient ST elevation
Unstable	Plaque disruption + partial thrombosis	Occurs with less exertion or at rest; part of ACS; precedes MI

Clinical Features of MI

Classic presentation: Severe, crushing substernal chest pain/pressure radiating to neck, jaw, epigastrium, or left arm; lasts minutes to hours; NOT relieved by nitroglycerin or rest
Silent infarcts: Up to 25% of MIs are entirely asymptomatic, especially in diabetics (autonomic neuropathy) and older adults
Associated features: Rapid weak pulse, diaphoresis, nausea (especially posterior wall MI), dyspnea (from impaired contractility/mitral valve dysfunction leading to pulmonary congestion)

Diagnosis

ECG: ST-segment changes, new Q waves
Cardiac biomarkers: Troponin I/T (most sensitive and specific), CK-MB; rise within hours, peak and fall over days
Imaging: Echocardiography (wall motion abnormalities), coronary angiography

Complications of MI

Complication	Timing	Notes
Arrhythmias	Minutes-hours	Most common early complication; VF is the most common cause of sudden death
LV failure / cardiogenic shock	Hours-days	Pump failure; 10-15% of hospitalized MIs
Myocardial rupture	3-7 days (peak softening)	Free wall → hemopericardium/tamponade; Septal rupture → VSD; Papillary muscle → acute MR
Pericarditis	2-3 days	Fibrinous/fibrinohemorrhagic; Dressler syndrome (autoimmune) at 2-10 weeks
Mural thrombus	Days-weeks	Risk of systemic embolism (stroke)
Ventricular aneurysm	Weeks-months	Paradoxical bulging; risk of thrombus, arrhythmia, CHF
Progressive CHF	Months-years	Infarct expansion + remodeling

Chronic IHD

Progressive cardiac decompensation that occurs after acute MI or through accumulated ischemic insults, eventually precipitating mechanical pump failure. Heart failure is typically severe and punctuated by new episodes of angina or infarction. Arrhythmias, CHF, and intercurrent MI account for most associated morbidity and mortality.

Sudden Cardiac Death (SCD)

Definition: Unexpected death from cessation of normal cardiac electrical activity with hemodynamic collapse
Incidence: ~450,000 deaths/year in the US
Underlying cause: 65-70% have coronary atherosclerosis/IHD; ~10% have other causes (hypertrophic cardiomyopathy, channelopathies)
Mechanism: Usually lethal arrhythmia - ventricular tachycardia, ventricular fibrillation, or asystole
Successful resuscitation = sudden cardiac arrest (SCA)

- Robbins & Kumar Basic Pathology, p. 368

Management Overview

Strategy	Examples
Risk factor modification	Smoking cessation, statin therapy, BP/diabetes control
Antiplatelet therapy	Aspirin, clopidogrel, ticagrelor
Anti-ischemic drugs	Beta-blockers, nitrates, calcium channel blockers
Reperfusion (acute MI)	Primary PCI (preferred), thrombolysis
Revascularization	PCI with stenting, CABG
Heart failure management	ACE inhibitors/ARBs, beta-blockers, diuretics, aldosterone antagonists
Arrhythmia prevention	ICD for high-risk patients

Since peaking in 1963, therapy advances have reduced IHD mortality by 50%. The greatest gains came from risk factor intervention (especially smoking cessation, statin use, hypertension treatment) with additional contributions from reperfusion therapies, stenting, and improved acute care.

Sources: Robbins & Kumar Basic Pathology (9780323790185); Braunwald's Heart Disease, 2-Volume Set (9780323722193)

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