Coronary Insufficiency – inadequate coronary circulation leading to anginal pain

• Ischemia manifests first in the subendocardium because due to its blood supply it is the most vulnerable to ischemia
• Stable Angina – due to blockage of a vessel there is ischemia during exercise or stress (times of Ý O₂ demand)
• Stenotic vessels, stable plaques occlude vessel lumen
• Clinical features: can be asymptomatic, angina with effort, arrhythmia, CHF, sudden death
• Unstable Angina – the formation of clots occludes the lumen of the vessels.
• Vulnerable plaques rupture and form clots
• Vulnerable plaques – thin endothelial layer overlying a large lipid deposit
• Stable plaques – thick fibrous cap overlaying small lipid core
• The plaques that rupture are usually occluding the vessel less than 50%.
• Plaques rupture at the edge, where inflammatory cells soften the plaque and make it more prone to rupture
• It is currently thought that inflammatory processes give rise to MI’s (the Chlamydia hypothesis)
• Clinical features: unstable angina, acute MI, arrhythmia, cardiogenic shock, sudden death
• Coronary Spasm – a.k.a. Prinzmetal’s Angina, Variant Angina, or Primary Angina
• A possible cause of unstable angina
• A non-atherosclerosed coronary artery that goes into spasm and it thereby stenotic.
• This spasm can be reversed with Nitroglycerine or calcium channel blockers; often it will resolve on its own.
• During the episode of angina there is ST segment elevation on the EKG
• Thought to be due to endothelial dysfunction (inability to produce vasodilators to counteract vasoconstrictors)
• Microvascular Angina – Syndrome X
• Myocardial ischemia with normal epicardial vessels
• Natural history: pain persists Þ disability but excellent survival
• Mechanism: intramyocardial arteriolar dysfunction (small vessels of the heart do not dilate properly)

• Anemia – ß [hemoglobin] means that there is not enough O₂ carrying capacity
• Tachycardia – ß diastolic filling
• Myocardial hypertrophy – ß perfusion because proliferation of vascular channels may not keep pace with the Ý in muscle mass or because the mechanical limitation of flow to the deeper transmural layers of the heart.
• Other causes of Angina
• Vasculitis, trauma, dissection of the coronary arteries, congenital defects, cocaine use (seen in young people with normal arteries)

 Clinical Evaluation of Coronary Stenosis

• history of angina
• angiography
• stress test
• functional studies
• Flow is normal at rest until a 80-90% block; maximum flow is impinged at 50-60%
• Symptoms
• Þ typically a substernal chest heaviness that radiates out (left > right) also shoulder, jaw, and throat.
• Þ The duration of the pain < 15 minutes after stopping exercising (if > 15 min "…get thee to a hospital")
• Þ the intensity is usually mild > severe ("I didn’t think it was a heart attack because the pain wasn’t so bad")
• Þ associated features: anxiety (sense of doom), SOB, diaphoresis, palpations, GI symptoms
• Stress Test – Ý the demand of the heart either by exercise (treadmill) or drugs (Dobutamine) and look at results
• Angiography – measure invasively, often clinician’s interpretation of the extent of the lesion differs from the pathologist’s because angles used in the test as well as the Glagoff phenomenon.
• Glagoff Phenomenon – the vessel dilates to accommodate the atherosclerotic plaque (up to 50% stenosis can be accommodated this way and is not apparent on angiography)
• Angioscope – look at the lesions directly with an invasive fiberoptic camera
• Flow reserve studies – use Doppler to measure velocities
• Also can measure the pressure on both sides of the plaques using little probes and compare