ANGINA
Heart cramps
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Angina is the reversible injury to cardiac myocytes that occurs with suboptimal blood flow. It causes chest pain.
Stable Angina occurs predictably with exercise. The cause is a large plaque (that occludes > 70% of the lumen). This is a chronic condition. Exercise makes it worse because the heart has to work harder during exercise. Relieved by rest (decreasing O2 demand), Nitroglycerine (opens veins to lower preload and O2 demand, also opens coronary arteries to a modest degree) or CCBs (open up arteries). Nitrates develop tolerance, so use a special Nitrate called Isosorbide Dinitrate to minimize this -- it can be taken once daily.
Unstable Angina is random anginal pain. It can occur at rest. The cause is a plaque rupture that leads to a clot formation. The clot only partially occludes the lumen. This is a highly concerning condition. High risk of progression to an MI. Probably needs a PCI in the next day or two.
NSTEMI is the same disease as Unstable Angina, but their Troponin is elevated. NSTEMI carries a worse prognosis than Unstable Angina, and requires a PCI in the next day or two. Classic NSTEMIs are caused by occlusions. But we are now increasingly aware that a lot of NSTEMIs are caused simply by stressful physiological conditions of the heart (anemia, severe hypertension, etc).
PRINZMETAL ANGINA
Coronary artery vasospasm
Prinzmetal Angina is a rare cause of angina that is due to vasospasm of the coronary arteries. It causes chest pain that starts randomly and lasts 10 to 15 minutes. The patient will be a smoker. The underlying problem is endothelial dysfunction (hence smoker) leading to coronary vasospasm. It’s theorized that the other causative component is a high Vagal tone. That’s why PA tends to flare up at night and in the early morning, and why it often improves with exercise.
The Vagus normally releases ACh into the heart. ACh does two (opposite) things in the coronaries. (1) The dominant action is to vasodilate. That’s because ACh tells the endothelial cells to produce NO. But if the endothelial cells are damaged (from smoking), then this effect will be lost. (2) The minor action is to vasoconstrict. That’s because ACh directly stimulates smooth muscle cells to contract. Smoking has no effect on this action. That’s why a parasympathetic surge can cause coronary vasospasm in a smoker! You can diagnose Prinzmetal by giving the patient a dose of ACh. In healthy people, ACh vasodilates the coronary arteries. But in patients with Prinzmetal, ACh will make the vasospasm worsen. Another weird test is with Ergots. Ergots activate serotonin receptors and lead to vasoconstriction. This is normally offset by NO, but these patients lack NO. So giving an ergot would worsen their symptoms too. Note that cocaine and sumatriptan may also cause Prinzmetals.
Prinzmetal Angina totally occludes the artery, so there will be transmural ischemia and transient ST elevation while their chest hurts. They will have a normal heart catheterization. Prolonged vasospasming can lead to an MI. The vasospasm is naturally relieved by vasodilators like Nitroglycerine and Calcium Channel Blockers. They should also quit smoking. They have to avoid Propranolol (and other nonselective beta-blockers), because blocking B2 can theoretically worsen the vasoconstriction.
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