Weatherly's Woes - Myocardial Infarction

MYOCARDIAL INFARCTION

Heart attack

A myocardial infarction is a heart attack. The idea of a heart attack seems to be a bit of a paradox to me. After all, the heart is full of blood. And yet the blood within its chambers can’t feed the hungry myocytes. Rather, the heart receives its nutrients from the coronary arteries, which splay across the outside of the heart, and dive down into the heart muscles to provide perfusion. The coronary arteries are fascinating blood vessels, as they play such a critical and unique physiological role. But whenever a coronary artery clogs up, the patch of heart muscle that it supplies will suffocate (ischemia) then die (infarction). Myocardiocytes cannot regenerate, so the damage is irreversible. An MI is usually due to plaque rupture of a coronary artery with complete occlusion of the coronary lumen. Other causes include prolonged Prinzmetal, emboli and vasculitis (Kawasaki).

It causes moderate-to-severe deep, crushing chest pain lasting longer than 20 minutes. Additional symptoms include diaphoresis, radiation to the arm / neck / jaw, SOB and nausea. These are the “classic” MI symptoms, which are more typical in men. In women and diabetics, heart attacks are more likely to be atypical. May present with dyspnea alone, jaw/back/abdominal pain alone or dizziness alone.

Labwork shows elevated Troponin about 2 - 4 hours after infarction. Troponin peaks at 24 hours, and returns to normal after a week or so. Troponin is a great test. It’s incredibly sensitive / specific. The only other cause of a really high Troponin is kidney failure (troponin accumulates when it can’t be excreted into the urine), and the EKG wouldn’t show ST elevation in kidney disease. The old labtest for an MI was CK-MB, but it was less sensitive / specific and it returned to normal after only 48 hours. There’s a niche role for CK-MB in detecting re-infarctions.

The treatment for an MI is a little complicated. Let's break it down into stages.

1st hour in the ER, give Aspirin / Heparin to limit additional thrombosis. Aspirin is the first thing you should do. Period. Some doctors recommend giving Nitrates to (a) open up veins to lower preload and O2 consumption, and (b) modestly open up arteries to restore flow to the heart. However Nitrates can make RV infarcts (Inferior STEMI) worse, so it may be wise to hold off on them. The old teaching was to give Morphine, Oxygen, Nitroglycerine and Aspirin (MONA) to every MI. It is no longer recommended that you give Morphine or Oxygen routinely, and Nitroglycerine is becoming increasingly controversial.

2nd hour in the Cardiac Cath Lab. PCI Angioplasty (stent placement) is the most important treatment. It restores blood to the dead heart tissue. Do it quickly, time is tissue. If the cath lab isn’t available, then thrombolysis (e.g., tPA) is adequate.

Hospital care over the next few days. ACE Inhibitors to prevent LV remodeling. Statins have been shown to improve outcomes. Give Beta blockers to (a) lower the HR and O2 consumption, and (b) suppress arrhythmias (a feared early complication).

If the EKG shows ST elevation in the setting of an elevated troponin, then we call this a STEMI, or ST Elevation Myocardial Infarction. This is a true "heart attack" involving tissue death of the entire thickness of the myocardium (transmural).

If the troponin is elevated, but the EKG does not show ST elevation, then we call it an NSTEMI.

Type 1 NSTEMIs are caused by a plaque rupture. It's essentially a mild STEMI.

Type 2 NSTEMIs are caused by stress. If the heart is weak overall, and then the patient suffers an acute illness (sepsis), then the perfusion of the heart can lag behind the demand for blood. This is called demand ischemia. The rise in troponin will typically be much milder than with a type 1.

LCX - Left Circumflex LAD - Left Anterior Descending RCA - Right Coronary Artery PDA - Posterior Descending Artery

Reperfusion injury is an unfortunate consequence that infrequently occurs after Angioplasty / Thrombolysis. When the heart tissue dies, the whole area becomes like a toxic wasteland. When blood returns to the dead tissue, the nasty environment will turn the influx of oxygen into free radicals. Free radicals can then spill into the adjacent living heart tissue, and kill them! Clinically, if a patient’s troponin continues to rise after a PCI, be suspicious for a reperfusion injury.

Contraction band necrosis is a histological finding. After a PCI, when calcium reaches the dead myocytes, some of them will contract. This produces a characteristic streaky pink pattern.

Coronary Steal Phenomenon- In stable angina, the vessels are occluded to 70% or more. Those vessels are already maximally vasodilated. Administering a vasodilator has ZERO effect on them. Instead, the vasodilators will open up every other blood vessel, sucking flow away from the stenotic vessel. This is the underlying principle behind chemical stress testing. Not everyone can walk on a treadmill (e.g., arthritis), so this is a commonly done procedure. The patient is given a tiny dose of a potent, short-acting vasodilator (Adenosine, Persantine, Regadenoson) to induce coronary steal, and the subtle drop in flow can be visualized with nuclear tracers. For some reason, coronary steal is not seen with nitrates or nifedipine.

STEMI COMPLICATIONS