That's all our cases for this specialty.

A Curious Case of Chest Pain

A 64 year old man presents to the emergency department with sudden onset chest pain. It is substernal, crushing in nature, and present at rest. He has not had this pain before; up until now he has had unlimited exertional capacity. He was given nitroglycerin by emergency medical providers with mild improvement in the chest pain. He has a medical history significant for hypertension and dyslipidemia. He has smoked a half-pack of cigarettes each day for the past 40 years. He takes HCTZ and Amlodipine for his hypertension and simvastatin for his dyslipidemia. His physical exam reveals vital signs of temperature 98.6 °F, heart rate 89, respirations 24, and blood pressure 126/67. He is in pain, but not diaphoretic or acutely dyspneic. The pain is not reproducible on palpation nor deep inspiration. He has no JVD or peripheral edema; his lungs are clear. EMS had performed a 12-lead ecg which shows non-specific t-wave changes without ST segment elevation or new bundle branch block.


The thing on the top of your mind should be Acute Coronary Syndrome. Whether its unstable angina, NSTEMI, or STEM is irrelevant at this point - just that you have, "heart attack," in mind. But anybody presenting with a sudden onset chest pain should also be considered for some other diseases.

In a clinical reasoning manner, most things that cause chest pain don't just BAM come on all of a sudden. Those that do are potentially dangerous. The two big killers (just because they’re more dangerous doesn't make them more common) are Pulmonary Embolism and Aortic Dissection. Assessing the Well's criteria can help with a PE (not included in this vignette means the question doesn't want you to go there). Tearing chest pain radiating to the back, asymmetric blood pressures arm to arm, and a widened mediastinum can help with dissection. The things that are more common, like GERD and Costochondritis, do not have a sudden crescendo pain. Of course there are others.

But I do not want you to miss the ACS.

Acute coronary syndrome: http://www.onlinemeded.org/cardiology/coronary-artery-disease
Approach to Chest Pain (intern Content): http://www.onlinemeded.org/intern-content/chest-pain

Troponins. You’ve said, "this could be ACS," and they’ve already gotten the 12-Lead which rules out a STEMI. Now the goal is to determine if it’s an NSTEMI or not, as that confirms the suspicion that the pain is myocardial in nature (which means definitely initiate therapy). However -

Aspirin. Would you really NOT give this guy aspirin? ACLS tells us to give everyone without obvious contraindications it. Of COURSE you’re going to do both in real life. You can treat and diagnose at the same time. See #4 for medications. For diagnosis, we cover that with 12-Lead and Troponins. 

You will NOT have to decide between Aspirin and Troponin on the exam; they’re both right. But if asked, give the aspirin to stabilize the clot. The troponin tells you, "I have to cath this person in 48 hours," while the aspirin says, "I just prevented this from becoming a STEMI."

Amlodipine and Simvastatin now have a black box warning. The combination apparently increases the risk of myopathy and hepatitis. Just remember it.

As for the meds in particular, diuretic + ccb is not a bad choice for someone who, "just has hypertension." Now that there are other things going on that’s going to change. But it’s a perfectly reasonable hypertensive regimen according to JNC-7.

MONA BASH. Morphine, Oxygen, Nitrates, Aspirin, Beta-Blockers, Ace-inhibitors, Statin, Heparin (i.e. therapeutic lovenox or a heparin gtt). You’ll also STOP the HCTZ and Amlodipine. While amlodipine is a good anti-anginal, it has no mortality benefit and can be looked at as the third medication to control blood pressure should additional meds be required after maximizing the beta blocker and ace-inhibitor.

Stress Test. You have to decide between modalities of testing (exercise or pharmacology) and evaluation (ECG, echo, nuclear).

In general, if a person can walk he/she gets on a treadmill. If FOR ANY REASON he/she can’t get on a treadmill, give him/her pharmacologic stress.

Generally, you want an ECG. But if there are baseline ECG abnormalities of any kind you have to go with an imaging technique. Most cardiologists actually perform stress tests with ECG and Echo analysis, but let's stick to the test. If ECG abnormalities, echo. If no ECG abnormalities, ECG. The nuclear comes in when the patient has either bundle branch block, baseline wall motion abnormalities, or when he/she has had a previous CABG.

This guy has some non-specific t-wave changes and no contraindication to ambulation. He should receive a treadmill (no contraindication) echocardiogram (baseline ECG defects) stress test.

Left Heart Catheterization. With the diagnosis of NSTEMI, the patient has 48 hours to get a cath. There’s no emergent need to rush him to the cath lab suspecting a total occlusion; that would be the case in a STEMI. He goes on all the medicines, including heparin gtt, and gets to the cath lab within 48 hours to evaluate the coronary vasculature.

CABG. This is a tricky one. There are only two vessels that are occluded - shouldn't that be stented? This is the classic example of a left mainstem equivalent: both the LAD and the Left Circumflex are occluded, which is the same as the left main since the only two branches of the left main are the LAD and the LCx. So, even though there are only 2 vessels, and CABG is performed in multi-vessel (3 or more) disease, CABG is the right choice because it’s mainstem equivalent. That’s good for step 2 – the next paragraph is for life.

In the real world the other way to look at this is to decide how important the vessel is against how big a lesion. Stents fail, get in-stent stenosis, and are actually a nidus for a new plaque to build up. So, if the vessel is big and important, and the lesion large, you might even want to graft a single vessel. But remember, when you do a CABG you harvest the Left Internal Mammary Artery (LIMA); you only have one to harvest (the other is needed for chest wall perfusion). The LIMA is an artery and you bypass an artery with an artery. You have one LIMA to use and it’s the best graft there is. Thus, you want to save the LIMA for a large and important vessel. Of course, other vessels will be grafted with a saphenous vein that will undergo arterialization.

Let’s consider more about CABG vs Stent in the next question.

Boards... CABG. Life... Stent. Wait wait wait. In #7 we CABG'd a guy with 2 vessel disease. Now, in #8 we want to stent a guy with multi vessel disease? What’s going on? For the USMLE Step 2 if it’s 3 or more vessels, CABG. But look at which lesions those are. There’s no big vessel. Are we going to waste the LIMA on a small distal branch? Or should we save it for an LAD lesion or a Left Cx? The decision to put in a stent or do a CABG has a lot more to do with the overall picture than <3 or > 3 vessels. It has to do with potential touch-down sites (where the wire will end up after passing the lesion, the amount of scar of the heart distal to the lesion, where the lesion is, how big the lesion is, how big the vessel is, and the skill of the operator).

The point is, that’s why there are interventional cardiologists who train for 4-5 years after internal medicine; they learn to make these decisions. YOU should know that, "it's more complicated than it looks," then follow the algorithm to decide CABG or Stent on the test based on left mainstem equivalent (CABG) or 3 or more vessels (CABG).

If CAD, the patient should be on: Beta-Blocker, Ace-inhibitor or Angiotensin receptor antagonist, Statin, and Aspirin. At the very least. If he gets a stent he needs clopidogrel. If he continues to experience angina, he should be on nitro.

So BB, Ace/Arb, ASA, Statin +/- Clopidogrel +/- Nitro

He most certainly has coronary artery disease: 64 years old now with atypical angina. He’s atypical only because he hasn’t had exertional chest pain previously. Refer to the diamond classification: substernal in nature, worsened by exertion, and relieved with nitroglycerin. He has 2/3, making it atypical (3/3 is typical, 1 or 0 out of 3 is nonanginal). He’s 64 with smoking, hypertension, and dyslipidemia. He has, with greater than 90% chance, coronary artery disease.

BUT

That's not what was asked. How sure are we that it was Acute Coronary Ischemia? He had this chest pain for the first time in his life. Which means he would have had to go from an asymptomatic plaque to sudden thrombosis of his coronary vessel. If this were the case, STEMI would be most likely (as it’s a supply issue). NSTEMI and Unstable angina are demand issues - once the demand is reduced the perfusion meets demand and the pain goes away. This would be the case if he had exertional dyspnea. Sudden onset and crushing chest pain that wakes someone from sleep (where the cardiac demand is lowest) speaks strictly to an acute thrombosis. You’d expect to see diaphoresis, hypotension, Lavigne sign, pallor, etc.

SO

In this man, he almost certainly had coronary artery disease from the start, but the cause of his chest pain was not necessarily acute coronary ischemia. However, given his age, risk factors, and nature of the pain you’d most certainly rule him out for acute coronary ischemia, treat it as though it were, and then consider alternative diagnoses when negative.

For more reading, check out TIMI score and its ability to predict 30 day mortality in patients presenting with STEMI, NSTEMI, or unstable angina. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1861157/