Published in the February 2017 issue of Today’s Hospitalist
DURING A PRESENTATION at a conference on managing hospitalized patients last fall, Dhruv S. Kazi, MD, MSc, MS, a cardiologist at Zuckerberg San Francisco General Hospital and an associate professor at University of California, San Francisco, presented his top take-home messages for hospitalists about the diagnosis and management of acute coronary syndrome (ACS).
“We assume,” said Dr. Kazi, “that ACS is equal to finding a ruptured plaque in the coronary arteries, which is true for the vast majority of acute coronary syndromes.” But there is an entire spectrum of coronary artery disease ranging from asymptomatic to ST-elevation MIs (STEMIs), he pointed out, and “this abrupt decrease in coronary flow can occur from other causes.”
STEMI, of course, is the “big bad” among ACS. Dr. Kazi spelled out its diagnostic criteria: ST elevations of 1 mm or more, with the exception of V2 and V3, which are 2 mm or more.
“We tend to obsess about STEMIs, but the fact is NSTEMI patients do just as poorly.”
~ Dhruv S. Kazi, MD, MSc, MS
Zuckerberg San Francisco General Hospital
“We believe ST elevations represent an occlusion or a critical stenosis in a large epicardial coronary artery such as the left anterior descending (LAD) or the circumflex,” he explained. These patients, he noted, benefit the most from early reperfusion, whether you give them thrombolytics or, more often, take them to the cath lab and open a vessel. ST elevations are also a marker of higher in-hospital mortality: While in-hospital mortality is 5% for all acute coronary syndromes, it’s 6% for patients presenting with a STEMI.
But that figure is only slightly lower (4%) for patients who present with a non-STEMI, and mortality among these patients “catches up to STEMI patients within a year.” Mortality at one year after a STEMI or a NSTEMI is “nearly identical,” Dr. Kazi said, and one mistake he believes doctors make is to discount NSTEMIs.
“We tend to obsess about STEMIs,” he said. “But the fact is that NSTEMI patients do just as poorly, so they need very close follow-up both in the hospital and out.”
Case No. 1: Left bundle branch block
In the first case Dr. Kazi presented, a 62-year-old woman with diabetes and hypertension presented with nausea and vomiting, as well as 4 out of 10 substernal discomfort and 6 out of 10 abdominal pain.
Her initial EKG was “characteristic of a left bundle branch block,” he pointed out. Dr. Kazi added that left bundle branch block was the “bane of my existence” as a cardiology fellow and the reason why more consults are generated in the hospital than for any other EKG.
The right bundle, he reminded the audience, is “a fragile, finicky structure.” The left bundle, on the other hand, is “this giant, fanlike structure that sits on the left side of the heart and is very resilient. Taking out the left bundle takes a substantial insult, which is the reason we worry about it.”
Moreover, “7% of patients with an acute MI have a left bundle on their presenting EKG, some of which will be new and some old,” he added. And “almost half these patients don’t have concomitant chest pain. They’re having an acute coronary syndrome but presenting with atypical symptoms for reasons that aren’t entirely clear.”But here’s the problem: “The STs we care about when diagnosing ACS are part of the repolarization of the left ventricle,” he noted. Because the depolarization and repolarization are abnormal in the setting of a left bundle branch block, “we can’t interpret the STT changes.”
The primary challenge is not that the left bundle branch block is equivalent to a STEMI, which it isn’t, he said. Instead, the big problem—and his take-home message no. 1—is that left bundle branch block can mask an ongoing MI. While a left bundle branch block can be caused by degenerative changes in the conducting system, it can also be due to an LAD infarct.
“This obsession that only a new left bundle matters is not true,” said Dr. Kazi. “Someone who has lived with a left bundle her whole life can still have an infarct, and we wouldn’t know it based on her EKG.”
And because patients present with atypical symptoms and an uninterpretable EKG, “it should come as no surprise that this often produces delays in diagnosis and treatment, which adversely affect outcomes.”
What do you do next?
When such a patient presents in the emergency room, Dr. Kazi said the key questions are: Do those symptoms represent a blockage in an epicardial coronary, and does the patient need to go to the cath lab emergently? When someone who is hemodynamically stable and has atypical symptoms presents with a left bundle branch block, he asked the audience, what should you do next?
Getting old EKGs from the patient’s primary care physician or repeat EKGs in the hospital “can occasionally be helpful.” But because most left bundles are stable, he explained, serial EKGs aren’t really a good option. And a stat echocardiogram is seldom helpful because the left bundle branch block itself can cause wall motion abnormalities.
The best course of action at this point is to send out for troponins and drill deeper into the patient’s history and clinical presentation. Positive troponins or hemodynamic instability “may push you toward urgent coronary angiography.” In any event, a left bundle branch block, said Dr. Kazi, “is an opportunity to think harder about the ACS.”
Case No. 2: Are you sure it’s an NSTEMI?
In the second case, a 68-year-old with obesity, hypertension, diabetes and a 30year smoking history was involved in a head-on collision.
He is hemodynamically stable in the ED, with multiple fractures of the pelvis and lower extremities. But on hospital day 4, he develops shortness of breath and new 7/10 substernal chest pain. He is tachycardic, normotensive, sating 94% on 2 liters NC, and his EKG shows sinus tachycardia and nonspecific STT changes.
“We talked about why getting to the bottom of ST elevations is important,” said
Dr. Kazi. “But in some settings, we’ve taken that to mean that non-STEMI syndromes don’t matter. I hope to change that thinking.”
If you see ST elevations in the initial EKG, send the patient to the cath lab. If you don’t see ST elevations but suspect ACS, he said, “keep looking for ST elevations with serial EKGs.”
Guidelines recommend getting one every 20 minutes. But “I think that’s too generous depending on the clini cal setting, so get and review them every 10 minutes,” he pointed out. And while an initial EKG will capture a certain number of leads, you have to look at others. You particularly need a right-sided EKG, looking for ST elevations in V4R, he explained, as well as a posterior EKG to look for ST elevations in V79.
ST elevations in V4R represent a right ventricular infarct. An inferior infarct that also involves the right ventricle is associated with three times the mortality of an inferior MI that does not, he pointed out. “Occasionally, you will see an insolated infarct of the right ventricle, without an inferior infarct,” he add ed. “This can be diagnostically challenging but, fortunately, it’s an uncommon event.”
A posterior infarct—which is one in the posterior wall of the left ventricle—can also complicate an inferior MI.
In both these cases, ordering a stat echocardiogram can help with the diagnosis because you might see wall motion abnormalities of either the right or posterior wall.
What do you do next?
Say you find no ST elevations, but you do have a positive troponin.
“Instead of immediately jumping to the conclusion of NSTEMI, this is where I spend time thinking,” said Dr. Kazi. “Is there a possible alternative explanation other than acute coronary syndrome? Is there something I’m missing that could cause this presentation?”
It is often tempting to skip this step, he added, which became his take-home message no. 2: Before diagnosing NSTEMI, exclude right-sided and posterior ST elevations, and rule out other causes of elevated troponins.
Patients’ decreased coronary blood supply, for instance, may be due to noncoronary syndromes such as shock, hypoxia or pulmonary embolism. (In fact, the patient in this particular case was found to have multiple PEs.) And “in my population,” he said, “we worry about cocaine and meth use, which are very prevalent.”
If after careful consideration you’re left with an NSTEMI, “you still may need early coronary angiography because there are high-risk NSTEMI patients”—his take-home message no. 3. (He defined “early” as within 24 to 72 hours.) High-risk NSTEMI patients include individuals with ongoing pain despite antiplatelet and anticoagulation therapy, those with electrical or hemodynamic instability, and patients with high GRACE or TIMI risk scores.
Also in the high-risk group: NSTEMI patients with heart failure. “You may not take them to the cath lab in the middle of the night,” said Dr. Kazi, “but it may help to do so sooner rather than later.”
Case No. 3: Who needs dual antiplatelets?
A 63-year-old man with diabetes who smokes a pack a day presents with chest pain that woke him up at 6 a.m. In the ED, he’s hemodynamically stable and free of chest pain, but the presenting EKG shows 2 mm ST depressions in II, III and aVF. (There are no ST elevations in the right-sided or posterior leads.) The troponin is 0.2 ng/dL.
“You diagnose NSTEMI and initiate aspirin, statin, heparin and metoprolol,” Dr. Kazi said. “Coronary angiography the next day reveals a 60% lesion of the mid-right coronary artery and 50% in the LAD.” Because an echo shows that LV systolic function is normal, you decide to medically manage the coronary artery disease without PCI.
But that raises this key question: Would this patient benefit from a second antiplatelet, even though he did not undergo PCI? While hospitalists in the audience were split about whether adding a second antiplate let was the right course, Dr. Kazi said that the correct answer is a strong “yes.”
“We know this very con vincingly from randomized trials as well as a host of other data,” he noted. “We also know that these patients should be on dual antiplatelets for at least a year.”
In fact, in addition to NSTEMI patients being medically managed without PCI, all of the following patients have lower rates of cardiovascular events with dual antiplatelets and need at least a year of such therapy: STEMI after PCI or fibrinolytics, unrevascularized STEMI, NSTEMI after PCI, unstable angina, and stable angina after PCI.
“This is one of the biggest evidence-practice gaps in acute coronary syndrome,” Dr. Kazi said. “It comes from the fact that we’ve obsessively tied antiplatelet use to stenting.”
While patients who undergo PCI with stent placement definitely need a year’s worth of dual antiplatelet therapy, “the data are just as clear about patients who don’t receive stents.”
The fact that you need to give medically-managed NSTEMI patients who don’t undergo PCI one year of dual antiplatelets was Dr. Kazi’s take-home message no. 4.
As for different antiplatelets, clopidogrel is the most well-studied, and “it is still a great choice,” Dr. Kazi pointed out. It’s also inexpensive and costs about $10 a month.
But patients with CYP2C19 polymorphisms are poor metabolizers of clopidogrel, so they “don’t achieve adequate platelet inhibition,” he noted. As a result, they have the highest recurrence rates. Approximately 20% of the general population have loss of function CYP2C19 polymorphisms, but this “varies very dramatically by ethnicity, going up as high as 50% in East Asian populations,” he noted.
Among these populations, you should consider clopidogrel alternatives, particularly after coronary stenting. While Dr. Kazi doesn’t currently screen patients for CYP2C19, “I expect that will change in a couple of years.”
As for other antiplatelet options: Prasugrel “is extremely potent and expensive.” Because it has a higher risk of bleeding, “you use it only in patients at very high risk of thrombosis,” said Dr. Kazi. “It’s indicated only among STEMI or NSTEMI patients who have undergone PCI.” Prasugrel is also contraindicated in patients with a prior history of stroke or transient ischemic attack because they appear to have an unacceptable risk of bleeding with the drug.
Ticagrelor has been studied in all ACS patients, regardless of whether they had PCI. Dr. Kazi pointed out, however, that between 3% and 5% of patients who begin ticagrelor therapy experience subjective dyspnea that is not related to changes in cardiovascular or pulmonary function. In the vast majority of these patients, the dyspnea goes away within 30 days. “You just have to coach them through it,” he said.
To choose between clopidogrel and ticagrelor for a year, “base your decision on cost and adherence,” he said. Ticagrelor appears to lower cardiovascular mortality without a substantial increase in bleeding, but it costs around $350 a month. It also requires twice-a-day dosing compared with once-a-day clopidogrel.
Phyllis Maguire is Executive Editor of Today’s Hospitalist.