Chest Pain Workup (Peng, 3/13/2024)

 A recording of this presentation is found HERE. 

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Thanks to Dr. Jonathan Peng for an excellent Grand Rounds this week on Chest Pain Workup. A recording of his presentation is above. My favorite favorite moment of the presentation was his last statement: "If it is important to the patient, it should be important to us." In other words, don't dismiss a patient's concerns. I love this mantra, and I so appreciate Dr. Peng's presentation -- he took us through a little history of medicine, some biostatistics, a bit of art history, and finally, the black box of cardiac stress testing.

Here are my notes:

Dr. Peng's  recipe for cardiac evaluation:

1. Evaluate the patient by their baseline characteristics (i.e. pretest probability).What are a patient's risks for CAAD? We should all be  aware that increasing age increases the likelihood.
2. Evaluate the patient with their symptoms (using risk scoring). How likely is it that the patient in front of me has chest pain that is ACS?
3. Evaluate the patient with testing (EKG, laboratories, stress testing, etc.)

Cardiologists love acronyms and scores!

There are two main calculators that help us predict cardiovascular risk using risk factors

1. ASCVD Risk Estimator (2019) predicts 10 year risk 
2. PREVENT Online Calculator (2024), new from AHA, predicts 10-30 year risk, in specific populations

There is additional score, called the HEART Score (2011) that helps to predict a patient's risk of ACS during an acute event. Factors include:

• History
• EKG
• Age
• Risk Factors
• Troponin

This HEART Score for Major Cardiac Events predicts a patient's 6-week MACE (Major Adverse Cardiac Event) risk. A score of 0-3 is low risk (1.7%), 4-6 is intermediate risk (16%) and 7-10 is high risk (50%). The authors suggested that a low HEART score excludes a short term MACE with a 98% certainty!

Once cardiologists have decided that a patient needs evaluation, they consider the following:

• indications: why am I ordering the test?
• contraindications: why should I NOT order the test?
• types of test: which one to choose?
• interpretation: what do the results mean?

Stress tests are ordered to rule out ischemia and to assess for cardiac viability, but also to assess functional capacity (eg. in valvular heart disease, hypertrophic cardiomyopathy, cardiac vs. lung dz and preop capacity if otherwise unclear), risk stratify specific patients after an acute MI (if cardiac cath not performed), and assess efficacy of medical therapy. 

Dr. Peng reminded us that many such tests are likely to be most  helpful for patients in the middle -- that is patients who have a low pretest probability will likely have normal tests, and patients with known severe CAD will have abnormal tests. 

Complications from stress tests are extremely rare, as are complications from pharmacological stress. Absolute contraindications include: severe AS, recent MI (within 2 days), unstable angina, decompensate heart failure, unstable arrhythmia, acute PE, suspected aortic dissection, inability to walk. Relative contraindications include: left main disease, moderate AS, HCM, electrolyte abnormalities, afib w/RVR, high degree AV block, and resting BP >200/110.

All stress tests involve a stress (either treadmill/exercise or pharmacologic) and follow-up imaging (EKG, echo, or nuclear med). See diagram below for the menu of stress tests:

What they are looking during the stress for something called the ischemic cascade; that is, as stress is put on the heart in the form of an exercise load, you can see a cascade of events that occur in the setting of decreasing coronary blood flow. I really LOVE this image Dr. Peng shared about how that manifests on perfusion scans, echocardiograms and EKGs, as well as symptoms. 

Exercise (i.e. treadmill testing) remains the stress test of choice -- it's cheap, you don't need special equipment, and it gives us an idea of a patient's functional capacity. It does have lower sensitivity/specificity than pharmacologic stress and there are some conditions that make a stress EKG uninterpretable (e.g. people with pacemakers, LBBB).

Pharmacologic testing options include adenosine (a vasodilator), dobutamine (a beta agonist), and lexiscan (most commonly used, shown to be safer, okay in people with BOPD).

Nuclear isotopes used in the nuclear portion of the stress test expose patients to 48 hours of high dose radiation. These types of nuc med tests can last anywhere between 2-4 hours and 2 days. Patients with higher BMI (>32-35) will often require a higher tracer dose and a longer test. 

example of nuc med imaging protocols

Stress imaging can be either via echocardiogram or nuclear med studies. Echo tends to be more specific (i.e. better for "ruling in" ischemia), nuclear med imaging tends to be more sensitives (i.e. better for "ruling out" ischemia). Other differences are seen in the table below. 

The next slide is probably my favorite from his talk, I'll call it a "Dummy's guide to stress testing". It is a flowsheet that takes us through the patient's clinical scenario and leads us down a path of which stress test to choose. Dr. Peng stressed that having good echo techs (which we do!) is an important caveat to which tests you order. 

att: Dr. Jonathan Peng, 3/13/2024

A treadmill EKG is 68% sensitive and 77% specific. In comparison, a treadmill echocardiogram has slightly increased sensitivity and specificity at 81% and 88%, respectively. A treadmill myoview has sen/spec of 87% and 70%. This makes me conclude that if we had a good echo tech to do the study, I would prefer a treadmill echo for myself (to avoid the radiation!).

What does an adequate study mean?

The results of stress tests don't always seem obvious. And this is because, you must first understand if the test was adequate before being able to interpret the results. Adequacy is defined as 1) patient being able to reach target heart rate,  (max predicted heart rates is traditionally defined as 220-age in years; the target heart rate is 85% of the max heart rate). A stress test is only negative IF the patient reached the target heart rate. 

On a related note, should we hold a beta blocker before a stress test?

It depends: for diagnosing ischemia then YES because you need to reach the target heart rate. For evaluation of medication efficacy then NO because we want to know if the meds are working correctly

It is also important to understand why a stress test was stopped. Absolute reasons for stopping include: ST elevations, BP drop >10mm hg with evidence of ischemia, mod/severe angina, dizziness/syncope, cyanosis/pallor, and sustained VT. Relative reasons for stopping the test early include: asymptomatic drop in BP, ST depressions >2mm, increasing chest pain, multiple PVCs, BP>220/115, fatigue/SOB/leg pain. 

Exercise time is prognostic! >8-9 minutes on the treadmill is a good prognostic sign. 

Of course, since we are talking cardiology, there are different scales to assess the outcomes of a treadmill tests and to use that to predict CV morbidity and mortality. These include the Duke Treadmill Criteria and the Cleveland Clinic score. The Duke score takes into account how long you were able to exercise, how bad the EKG changes, and whether or not you had chest pain during the test. The higher the number, the higher the CV risk.

High risk stress tests involve people with short time to symptom (3 minutes or less), induced hypotension, and prolonged time to recovery. The notion that having your heartrate return to baseline with relative quickness predicts the severity of your cardiac disease. For more high risk stress test outcomes, see the image below.

Unsurprisingly, exercise ability predicts prognosis -- that is, the more you can exercise (i.e. the higher METS you  achieve), the better your prognosis, regardless of your comorbidities. This is a reminder to us all to move move move our bodies as much as we possibly can! Stay in shape. 

Dr. Peng spent just a few minutes at the end talking about CT coronary angiography, a relatively new imaging study for intermediate and low-risk patients, those who are younger, have a lower BMI. It exposes people to much less radiation than a nuclear med study and decreases a need for unnecessary cardiac catheterization in the lower risk population. 

And finally, Dr. Peng ended the way I began this blog --with a plea to listen to patients: "When I was a younger clinician, I used to ignore my patients, sometimes disregard their symptoms. They would complain of pain or shortness of breath, and I would think 'oh, that isn't cardiac'. With time, I have learned to listen to my patients. If it is important to them, it should be important to us."

Amen. Dr. Peng.

Go forth and listen to your patients. 

Pulmonary Hypertension (Wang - 8/2/23)

 A recording of this presentation can be viewed HERE.

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Dr. Helena Wang gave an excellent Grand Rounds this week on Pulmonary Hypertension. It is worth watching!

We currently have at least three patients on our adult medicine service that we are evaluating for this condition after getting a TTE to look at their heart failure status. Pulmonary hypertension is such an interesting intersection between the lungs and the heart and a good opportunity to review basic physiology too! Dr. Wang gave an earlier version of this presentation 2 1/2 years ago, and I felt then, as I did this week, that I could watch it over and over. You can! 

But for those who prefer the written word:

The definition of pulmonary hypertension (pHtn) is simple enough: a mean PAP of > 20mmHg at rest.

Dr. Wang likens the pulmonary artery to something like a six lane highway (think of the 101 going north from Novato into Petaluma). When the lanes decrease from six to two in northern Novato, there is suddenly a lot of congestion, and all the cardiac output has to move through that smaller space at higher pressures. Voila! Elevated PAP.

Pulmonary arterial hypertension is rare, but not that rare, 15-50 cases/million, and more common in people with HIV (regardless of CD4 count or duration), connective tissue disease, and portal hypertension. For patients with any of these diagnoses, should be screened annually for pHtn with an echocardiogram (TTE).

Symptoms of pHtn include dyspnea on exertion, fatigue, edema, bloating, and syncope (obviously pretty non-specific). 

On exam, you can see elevated JVP (check the neck veins!), hear a split S2, and see peripheral edema.

Chest imaging reveals often a dilated R pulmonary artery on CXR, and even sometimes a prominent L pulmonary artery. Also, look for the "banana and egg sign" on CT, in which the aortic arch and the pulmonary artery are a little too close in size for comfort. The aortic arch is the banana; the pulmnoary artery is the egg.

Banana and egg sign (photo credit: CHEST Journal)

Okay, what about the TTE??

Oh, reminds the pulmonologist and the family physician, don't forget to pay attention to the right side of the heart in the echocardiogram! Dr. Wang urged us to scroll down, skip the conclusion,  and look at the text (often the third paragraph). Is the RV big? What is the velocity of the regurgitant jet? What is the TAPSE?

A first hint of pulmonary hypertension on a TTE comes on apical 4 chamber view where the R ventricle shows turbulent flow back into the R atrium

RVSP (right ventricular systolic pressure) is an estimate reported on most echo reports and can be very challenging for the Echo tech to calculate. However, a calculated RVSP>25 is considered HIGH right sided pressure and increases your suspicion for pHtn.

The R ventricle is often very plump and dilated under high pressure (so. . .a big chubby RV on echo is another clue that you might have pulmonary hypertension)

Tricuspid Annular Plane Systolic Excursion (TAPSE): RV contracts in a twisting motion with each contraction as RV shortens. Normal excursion is 1.5cm. If RV is volume overloaded and dilated, cannot squeeze as well, not shortening, TAPSE drops <1.5cm on echo

And finally, right heart catheterization is still gold standard for measuring R sided pressures, but really this should be done after you have done a full evaluation (see below) once you are pretty certain you have primary pulmonary hypertension (WHO Group 1). And, due to changes in insurance, it is no longer required always for diagnosis.

WHO Classification of Pulmonary Hypertension

• WHO Class 1: Pulmonary ARTERIAL Hypertension (pressure goes up, fluid backs up)
• WHO Class 1 has the worst outcome: 5 year survival 61%
• only diagnosed once other causes of pulmonary hypertension are identified and treated
• Seen in patients with HIV (regardless of viral load, duration), connective tissue disease (e.g. scleroderma), and portal hypertension
• All other WHO classes are actually pulmonary VENOUS hypertension (something downstream to the lungs causing poor forward flow, back up of blood, then high pressure on R side of heart). These include
• WHO 2: L heart disease (LV systolic or diastolic dysfunction, valvular disease, s/p TAVR, myxomatous disease)
• WHO 3: bad lung disease or hypoxia (COPD, inadequately treated asthma, ILD, sleep disordered breathing (OSA), OHS, chronic exposure to high altitute, developmental lung disease. Consider high resolution CT (with very thin cuts with and without contrast), home sleep test, pulmonary function tests.
• WHO 4: chronic thromboembolic pulmonary hypertension (small, little tiny chronic). You cannot see this on typical PE protocol CT scan. You need a VQ scan to evaluate chronic thromboembolic disease.
• WHO 5: potpourri

Once Pulmonary Hypertension is identified, the next question is DOES the patient have pulmonary hypertension that is primary or secondary

Ddx pulmonary arterial hypertension (WHO Group 1)

• idiopathic
• heritable (no current gene therapies)
• drug and toxin induced (fen fen, methamphetamines including stimulant medications prescribed)
• connective tissue disease (scleroderma)
• HIV
• portal hypertension
• congenital heart disease
• Schistosomiasis (#1 cause of pulmonary hypertension outside the US)

A quick interruption to review the three types of CT chest you might consider to evaluate the lungs:

• CT angiogram (aka CTA) is a very quick scan from feet to head chasing the dye, itskips very low bases and apices of lungs and should never be used to assess for interstitial lung disease. Great for acute PE asessment.
• A High Resolution CT Chest: much thinner cuts (2mm) than a CTA starting at apices and going all the way to the bases. 
• Very high detail of parenchyma
• Ground glass opacities can be atelectasis vs. ILD--> flip when prone to see if atelectasis resolves while doing high res scan
• CT w/wo contrast (e.g. nodule) 
• can see 4 generations of branches of bronchial tree, but keep in mind that there are 17, so you cannot see filling defects in the small peripheral vessels

Treatment of Pulmonary Arterial Hypertension (PAP)

1. First identify if the patient has any WHO 2-5 diagnoses that may be influencing their pHtn and treat them maximally, then repeat TTE to check for PAP
2. If they still display pHtn on TTE, they now meet criteria for pulmonary arterial hypertension (PAP).
3. Consider pulmonary vasodilator therapy (obviously in conjunction with pulmonologist). These, while still very expensive, are coming down in price. The meds range currently between $40,000 to $100,000 per year.

When to treat Pulmonary Arterial Hypertension?

There is NO specific number for pressure goals. Look at patients functional class, 6 minute walk, and Echo

Treatment goals:

• Functional class: symptoms at rest (class IV), normal (class I): goal is 2 or less
• 6 minute walk test: goal is 400mg in 6 minutes ("please walk as far as you can in 6 minutes", not "as fast as you can walk")
• BNP: can be elevated in R heart strain, goal is normal
• Echo: goal is RV not fat and chubby, decompressed and slender, TAPSE moving nicely

Pulmonary Hypertension Therapy

• Endothelin pathway: block (bosentan (black box liver toxicity, no longer used), ambrisentan, macicentan: side effects: edema, check LFTs, watch for rare malignant facial edema
• Nitric oxide pathway: enhance (sildenafil TID, tadalafil QD, no lab monitoring, can get blue green colorblindness, rare complication anterior ischemic optic neuropathy (sudden blindness one eye, reversible when stop), riociguat (TID, more systemic hypotension)
• Prostacyclin pathway: enhance (potent, short half life and unstable)
• epoprostenol: IV infusion, tubing connected to a pump, best mortality data, very labor intensive
• treprostinil: IV vs. sq (like insulin pump) and inhaled QID (takes a lot of time, breathing treatment like nebulizer, 20-30 minutes per treatment
• iloprost: inhaled 6-9 times/day
• selexipag: oral BID, no labs but unrealistic uptitration protocol

Guidelines for treatment are based on functional class. The ultimate goal is minimal symptoms with regular activity

If functional class IV-->  needs prostacyclins right away

If functional class III-->  can start with orals (e.g. tadalafil and macicentan)

Any questions? Email or staff message Dr. Helena Wang at: helena.wang@sutterhealth.org