Patients occasionally do not tell us the truth, especially about their compliance with medications, either because they are embarrassed to admit they are not taking the medicines or for other reasons. So, it’s important that clinicians develop ways to verify that patients are actually taking their medicines. We discussed using chloride levels as an indicator as to whether or not a patient with chronic heart failure is taking the diuretic.1 I admit to a love affair with serum chloride levels not only to indicate when patients are taking their medications, but also as one component of deciding when they have been diuresed enough. I also always check heart rate in patients treated with beta-blockers to reassure me that they are taking their medication. If the heart rate is higher than expected, perhaps they are not taking the beta-blocker. I will never forget one of my Stanford clinic patients, who had difficult-to-control hypertension because she did not take her medications. Our attendings staffed the clinic when the fellows were away. One of the attendings covering for me did a pheochromocytoma workup on this woman because her heart rate was high and she said she was taking her propranolol.
There are other little tip-offs that can be used with lipid-lowering medications. Bile acid sequestrants like colesevalam and cholestyramine usually increase the triglyceride levels slightly as we discussed previously2. That’s because bile salts are reabsorbed, pass into the portal circulation, and come back to the liver to suppress triglyceride production. Bile sequestrants bind bile salts and take them out the “poop shoot” (that’s the medical term) so they cannot go to the liver to suppress triglyceride synthesis. Both fibric acid and bempedoic acid produce slight increases in the creatinine because they block renal tubular creatinine excretion. So, I watch creatinine in some patients with severe hypertriglyceridemia and occasional medicine non-compliance as an additional way to assess their adherence. If their triglycerides are high again, I glance at their creatinine. It helps let me know if they need a “come to Jesus” lecture.
Missing their beta-adrenergic blockers can cause patients to present with worsening symptoms of cardiac ischemia. The number and activity of beta-adrenergic receptors increases when patients are a beta-blocker so withdrawing the drug suddenly leads to an increase in sensitivity to their endogenous catecholamines. Always think of the possibility that a patient with worsening ischemic symptoms, resting tachycardia, atrial fibrillation more rapid than usual, or an increase in ventricular extrasystoles is not taking their beta blocker. Knowing about the issue of beta-blocker withdrawal is especially important when consulting on hospitalized patients. The beta blockers are often stopped for various reasons, and many clinicians are unaware that abrupt beta-blocker withdrawal can have deleterious effects. Looking at the heart rate and asking if it’s low enough for that dose of beta blocker can help accept or dismiss that possibility.
Some patients have decreased their medication dose without knowing it. Generic medications are wonderful because they cost far less for patients and for the healthcare system, but there is a possible downside. Some generic drugs do not have the same absorption and bioavailability as the original compound. That means that the patient who is stable on one formulation of a drug may get a different response when switched to a generic or to a different generic. Similarly, a hypertensive patient, well-managed with a specific anti-hypertensive agent, may suddenly become hypertensive again if the manufacturer of their hypertensive medications is changed. Whenever a stable patient changes or develops new symptoms, always ask if they have recently refilled their prescription and if there has been a change in the appearance of their medications. The switch from one generic to another is not always benign.
And then there’s cocaine. Everyone lies about their cocaine use, but cocaine is the drug of choice for cardiologists because it generates so much business. You name a vascular problem and cocaine can cause it: myocardial infarction (MI), cardiomyopathy, aortic dissection, arrhythmias, stroke, malignant hypertension, and placenta abruption. I reported what we thought was the second MI with cocaine at a time when it was still considered a safe drug.3 Jeff Isner, MD, my medical school classmate now deceased, myself and others reported other cardiac conditions, including cardiomyopathy, that were linked to cocaine.4 So, I often measure urinary cocaine levels in patients with any cardiac issue, especially if the event happened on the weekend. And you don’t have to think of cocaine and measure it immediately. If taken nasally cocaine can be detected in the urine for up to 7 days because it causes vascular constriction in the nares that slows its absorption.5 That’s why the otolaryngologists loved it. It was an anesthetic, but produced vasoconstriction so reduced bleeding. But if you chronically use it nasally, it also produced septal perforations, where you can put your nose ring. How long cocaine is detectable after smoking or injecting is much shorter than intranasally, but I do not know exactly how long. The point is to think about the possibility of cocaine and test for it in the urine.
By the way, did you know Coca-Cola actually contained cocaine up until 1903, and that it still contains cocaine-free coca leaf extract.6
So, here are the rules:
-Patients lie.
-To verify compliance, use chloride levels for diuretics, heart rates for beta-blockers, triglycerides for bile-acid sequestrants, and creatinine for fenofibrate and bempedoic acid.
-Don’t forget about beta-blocker withdrawal especially in hospitalized patients.
-Lots of people who uses cocaine deny it, so test for it. I guess that’s called, “Don’t Trust and Verify”.
1, https://pauldthompsonmd.substack.com/p/pissing-away-the-chloride?utm_source=profile&utm_medium=reader2 (accessed April 21, 2024)
2. https://pauldthompsonmd.substack.com/p/the-law-of-diagnostic-parsimony?utm_source=profile&utm_medium=reader2 (accessed April 21, 2024)
3. Schachne JS, Roberts BH, Thompson PD. Coronary-artery spasm and myocardial infarction associated with cocaine use. N Engl J Med. 1984 Jun 21;310(25):1665-6. PMID: 6727939
4. Isner JM, Estes NA 3rd, Thompson PD, Costanzo-Nordin MR, Subramanian R, Miller G, Katsas G, Sweeney K, Sturner WQ. Acute cardiac events temporally related to cocaine abuse.
N Engl J Med. 1986 Dec 4;315(23):1438-43. PMID: 37852955. https://www.crestviewrecoverycenter.com/addiction-blog/how-long-does-cocaine-stay-in-your-system/ (accessed April 21, 2024)
6. https://en.wikipedia.org/wiki/Coca-Cola#:~:text=In%201903%2C%20it%20was%20removed,cocaine%2Dfree%20coca%20leaf%20extract. Accessed 21 April 2024
that is so true Dr. Thompson- I found this out by chance when I ordered drug screen in a patient who had HFrEF, though he denied using drugs; but to my surprise his drug screen came back positive and since then I order UDS especially in younger patients with chest pain or HFrEF. I order it even if they say that eat greens all the time.