Torsades de Pointes

• “Twisting of the ribbons”
• Polymorphic ventricular tachycardia with prolonged QT
  • The QT prolongation is important, since there are other polymorphic VTs that aren’t Torsades and need very different Tx
  • DISCLAIMER: Addie may have been sloppy in past episodes with calling certain polymorphic tracings “Torsades” when in face they weren’t Torsades by definition
• Tx? Empiric IV Mg. (And possibly K, since → “HypoMag is HypoK” → Phrase Addie has heard a bunch from Corey Slovis; see more from Whang and colleagues, 1992.)
  • Why give empirically?
    • “Serum concentrations of magnesium do not correlate with intracellular concentrations.” –Reinhart, 1992, Ann Emerg Med.
    • Serum Mg is usually measured in the non-active (non-ionized) form; one study found 82% of patients with “low” serum Mg actually had normal ionized (active) Mg [citation]

Clinical Pearl

Atrial fibrillation does not generally create a pulse that is palpable at the radial artery. I always palpate a radial pulse while also auscultating the heart. This way, if I detect “irregularly irregular” beats, I also have some sense whether those beats are a-fib or another rhythm. [Systematic review of radial palpation in a-fib]

Second Clinical Pearl?

The first sign of [which endocrine disorder] may be a-fib? (Supposedly a-fib is like 4x as common in this case.) [Answer: hyperthyroidism]

Hyperlipidemia & Atherosclerosis

Second topic goes here. Probably something related to hyperlipidemia or atherosclerosis? Thoughts?

We know that cholesterol in our diet causes blood cholesterol levels to rise. That said, there are a number of studies (and thus a lot of physicians) that say that dietary cholesterol is not related to blood cholesterol. Why is that? Well we see that blood cholesterol rises after eating cholesterol heavy foods, but this is usually transient in nature. Typically within 6-8 hours we are back to our “baseline” cholesterol (https://doi.org/10.1177/000456329002700512).

The majority of the time when individuals are getting a lipid panel they are told to fast before their panel is drawn. Why is that? We know that transiently there is a change in blood cholesterol following cholesterol intake (sort of like a cholesterol bolus), but the idea is that this is temporary and thus does not represent an individuals baseline/true levels. (PMID:7868978)

You can think of this similarly to glucose. If I ate a bag of candy, you wouldn’t immediately look at my glucose and come to a conclusion about whether I had diabetes, (unless I was above 200). Instead you would look at an A1c (in addition to one of those other numbers).

The issue with cholesterol is that a few papers have shown (using human and animal models) that atherogenesis occurs in the post-prandial period (https://doi.org/10.1161/01.CIR.60.3.473). This means that we may not actually be interested in those baseline cholesterol levels, but rather, we are interested in the cholesterol levels after a meal. This is particularly important when we think about the fact that we are more often than not in a post prandial state (since we eat every 8 hours or more frequently).

Addie also mentioned fibrates lower cholesterol but do nothing for mortality. And of course a citation was promised, so here is a Cochrane Review paper → Wang D, et al. “Fibrates for secondary prevention of cardiovascular disease and stroke.” Cochrane Database Syst Rev. 2015. https://www.ncbi.nlm.nih.gov/pubmed/26497361 … But really this is true of all the “extra” drugs Franke was talking about, not just fibrates. See below.

“The table [below] summarizes 29 major RCTs of cholesterol reduction … Notably, only 2 of these 29 studies reported a mortality benefit, while nearly two-thirds reported no cardiovascular benefit at all. These unfavorable outcomes and inconsistent results suggest that the lipid hypothesis has failed the test of time.” — Dubroff R. “A Reappraisal of the Lipid Hypothesis.” Am J Med. https://www.amjmed.com/article/S0002-9343(18)30404-2/fulltext

“The 2014 AHA/ACC guideline on the management of non-ST-elevation acute coronary syndromes (NSTE-ACS) states, ‘Therapy with statins in patients with NSTE-ACS reduces the rate of recurrent myocardial infarction, coronary heart disease mortality, need for myocardial revascularization, and stroke.’ Not referenced in this guideline was the Cochrane meta-analysis of 18 RCTs of statins for acute coronary syndrome that reported no benefit in 14,303 patients. Similarly, the National Lipid Association Statin Diabetes Safety Task Force concluded that the cardiovascular benefits of statin therapy outweigh the modest risk of developing diabetes. By reviewing only short-term statin studies, they overlooked the impact of long-term exposure.

→ NNT for statins in primary prevention?

• Number varies a lot depending on the trial and the outcome (all cause mortality vs cardiac mortality vs composite outcome of various things, etc).
• USPSTF systematic review [link]:
  • All-cause mortality → Across 15 studies, “the NNT ranged from 47 to 294 over 2 to 6 years in nine trials, and six trials reported no benefit from statins; the pooled NNT was 250.“
  • Cardiac mortality → “…the pooled NNT was 500 (range, 76 to 1,111 in 8 trials; 2 trials found no benefit with statin therapy)”

Vocab

The vocab word of the episode is → Lancinating

“Precordial catch syndrome is a short, lancinating chest pain occurring in bunches lasting 1 to 2 minutes near the cardiac apex…” — Tintinalli’s Emergency Medicine, A Comprehensive Study Guide

“Over time, neuropathic pain may become independent of the inciting injury, becoming burning, lancinating, or shock-like in quality…” — Bates’ Guide to Physical Examination and History Taking

Step1 Q

A 67 year old female with a history of osteoarthritis, hyperlipidemia, and chronic a-fib is evaluated in the urgent care setting for a two day history of dysuria and urinary frequency. The patient’s workup includes a complete history, CBC, BMP, and urine analysis which is positive for nitrites. Three days later she is evaluated in a the same health system’s emergency department, secondary to a fall sustained at home. The patient requires transfusion of 5 units of FFP. The hospital system’s medical malpractice committee reviews the case. They are most likely to find:

1. The urgent care provider should have prescribed an antibiotic
2. The urgent care provider did not appropriately adjust the dose of the patient’s antibiotic
3. The urgent care provider did not choose the correct antibiotic for this patient
4. The urgent care provider delivered excellent care that exceeded current professional standards

EBM

Today’s EBM discussion looks at the results of: Schwartz L.M & Woloshin S. “Communicating Uncertainties About Prescription Drugs to the Public.” Archives of Internal Medicine. 2011. doi:10.1001/archinternmed.2011.396 → https://www.ncbi.nlm.nih.gov/pubmed/21911629

“A total of 2944 participants were randomized to receive 1 of 3 explanations about a pair of cholesterol drugs (1 approved based only on a surrogate outcome [lower cholesterol] and 1 based on a patient outcome [reduced myocardial infarctions]).”

General findings:

• “Thirty-nine percent mistakenly believed that the FDA approves only ‘extremely effective’ drugs”
• “25% mistakenly believed that the FDA approves only drugs without serious side effects.”
• “Which [heartburn] drug do you believe is safer”
  • Two hypothetical drugs; one newly approved, one on market 8 years → 69% believed newer drug is safer

Outcomes-oriented findings:

• “Imagine you had vascular disease. You could take QUESTOR—the drug that lowered cholesterol and reduced heart attacks or CHOLESTAT [which is shown to reduce cholesterol]. If both drugs were free, which would you rather take?” → 41% of controls preferred the surrogate-outcome-only drug (‘CHOLESTAT’).
  • In the experimental group, which was also told, “CAUTION: CHOLESTAT has only been shown to lower cholesterol levels. It is not known whether it will help patients feel better or live longer” → 29% wanted ‘CHOLESTAT’ over ‘QUESTOR’

 

 

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— Episode credits —

Hosted by Addie, Kim, and Alex.
Audio production and editing by Addie.
Show notes written by Addie (with a little bit of Alex).