Statins…the best thing since sliced bread?

Thank you to Dr Paul Williams for the many words of wisdom!

Check it out on Class Capture through our Lecture Database.

“Lipids. What are they good for? Absolutely nothin’. Huh”

Hypercholesterolemia leads to LDL accumulation in vessel intima, results in oxidative modification of lipoproteins, which triggers an inflammatory response. Monocytes invade the intima and become foam cells which also trigger smooth muscle cells to migrate from the media to intima.

Rupture of the plaque causes there to be contact of coagulation factors in the blood with the thrombogenic tissue factors.

Statin Drug Information

Statins lead to decreased cholesterol synthesis and hepatic cholesterol concentrations by inhibiting HMG-CoA reductase. They may also have anti-inflammatory effects by acting on Ras and Rho synthesis.

Statin intolerance can be manifested by myalgia, asymptomatic myopathy, myositis, and rhabdomyolysis. Risk factors include age >80, female sex, frailty, hypothyroidism, CKD, DM-2, EtOH abuse, infection, high doses of statins. If there is an elevated CK, statin should be avoided if CK >10 times upper limit of normal. ACC/AHA recommends niacin or cholestyramine if this occurs. Patients with normal CK and myalgias can stop the statin for two weeks and then restart to see if symptoms recur or reduce the dosage or change to fluvastatin or rosuvastatin.

Statins can also modestly increase the incidence of type 2 diabetes, in patients with risk factors for diabetes (metabolic syndrome, impaired fastin glucose, BMI >30, A1c >6%)

Guidelines

Current statin therapy are influenced by the 2013 ACC/AHA practice guidelines. Takeaway points include:

  • patients with clinical ASCVD should be on a high-intensity statin
  • those with an LDL >190 mg/dL should be on a high intensity statin
  • patients with diabetes with LDL between 70-190 should be on a moderate intensity statin (if 10 year ASCVD risk >7.5% should be on a high intensity statin)
  • patients with a 10 year ASCVD risk >7.5% should be on a moderate or high intensity statin.

Basics of EKG, Part 1

Dr Greenberg started off our EKG series with an overview of how to read EKG’s.

Click here for the lecture powerpoint. Audio/video coming soon!

The most important point? If he, an electrophysiologist who has read thousands of EKG’s, still uses the following method to read every EKG.

  1. Rate
    • Count big boxes between each RR interval. For each big box in R-R interval, count down: 300bpm-> 150bpm->100bpm->75bpm->60bpm->50bpm…, or
    • Count QRS complexes in a 10s rhythm strip, multiply by 6
  2. Rhythm
    • p wave precedes each QRS?
    • QRS after every p wave?
    • Are the p waves and QRS complexes regular?
    • Is the PR interval constant?
  3. Axis (ventricular)
    1.  Simple limb lead method (not 100% but gets almost all)
      1. Normal: up in I and AVF.  OR: up in I, down in AVF, up in II
      2. L Axis: up in I, down in AVF, down in II
      3. R Axis: down in I
    2. R wave progression: RS complex should be isoelectric by V3-V4
  4. Intervals
    1. PR = atrial depolarization: normal 120-200msec
    2. QRS: normal 80-100msec (100-120msec: slightly wide; >120msec: wide)
    3. QTc: Normal <440msec (males) or <460msec (females)
      1. Rough estimate–normal less than 1/2 the RR interval
      2. Bazett calculation (QT / (sq root of RR interval in seconds)
  5. Morphologies
    1. P wave
    2. QRS Complex
    3. ST – T wave (ST depression, ST elevation, T wave changes)
    4. U wave

Other notables:

  • 1 small box = 0.04s (40msec)
  • 1 big box = 5 small boxes = 0.2s (200msec)