Hypercholesterol-emia in Postmenopausal Women
Postmenopausally, women’s risk of cardiovascular disorders rises steeply. Both estrogen replacement and lipid lowering are associated with reductions in cardiovascular end points in these women, though they have not been compared in a head-to-head trial.
Darling et al performed a randomized crossover trial in 58 menopausal women with marked hyperlipidemia (mean total cholesterol = 305 mg/dL) of simvastatin (10 mg/d) vs. combination hormone replacement therapy (HRT) in the form of oral conjugated equine estrogens (up to 1.25 mg/d) plus medroxyprogesterone acetate (5 mg/d) for eight weeks.
Both interventions were associated with favorable lipid changes. The mean decrease in total cholesterol was almost twice as great with simvastatin as HRT (26% vs 14%); similarly, LDL reductions were more dramatic with simvastatin (36% vs 24%). On the other hand, HDL levels were altered favorably to an equal degree (increased 7%) by either treatment.
Although typically not measured in clinical practice, serum Lp(a) levels are a powerful predictor of coronary heart disease. In this trial, HRT, but not simvastatin, substantially reduced Lp(a) levels.
Most of the beneficial effect of HRT has been attributed not to changes in lipid levels, but rather to vasculotonic effects of estrogen on the vessel wall and renewal of nitric oxide production by the endothelium. Nonetheless, it is of value to confirm the salutary effect of HRT on relevant lipid fractions.
Darling G, et al. N Engl J Med 1997; 337:595-601.
Clinical Scenario: The figure shows a 12-lead ECG obtained from an older woman with suspected coronary disease. Can you explain the events in the simultaneously recorded lead II rhythm strip that appears below the 12-lead ECG shown in the figure (i.e., what are beats #7 and #8)?
Interpretation: The underlying rhythm is sinus, as seen from the obviously upright P wave in lead II. This tall, peaked P wave is consistent with right atrial abnormality (RAA). Otherwise, there are minimal nonspecific ST-T wave changes on the 12-lead tracing that do not appear to be acute.
The first six beats in the lead II rhythm strip are sinus with slight variability in heart rate (sinus arrhythmia). The advantage of using simultaneous lead recording is evident from beat #7, which looks narrow in this lead II rhythm strip. In reality, this beat is wideas seen from simultaneously recorded leads V1, V2, and V3. Beat #7 is therefore a premature ventricular contraction (PVC). A retrograde P wave is seen in the rhythm strip as the small peaked negative deflection that follows this QRS complex.
There is then a short pause that ends with a narrow complex (beat #8). Note that beat #8 is slightly different in appearance than all other sinus-conducted beats on this rhythm strip. Beat #8 is therefore a junctional escape beat. I, too, is followed by a retrograde P wave (the notch at the J point of beat #8) that manifests an even shorter RP interval than the retrograde P wave that followed the PVC. This makes sense because the retrograde distance to arrive at the atria is less for a junctional beat than it is for a ventricular beat.
Beats #9 and #10 suggest resumption of the rhythm with sinus bradycardia. The reason the rate is so slow for these beats may be the result of retrograde conduction (from beats #7 and #8) having delayed sinus node recovery.