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Lescol in Severe Atherosclerosis Trial - LISA
Description:
The Lovastatin in Severe Atherosclerosis (LISA) trial was designed to assess whether aggressive treatment with the HMG-CoA reductase inhibitor fluvastatin was associated with reduced cardiovascular events within one year for patients with symptomatic coronary artery disease (CAD) and hypercholesterolemia.
Hypothesis:
Fluvastatin will be associated with a reduction in cardiac death, nonfatal myocardial infarction (MI), and unstable angina compared with placebo in patients with CAD established by stress testing.
Study Design
Study Design:
Patients Screened: 572
Patients Enrolled: 365
Mean Follow Up: One year
Mean Patient Age: Fluvastatin 59.4 ± 7.5 years
Female: 38
Patient Populations:
1. Adults aged 40-70.
2. Screening total cholesterol ≥250 mg/dl.
3. Stable symptomatic CAD with abnormal exercise ECG.
4. LDL >160 mg/dl and triglycerides ≤300 mg/dl.
Exclusions:
1. Percutaneous transluminal coronary angioplasty (PTCA) during the previous six months.
2. Planned PTCA or CABG.
3. New York Heart Association class III or IV chronic heart failure.
4. Allergy or intolerance to HMG-CoA reductase inhibitors.
5. Abnormal liver function tests.
6. Pregnant or lactating women.
Primary Endpoints:
Combined cardiac death, nonfatal MI, coronary artery bypass graft surgery (CABG), or unstable angina at one year
Secondary Endpoints:
1. Incidence of unstable angina.
2. Frequency of nitrate use.
3. Exercise tolerance.
4. Carotid artery intimal-medial thickness.
Drug/Procedures Used:
Patients were randomized to fluvastatin 40 mg daily or placebo. If the low-density lipoprotein (LDL) was reduced by ≤30%, the dose was increased to 40 mg twice a day (and placebo twice daily).
Concomitant Medications:
By group (fluvastatin vs. placebo):
Angiotensin-converting enzyme inhibitors (18.7% vs. 21.9%)
Calcium antagonists (31.6% vs. 33.7%)
Beta-blockers (23.0% vs. 18.6%)
Nitrates (52.9% vs. 59.0%)
Aspirin (43.9% vs. 40.4%)
Diuretics (7.5% vs. 5.6%)
Principal Findings:
From baseline to one year, total cholesterol and LDL cholesterol were reduced by 17.4% and 26.9%, respectively, in the fluvastatin arm as compared to 4.9% and 8.0% reductions with placebo. The primary endpoint was reached by 1.6% (3/187) of fluvastatin patients versus 5.6% (10/178) of placebo (p<0.05). Half of the primary endpoints in the placebo group were unstable angina. Anginal episodes were reduced from 2.0 per week to 1.0 per week with fluvastatin and from 2.3 per week to 1.6 per week on placebo (p=NS for comparison). Carotid intimal-medial thickness was minimally changed in fluvastatin (change -0.02 mm) and placebo (change -0.03 mm) groups (p=NS for comparison).
Interpretation:
Among patients with high total and LDL cholesterol, stable angina, and abnormal exercise ECGs, fluvastatin was associated with a reduction in the combined incidence of cardiac death, nonfatal myocardial infarction (MI), and unstable angina compared with placebo at one year, although half of the endpoint events in the placebo arm were unstable angina.
References:
Riegger G, Abletshauser C, Ludwig M, et al. The effect of fluvastatin on cardiac events in patients with symptomatic coronary artery disease during one year of treatment. Atherosclerosis 1999;144:263-70.
Keywords: Myocardial Infarction, Coronary Artery Disease, Atherosclerosis, Lovastatin, Angina, Stable, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Fatty Acids, Monounsaturated, Electrocardiography, Hypercholesterolemia, Lipoproteins, LDL, Indoles, Triglycerides
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