dl

Eur Heart J 1989;10:106&1074. 9. Huikari HV, Kessler KM, Terracall E, Catellanos A, Liialuoto MK, Myerbq RJ. Reproducibility and circadian rhythm of heart rate variability in healthy subjects. Am J Cardiol 1990;65:391-393. 10. Kleiger RE, Bigger JT, Bosner MS, Chug MK, Cook JR, Rolnitzki LM, Steinman R, Fleiss JL. Stability over time of variables measuring heart rate variability in normal subjects. Am J Cardiol 1991;68:626-630. 11. Van Hoogenhuyze D, Weinstein N, Martin GJ, Weiss JS, Schaad JW, Sabyouni N, Fintel D, Remme WJ, Singer DH. Reproducibility and relation to mean

Effect of Lovastutin Other Day on Serum Cholesterol Joseph

P. Rindone,

Administered Every Low-Density Lipoprotein > 160 mg/dI

PharmD, Roland0

he efficacy and safety of lovastatin in treating‘hyperT lipidemia is well estab1ished.l Its apparent advantages in treating patients with hyperlipidemia are partially offset by its acquisition cost. At a dose of 20 mg/ day, the yearly cost of lovastatin approaches $1,000 (average wholesale price plus pharmacy markup). One strategy to lower the cost of lovastatin is to administer a smaller dose. Studies have shown that lovastatin 10 mg/day significantly reduces low-density lipoprotein (LDL) cholesterol in patients with elevared serum cholesterol.2A Lovastatin is available as a 10 mg tablet, but the cost is comparable to the 20 mg size. To reduce cost, lovastatin 20 mg tablets could be cut in half, but the tablets are not scored and cutting a 20 mg tablet in half may be problematic for patients. We therefore undertook a pilot study examining the efficacy of administering lovastatin 20 mg every other day in patients with hypercholesterolemia. . . . Patients who had LDL of >160 mg/dl despite following a 3-month trial of an American Heart Association phase I diet were recruited into the study. Compliance to the diet was assessed by diet history and any changes in weight. Patients were excluded if they had any evidence of liver disease, a serum triglyceride level of >400 mg/dl, a previous i,ntolerance to lovastatin, or if they were taking concurrent hypolipidemic medication. All eligible patients received lovastatin 20 mg every other day for 6 weeks. Patients were instructed to take lovastatin with their evening meal. Serum cholesterol, triglycerides, high-density lipoprotein cholesterol, and liver function tests were determined before and after 6 weeks of lovastatin therapy. LDL was calculated by using standard published forTABLE I Effect of mulas.5 Compliance to lovastatin was assessed by tablet count. Data were analyzed by comparing mean total se-

From the Departments of Pharmacy and Medicine, Veterans Affairs Medical Center, Prescott, Arizona 863 13. Manuscript received February 2, 1995; revised manuscript received and accepted May 22, 1995.

312

THE AIyIERlCAN

JOURNAL

OF CARDIOLOGYa

heart rate of heart rate variability in normal subjects and in patients with congestive heart failure secondary to coronary artery disease. Am J Cardiol 1991;68: 1668-1676. 12. Hohnloser SH, Klingenheben T, Zabel M, Schroder F, Just H. Intraindividual reproducibility of heart rate variability. PACE 1992;15:2211-2214. 13. Bigger JT Jr, Fleiss JL, Rolnitzky LM, Steimnan RC, with data contributed by the CAPS and ESVEM Investigators. Stability over time of heart period variability in patients with previous myocardial infarction and ventricular arrhythmias. Am J Cardiol 1992;69:718-723.

Total cholesterol LDL Triglycerides HDL

Achacoso,

76

Ray Bledsoe,

MT

rum cholesterol, triglycerides, high-density lipoprotein cholesterol, and LDL before and after lovastatin therapy. Statistical analysis was performed using a paired t test. An CYof 0.05 was considered statistically signticant. Twenty-one patients were entered into the study. One patient developed angioedema during lovastatin therapy and was withdrawn from the study. Another patient was lost tb follow-up. Nineteen patients (17 men and 2 women, mean age 66 f 8 years) completed the study. Nine patients had a history of coronary artery disease. The effects of lovastatin on lipid components are depicted in Table I. The mean reduction in cholesterol and LDL was 15% and 20%, respectively. There were no statistically different changes in triglycerides and HDL. No change in weight was noted before or after lovastatin. Lovastatin was well tolerated, although 1 patient developed muscle cramping toward the end of the study. No evidence of hepatitis occurred in any patient. Compliance to lovastatin ranged from 90% to 100% (mean 98%). . . . These data show that lovastatin 20 mg administered every other day is effective in reducing LDL. This is slightly less than the 24% reduction in LDL reported when lovastatin 20 mg/day was administered.l Our results are consistent with other studies reporting a 17% to 25% reduction in LDL when lovastatin was administered as either 5 mg twice daily, or 10 mg once daily.2-4 Compliance to lovastatin was excellent in our study despite many patients taking multiple medications. In conclusion, lovastatin administered as 20 mg every other day is effective in lowering LDL levels in patients with serum LDL >160 mg/dl. Lovastotin

on Lipid Components

Baseline

At 6 Weeks of Therapy (mg/dl)

h/4

270

f 20

230

191 185 41

zt 18 zt 69 it0

153 170

Values are expressed as mm HDL = highdensity lipoprotein;

VOL.

MD, and

AUGUST

A 27

zt 28 f 73 43 f 11

* SD unless otherwise indicated. LDL = low-density lipoprotein.

1, 1995

% Change

p Value

-15

0.001 0.001

-20 -8 +5

0.07 0.52

1. Bradford RH, Shear CL, Chermos AN, Dujovne C, Downton M, Franklin FA, Gould AL, Haney M, Higgins J, Hurley DP, Langendorfer A, Nash DT, Pool JL, Schnaper H. Expanded clinical evaluation of lovastatin (EXCEL) study results. Arch Intern Med 1991;151:151-143. 2. Rubinstein A, Lmie Y, Groskop I, We&rob M. Cholesterol-lowering effects of a 10 mg daily dose. of lovastatin in patients with initial total cholesterol levels 200 to 240 mg/dl. Am J Cardiol 1991;68:1123-1126. 3. The Lovastatin Study Group. Therapeutic response to lovastatin (Mevinolin) in

Systolic Percutaneous Douglass

Morrison,

nonfamilial hypercholesterolemia. JAMA 1986;256:2829-2834. 4. Have1 RJ, Humtinghake DB, Illingworth DR, Lees RS, Stein EA, Tobert JA, Bacon SR, Bolognese JA, Frost PH, Lamkin GE, Lees AM, Leon AS, Gardner K, Johnson G, Mellies MJ, Rhymer PA, Ton P. Lovastatin (Mevinolm) in the treatment of heterozygous familial hypercholesterolemia. Ann Intern Med 1987;107:609-615. 5. Summary of the second report of the National Cholesterol Education Program (NCEP). Expert panel of detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel II). JAMA 1993;269:3015-3023.

Blood Pressure Response to Transluminal Coronary Angioplasty for Cardiogenic Shock

MD, Stephen

T. Crowley,

MD, Roger Bies, MD, and Charles

ardiogenic shock complicates 5% to 15% of acute myocardial infarctions. 1 A number of consecutiveC case series have strongly suggested that percutaneous transluminal coronary angioplasty (PTCA), especially when it results in patency of the infarct-related artery, may be associated with improved in-hospital and shortterm survival.26 This study reports a small series of patients with cardiogenic shock who underwent PTCA, and suggests that the blood pressure response to successful dilatation of the infarct-related artery may predict hospital discharge. . . . Patients with cardiogenic shock met 4 criteria: (1) acute myocardial infarction by chest pain, electrocardiogram, and enzymes within 96 hours of coming to the catheterization laboratory; (2) sustained systolic blood pressure ~90 mm Hg; (3) pulmonary wedge pressure >18 mm Hg; and (4) some evidence of tissue hypoperfusion (altered mental status or obtundation, oliguria, rising creatinine, cool extremities, metabolic acidosis). These patients constitute 1.9% (17 of 902) of PTCAs performed between 1988 and July 1994 at our institution. Table I summarizes clinical variables seen in this cohort. In this series, most patients were elderly (71% >65 years of age) and had 3-vessel coronary artery disease (65%). Conventional balloon angioplasty was performed in all of these patients. Systolic blood pressure was measured in the central aorta using the fluid-filled guiding catheter connected to a pressure transducer. Changes refer to the pressures before and after dilatation of the coronary Jesion without a change in intraaortic balloon counterpulsation or pressor drug support. Successful angioplasty (~50% residual stenosis) was obtained in the culprit or infarct-related artery in 12 patients (71%). In 8 of 12 patients and in 8 of 8 hospital survivors, a successful angioplasty result was associated with an increase in systolic BP of >lO mm Hg. Three patients had a successful PTCA result but no change in systolic blood pressure, and all died before hospital discharge. Patient From the Cardiolog Section, Denver Veterans Affairs Medical Center and University o Y Colorado Health Sciences Center, 1055 Clermont Street, Denver, Colorado 80220. Manuscript received March 28, 1995; revised manuscript received and accepted May 17, 1995.

TABLE I Clinical

and

Characteristic

Angiographic

RN

1

Characteristics

Entire Group (n = 17) 12 13 9 11 11

C. Barbiere,

(71) (76) (53) (65) (65)

Increased (n !‘B)

2 (25)

No

Change in BP (n = 9)

Age 265 years Q-wave infarct Remote infarct 3-vessel disease Congestive failure Ventricular fibrillation IABP Right heart catheter

17 (100) 17 (100)

8 (100) 8 (100)

9 (100) 9 (100)

Pressor drugs Survived hospitalization

10 (59) 8 I471

4 WI 8 (100)

6 (67) 0

6 6 6 5

(75) (751, (751 (63)

8 7 3 5 6

(89) (781 (331 (561 (67)

Values are expressed as number (%). IABP = intraaortic balloon counterpulsation.

mortality occurred in 9 of 17 patients (53%): 6 of 6 patients with unsuccessful and in 3 of 12 with successful PTCAs. All patients (9 of 9) without improvement in systolic blood pressure died during index hospitalization. . . . Cardiogenic shock after acute myocardial infarction is associated with a very high in-hospital mortality.1,2 A number of recent studies have suggested that PTCA, particularly if it is successful in terms of achieving infarctrelated artery patency and flow, may favorably influence the outcome of patients with cardiogenic shock.26 To date, every patient taken to our catheterization laboratory in cardiogenic shock who has survived to leave the hospital has responded to successful dilatation of the infarct-related artery, with an acute increase in systolic blood pressure of >10 mm Hg; most have had an increase of >20 mm Hg. The same response has been seen in many hemodynamically compromised patients, and in some patients with angina at rest. Failure of blood pressure to increase after a technically successful PTCA in a patient in cardiogenic shock has uniformly been associated with mortality within 96 hours, despite intraaortic balloon counterpulsation and pressor drugs. This study reports that an improvement in systolic blood pressure of >lO mm Hg after PTCA in patients with cardiogenic shock was associated with in-hospital survival (8 of 8 patients). Failure to achieve infarct artery patency (6 of 6) or technically

BRIEF REPORTS

313