The Canadian Journal of Hospital Pharmacy (CJHP) / Le Journal canadien de la pharmacie hospitalière (JCPH)

Offman, E.M.

Sabawi, N.

Melendez, L.J.

Volume 51, N° 5 octobre 1998 Le Journal canaclien de la pharmacie hospitaliere ~ 233 
Suspected pravastatin-induced rhabdomyolysis in a 
patient experiencing a myocardial infarction 
E.M. Offman, N. Sabawi and L.J. Melendez 
Can J Hosp Pharm 1998;51: 233-235 
HMG-CoA reductase inhibitors have become the first-line 
agents for treating hyperlipidemia associated with 
increased LDL. While they have been proven to be 
effective in reducing LDL and total cholesterol, and 
increasing HDL cholesterol, potentially serious adverse 
effects may occur in some patients. Rhabdomyolysis is 
one such adverse effect observed in patients treated with 
this class of medications. The purpose of this paper is to 
report a case of a patient presenting with severe ischemic-
type chest pain in whom the timing and magnitude of 
serum enzyme changes are strongly suggestive of 
pravastatin-induced rhabdomyolysis. 
CASE 
A67-year-old obese male presented to the emergency room in May 1997 with shortness of breath and 
severe retrosternal pain radiating to his left arm. During 
the previous 48-72 hours, he had experienced chills, 
sweating, rigors, and he had complained of a 
nonproductive cough over the preceding week. His 
cardiac history was significant for 3 previous myocardial 
infarctions (2 in 1996 and 1 in 1979), coronary artery 
bypass surgery in 1982, congestive heart failure and 
hypercholesterolemia. His medications just prior to 
admission were amlodipine 10 mg daily, furosemide 80 
mg in the morning and 120 mg in the afternoon., 
isosorbide dinitrate 10 mg 3 times daily, ASA 80 mg 
daily, losartan 50 mg daily, digoxin 0.25 mg daily, 
pravastatin 20 mg nightly for the last 9 months, warfarin 
5 mg daily, and cisapride 10 mg 3 times daily. 
Elliott M. Offman, BScPharm, is engaged in graduate 
studies at the Robarts Research Institute, University of 
Western Ontario, London, Ontario. 
N. Sabawi, MD, is a Clinical Nephrology Fellow at the 
London Health Sciences Centre, London, Ontario. 
L.J. Melendez, MD, FRCPC, is a cardiologist at the London 
Health Sciences Centre, London, Ontario. 
Address corespondence to Elliot Offman, c/o Dr. D.C. 
Freeman, Robarts Research Institute, University of Western 
Ontario, 100 Perth Drive, London ON N6A 5K8. 
On examination, the patient's temperature was 39°C, 
his blood pressure was 130/70, his heart rate was 80 beats 
per minutes and and his respiratory rate 20 breaths per 
minute. He had an elevated venous pressure and palpable 
cardiomegaly. His ECG revealed a normal sinus rhythm, 
with a first degree heart block, and no ST segment 
changes. Blood tests showed an elevated leukocyte count 
of 13.1 (normal 4-10 x 109/L) as well as an elevated 
myoglobin at 5500 U/L (normally negative), creatine 
phosphokinase (CK) at 7405 U/L (35-230 U/L), troponin 
I at 13.1 µg/L (0-1 µg/L), and LOH at 444 U/L (88-177 
U/L). The admitting diagnosis was a new acute 
myocardial infarction, though rhabdomyolysis secondary 
to pravastatin was considered and this drug was withheld. 
By the third day after admission, the patient's serum 
creatinine and blood urea nitrogen (BUN) had risen from 
182 ~Lmol/L (70-120 µmol/L) and 7 mmol/L (3.5-7 
mmol/L) to 268 and 19 .4 respectively, with a decreased 
urine output. Serial cardiac enzymes revealed a continued 
increase in total CK despite decreasing troponin I levels. 
By the sixth day following admission, the serum troponin 
had nearly normalized despite the total CK peaking at 
9150 IU/L. Concurrently, the serum creatinine and BUN 
were 324 µmol/L and 33.2 mmol/L respectively. 
The patient received a furosemide infusion in 
combination with oral metolazone to enhance diureses. 
The total CK, serum creatinine and BUN began to 
decrease, and were at levels of 335 IU/L, 174 µmol/L, 
and 35.2 mmol/L respectively by the tenth day post 
admission. At this point, the patient was feeling well with 
his only complaint being fatigue. 
The patient's laboratory results in June 1997 revealed 
a total CK of 90 U/L, a serum creatinine of 119 µmol/L, 
and a BUN of 7.9 µmol/L. 
DISCUSSION 
The marked and persistent elevation in total CK measured in this patient is strongly suggestive of 
extra-cardiac ongm, specifically rhabdomyolysis 
secondary to pravastatin. I However, since there was also 
an elevation of troponin I ( considered of higher 
specificity for cardiac origin) and severe ischemic-type 
234 ~ The Canadian journal of Hospital Pharmacy 
chest pain was present on admission, it is likely that the 
patient also had a non-Q wave myocardial infarction.2,3 
The elevated blood urea and creatinine may have been 
the result of rhabdomyolysis-related renal failure as they 
decreased with continuation of furosemide diuresis. A 
review of the product monographs of the patients 
concomitant medications did not reveal elevation of CK 
or rhabdomyolysis as a potential adverse effect.4 
The HMG-CoA reductase inhibitors, and the fibric 
acid derivatives have been implicated in causing 
rhabdomolysis in the literature.s-10 
In 2 large pravastatin trials involving over I 0,000 
subjects, there were no reports of rhabdomyolysis in the 
safety analysis.10,11 In the WOSCOP trial, 20 of the 3302 
patients receiving pravastatin (0.6%) reported myalgias, 
97 subjects (2.9%) reported muscle aches and 3 patients 
(0.09%) presented with an asymptomatic elevation in CK 
(> 10 times the upper limits of normal). None of these 
incidences were signficantly different from placebo. I I In 
the CARE trial, there were 12 cases (0.6%) of CK 
elevation in the 2081 pravastatin patients (incidence not 
significantly different from placebo), with no reports of 
myalgia or muscle aches.12 
According to manufacturer data, myalgia was 
associated with pravastatin therapy in 2. 7% (n=900) 
compared to 1 % in placebo-treated individuals (n=4 l l ). 
Again, these differences were not statistically 
significant. IO 
Myopathy without renal sequelae has been 
demonstrated in case reports. Although serious myopathy 
is considered rare, one report revealed a severe myopathy 
in a 69-year-old male taking pravastatin for 5 months for 
hypercholesterolemia. The patient, who was also 
suffering from non-insulin-dependent diabetes mellitus, 
was unable to stand, and his skin showed an 
erythematous rash on his thighs. The patient also had 
extreme pain and tenderness in his lower limbs. The 
patient's CK peaked at 1892 U/L, and a biopsy of the 
patient's gastrocnemius ( calf muscle) showed an 
inflammatory infiltrate of lymphocytes, macrophages, 
and eosinophils. Phagocytosis and degenerative changes 
of the muscle were evident.6 
Despite the lack of rhabdomyolysis reported in 
clinical trials, there have been case reports of pravastatin-
associated rhabdomyolysis. One case involves 61-year-
old female who had been taking clofibrate, and was 
switched to pravastatin. Three weeks later she developed 
severe pain in her subscapular region, and her CK levels 
attained a peak level of 682 U/L. The drug was removed, 
and the myalgia disappeared completely 10 days later. 5 
Volume 51, No. 5 October 1998 
Another case in the literature reported a 63-year-old 
female using pravastatin 10 mg per day for her 
cholesterol, as well as famotidine and prednisilone (for a 
mixed connective tissue disorder). Four months after 
starting pravastatin, she presented with muscle pain and 
weakness, fever and dark urine. Her peak CK was 8280 
U/L, and her urine myoglobin level was 1227 µg/L. 
Pravastatin was discontinued, and her CK decreased to 39 
U/L within 7 days. Her renal function, and myalgias 
improved over the ensuing month, without an increase in 
her prednisilone dosage. 7 
Although this adverse event is rare, it is not 
surprising. Both myopathy and rhabdomyolysis have 
been associated with hypercholesterolemia treatment. 
This reaction was initially described with the fibric-acid 
derivatives, but has been demonstrated by the HMG-CoA 
reductase inhibitors. Lipid lowering medication-
associated rhabdomyolysis characteristically occurs 
within the first 2-5 months of treatment; however, the 
patient described in this case had been taking his lipid-
lowering agent for approximately 9 months.5 Factors 
associated with its development include moderate to 
severe renal insufficiency, nephrotic syndrome associated 
hypoalbuminemia, combining HMG-CoA reductase 
inhibitors with fibric-acid derivatives, and 
hypothyroidisms,s As well, the frequency is increased in 
the presence of other drugs such as cyclosporine, 
erythromycin, nicotinic acid, and fibric acid derivatives.5 
The actual cause of the rhabdomyolysis is complex 
and not completely understood. The acute muscle 
damage that occurs often leads to renal damage, which is 
thought to occur via 3 proposed mechanisms.13 The first 
is impairment of renal vascular flow due to sympathetic 
nervous overactivity, followed by activation of the renin-
angiotensin system, alteration of prostaglandin synthesis, 
high circulating levels of antidiuretic hormone and the 
deposition of microthrombi. The second mechanism 
includes tubular obstruction by myoglobin casts or 
crystals of uric acid, with passive diffusion of glomerular 
filtrate. Myoglobin and uric acid are filtered through the 
kidneys and give the urine a reddish-brown colour. 
Lastly, it is thought that ferrihemate (a product of the 
dissociation of myoglobin at pH<5.6) causes direct 
toxicity. Ferrihemate has been shown in animals to 
produce a dose-dependent deterioration in renal function, 
with depression of renal transport mechanisms, cell 
swelling and death. 
As was evident in the patient described in this case, 
renal failure can follow myoglobinuria. Other sequelae 
include hyperphosphatemia, marked hyperuricemia, 
\ 
8 Volume 51, N° 5 octobre 1998 
severe hypocalcemia, metabolic acidosis and 
disseminated intravascular coagulopathy (DIC).13 Our 
patient presented with an anion gap of 16 (normal 8-14) 
on admission, and a calcium of 1.95 mmol/L (2.12-2.62 
mmol/L), and albumin of 32 g/L (35-50) and a phosphate 
of2.20 mmol/L (0.8-1.45 mmol/L) measured on the third 
day of admission. 
Aside from furosemide, other diuretics have been 
used in the treatment of rhabdomyolysis. Mannitol has 
been used to promote diuresis. The increase in 
glomerular filtration leads to an increased intratubular 
flow, followed by a decrease in the tubular obstruction. 
As well, the increased flow flushes out the nephrotoxic 
substances. Manni to I itself has the disadvantage of being 
nephrotoxic at doses greater than 200 grams per 
day.13,14,15 Sodium bicarbonate infusions can also be 
used, as myoglobin and urate crystals are more soluble in 
alkalinized urine, and alkalinization prevents the 
dissociation of myoglobin to its nephrotoxic metabolite 
ferrihemate. Using a sodium bicarbonate infusion 
however, can lead to metabolic alkalosis. 
Once the offending agent is withdrawn, the signs and 
symptoms of myalgia nonnally disappear. Normalization 
of the CK can, however, take 1-2 weeks.5 In our case, the 
patient did not have any overt muscle pain; however, he 
did complain of extreme weakness both during and after 
the episode. It is difficult to determine whether this 
weakness was a result of an adverse reaction or 
secondary to the myocardial infarction. As can be 
expected, this patient's CK levels did not fall until the 
patient recovered from the acute renal effects. The patient 
experienced oliguria, treated by a combination of high-
dose furosemide plus metolazone. 
Patients who develop rhabdomyolysis may benefit 
from lipid-lowering therapy from another class of agents. 
In a case of simvastatin-induced rhabdomyolysis, the 
drug was discontinued and, at least 6 months later, 
gemfibrozil was instituted with no adverse effects by 7 
months. 16 
The literature suggests that any patients starting lipid-
lowering therapy with either an HMG-CoA reductase 
inhibitor or a fibric-acid derivative should be evaluated 
for baseline CK levels and thyroid function. 8, 1 o If not 
identified early, rhabdomyolysis can be a serious adverse 
effect. Therefore, patients taking HMG-CoA reductase 
inhibitors who present with complaints of muscle 
weakness or pain, with elevated CK levels (approximately 
10 or more times their baseline value) should be 
suspected of having a drug-induced myopathy, and have 
the medication discontinued. 
Le Journal canadien de la pharmacie hospitaliere ~ 235 
REFERENCES 
1. Mullner M, Sterz F, Binder M, Brunner M, Hirschi MM, 
Mustafa G, et al. Creatine kinase and creatine kinase-
MB release after non-traumatic cardiac arrest. Am J 
Cardiol 1996;77:581-585 
2. Adams J, Geza B, Davila-Roman V, Delmez J, Apple F, 
Ladenson J, et al. Cardiac troponin I. A marker with high 
specificity for cardiac injury. Circulation 
1993;88:101-106 
3. Adams J, Abendshein DR, Jaffe AS. Biochemical 
markers of myocardial injury. Is MB creatine kinase the 
choice for the 1990s? Circulation 1993;88:750-763 
4. Compendium of Pharmaceuticals and Specialties, 33rd 
edition. M. Claire Gillis (ed.). Canadian Pharmacists 
Association. Ottawa, 1998 
5. Decloux E, Millaire A, de-Groote P, Mahieux G, Ducloux 
G. Rhabdomyolyse sous pravastatine et 
macrocreatinine kinase de type I (in French). Ann 
Cardiol Angeiol 1993;42:267-9 
6. Hino I, Akama H, Furuya T, Ueda H, Taniguchi A, et al. 
Pravastatin-induced rhabdomyolysis in a patient with 
mixed connective tissue disease. Arthritis Rheum 
1996;39: 1259-60 
7. Scalvini T, Marocolo D, Cerudelli B, Sleiman I, 
Balestrieri GP. Pravastatin-associated myopathy: report 
of a case. Adis Reactions Weekly. 29 July, 1995 
8. Gouton M. Hypoparathyroidism, Lipid lowering drugs 
and rhabdomyolysis. Arch Mal Coeur, Vaiss 
1993;86:1761-4 
9. Raimondeau, J., Lemarec, H., Chevallier, J.C., Bouhour, 
J.B. Biological myolysis after replacing fenofibrate by 
pravastatin treatment. Presse Med 1992;21(14):663-4 
10. Pravastatin Product Information. Compiled by Bristol-
Myers Squibb, Medical Information. Montreal, Quebec. 
1997 
11. Shepherd J, Cobbe S, Ford I, Isles C, Lorimer A, 
Macfarlane P, et al. Prevention of Coronary heart 
disease with pravastatin in men with 
hypercholesterolemia. N Engl J Med 
1995;333:1301-1307 
12. Sacks F, Pfeffer MA, Moye L, Roleau J, Rutherford J, 
Cole T, et al .. The effect of pravastatin on coronary 
events after myocardial infarction in patients with 
average cholesterol levels. N Engl J Med 
1996;335:1001-1009. 
13. Predergast BO, George CF Drug-induced 
rhabdomyolysis - mechanisms and management. 
Postgrad Med J 1993;69:333-6 
14. Tuckey J. Bilateral compartment syndrome complicating 
prolonged lithotomy position. Br J Anaesth 
1996;77:546-549 
15. Ball DR, Management of rhabdomyolysis (letter). Br J 
Anaesth 1997;78:340-341. 
16. Deslypere, J.P., Verneulen, A. Rhabdomyolysis and 
simvastatin. Ann Intern Med 1991;114(4):342. • 


English

Suspected pravastatin-induced rhabdomyolysis in a patient experiencing a myocardial infarction

Paton, Thomas W

Teaching and Learning Strategies in Pharmacy Ethics (2nd edition)

Authors, Various

AGM 1998 Poster abstracts

Welcome to the Newfoundland and Labrador Branch of CSHP

Bailey, Caroline L.

Smith, Reginald E.

Volume 50, No. 2, April 1997 The Canadian Journal of Hospital Pharmacy 79 
Intermittent Intravenous Nitroglycerin Boluses for Acute 
Puhnonary Edema 
Caroline L. Bailey and Reginald E. Smith 
INTRODUCTION 
C 
ardiogenic pulmonary edema ( CPE) occurs when 
the pulmonary capillary pressure exceeds the 
forces that maintain f1uid within the vascular 
space. Initial treatment includes maintenance of a pat-
ent airway, administration of 100% oxygen, and secur-
ing intravenous (IV) access. Pharmacologic treatment is 
often instituted with vasodilator therapy. 1-3 Paramedi-
cal staff will typically administer IV furosemide, IV mor-
phine sulphate, and oral, sublingual or topical nitrates. 
Furosemide IV has a direct venodilating effect with an 
onset of vascular effect within five minutes. 2 Effects of 
morphine are, in part, produced by decreased arterial 
resistance and pressure secondary to a reduction of cen-
trally mediated sympathetic neural tone. 1 Nitrates have 
a profound venodilating effect that even at low doses 
result in an increase in vascular capacitance, thus lower-
ing preload and pulmonary capillary pressure. Evidence 
also supports that nitrates have a relaxing effect on col-
la_teral vascular channels, particularly coronary collateral 
vessels, 1 making these agents the therapy of choice if 
CPE occurs as a result of myocardial ischemia. 3 
If the above measures fail, continuous infusion of ni-
troglycerin has been advocated for the treatment of acute 
CPE. 1 However, little information is available regarding 
the use of IV bolus nitroglycerin therapy. We report a 
case in which intermittent nitroglycerin boluses were 
used to treat acute CPE. 
CASE 
A 74 year-old, 52 kg, female developed sudden on-set of shortness of breath at rest and was brought 
into the emergency department by the paramedical serv-
ices. En route to hospital she received 60 mg furosem-
ide IV, morphine 2.5 mg IV, and five doses of sublin-
gual nitroglycerin 0.6 mg. Her medications at home prior 
to admission were isosorbide dinitrate 30 mg PO tid, 
furosemide 20 mg PO daily, and hydralazine 50 mg PO 
tid. Her past medical history included congestive heart 
failure, mild aortic stenosis, hypertension, and a silent 
anteroseptal myocardial infarction. 
On admission, she had a pulse of 121 beats per minute, 
a respiratory rate of 32/min, and a blood pressure of 
200/90 mmHg. She could only speak in short sentences. 
Oxygen by face mask was started at 10 Umin. She re-
ceived nitroglycerin 2 mg IV bolus. This dose was re-
peated after five minutes and a third dose was given two 
minutes later. At this point her vital signs were not sub-
stantially changed. She received an additional IV bolus 
dose of 1 mg nitroglycerin. Her chest x-ray showed car-
diomegaly, small bilateral pleural effusions and wide-
spread pulmonary edema. After 30 minutes of observa-
tion her vital signs improved to a heart rate of 86 beats 
per minute, a respiratory rate of 22/min, and a blood 
pressure 165/67 mmHg. Dyspnea was improved and 
she was admitted to CCU with a diagnosis of CPE. A 
subsequent coronary angiogram showed normal large 
coronary arteries. A nuclear ventriculogram showed a 
dilated left ventricle, hypokinesis of the anterolateral wall, 
and a left ventricular ejection fraction of 41 %. Her furo-
semide dose was increased and she was discharged home 
five days later. 
DISCUSSION 
Nitroglycerin IV is considered part of standard therapy of CPE. 3 However, delivery by IV bolus (over one 
minute or less) has not been widely discussed. 1.2 Al-
though postulated as a possible mode of administration 
in a review published approximately 15 years ago, little 
additional information is available. Continuous infusions 
are generally begun at 5 mcg/min and then increased in 
increments of 5 mcg/min every three to five minutes 
Caroline L. Bailey, MSc, is a Project Pharmacist, Department of Pharmacy, 
Greater Victoria Hospital Society, Victoria, BC. 
Reginald E. Smith, Pharm D, is a Critical Care Specialist, Cardiology and Car-
diac Services, Department of Pharmacy, Greater Victoria Hospital Society. 
Address correspondence to: Caroline L. Bailey MSc, Department of Phar-
macy, Victoria General Hospital, 35 Helmcken Rd, Victoria, BC V8Z 6R5. 
Acknowledgements: The authors wish to acknowledge William McCauley, MD, 
Department of Medicine, Division of Emergency Medicine, University of West-
ern Ontario, for his assistance in the preparation of this manuscript. 
80 Le Joumal canadien de la pharmacie hospitaliere 
until the desired clinical response is achieved or adverse 
effects occur.J 
A review of the literature (MED LINE 1961-1996) iden-
tified only two reports of bolus doses of nitroglycerin 
for CPE, both open trials.'5·6 Bose et al, used 3 mg bolus 
doses to treat CPE in 35 patients. Twenty-seven patients 
(71 %) showed a marked improvement within five min-
utes of a single dose. Five patients (13%) experienced 
hypotension (SBP :s; 90 mmHg). One of these was a pa-
tient who weighed 35 kg, another was a 91 year-old man, 
and a third patient received 5 mg in error. None of the 
hypotensive episodes required treatment with inotropes 
or vasopressors. One patient developed hypotension and 
bradycardia, and required atropine. 
In the report by Nashed et al, patients were treated 
with IV nitroglycerin boluses of 0.05 to 0.4 mg depend-
ing on the patient's systolic blood pressure as shown in 
Table l. 6 This was followed by an infusion of nitroglyc-
erin with additional nitroglycerin boluses repeated every 
five minutes as required. Twenty of the 24 cases (83%) 
responded within 30 minutes and in none of the cases 
did hypotension occur. One patient developed symptomatic 
bradycardia without hypotension, which resolved sponta-
neously after 10 minutes. A second patient experienced 
supraventricular tachycardia which responded to verapamil. 
We believe that the benefit of a bolus technique, as 
suggested by Nashed et al, 6 is that more drug is deliv-
ered early in treatment with more rapid resolution of 
Table I. Nitroglyceria Dosing Regimens 
·.·Stst§li~:£1n·:••·•,:.\ 
BP;:: 180 
140 ~BP< 180 
110 ~BP< 140 
95~BP<110 
''en1u~:l~~e···· 
0.4 mg 
0.3 mg 
0.15 mg 
0.05 mg 
Malnt~·nance.rati 
17µg/min 
10µg/min 
6.7 µg/min 
3.3 µg/min 
Adapted from Nashed et al, 6 and reproduced with permission. 
Volume 50, NO 2, avril 1997 
symptoms. However, in contrast to this group, we use a 
larger bolus dose and do not always start an infusion at 
the same time. 
Currently, there is no standardized protocol in our 
emergency department for the treatment of CPE and the 
initial dose of nitroglycerin employed varies among cli-
nicians. If additional doses of IV nitroglycerin are re-
quired, these are repeated at five to ten minute intervals 
and if multiple, repeat bolus doses are required a con-
tinuous infusion should be considered. 
In conclusion, it appears from our experience and other 
limited reports 5·6 that nitroglycerin IV bolus is a safe and 
effective method of treating acute CPE especially in pa-
tients with significant hypertension. Further study is 
needed to determine the optimal dose and whether such 
therapy is superior to other regimens. 
REFERENCES 
1. Cohn JN. Drugs used to control vascular resistance and 
capacitance. In: Schlant RC, Alexander RW, eds. Hurst's the 
heart: arteries and veins. 8th ed. New York, NY: McGraw-Hill; 
1994:611-20. 
2. Emergency cardiac care committee and subcommittees, 
American Heart Association. Guidelines for cardiopulmonary 
resuscitation and emergency cardiac care. Part Ill. Adult 
advanced cardiac life support. JAMA 1992; 268:2199-241. 
3. Ratner K: Pulmonary edema (Disease and Trauma Monograph 
for Acute Care) in Honigman Band Rumack BH (eds): 
Emergindex® Information System. Micromedex®, Inc., Denver, 
Colorado (edition expires 12/96). 
4. Hill NS, Antman EM, Green LH, Albert JS. Intravenous 
nitroglycerin. A review of pharmacology, indications, therapeu-
tic effects and complications. Chest 1981; 79:69-76. 
5. Bose E, Bertinchant JP, Hertault J. Utilisation de la trinitrine 
injectable (bolus de 3 mg) dans le traitement de l'oedeme 
pulmonaire cardiogenique. Ann Cardiol Angeiol 1982; 31 :477-80. 
6. Nashed AH, Allegra JR. Intravenous nitroglycerin boluses in 
treating patients with cardiogenic pulmonary edema. Am J 
Emerg Med 1995; 13:612-3. Letter. 
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Intermittent Intravenous Nitroglycerin Boluses for Acute Pulmonary Edema

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