You are on page 1of 3

Circ J 2005; 69: 1000 – 1002

Acute Myocardial Infarction in a Patient


With Essential Thrombocythemia
Successful Treatment With Percutaneous
Transluminal Coronary Recanalization

Einosuke Mizuta, MD; Shin-ichi Takeda, MD*; Norihito Sasaki, MD*;


Junichiro Miake, MD; Toshiriro Hamada, MD*; Masaki Shimoyama, MD*;
Fumihito Tajima, MD**; Osamu Igawa, MD*;
Chiaki Shigemasa, MD*; Ichiro Hisatome, MD

A 65-year-old woman with essential thrombocythemia (ET) was admitted to hospital where she was diagnosed
as acute myocardial infarction (AMI). Because of abundant thrombus of right coronary arteries, percutaneous
transluminal coronary recanalization by administration of urokinase was selected as the reperfusion therapy,
resulting in successful revascularization with Thrombolysis in Myocardial Infarction grade III coronary flow.
The maximum creatine kinase reached 507 IU/L, and left ventriculography performed at 1 month after initiation
of both anticoagulant and antiplatelet therapies revealed reduced motion in the inferior wall with an ejection
fraction of 57%. Despite good recovery of left ventricular function, bleeding complications, such as epistaxis or
ecchymoma, which did not require blood transfusion, occurred during the clinical course. Because ET causes not
only thrombus formation but also bleeding tendency, it is very important to carefully follow-up any clotting
abnormality in AMI patients with ET. (Circ J 2005; 69: 1000 – 1002)
Key Words: Acute myocardial infarction; Essential thrombocythemia; Percutaneous transluminal coronary
recanalization

E
ssential thrombocythemia (ET) is a clonal myelo- Several agents are now available for initial treatment of
proliferative disorder of unknown origin, charac- ET to prevent thrombus.8 There is evidence that hydrox-
terized by a persistent increase in the platelet yurea, which controls platelets, is effective in preventing
count. In the past, ET was described as hemorrhagic throm- thrombus in ET patients at high risk for systemic artery
bocytosis,1–3 but recent studies have reported that thrombo- disease.9 Low-dose aspirin therapy (100 mg/day) reduces
embolic complications, especially thrombus in the cerebral, coronary thrombosis without increasing bleeding complica-
coronary, and peripheral arteries, were more frequent than tions in patients with elevated platelet count and common
hemorrhages in patient with ET.4,5 Pulmonary embolism atherosclerotic risk factors.7 There are many reports about
and deep-vein thrombosis were less frequent than arterial the efficacy of drug therapy for preventing coronary artery
thrombus.6 The incidence of acute coronary disease in disease in patients with ET, but no guidelines to treat AMI
patients with ET was reported as 9.4% and that of acute in such patients, as ET causes the high-risk complications
myocardial infarction (AMI) as more frequent in patients of thrombosis, as well as hemorrhage, during acute treat-
older than 40 years.7 Smoking and hypertension are risk ment of AMI.
factors of arterial ischemic complications, including AMI, We present a case of ET accompanied by AMI which
in patients with ET. was characterized by both coronary artery thrombus and
bleeding during the clinical cause.
(Received December 27, 2004; revised manuscript received April 27,
2005; accepted May 25, 2005) Case Report
Divison of Genetic Medicine and Regenerative Therapeutics, Depart-
ment of Regenerative Medicine and Regenerative Therapeutics, A 65-year-old woman visited the Emergency Depart-
Institute of Regenerative Medicine and Biofunction, Tottori Graduate ment of Tottori University Hospital because of severe chest
School of Medical Science, Tottori University, *Department of
Molecular Medicine and Therapeutics, Division of Multidisciplinary
pain lasting for 3 h. She was a smoker and had a past histo-
Internal Medicine, Division of Multidisciplinary Internal Medicine, ry of hypertension, chronic renal failure, and ET, but did
Tottori University Faculty of Medicine and **Department of Medi- not have a family history of heart disease or hemorrhagic
cine and Clinical Science, Division of Multidisciplinary Internal disorder. She had been already treated with hydroxyurea
Medicine, Tottori University, Tottori, Japan and ticlopidine because of the previous diagnosis of ET
Mailing address: Einosuke Mizuta, MD, Division of Genetic Medi- when her platelet count was 1,500,000 /mm3. The vital
cine and Regenerative Therapeutics, Department of Regenerative
Medicine and Regenerative Therapeutics, Institute of Regenerative
signs on admission were as follows: blood pressure,
Medicine and Biofunction, Tottori Graduate School of Medical 140/76 mmHg; pulse rate, 64 beats/min, regular; tempera-
Science, 86 Nishicho, Yonago 683-8503, Japan. E-mail:einosuke@ ture, 35.4°C. Laboratory results were as follows: white
grape.med.tottori-u.ac.jp blood cell count, 13,400 /mm3; hemoglobin, 12.3 g/dl;

Circulation Journal Vol.69, August 2005


MI and Thrombocythemia 1001

Fig 1. Angiography of the right coronary artery before PTCR. Fig 2. Angiography of the right coronary artery after the procedure.

platelet count, 469,000 /mm3; serum sodium, 143 mmol/L; remarkable complications did not occur during her clinical
serum potassium, 4.1 mmol/L; chlorine, 102 mmol/L; blood course other than ecchymoma at the puncture site of the
urea nitrogen 29 mg/dl; serum creatinine, 1.61 mg/dl; serum right femoral artery, which did not appear until the day
glutamate oxaloacetate transaminase, 15 IU/L; serum after angiography. Epistaxis occurred frequently, but was
glutamate pyruvate transaminase, 18 IU/L; serum lactate stopped by compression of the nose for a few minutes. The
dehydrogenase, 458 IU/L; serum creatine kinase (CK), size of the ecchymoma did not increase and vascular echo
173 IU/L; CK-MB, 17 IU/L; blood sugar, 144 mg/dl; C study showed extravasation of blood had already stopped.
reactive protein, 0.08 mg/dl; serum troponin T levels were These complications did not cause a severe anemia that re-
high. No pulmonary congestion was observed on chest X- quired blood transfusion. Von Willebrand factor is known
ray. Electrocardiography revealed heart rate, 52 beats/min, to play crucial role in the onset of arterial thrombosis11–15
sinus rhythm; ST segment elevation in leads II and III, and and her plasma von Willebrand factor was high at 184%.
augmented voltage foot (aVF); poor R progression in leads One month later, the ecchymoma had disappeared, and
III and aVF. Echocardiography showed that the inferior so a treadmill test and repeat CAG were performed. The
wall motion was severely reduced. These findings were treadmill test showed no ischemic change under sufficient
compatible with AMI accompanied by ET, so intravenous load. Although there was still moderate stenosis in the mid
heparin (3,000 U), intravenous and oral nitroglycerin RCA (Fig 2), CAG revealed that blood flow had dra-
(2.5 mg), and oral aspirin (200 mg) were initiated and matically improved and the thrombus had disappeared as
emergency coronary catheterization was performed. When expected. Left ventriculography showed that inferior wall
she arrived at the catheter laboratory, her chest pain had motion had improved. Her platelet count was kept stable at
entirely disappeared, and the ST segment elevation had approximately 600,000 /mm3.
recovered and an inverted T wave appeared in leads II, III,
and aVF. Coronary angiography (CAG) revealed that the
mid region of the right coronary artery (RCA) was ob- Discussion
structed by abundant thrombus with Thrombolysis in Myo- ET is a myeloproliferative disorder characterized by
cardial Infarction (TIMI) grade II flow (Fig 1). Because the abnormal proliferation of megakaryocytes and it causes
thrombus was mainly composed of platelet and fibrin,10 thrombus formation in systemic arteries including the coro-
percutaneous transluminal coronary recanalization (PTCR) nary arteries. In AMI associated with ET, the affected coro-
with intra-right coronary injection of urokinase (240,000 nary artery is often occluded with a large amount of throm-
units) was selected as the early reperfusion therapy, result- bus, thus a careful therapeutic strategy is required for
ing in improving RCA flow from TIMI grade II to TIMI successful revascularization. We report here that PTCR
grade III. followed by sufficient antiplatelet and anticoagulant thera-
Subsequently, she was treated with anticoagulant and py resulted in a good clinical course of AMI in a patient
antiplatelet drugs, such as heparin, aspirin, ticlopidine, and with ET.
warfarin, to prevent the formation of new thrombus and to We selected PTCR for the early reperfusion therapy
dissolve the existing multiple thrombi. Hydroxyurea was rather than balloon angioplasty because the occlusion was
continued to control the platelet count. As a result, bleeding caused by abundant thrombus. In addition, we thought that
time was prolonged to 8 min and the platelet aggregation the peripheral blood circulation might recover spontane-
test showed that 10μmol/L ADP-induced secondary aggre- ously when cardiac catheterization began, because by that
gation was inhibited. The maximum concentration of CK time her chest pain had disappeared with recovery of ST
was 507 IU/L at 24 h after the onset of chest pain, and no segment elevation.

Circulation Journal Vol.69, August 2005


1002 MIZUTA E et al.

We consider that it is rational to carefully monitor of the 3. Silverstein MN. Primary or hemorrhagic thrombocythemia. Arch
Intern Med 1968; 122: 18 – 22.
inhibition of platelet aggregation in patient with ET be- 4. Bellucci S, Janvier M, Tobelem G. Essential Thrombocythemia:
cause the complications of ET are not only thrombus but Clinical evolutionary and biological data. Cancer 1986; 58: 2440 –
also hemorrhage. Regarding the anticoagulation therapy for 2447.
patient with ET, we treated with aspirin, ticlopidine and 5. Preston FE. Essential thrombocythemia. Lancet 1982; 1: 1021.
warfarin and the patient’s bleeding time was increased to 6. Lofvenberg E, Nordenson I, Wahlin A. Cytogenetic abnormalities
and leukemic transformation in hydroxyurea-treated patients with
8 min and ADP-induced secondary aggregation was in- Philadelphia chromosome negative chronic myeloproliferative dis-
hibited. ease. Cancer Genet Cytogenet 1990; 49: 57 – 67.
Moreover, we treated with hydroxyurea to decrease the 7. Rossi C, Randi ML, Zervinati P, Rinaldi V, Girolami A. Acute coro-
platelet count. Platelets are a major source of von Willebrand nary disease in essential thrombocythemia and polycythemia vera.
J Intern Med 1998; 244: 49 – 53.
factor,11–15 which is known to play a major role in the onset 8. van Genderen PJJ, Michiels JJ. Primary thrombocythemia: Diagno-
of coronary arterial thrombosis. In the present patient, von sis, clinical manifestations and management. Ann Hematol 1993; 67:
Willebrand factor was high (184%), emphasizing the need 57 – 62.
to control the platelet count. 9. Cortelazzo S, Finazzi G, Ruggeri M, Vestri O, Galli M, Rodeghiero
F, et al. Hydroxyurea for patients with essential thrombocythemia
It is also important to control the risk factors for prevent- and a high risk of thrombosis. N Engl J Med 1995; 332: 1132 – 1136.
ing ischemic heart disease in patients with ET, especially 10. Nagata Y, Usuda K, Uchiyama A, Uchikoshi M, Sekiguchi Y, Kato
arterial blood pressure and cigarette smoking, because a H, et al. Characteristics of the pathological images of coronary artery
previous study has shown that they have strong relation thrombi according to the infarct-related coronary artery in acute
with the thromboembolic complications of ET.7 It has been myocardial infarction. Circ J 2004; 68: 308 – 314.
11. Goto S. Understanding the mechanism and prevention of arterial
reported that in patients with ET who also have hyperten- occlusive thrombus formation by anti-platelet agents. Curr Med
sion or who smoke, the blood platelets facilitate the Chem Cardiovasc Hematol Agents 2004; 2: 149 – 156.
endothelial injury, which increases the possibility of throm- 12. Dardik R, Ruggeri ZM, Savion N, Gitel S, Martinowitz U, Chu V,
bosis.16 The present patient was a habitual smoker and had et al. Platelet aggregation on extracellular matrix: Effect of a recom-
binant GPIb-binding fragment of von Willebrand factor. Thromb
apast history of hypertension, so we persuaded her to quit Haemost 1993; 70: 522 – 526.
smoking immediately and monitored her blood pressure 13. Kumagai K, Fukuchi M, Ohta J, Baba S, Oda K, Akimoto H, et al.
very carefully. Expression of the von Willebrand factor in atrial endocardium is
In summary, a case of ET had a good clinical course increased in atrial fibrillation depending on the extent of structural
remodeling. Circ J 2004; 68: 321 – 327.
after AMI treated by PTCR followed by anticoagulant and 14. Marchese P, Murata M, Mazzucato M, Pradella P, De Marco L,
antiplatelet therapy. Careful follow-up of any clotting Ware J, et al. Identification of three tyrosine residues of glycoprotein
abnormality is necessary for AMI patients with ET. Ib alpha with distinct roles in von Willebrand factor and alpha-
thrombin binding. J Biol Chem 1995; 270: 9571 – 9578.
15. Murata M, Matsubara Y, Kawano K, Zama T, Aoki N, Yoshino H,
References et al. Coronary artery disease and polymorphisms in a receptor medi-
ating shear stress-dependent platelet activation. Circulation 1997;
1. Epstein E, Goedel A. Hamorrhagische Thrombozytamie bei vasku- 96: 3281 – 3286.
larer Schrumpfmils. Virchows Arch Pathol Anat 1934; 292: 233 – 16. Fuster V, Badimon L, Chesebro JH. The pathogenesis of coronary
248. artery disease and the acute coronary syndromes. N Engl J Med
2. Gunz FW. A critical review. Blood 1960; 15: 706 – 723. 1992; 326: 242 – 250, 310 – 318.

Circulation Journal Vol.69, August 2005

You might also like