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Development of acute myocardial infarction in a young female patient with essential thrombocythemia treated with anagrelide: a case report.

Lim YH, Lee YY, Kim JH, Shin J, Lee JU, Kim KS, Kim SK, Kim JH, Lim HK - Korean J Hematol (2010)

Bottom Line: However, patients treated with anagrelide might experience cardiovascular adverse effects including myocardial infarction (MI), although these events are rare.There has no found any cardiovascular risk factors in this ET patient, strongly suggesting that anagrelide might be the cause of MI.Therefore, cardiovascular function should be monitored in those patients prescribed with anagrelide.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Department of Internal Medicine, College of Medicine, Hanyang University, Seoul, Korea.

ABSTRACT
Essential thrombocythemia (ET) is a chronic myeloproliferative disorder with a prolonged clinical course. Since this disorder is considered to be at increased risk of thromboembolism, therapy is mainly focused on the decreased risk of thrombohemorrhagic events by use of cytotoxic agents. Anagrelide is a phosphodiesterase III inhibitor which is utilized in the treatment of ET for the reduction of platelets. However, patients treated with anagrelide might experience cardiovascular adverse effects including myocardial infarction (MI), although these events are rare. Herein, we report a case of a 30-year-old female with well controlled ET by anagrelide, who eventually developed an acute non-ST elevation myocardial infarction (MI). There has no found any cardiovascular risk factors in this ET patient, strongly suggesting that anagrelide might be the cause of MI. Therefore, cardiovascular function should be monitored in those patients prescribed with anagrelide.

No MeSH data available.


Related in: MedlinePlus

Coronary angiography (CAG) and intravascular ultrasound (IVUS). (A) Left CAG before intracoronary nitroglycerin injection. (B) Left CAG after intracoronary nitroglycerin injection. (C) Plaque rupture and thrombus formation in an IVUS image.
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Figure 2: Coronary angiography (CAG) and intravascular ultrasound (IVUS). (A) Left CAG before intracoronary nitroglycerin injection. (B) Left CAG after intracoronary nitroglycerin injection. (C) Plaque rupture and thrombus formation in an IVUS image.

Mentions: A 30-year-old female patient presented to the emergency department with dyspnea on exertion and severe left anterior chest pain that had begun about 30 minutes prior to arrival, and which increased in intensity over time. She reported a history of exertional chest pain that had begun 10 days prior to her presentation. Previous studies, including electrocardiography (ECG), cardiac biomarkers, echocardiography, and an exercise treadmill test had shown no abnormalities. Her chest pain had been slightly alleviated by sublingual nitroglycerine. The patient had no smoking history and had no cardiovascular risk factors such as hypertension, dyslipidemia, or diabetes mellitus. The patient had been diagnosed with ET 6 months previously at a workplace health screening, and was being treated with 100 mg aspirin, 500 mg hydroxyurea twice a day, and 1 mg anagrelide three times daily. Her ET was relatively well controlled without any other complications, and her platelet counts had been within the normal range. Initial vital signs were stable, with a blood pressure of 110/80 mmHg, a heart rate of 78 beats/min, and a respiratory rate of 18 breaths/min. S1 and S2 were normal and S4 was faintly audible at the apex. An ECG showed T-wave inversions in leads I, aVL, and in V2 through V5, which were consistent with myocardial ischemia (Fig. 1). Neither cardiomegaly nor pulmonary congestion was noted on a chest X-ray. The MB fraction of creatinine phosphokinase (CK-MB) was 8.5 ng/mL and cardiac troponin I was 3.08 ng/mL (upper normal limit, 0.07 ng/mL). B-type natriuretic peptide (100 pg/mL) was also slightly elevated. A complete blood count showed the following: a leukocyte count of 3.70×103/µL, hemoglobin of 10.5 g/dL, and a platelet count of 388×103/µL. Low density lipoprotein (LDL) cholesterol level was 54 mg/dL. An echocardiograph revealed hypokinesis in the anteroseptal wall and a left ventricular ejection fraction of 55%. These results were compatible with an acute, non-ST-elevation MI. Immediately, the patient was treated with anti-platelet therapy (300 mg aspirin and 600 mg clopidogrel). In addition, according to the early invasive strategy, coronary angiography was performed, which revealed significant segmental stenosis (90%) of the mid left anterior descending artery (LAD) (Fig. 2A). The segmental lesion in the mid LAD did not respond to intracoronary nitroglycerin injection, which excluded coronary spasms as the causative factor (Fig. 2B). An intravascular ultrasound (IVUS) scan showed a focal soft plaque with a ruptured cap and thrombus formation (Fig. 2C). Percutaneous coronary angioplasty and stenting (Promus, 3.5×18 mm) were performed successfully. After coronary angioplasty, the chest pain and T-wave inversions on ECG disappeared. Anagrelide was discontinued, anti-platelet and anti-anginal agents were added to the treatment, and the patient was discharged without further cardiac symptoms.


Development of acute myocardial infarction in a young female patient with essential thrombocythemia treated with anagrelide: a case report.

Lim YH, Lee YY, Kim JH, Shin J, Lee JU, Kim KS, Kim SK, Kim JH, Lim HK - Korean J Hematol (2010)

Coronary angiography (CAG) and intravascular ultrasound (IVUS). (A) Left CAG before intracoronary nitroglycerin injection. (B) Left CAG after intracoronary nitroglycerin injection. (C) Plaque rupture and thrombus formation in an IVUS image.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2983030&req=5

Figure 2: Coronary angiography (CAG) and intravascular ultrasound (IVUS). (A) Left CAG before intracoronary nitroglycerin injection. (B) Left CAG after intracoronary nitroglycerin injection. (C) Plaque rupture and thrombus formation in an IVUS image.
Mentions: A 30-year-old female patient presented to the emergency department with dyspnea on exertion and severe left anterior chest pain that had begun about 30 minutes prior to arrival, and which increased in intensity over time. She reported a history of exertional chest pain that had begun 10 days prior to her presentation. Previous studies, including electrocardiography (ECG), cardiac biomarkers, echocardiography, and an exercise treadmill test had shown no abnormalities. Her chest pain had been slightly alleviated by sublingual nitroglycerine. The patient had no smoking history and had no cardiovascular risk factors such as hypertension, dyslipidemia, or diabetes mellitus. The patient had been diagnosed with ET 6 months previously at a workplace health screening, and was being treated with 100 mg aspirin, 500 mg hydroxyurea twice a day, and 1 mg anagrelide three times daily. Her ET was relatively well controlled without any other complications, and her platelet counts had been within the normal range. Initial vital signs were stable, with a blood pressure of 110/80 mmHg, a heart rate of 78 beats/min, and a respiratory rate of 18 breaths/min. S1 and S2 were normal and S4 was faintly audible at the apex. An ECG showed T-wave inversions in leads I, aVL, and in V2 through V5, which were consistent with myocardial ischemia (Fig. 1). Neither cardiomegaly nor pulmonary congestion was noted on a chest X-ray. The MB fraction of creatinine phosphokinase (CK-MB) was 8.5 ng/mL and cardiac troponin I was 3.08 ng/mL (upper normal limit, 0.07 ng/mL). B-type natriuretic peptide (100 pg/mL) was also slightly elevated. A complete blood count showed the following: a leukocyte count of 3.70×103/µL, hemoglobin of 10.5 g/dL, and a platelet count of 388×103/µL. Low density lipoprotein (LDL) cholesterol level was 54 mg/dL. An echocardiograph revealed hypokinesis in the anteroseptal wall and a left ventricular ejection fraction of 55%. These results were compatible with an acute, non-ST-elevation MI. Immediately, the patient was treated with anti-platelet therapy (300 mg aspirin and 600 mg clopidogrel). In addition, according to the early invasive strategy, coronary angiography was performed, which revealed significant segmental stenosis (90%) of the mid left anterior descending artery (LAD) (Fig. 2A). The segmental lesion in the mid LAD did not respond to intracoronary nitroglycerin injection, which excluded coronary spasms as the causative factor (Fig. 2B). An intravascular ultrasound (IVUS) scan showed a focal soft plaque with a ruptured cap and thrombus formation (Fig. 2C). Percutaneous coronary angioplasty and stenting (Promus, 3.5×18 mm) were performed successfully. After coronary angioplasty, the chest pain and T-wave inversions on ECG disappeared. Anagrelide was discontinued, anti-platelet and anti-anginal agents were added to the treatment, and the patient was discharged without further cardiac symptoms.

Bottom Line: However, patients treated with anagrelide might experience cardiovascular adverse effects including myocardial infarction (MI), although these events are rare.There has no found any cardiovascular risk factors in this ET patient, strongly suggesting that anagrelide might be the cause of MI.Therefore, cardiovascular function should be monitored in those patients prescribed with anagrelide.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Department of Internal Medicine, College of Medicine, Hanyang University, Seoul, Korea.

ABSTRACT
Essential thrombocythemia (ET) is a chronic myeloproliferative disorder with a prolonged clinical course. Since this disorder is considered to be at increased risk of thromboembolism, therapy is mainly focused on the decreased risk of thrombohemorrhagic events by use of cytotoxic agents. Anagrelide is a phosphodiesterase III inhibitor which is utilized in the treatment of ET for the reduction of platelets. However, patients treated with anagrelide might experience cardiovascular adverse effects including myocardial infarction (MI), although these events are rare. Herein, we report a case of a 30-year-old female with well controlled ET by anagrelide, who eventually developed an acute non-ST elevation myocardial infarction (MI). There has no found any cardiovascular risk factors in this ET patient, strongly suggesting that anagrelide might be the cause of MI. Therefore, cardiovascular function should be monitored in those patients prescribed with anagrelide.

No MeSH data available.


Related in: MedlinePlus