Resolution of mid-ventricular thrombus in a patient with heart failure and high hematocrit

Excerpt

A 48-year-old male smoker visited our hospital because of persistent cough for 3 months. He had no previous history and had been prescribed anti-allergic drugs including 0.05 mg of betamethasone for cough. His blood pressure was 149/106 mmHg and his pulse rate was 110 beats per minute. Auscultation revealed normal respiratory sounds and a gallop rhythm. Results of blood testing showed a hematocrit (Ht) of 47 % and b-type natriuretic peptide (BNP) level of 669 pg/mL. Levels of serum glucose, lipids, and C-reactive protein were within normal range. A chest radiograph showed a cardiothoracic ratio of 60 % with pulmonary congestion and bilateral pleural effusions. A 12-lead electrocardiogram showed sinus rhythm with left atrial and left ventricular (LV) overload. Transthoracic echocardiography showed LV enlargement and hypokinesis (end-diastolic dimension of 69 mm, end-systolic dimension of 62 mm, and ejection fraction of 21 %). LV wall was not edematous, and the thickness of the interventricular septum and LV posterior wall was 10 and 9 mm, respectively. Doppler echocardiography showed there was no significant valvular heart disease. He was treated for heart failure with diuretics, human atrial natriuretic peptide, furosemide, spironolactone, imidapril, and carvedilol. One week later, his body weight decreased by 8 kg. The results of blood sampling showed markedly an elevated Ht of 57 % and a lowered BNP level of 72 pg/mL. Follow-up echocardiography revealed a newly developed mass at the mid-ventricular septum (Fig. 1, arrow). This oval mass measured 27 mm × 17 mm × 15 mm, and its interior was homogeneous. This mass was considered to be a thrombus, and anticoagulation with heparin followed by warfarin was started. After 1 week, the thrombus was markedly smaller and the interior became hypoechoic (Fig. 2, arrow). A cardiac catheterization showed there was no significant coronary artery stenosis. The thrombus eventually disappeared 1 month later. Follow-up echocardiography 3 months later revealed that the LV wall motion had returned to normal.

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