Most of the patients had an acute onset of symptoms.
The time interval from onset to presentation was reported in 21 patients: 17 patients (81.0%) presented
within 24 hours and four patients (19.0%) presented
two days to six months after onset. The mean interval
was 254.7±944.7 (range, 0.5-4320; median, 3) hours
(n=21). Chest pain was the prevailing onset symptom
accounting for 75.6% (Table 1
Table 1: Onset symptoms
Heart murmur was reported in two patients.[29,36]
Serum troponin was detected in 16 patients (33.3%)
including troponin I in 11 (68.8%) and troponin T
in four (25%), while troponin type was unknown in
one patient (6.3%). The troponin I on admission was
normal in five patients (45.5%) and elevated in six
(54.5%) with a mean of 67.6±177.3 (range, 0.00189-570;
median, 3.135) μg/L (n=10). Two of these patients had a
remarkably elevated troponin I to 307.6 and 31.21 μg/L
during the hospitalization. The troponin T values were
positive in all four patients with a mean of 3.5±4.3
(range, 0.31-9.37; median, 2.14) μg/L (n=4). Elevated
serum enzymes including lactate dehydrogenase
1063.9±754.4 (range, 225-6245; median, 978) U/L
(n=8), creatinine phosphokinase 1314.5±1239.8 (range,
45-4000; median, 739.5) U/L (n=16), and creatine
kinase MB (CK-MB) 133.3±155.8 (range, 4.5-500;
median, 57) U/L (n=10) were also noted.
Three patients (6.3%) had a previous history of
cerebral infarct and four patients (8.3%) presented
with embolic events (cerebral and multiple peripheral
in two, cerebral in one, and femoral embolic events in
Four patients (8.3%) deteriorated into cardiogenic
shock (which required intraaortic balloon pump) with
pneumonia, severe pulmonary edema, multiple organ
failure or ventricular tachycardia in each (25%).
Locations of AMI were evident by electrocardiogram
in 37 patients, where the most frequent site of
AMI was the inferior wall followed by the anterior
(Figure 1). Echocardiography was inspected before coronary angiogram in 31 (70.5%) (coronary angiogram
was not performed in one of them), coronary angiogram
first in 12 (27.3%), and coronary computed tomographic
angiogram first without coronary angiogram in one
(2.3%) patient. Three (25%) of the patients with
coronary angiogram first had a delayed diagnosis of
cardiac myxoma, and one (33.3%) of them deteriorated
rapidly. In two patients, embolectomy was performed
for the peripheral embolic events and pathologically
myxomatous nature of the excavated samples led to the
suspicion of cardiac myxoma.
Figure 1: Distribution of myocardial infarction sites. NST: Non-
ST segment elevation myocardial infarction.
Coronary lesion was confirmed by autopsy in two
patients and by coronary angiogram in 39 patients.
A normal coronary artery was found in 20 patients
(48.8%) and coronary occlusive lesion in 21 patients
(51.2%). The culprit coronary arteries included eight
circumflex arteries (38.1%), six right coronary arteries
(28.6%), five left anterior descending coronary arteries
(23.8%), one left anterior descending coronary artery
and right coronary artery (4.8%), and one not stated
culprit coronary artery (4.8%). Neovascularization
of the cardiac myxomas was noted in eight patients
(66.7%) who underwent a coronary angiogram with a
supplying artery of the right coronary artery in (62.5%)
patients, circumflex artery in two (25%) patients, and
in one (12.5%) patient whose supplying artery was
Of the 20 patients with a normal coronary
angiogram, seven were males and 13 were females with
no sex predominance (c2=3.6, p=0.113). The patients
with a normal coronary angiogram was younger than
those with a myxoma thrombosed coronary artery
with no statistical significance (42.9±15.6 years vs.
48.6±17.4 years, p=0.324).
Cardiac myxoma was diagnosed by transthoracic
echocardiography in 36 (83.7%), transthoracic and
transesophageal echocardiography in four (9.3%) (inconsistent results of both transthoracic and
transesophageal echocardiogarphy were noted in
one patient), and computed tomography aortogram,
transthoracic and transesophageal echocardiography
and magnetic resonance imaging and intraoperative
transesophageal echocardiography in one (2.3%) each.
Hypo- and/or akinesis of the ventricular wall was
observed by echocardiography in 28 patients (45.9%),
the inferior wall being the most frequently involved
(Figure 2). Moreover, five patients (10.4%) had urgent
coronary angiography[2,13,18,21,40] and one patient (2.1%)
had urgent cardiac computed tomography done for
the diagnostic purpose of the coronary lesions.
Figure 2: Distribution of hypo- and/or akinesis of the
ventricular wall observed by echocardiography.
Of the 45 cardiac myxomas with a location
reported, 42 (93.3%) were in the left atrium (one of
them was on the mitral valve) and one (2.2%) each in
the left ventricle, both left atrium and right atrium,
and on the aortic valve. Nineteen (44.2%, 19/43) of
the atrial myxomas prolapsed into the left ventricle
during diastole. At least 13 (27.1%) myxomas were
pedunculated. Fourteen (82.4%) myxomas were regular
and three (17.6%) irregular on gross appearance.
Dimension of the myxomas was 44.7±19.5 (range,
10-90; median; 46) mm (n=31). Three patients (6.3%)
had a hemorrhagic myxoma.
Conservative management strategies were
described in 17 patients (35.4%). Ten (58.8%) of
them were performed thrombolysis with recombinant
tissue plasminogen activator (n=3), streptokinase (n=2),
tenecteplase (n=2), urokinase (n=1), and agent unknown
(n=2). In one patient, thrombolytic therapy failed in
recanalization of the coronary artery and heparin was
used instead. In the patient who was administered
bisoprolol, acetylsalicylic acid, perindopril, fragmin,
and atorvastatin were used thereafter. In the seven
patients without receiving a thrombolytic therapy, a coagulate therapy by acetylsalicylic acid, heparin,
acetylsalicylic acid, clopidogrel, fragmin, or fibrinolytic
agents was given.
Treatment was not described in two patients. Of the
remaining 46 patients, two patients (4.2%) died suddenly
and without an opportunity of surgical treatment.
A surgical resection of the myxoma was performed in
44 patients (95.7%): a sole resection of the myxoma in
24 (54.5%), with concurrent coronary artery bypass
grafting in six (13.6%), with concurrent percutaneous
coronary intervention in five (11.4%), with concurrent
coronary artery bypass grafting and atrial septal defect
closure in one (2.3%), coronary artery bypass grafting
and staged surgical embolectomy in one (2.3%), and
staged surgical embolectomy in seven (15.9%) patients.
An urgent cardiac surgery was performed in two
patients (4.2%).[15,42] A delayed myxoma resection was
performed in at least 10 patients (22.7%) for 19.6±10.8
(5-35; 19.5) days. Totally, eight patients had a staged
surgical embolectomy, for the embolized femoral
artery in two (25%), and for the emboli of the aorta, left
anterior descending coronary artery, circumflex artery,
right coronary artery, extremity artery and multiple
sites in one (12.5%) each. In addition, there were three
amputations, two fasciotomies, and one left ventricular
aneurysmectomy. Percutaneous coronary intervention
failed in two patients.
Five patients were under postoperative follow-up
with a mean of 21.0±11.6 (range, 7-36; median, 24)
months (n=5). Prognoses of 43 patients were presented,
with 38 (88.4%) event-free survivals, three (7.0%)
survivals with disabilities, and two (4.7%) deaths.