Case 2 -
Right Ventricular Infarction Secondary to Massive Pulmonary Embolism
Carmela Tan, Cleveland Clinic, Cleveland, OH
Click on slide thumbnail images for an enlarged view.
If you have any difficulties viewing these slides, email the webmaster.
A 72-year-old woman with history of dementia had been bedbound at home for the past six months. She
was recently admitted for treatment of a urinary tract infection and discharged to a skilled nursing
facility. Four days later, she was brought to the Emergency Department after having been found
unresponsive. Postmortem examination revealed a thrombus within the pulmonary trunk extending into the
right pulmonary artery.
Case 2 - Figure 1
Nitroblue tetrazolium staining showing a right ventricular infarct.
Case 2 - Figure 2
High-power view of right ventricular myocardium showing contraction band necrosis.
Case 2 - Figure 3
High-power view of right ventricular myocardium showing polymorphonuclear cell infiltrates.
Pathological/Microscopic Findings and any Immunohistochemical or Other Studies:
The heart weighed 505 grams. There was mild dilatation of the left ventricle and concentric left
ventricular hypertrophy. The right ventricle was not dilated and the free wall measured 0.4 cm. The
ventricles were serially sectioned parallel to the atrioventricular groove. The slices were incubated
for 30 minutes in 0.5% nitroblue tetrazolium solution to visualize signs of early infarction. As can be
seen in Figure 1, nitroblue tetrazolium stains viable myocardium dark blue while infarcted myocardium
without dehydrogenases appear unstained. Examination of the coronary arteries showed a focal 80%
stenosis of the proximal right coronary artery without plaque rupture or thrombus formation.
Histologic sections of the right ventricle (Figure 2 and 3) showed contraction band necrosis and
polymorphonuclear infiltrates in focal areas. There was no evidence of left ventricular ischemia or
infarction in this case despite the presence of coronary atherosclerosis.
The differential diagnoses of unexpected death in the elderly include coronary atherosclerosis,
stroke, aortic rupture and noncardiac causes. The risk of sudden death in adults closely reflects the
incidence of coronary heart disease. In contrast, the common causes of sudden death in young adults
include cardiomyopathies, coronary artery anomalies, arrhythmogenic disorders and drug abuse .
Most sudden deaths are secondary to ventricular tachyarrhythmias. Underling cardiac structural
abnormalities that are potential substrates for ventricular arrhythmias include coronary thrombosis,
myocardial scars, left ventricular hypertrophy, inflammation and interstitial fibrosis. Around 5-10% of
patients who suffer from sudden cardiac death will have structurally normal hearts.
The cause of death in this case was massive pulmonary embolism (PE). The patient's risk of developing
PE was likely related to inactivity secondary to dementia. This catastrophic event usually results in
acute right ventricular failure secondary to ischemia and necrosis.
Right Ventricular Infarction Secondary to Massive Pulmonary Embolism
Right ventricular infarction is most commonly associated with transmural posterior left ventricular
infarction. On the other hand, isolated right ventricular infarction is found in less than 3% of cases
of myocardial infarction in autopsy series . The low incidence of right ventricular infarction is
thought to be due to a lower myocardial oxygen demand/supply ratio compared to the left ventricle. The
lower right-sided pressures require lower work load and consequently lower oxygen demand. Favorable
coronary perfusion is related to the thinness of the wall, lower coronary vascular resistance, and
collaterals from the left coronary circulation. The lower right ventricular wall tension results in
minimal compression of the microvasculature, thereby allowing for coronary blood flow to occur
continuously throughout systole and diastole.
In massive PE, there is a sudden increase in right ventricular afterload. Acute right ventricular
compensatory response is limited. Sympathetic stimulation result in an increase in systolic pressure
which increases oxygen demand. The right ventricular response to outflow obstruction is predominantly
ventricular dilatation to maintain stroke volume. Right ventricular oxygen consumption further increases
due to increased enddiastolic volume. While oxygen demand increases, oxygen supply decreases because
higher intracavitary filling pressures diminish transmural perfusion and limit coronary flow during
diastole. Obstruction of the pulmonary arteries leads to a decrease in transpulmonary delivery of left
ventricular preload. Furthermore, right ventricular dilation also causes the interventricular septum to
shift to the left, which decreases left ventricular compliance contributing to inadequate left
ventricular filling. A decrease in left ventricular output reduces coronary perfusion of the right
ventricle. Systemic hypotension results once forward cardiac output can no longer be sustained. The
imbalance in oxygen demand and supply, in combination of hypotension and hypoxia, produces right
ventricular ischemia and dysfunction.
The histologic features of right ventricular infarction are similar to those of left ventricular
infarction. However, identification of very early myocardial infarcts (duration less than 6 hours)
remains challenging as unequivocal gross pathologic changes are not recognizable until at least 24 hours
of infarction. Diagnosis can be missed when only random sections are taken for microscopic examination.
One method employed in this case was the use of nitroblue tetrazolium staining. Nitroblue tetrazolium is
an oxidation-reduction indicator that produces a dark blue formazan pigment visible in viable myocardium.
The absence of pigment indicates substrate depletion during periods of ischemia and loss of
dehydrogenases in necrotic myocardium. It also accurately outlines recent, healing and healed infarcts.
Therefore, it facilitates three-dimensional mapping of the infarcted areas by incubating sequential
slices of the ventricles. Using the nitroblue tetrazolium method, infarcts can be recognized as early as
2 hours after arterial ligation in dogs . Studies with human hearts report detection of infarcts as
early as 1 hour to 3 ½ hours of presumed clinical onset
False positive reactions can be seen
with poor technique and in cases with autolysis (more than 72 hours) .
Review of the Literature/Treatment Options:
Infarction of the right ventricle is usually a direct result of an occlusion of the right coronary
artery by plaque rupture and/or thrombus formation. Occlusion of the proximal segment of a dominant
right coronary artery can result in infarction of the right ventricular free wall with extension to the
posterior interventricular septum and adjoining posterior wall of the left ventricle. Occlusion of the
proximal left anterior descending artery or conus branch of the right coronary artery can result in an
anterior right ventricular infarction .
Less commonly, right ventricular myocardial infarction has been reported secondary to right coronary
artery dissection , anomalous origin of the right coronary artery
 and side branch occlusion during
stenting of the right coronary artery .
In the absence of significant coronary artery disease, right ventricular infarction has been reported
in the setting of right ventricular hypertrophy. A relationship between right ventricular infarction and
pulmonary hypertension has been observed in several studies
Patients with chronic
obstructive pulmonary disease may also be more susceptible to right ventricular infarction due to
associated right ventricular hypertrophy
The increased right ventricular mass and elevated
right ventricular enddiastolic pressure not only increases oxygen demand but also cause compression of
flow to the right coronary system.
Isolated right ventricular infarction is rare. In addition to proximal right coronary artery
occlusion, right ventricular infarction may also occur secondary to acute pulmonary hypertension in the
setting of massive PE. Cases of right ventricular infarction have also been reported in patients with
right ventricular hypertrophy due to chronic pulmonary hypertension and chronic obstructive pulmonary
Early diagnosis of myocardial infarction can be challenging. One valuable method for macroscopic
identification of early myocardial infarction is the use of nitroblue tetrazolium staining to delineate
the location and extent of infarct.
- Adabag AS, Luepker RV, Roger VL, Gersh BJ. Sudden cardiac death: epidemiology and risk factors. Nat Rev Cardiol. 2010 Apr;7(4):216-25.
- Wartman WB, Hellerstein HK. The incidence of heart disease in 2,000 consecutive autopsies. Ann Intern Med. 1948 Jan;28(1):41-65.
- Nachlas MM, Shnitka TK. Macroscopic identification of early myocardial infarcts by alterations in dehydrogenase activity. Am J Pathol. 1963 Apr;42:379-405.
- Derias NW, Adams CW. Nitroblue tetrazolium test: early gross detection of human myocardial infarcts. Br J Exp Pathol. 1978 Jun;59(3):254-8.
- McVie JG. Postmortem detection of inapparent myocardial infarction. J Clin Pathol. 1970 Apr;23(3):203-9.
- Andersen JA, Hansen BF. The value of the nitro-BT method in fresh myocardial infarction. Frequency and location of fresh myocardial infarction in a consecutive series of autopsies. Am Heart J. 1973 May;85(5):611-9.
- Andersen HR, Falk E, Nielsen D. Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Coll Cardiol. 1987 Dec;10(6):1223-32.
- Atkinson JB, Barnhill J, Virmani R. Isolated right ventricular infarction: a rare complication of coronary artery dissection. South Med J. 1986 May;79(5):619-22.
- Saremi F, Gurudevan SV, Harrison AT.Isolated right ventricular infarction owing to anomalous origin of right coronary artery: role of MR and CT in diagnosis. J Thorac Imaging. 2009 Feb;24(1):34-7.
- Coosemans M, Koevoets R, Vydt T. A right ventricular infarction disguised as an anterior infarction due to an occluded isolated right ventricular branch. Acta Cardiol. 2008 Oct;63(5):641-5.
- Wade WG. The pathogenesis of infarction of the right ventricle. Br Heart J. 1959 Oct;21(4):545-54.
- Forman MB, Wilson BH, Sheller JR, Kopelman HA, Vaughn WK, Virmani R, Friesinger GC. Right ventricular hypertrophy is an important determinant of right ventricular infarction complicating acute inferior left ventricular infarction. J Am Coll Cardiol. 1987 Dec;10 (6):1180-7.
- Carlson EB, Reimer KA, Rankin JS, Peter RH, McCormack KM, Alexander LG. Right ventricular subendocardial infarction in a patient with pulmonary hypertension, right ventricular hypertrophy, and normal coronary arteries. Clin Cardiol. 1985 Sep;8(9):499-502.
- Kopelman HA, Forman MB, Wilson BH, Kolodgie FD, Smith RF, Friesinger GC, Virmani R. Right ventricular myocardial infarction in patients with chronic lung disease: possible role of right ventricular hypertrophy. J Am Coll Cardiol. 1985 Jun;5(6):1302-7.
- Middelhoff CJ, Büthker W, Becker AE. Pure right ventricular infarction. Eur Heart J. 1980 Oct;1(5):369-74.