RESIDENTS’ CLINIC

86-Year-Old Man With Sharp Chest Pain

and Dyspnea
Nikhil Kolluri, MD; Michael D. Klajda, MD; and Nandan S. Anavekar, MB, BCh

A
See end of article for n 86-year-old man with a history of mg/dL (0.8-1.3 mg/dL); international normal-
correct answers to coronary artery disease after 3-vessel ized ratio, 3.1 (0.9-1.1); and troponin T,
questions. coronary artery bypass grafting (left 1.74 ng/mL (<0.01 ng/mL).
anterior descending coronary artery, first and
Resident in Internal Medicine,
Mayo Clinic School of Grad- second obtuse marginal branches) in 2000, 1. Based on the initial presentation, which
uate Medical Education, hypertension, and atrial fibrillation with one of the following is the most likely
Rochester, MN (N.K., M.D.K.); tachycardia-bradycardia syndrome after per- etiology of this patient’s symptoms?
Advisor to residents and
Consultant in Cardiovascular manent pacemaker placement in 2015 pre- a. Pulmonary embolism (PE)
Diseases, Mayo Clinic, sented to his physician with new-onset b. Pericarditis
Rochester, MN (N.S.A.). nonexertional sharp chest pain with radiation c. Pneumonia
to his neck for 1 day. His chest pain was associ- d. Non-ST elevation myocardial infarction
ated with diaphoresis and dyspnea. Before his (NSTEMI)
presentation to the hospital, he had taken 5 e. Unstable angina
baby aspirin tablets and called emergency med-
ical services. He was given nitroglycerin with The clinical presentation of a PE would
temporary relief of symptoms en route to the consist of tachycardia, tachypnea, pleuritic
hospital. In the setting of ongoing chest pain chest pain, hypoxia, and potentially hemopty-
in the hospital, he was admitted to the cardiac sis, which did not fit this patient’s presentation.
intensive care unit for further management. He also lacked any evidence of a deep venous
Physical examination revealed a tempera- thrombosis on examination, and ECG did not
ture of 36.9 C, heart rate of 64 beats/min, blood reveal the classic S1Q3T3 pattern, although
pressure of 95/75 mm Hg, and oxygen satura- this is not a highly sensitive ECG finding for a
tion of 93%. He was in no acute distress. Mildly PE and is even less so in the setting of a paced
increased jugular venous distention was ECG.1 Cardiac biomarker elevation may also
observed. Cardiac examination revealed a regu- be observed in a PE, but it would typically be
lar rhythm without murmurs, rubs, or gallops. lower than this patient’s value. Therefore, a
Lung examination was notable for basilar search for other etiologies for such a large car-
crackles and mild wheezing. His abdomen diac troponin elevation should be prompted.
was nontender, and his extremities had no Pericarditis would typically present with acute
edema or signs of a deep venous thrombosis. retrosternal pleuritic chest pain. The pain is
Chest radiography revealed cardiomegaly typically exacerbated when the patient is in a
with increased bilateral pulmonary edema, supine position, with inspiration, and with
calcified pleural plaques, and pacemaker leads. coughing and improves with sitting up or
Electrocardiography (ECG) was notable for a leaning forward. Cardiac biomarker elevation
ventricular paced rhythm of 61 beats/min could also be seen in acute pericarditis, but it
with underlying atrial fibrillation. Laboratory would only be expected to be mild. Electrocar-
studies revealed the following (reference diography would also classically show wide-
ranges provided parenthetically): hemoglobin, spread ST-segment elevations and PR-segment
13.4 g/dL (13.5-17.5 g/dL); leukocytes, 6.0  depressions.2 Pneumonia would typically pre-
109/L (3.5-10.5  109/L); platelet count, sent with a cough, fever, an infiltrate on chest
135 109/L (150-450 109/L); sodium, 141 radiography, and leukocytosis, none of which
mmol/L (135-145 mmol/L); potassium, are present in this patient. A NSTEMI typically
4.7 mmol/L (3.6-5.2 mmol/L); chloride, 104 presents with chest pain, diaphoresis, dyspnea,
mmol/L (98-107 mmol/L); creatinine, 1.6 and elevated cardiac biomarkers. This scenario

1320 Mayo Clin Proc. n September 2018;93(9):1320-1324 n https://doi.org/10.1016/j.mayocp.2018.01.029

www.mayoclinicproceedings.org n ª 2018 Mayo Foundation for Medical Education and Research
RESIDENTS’ CLINIC

is most consistent with the patient’s initial pre- because artifact from existing calcium deposits
sentation, especially in the context of known could make it challenging to accurately assess
coronary artery disease, and should be the first the coronary arteries. Chest radiography is typi-
consideration in the differential diagnosis for cally used for evaluation of pulmonary problems
this patient. An elevation of cardiac troponins including pneumonia and pulmonary edema.
distinguishes this patient’s NSTEMI from a pre- We immediately initiated medical therapy
sentation of unstable angina.3 with aspirin (81 mg) and atorvastatin (80 mg),
Although the differential diagnosis was and urgent TTE was obtained to assess left
broad, the most likely diagnosis for this initial ventricular function, regional wall motion ab-
presentation was an NSTEMI, and medical normalities, and other cardiac complications.
therapy was instituted. Early in the hospital Invasive coronary angiography was deferred
course, the patient’s chest pain had recurred initially given the patient’s clinical stability
and was responsive to intravenous nitroglyc- and presence of a relative contraindication to
erin infusion in the cardiac intensive care unit. invasive coronary angiography (supratherapeu-
tic international normalized ratio, >3), with the
2. Which one of the following is the most contingency plan of reconsidering an invasive
appropriate next test/procedure in the assessment as dictated by changes in his clinical
evaluation of this patient in this clinical course or based on the TTE findings. Transtho-
scenario? racic echocardiography revealed an anterior,
a. Cardiac magnetic resonance imaging loculated, heterogeneous (fluid/thrombus)
(MRI) pericardial fluid collection, left ventricular ejec-
b. Transthoracic echocardiography (TTE) tion fraction of 46%, regional wall motion
c. Transesophageal echocardiography abnormalities in the mid anterior left ventricu-
d. Computed tomographic angiography lar segments, and apical anterior, posterior,
e. Chest radiography and septal segments with normal right ventric-
ular function.
Although cardiac MRI is used to characterize
myocardial infarction (MI), its greatest utility is 3. Based on the patient’s imaging findings,
in the post-MI risk stratification assessment which one of the following is the most
rather than in the initial diagnostic work-up. concerning complication of the acute MI
Furthermore, cardiac MRI is not always feasible experienced by this patient?
or available. It would not be the first step in eval- a. Interventricular septal rupture
uating a patient with an MI. Transthoracic echo- b. Post-MI syndrome
cardiography is an effective diagnostic tool in c. Papillary muscle dysfunction
the evaluation of patients presenting with an d. Thrombus embolization
MI because it can accurately identify the location e. Left ventricular free wall rupture
and extent of any wall motion abnormalities that
can correlate with current and past infarcts. Interventricular septal rupture would pre-
Hypokinesis seen on TTE may include suben- sent with hemodynamic compromise, biven-
docardial infarcts, while regional akinesis or tricular failure, a new harsh holosystolic
dyskinesis is more concerning for a transmural murmur, and shunting between the ventricles
infarction.4 Transesophageal echocardiography would be appreciated on TTE.6 Post-MI syn-
is a semi-invasive procedure and is not consid- drome, otherwise known as Dressler syndrome,
ered a first-line diagnostic imaging test in the is an immune-mediated pericarditis against car-
setting of an acute coronary syndrome. diac antigens exposed during myocardial injury
Computed tomographic angiography has been and usually presents weeks to months after an
found to be effective in detecting stenosis of MI.7 Papillary muscle dysfunction would result
the coronary arteries, but it is also not indicated in acute mitral regurgitation seen on TTE, a new
when cardiac biomarker elevations are already mitral regurgitation murmur, pulmonary
noted, unless the suspicion for coronary artery edema, hypotension, and cardiogenic shock.6
disease is very low.5 Moreover, computed tomo- Thrombus embolization would present with
graphic angiography in patients with known signs of stroke or ischemia in various parts of
coronary artery disease could be less than ideal the body. The patient’s physical examination

Mayo Clin Proc. n September 2018;93(9):1320-1324 n https://doi.org/10.1016/j.mayocp.2018.01.029 1321

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 MAYO CLINIC PROCEEDINGS

was negative for these findings. Left ventricular goals.8 Percutaneous closure of the rupture
free wall rupture, classified as early-phase site is on the horizon of consideration, espe-
rupture (slit-like tear in infarcted myocardium) cially in the setting of high surgical risk. There
vs late-phase rupture (infarct expansion) leads are no studies to prove this approach as being
to extravasation of blood into the pericardial efficacious, and as such, it cannot be recom-
sac, cardiac tamponade, or electromechanical mended as a first-line form of therapy for a
dissociation and sudden death. The TTE for free wall myocardial rupture at this time.
this patient was most concerning for a con- After interpreting the TTE and computed
tained left ventricular free wall rupture. tomographic angiography results, the cardio-
Cardiovascular surgery was immediately vascular surgery service expressed concern
consulted to assess candidacy for urgent surgi- that although a surgical repair would be the ideal
cal repair. At the bequest of the surgical approach, the patient would be a high-risk
consultative service, cardiac computed tomog- surgical candidate considering his advanced
raphy was performed to delineate the extent of age, prior coronary artery bypass grafting, cur-
rupture and patency of the graft vessels. The rent MI, acute heart failure, and progressive
study revealed a left ventricular anterolateral renal insufficiency. Palliative care was con-
wall rupture with active extravasation of sulted, and a multidisciplinary team discussed
contrast medium within the pericardial space the options available with the patient and his
as well as marked left ventricular hypokinesis. family. Eventually, he decided to forgo surgery.
A do-not-resuscitate/do-not-intubate order was
4. Which one of the following is the initiated with a contingency plan of pericardio-
definitive treatment for this patient’s left centesis to relieve some of the symptoms of peri-
ventricular free wall rupture? cardial tamponade. He was transferred from the
a. Pericardiocentesis cardiac care unit to the general medical ward
b. Surgical repair with goals of symptom management. All anti-
c. Medical management (fluids, platelet and anticoagulation medications were
vasopressors) discontinued. Transthoracic echocardiography
d. Percutaneous coronary intervention performed 7 days after initial admission revealed
e. Percutaneous closure of the rupture site a larger anterolateral rupture with systolic and
end-diastolic flow through the defect, a left ven-
Pericardiocentesis can be performed as a tricular pseudoaneurysmal cavity, free-flowing
way to confirm that a pericardial fluid pericardial effusion, left ventricular ejection
collection is indeed blood, signifying a free fraction of approximately 30%, and mild right
wall rupture. However, in the setting of a ventricular dysfunction.
free wall rupture, pericardiocentesis is only a
temporizing measure and can be associated 5. Which one of these conservative
with increased tension on the damaged management techniques would be most
myocardium leading to extension of the effective in improving the patient’s survival?
rupture, and therefore, in many circles, it is a. Strict blood pressure control
considered relatively contraindicated.6 Imme- b. Inotropes
diate surgical repair in an ideally selected c. Pericardiocentesis
candidate is the definitive treatment for a left d. Intravenous fluids
ventricular free wall rupture. Surgical repair e. Aspirin and clopidogrel
can either be done with direct suture of the
rupture with a Teflon strip reinforcement or Keeping systolic blood pressure between
using a bovine pericardial patch.6 Medical 100 and 120 mm Hg, along with strict bed
management with fluids, vasopressors, and rest for at least 10 days, has been found to
general hemodynamic stabilizing measures improve survival.9 This therapy is done prefer-
are typically used until a patient can undergo ably with the use of b-blockers, but a combi-
a definitive repair. Percutaneous coronary nation of medications including vasodilators
intervention can be performed early after diag- and laxatives to prevent obstipation/constipa-
nosis of an MI to reduce the risk of a rupture tion lead to reduced stress on an already
or after surgery to achieve revascularization weak myocardium and subsequently reduce

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RESIDENTS’ CLINIC

the chance of a secondary rupture.9 Although cardiac tamponade with rapid irreversible elec-
inotropes were used in the initial attempts at tromechanical dissociation.11 Fortunately, a
maintaining blood pressures, they are not the subset of people that experience a free wall
ideal choice for long-term medical manage- rupture present with a subacute cardiac rupture
ment of free wall rupture.9 Pericardiocentesis that is well contained within the pericardial sac.
is used mostly for symptom management These patients may survive several hours,
and reduction of tamponade physiology if which allows for diagnostic imaging as well as
clinically necessitated.6 From clinical experi- implementation of therapeutic measures.11
ence, it seems that if pericardiocentesis is Typical risk factors that predispose to a
mandated by clinical deterioration, the goal free wall rupture include female sex, older
would be to evacuate enough of the pericardial age (>65 years old), first transmural MI,
contents to improve hemodynamic parameters severe 1-vessel coronary artery disease with
rather than to evacuate the entire pericardial the lack of collateral formation, and the
contents as would be done in a pericardial absence of previous angina. Although these
effusion with tamponade physiology. Intrave- features are generally considered to be some
nous fluids are used initially for hemodynamic of the most important risk factors, it is impor-
stability but are not a long-term option for tant to keep in mind that each patient is
increasing survival. Aspirin and clopidogrel different and one size never fits all. Interest-
have no role in the management of a free ingly, a history of multivessel disease or prior
wall rupture and may worsen the clinical angina might be a protective factor because
situation. of the development of collateral vessels in
The patient was stabilized and discharged to response to cardiac stress.11,12 The pathophys-
a skilled nursing facility. He returned to the iology of a free wall rupture usually revolves
hospital a month later because of increased dys- around a modest-sized infarction leading to
pnea, hypoxemia, and pleural effusions. Thora- necrosis and thinning of the myocardial wall
centesis revealed an exudative pleural effusion, with poor collateral flow. This scenario makes
which was likely multifactorial in nature the already thin wall susceptible to the
considering the patient’s impaired cardiac func- shearing as the surrounding areas of normal
tion and postecardiac injury inflammation. myocardium contract rigorously against the
Transthoracic echocardiography revealed the stiffened, necrotic area. This process can lead
same-sized left ventricular anterolateral wall to the dissection of blood through the myocar-
rupture with moderate-sized pericardial effu- dium into the pericardium.13
sion and associated hematoma/coagulum and The clinical presentation of an acute free
left ventricular ejection fraction of 30%. His wall rupture is usually devastating and irrevers-
condition was medically optimized, and he ible, with chest pain, electromechanical dissoci-
was discharged to a skilled nursing facility ation, shock, and death occurring shortly after
with a regimen of furosemide, metoprolol, sim- rupture. The transmural tear leads to a severe
vastatin, spironolactone, and valsartan and pericardial tamponade with limited cardiac
encouraged to closely monitor his blood output and immediate death.11 However, a sub-
pressure. acute rupture usually leads to a slower, more
contained hemopericardium with a limited tam-
DISCUSSION ponade physiology. This condition can present
Although the mortality from an acute MI con- with chest pain, hypotension, syncope, muffled
tinues to decline in this era of expeditious reper- heart sounds, and hypoxemia.11 In some in-
fusion therapy, left ventricular rupture is still stances, much like what happened with our pa-
one of the most serious mechanical complica- tient, the subacute free wall rupture leads to a
tions of an acute MI with associated marked sealed rupture with pseudoaneurysm forma-
mortality. Within the subclasses of left ventric- tion. These patients can be relatively stable and
ular rupture (ventricular septal rupture vs left asymptomatic. Transthoracic echocardiography
ventricular free wall rupture), left ventricular is the test of choice to establish the diagnosis of
free wall rupture has an incidence rate of 2% myocardial rupture with findings of pericardial
to 4%.10 Furthermore, it can account for up effusion and tamponade physiology.11 The
to 15% of in-hospital mortality as a result of absence of a pericardial effusion has a high

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 MAYO CLINIC PROCEEDINGS

negative predictive value and excludes cardiac REFERENCES

rupture in many patients.11 1. Bĕlohlávek J, Dytrych V, Linhart A. Pulmonary embolism,
Early reperfusion in the setting of acute cor- part I: epidemiology, risk factors and risk stratification,
pathophysiology, clinical presentation, diagnosis and non-
onary syndrome has been found to be the thrombotic pulmonary embolism. Exp Clin Cardiol. 2013;
prevailing force in the observed reduced inci- 18(2):129-138.
dence of myocardial rupture in contemporary 2. Snyder MJ, Bepko J, White M. Acute pericarditis: diagnosis and
management. Am Fam Physician. 2014;89(7):553-560.
practice.11 There is also some evidence for pre- 3. Thygesen K, Alpert JS, Jaffe AS, et al. Third universal defi-
vention of a free wall rupture in high-risk nition of myocardial infarction. Circulation. 2012;126(16):
patients that relies on strict blood pressure 2020-2035.
4. Douglas PS, Garcia MJ, Haines DE, et al. ACCF/ASE/AHA/
control with b-blockers and angiotensin- ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appro-
converting enzyme inhibitors to reduce wall priate Use Criteria for Echocardiography: a report of the
stress.10 Once the rupture is diagnosed, howev- American College of Cardiology Foundation Appropriate Use
Criteria Task Force, American Society of Echocardiography,
er, surgical repair is the definitive treatment of American Heart Association, American Society of Nuclear
choice.7,12 Close follow-up is recommended Cardiology, Heart Failure Society of America, Heart Rhythm
for those with subacute/contained ruptures to Society, Society for Cardiovascular Angiography and In-
terventions, Society of Critical Care Medicine, Society of Car-
assess for hemodynamic stability and therapeu- diovascular Computed Tomography, and Society for
tic pericardiocenteses.12 Regardless of manage- Cardiovascular Magnetic Resonance. J Am Coll Cardiol. 2011;
ment (surgical repair vs conservative therapy), 57(9):1126-1166.
5. Stein PD, Yaekoub A, Matta F, Sostman H. 64-Slice CT for
tight control of the patient’s hemodynamic diagnosis of coronary artery disease: a systematic review. Am J
status and the severity of cardiogenic shock Med. 2008;121(8):715-725.
seem to be the biggest components that deter- 6. Kutty RS, Jones N, Moorjani N. Mechanical complications of
acute myocardial infarction. Cardiol Clin. 2013;31(4):519-531.
mine survival in patients with cardiac rupture 7. Imazio M, Hoit BD. Post-cardiac injury syndromes: an
after MI. Most importantly, it is crucial to align emerging cause of pericardial diseases. Int J Cardiol. 2013;
therapeutic options in the context of a patient’s 168(2):648-652.
8. Cheriex EC, de Swart H, Dijkman LW, et al. Myocardial rupture
comorbidities. In the current clinical circum- after myocardial infarction is related to the perfusion status of
stance, surgical risk was exceedingly high and the infarct-related coronary artery. Am Heart J. 1995;129(4):
predicted a prolonged recovery, both of which 644-650.
9. Figueras J, Cortadellas J, Evangelista A, Soler-Soler J. Medical
were against the wishes of the family. In the management of selected patients with left ventricular free wall
appropriate clinical setting, medical therapy rupture during acute myocardial infarction. J Am Coll Cardiol.
alone may be the best alternative to provide a 1997;29(3):512-518.
10. Nozoe M, Sakamoto T, Taguchi E, Miyamoto S, Fukunaga T,
balance between the risk of mortality on one Nakao K. Clinical manifestation of early phase left ventricular
hand and the ability to maintain a level of inde- rupture complicating acute myocardial infarction in the primary
pendence and comfort on the other. At the time PCI era. J Cardiol. 2014;63(1):14-18.
11. Solis C, Pujol D, Mauro V. Left ventricular free wall rupture
this report was written, our patient continued after acute myocardial infarction. Rev Argent Cardiol. 2009;77(5):
to improve from a clinical standpoint and was 395-404.
being well maintained on medical therapy. 12. Sulzgruber P, El-Hamid F, Koller L, et al. Long-term outcome
and risk prediction in patients suffering acute myocardial
Potential Competing Interests: The authors report no infarction complicated by post-infarction cardiac rupture. Int J
competing interests. Cardiol. 2017;227:399-403.
13. Vanezis AP, Quadery R, Wasil M, Azher M. An unusual pre-
Correspondence: Address to Nandan S. Anavekar, MB, sentation of left ventricular free wall rupture following a silent
myocardial infarction. Br J Med Pract. 2009;2(1):41-43.
BCh, Division of Cardiovascular Diseases, Mayo Clinic,
200 First St SW, Rochester, MN 55905 (anavekar.
nandan@mayo.edu). CORRECT ANSWERS: 1. d. 2. b. 3. e. 4. b. 5. a.

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