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Figure 1 Shown here are pictures of aortic valves with portions of ascending aorta
excised surgically: a. Case #1, b. Case #2. In case #1, the aortic valve is 3-cuspid and
in case #2, bicuspid, and the black pigment is present only in the calcic deposits. In
case #1, the pigment in the aorta is extensive and in case #2, minimal.
the cardiac valve. Although previously reported, ochronotic pigment in a stenotic
congenitally unicuspid
unusual. Congenitally bicuspid aortic valves have an estimated frequency of about 1
in 100 adults
250,000 to 1,000,000,
68
and clinically manifest ochronosis has an estimated frequency of 1 in
69
such that the occurrence of both conditions in the same person
is indeed unusual. Ochronotic pigment in atherosclerotic plaques, as occurred in
our patient #2, was rst recognized by Virchow and observed subsequently by many
other investigators (Table 1). It appears that cardiovascular ochronosis causes no
functional derangement and only exists in previously abnormal cardiac valves or
arteries (previous atherosclerosis).
Ochronosis occurs in both primary and secondary forms. The most common
secondary form is associated with phenols, a class of chemicals containing
a hydroxyl group (-OH) bonded to an aromatic (presence of a benzene ring)
hydrocarbon group. Secondary or exogenous ochronosis can be secondary to the
topical application of hydroquinone, phenol, resorcinol, or oral administration of
antimalarials.
70
Minocycline, one of the tetracyclines, consumed by both patients
300
53
or bicuspid
6, 52
aortic valve, as in our patient #2, is most
CASE 1753 CARDIOVASCULAR OCHRONOSIS
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Figure 2 Case # 1. Photomicrograph of a section of aortic valve showing a liner
row of dark-staining cells consistent with ochronosis pigment. The pigment stains
lightly probably because the tissue was decalcied before processing and staining.
Fontana-Masson stain, x25.
described herein, has been recognized, if used chronically, as an exogenous cause of
ochronosis.
joint pains and in case #2, for neuropathic pain.
6, 22, 25, 32, 43, 46, 49, 53, 55, 71
In case #1, this drug was administered for chronic
71
Whether the minocycline in our 2
patients was the cause of the ochronosis in them is unclear (Figure2).
DECLARATION OF COMPETING INTEREST
None.
FUNDING
This research did not receive any specic grant from funding agencies in the public,
commercial, or not-for-public sectors.
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304
CASE 1760 VIRTUALLY ALL COMPLICATIONS OF ACTIVE INFECTIVE ENDOCARDITIS
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Case 1760 Virtually All Complications of Active
Infective Endocarditis Occurring in a Single Patient
William C. Roberts, MDa*, Divya Kapoor, MDb, and Michael L. Main, MD
b
Described herein is a 49-year-old black man with advanced polycystic renal
disease, on hemodialysis for 6years, who during his last 12 days of life had his
vegetations on the aortic valve extend to the mitral and tricuspid valves, through
the aortic wall to produce diffuse pericarditis, to the atrioventricular node to
produce complete heart block, and embolize to cerebral arteries producing
multiple brain infarcts, to a branch on the left circumex coronary artery
producing acute myocardial infarction, and to mesenteric arteries producing
bowel infarction. © 2020 Published by Elsevier Inc.
(Am J Cardiol 2020;137:127–129)
Vegetations dangling on one or more aortic valve cusps (active infective
endocarditis) are life threatening because they may extend to adjacent tissues (ring
abscess) and/or embolize to arteries causing infarction. It is unusual for aortic valve
vegetations to extend to 2 other cardiac valves or to embolize to multiple arteries or
to cause septic pericarditis. Such was the case in the patient to be described herein.
CASE DESCRIPTION
A 49-year-old black man with known advanced polycystic renal disease on
hemodialysis (for 6years), diabetes mellitus, systemic hypertension, and obstructive
sleep apnea (without obesity—body weight 176 lbs.) had been in h is usual health until
he developed epigastric, back, and vague chest pain 3 days before hospitalization.
Examination in the emergency room disclosed a grade 2/6 systolic murmur along
the lower left sternal border. The patient indicated that his chest pain worsened
when lying at. The electrocardiogram was consistent with posterior wall acute
myocardial infarction (Figure1). His troponin level was 1.7 rising to 76 mg/L the
next day. From the emergency room he was taken to the cardiac catheterization
laboratory where coronary angiogram showed normal right (nondominant), left
main, left anterior descending, and left circumex coronary arteries, and a totally
occluded third marginal coronary artery, which could not be opened. The following
pressures in mmHg were recorded: pulmonary artery 47/24; pulmonary arterial
wedge a 28, v 37, mean 24; aorta 82/54. Blood drawn for culture later disclosed
methicillin-sensitive Staphylococcus aureus.
Despite appropriate antibiotic therapy his condition progressively worsened.
Because of continued abdominal pain, abdominal imaging was performed which
revealed bowel necrosis. Laparoscopic bowel resection was performed the day
after admission and a 5 cm portion of necrotic ileum was resected. He became
progressively more confused and magnetic resonance imaging of the brain
showed several cerebral infarcts. During his 9 days in the hospital he progressed
a
Baylor Scott& White Heart Institute, Baylor University Medical Center, Dallas, Texas; and
b
Saint Luke’s Mid American Heart Institute, Kansas City, Missouri. Manuscript received
July7, 2020; revised manuscript received and accepted September23, 2020.
*
Corresponding author.
E-mail address: William.Roberts1@BSWHealth.org (W.C. Roberts).
DOI: 10.1201/9781003409281-63 305
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Figure 1 Electrocardiogram shortly after admission with ndings of acute myocardial infarction.
Figure 2 Heart showing acute diffuse pericarditis.
306
CASE 1760 VIRTUALLY ALL COMPLICATIONS OF ACTIVE INFECTIVE ENDOCARDITIS
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from sinus tachycardia with prolonged PR interval to second degree heart block
(Wenckebach), to complete heart block (pacemaker inserted), and nally to fatal
ventricular brillation.
At necropsy, the pericardial surfaces were diffusely covered by brin deposits
(brinous “pericarditis”) (Figure 2). The heart weighed 720g (normal < 350g). The
aortic valve was 3 cuspid. Vegetation was present on each of the 3 cusps and calcic
deposits were present in the left cusp. The vegetations extended through the wall
of aorta to the space between the walls of the aorta and left atrium. The aortic
vegetations extended on to the anterior mitral leaet and into the calcium of the
mitral annulus (Figure3). The infection at the aortic and left atrial wall extended
into the atrial septum to destroy the atrioventricular node and infect the adjacent
Figure 3 Views of the heart. (a) left parasagittal view showing the infection
involving the aortic and mitral valves and the posterior wall acute infarct, a close-up
of which is shown in (b). (c). Aclose-up view of the aortic and mitral valves showing
vegetations on each. Ao=aorta; LA=left atrium. (d). Right parasagittal view showing vegetation in the area of the atrioventricular node with extension into the septal
tricuspid valve leaet.
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tricuspid valve leaet. All epicardial coronary arteries were wide open except for
the third obtuse marginal which was totally occluded by a septic embolus. Alarge
acute myocardial infarct involved the posterior left ventricular free wall and the
posteromedial papillary muscle (Figure 3). Septic emboli were found in several
small intracerebral arteries and in several mesenteric arteries.
DISCUSSION
Of the various cardiac valves affected by infective endocarditis, the aortic by far is the
most common and it also is associated with the most complications.
1
Chronic renal
disease, as in the present patient, is a major risk factor for infective endocarditis.
These complications include destruction of the aortic valve cusps causing aortic
regurgitation, extension of the cuspal infection to adjacent tissues (ring abscess),
including the anterior mitral leaet and its chordae tendinea producing mitral
regurgitation; to the atrioventricular node or bundle or both producing heart block;
to the atrial septum (or membranous ventricular sept um) to infect the tricuspid valve;
through the aortic wall to produce pericardial disease, and to embolize to multiple
systemic arteries. The patient described herein had all of these complications. The
least common is pericardial disease.
REFERENCES
1. Roberts WC, Oluwole O, Fernicola DJ. Comparison of active infective endocarditis
involving a previously stenotic versus a previously nonstenotic aortic valve. Am J
Cardiol 1993;71:1082–1088.
2. Roberts WC, Taylor MA, Shirani J. Cardiac ndings at necropsy in patients with
chronic kidney disease maintained on chronic hemodialysis. Medicine (Baltimore)
2012;91:165–178.
2
308
CASE 1763 ISOLATED MITRAL VALVE ENDOCARDITIS WITH RING ABSCESS AND PERICARDITIS
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Case 1763 Isolated Mitral Valve Endocarditis with Ring
Abscess and Pericarditis in End-Stage Renal Disease
William Ryan Sovic, MDa, Quynh Ngo, MDa, Srikant Patlolla, MDa, Joseph M.
Guileyardo, MD
b
, and William C. Roberts, MD
a,b,c
Described herein is a 68-year-old man with end-stage renal disease on
hemodialysis who was found to have methicillin-sensitive Staphylococcus
aureus endocarditis with an associated ring abscess that extended into the
left atrioventricular sulcus and ruptured into the pericardial space causing
pericardial effusion. In contrast to the frequency of infective endocarditis
involving the aortic valve, ring abscess associated with infection of the mitral
valve is uncommon.
Infective endocarditis (IE) with ring abscess occurs mainly with infection involving
the aortic valve.
1, 2
IE with a ring abscess isolated to the mitral valve is uncommon,
but such was the case in the patient described herein.
CASE REPORT
A 68-year-old Hispan ic man with end-stage renal disease presented to the emergency
department with several days of altered mental status, chest pain, dizziness, nausea,
and chills. Aweek earlier he had transitioned from a temporary catheter to an upper
extremity stula for hemodialysis. In the emergency depart ment, he was hypotensive
and in atrial brillation with a ventricular rate of 134 beats/min. His blood lactate
was 6.7 mmol/L, troponin 6.6 ng/mL, D-dimer 14.67 mcg/mL, and C-reactive
protein 21.5 mg/dL. He was given uids, antibiotics, and heparin intravenously.
Blood cultures from admission grew methicillin-sensitive Staphylococcus aureus.
On the third day of hospitalization, the patient had cardiac arrest; resuscitation
was successful. An echocardiogram after the cardiac arrest disclosed a pericardial
effusion. A subsequent cardiac arrest was fatal. Autopsy revealed mitral valve
endocarditis with a ring abscess extending into the left atrioventricular sulcus with
rupture into the pericardial space producing hemorrhagic pericardial effusion
(Figure1).
DISCUSSION
The patient described herein required hemodialysis for end-stage renal disease,
initially with a temporary catheter and recently with an arteriovenous stula.
Patients on chronic hemodialysis have a high incidence of IE. The Danish National
Patient Registry reported a frequency of IE in patients undergoing hemodialysis of
1092 per 100,000 person-years.
a
Department of Internal Medicine, Baylor University Medical Center, Dallas, Texas; bDepartment of Pathology, Baylor University Medical Center, Dallas, Texas;
Institute, Dallas, Texas
Corresponding author: William C. Roberts, MD, Baylor Heart and Vascular Institute, 621 N.
Hall Street, Ste. H030, Dallas, TX 75246 (e-mail: William.Roberts1@BSWHealth.org)
The authors report no conicts of interest. Before his death, the patient gave permission
for use of his medical information for educational purposes. Received November 19, 2020;
Revised December30, 2020; Accepted January19, 2021.
DOI: 10.1201/9781003409281-64 309
3
The risk of IE in patients with central venous catheters
c
Baylor Heart and Vascular
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