Lyme Disease and the heart

Topics with information and discussion about published studies related to Lyme disease and other tick-borne diseases.
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Yvonne
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Re: Lyme Disease and the heart

Post by Yvonne » Fri 8 Jan 2010 18:01

http://www.springerlink.com/content/b8x4742136623114/

Presence of Borrelia burgdorferi in endomyocardial biopsies in patients with new-onset unexplained dilated cardiomyopathy
Abstract Dilated cardiomyopathy (DCM) represents the third most common cause of heart failure and the most frequent cause of heart transplantation. Infectious, mostly viral, and autoimmune mechanisms, together with genetic abnormalities, have been reported as three major causes of DCM. We hypothesized that Lyme disease (LD), caused by spirochete Borrelia burgdorferi (Bb), might be an important cause of new-onset unexplained DCM in patients living in a highly endemic area for LD such as the Czech Republic. We performed endomyocardial biopsy (EMB) in 39 consecutive patients presenting with symptomatic unexplained left ventricular (LV) systolic dysfunction lasting no more than 12 months. In eight subjects (21%), Bb was detected in the EMB sample by polymerase chain reaction or by electron microscopy. None of these patients exhibited any form of atrioventricular block or other extracardiac manifestation of Bb infection. Serological testing identified IgG antibodies against Bb in only two cases and IgM antibodies in none. All affected patients were treated with intravenous ceftriaxone for 3 weeks. At 6 months follow-up, LV morphology and function as well as functional status of these patients significantly improved. In conclusion, Bb infection may represent an important cause of new-onset unexplained DCM in patients living in endemic regions such as the Czech Republic. Because the antibiotic treatment appears to be markedly effective and serological examination does not provide a tool for diagnosing the disease, EMB focused on the detection of Bb should be performed in all patients from endemic areas with new-onset unexplained DCM not responding to conventional therapy.
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Re: Lyme Disease and the heart

Post by Yvonne » Fri 19 Mar 2010 18:29



Int J Cardiol. 2010 Mar 10. [Epub ahead of print]

Atrio-ventricular block as the first presentation of disseminated Lyme disease.

Panic G, Stanulovic V, Popov T.

Institute of Cardiovascular Diseases of Vojvodina, Clinic of Cardiology, Sremska Kamenica, Serbia.

A 36year old male patient presented to emergency cardiology department because of fatigability. ECG revealed high grade II atrio-ventricular block and bradycardia of 31beats/min. An erythema increasing in size to up to 7-8cm in diameter appeared a month earlier and spontaneously resolved within 10days. ELISA testing for antibodies against Borrelia burgdorferi IgM was positive and IgG titer was 1:40. Intravenous ceftriaxone 2g qod, and 0.5g metronidazole tid lead to regression of grade II block to grade I block within 2days. Grade I block persisted for an additional 10days. This is a relatively rare case of early occurrence of Lyme carditis within one month of exposure as the first sign of Lyme disease dissemination.
Copyright © 2010. Published by Elsevier Ireland Ltd.

PMID: 20226549
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Re: Lyme Disease and the heart

Post by Yvonne » Sat 1 May 2010 12:43

http://iai.asm.org/cgi/content/full/75/ ... d=17101663

Recruitment of Macrophages and Polymorphonuclear Leukocytes in Lyme Carditis
ABSTRACT

Lyme arthritis, caused by the spirochete Borrelia burgdorferi, can be recurrent or prolonged, whereas Lyme carditis is mostly nonrecurring. A prominent difference between arthritis and carditis is the differential representation of phagocytes in these lesions: polymorphonuclear leukocytes (PMN) are more prevalent in the joint, and macrophages predominate in the heart lesion. We have previously shown differential efficiency of B. burgdorferi clearance by PMN and macrophages, and we now investigate whether these functional differences at the cellular level may contribute to the observed differences in organ-specific pathogenesis. When we infected mice lacking the neutrophil chemokine receptor (CXCR2–/– mice) with spirochetes, we detected fewer PMN in joints and less-severe arthritis. Here we have investigated the effects of the absence of the macrophage chemokine receptor CCR2 on the development and resolution of Lyme carditis in resistant (C57BL/6J [B6]) and sensitive (C3H/HeJ [C3H]) strains of mice. In B6 CCR2–/– mice, although inflammation in hearts is mild, we detected an increased burden of B. burgdorferi compared to that in wild-type (WT) mice, suggesting reduced clearance in the absence of macrophages. In contrast, C3H CCR2–/– mice have severe inflammation but a decreased B. burgdorferi burden compared to that in WT C3H mice both at peak disease and during resolution. Histopathologic examination of infected hearts revealed that infected C3H CCR2–/– animals have an increased presence of PMN, suggesting compensatory mechanisms of B. burgdorferi clearance in the hearts of infected C3H CCR2–/– mice. The more efficient clearance of B. burgdorferi from hearts by CCR2–/– versus WT C3H mice suggests a natural defect in the recruitment or function of macrophages in C3H mice, which may contribute to the sensitivity of this strain to B. burgdorferi infection.
DISCUSSION

In Lyme disease, infection of joints and the heart with the same organism in the same host results in quite distinct courses of disease: macrophages predominate in the heart lesion and PMN in infected joints (2, 5, 6, 28). We have shown that macrophages infiltrating the heart are appropriately activated (35) and clear spirochetes efficiently through largely intracellular killing mechanisms (29, 30, 32). Myocarditis resolves at day 30 to 45, and spirochetes are rare at late intervals

The differential recruitment of phagocytic cells to the site of infection is likely to be mediated by specific chemokines. We have previously shown for B. burgdorferi infection of CXCR2–/– mice that PMN do not enter the joint and arthritis development is attenuated (8). In the current study, we have examined the development of macrophage-mediated Lyme carditis in CCR2-deficient mice, for whom recruitment of macrophages is impaired (23, 24). We show here that B. burgdorferi burdens are significantly increased in infected hearts of B6 CCR2–/– animals at peak disease, confirming the anticipated role for macrophages in the clearance of B. burgdorferi in Lyme carditis. However, the elevation of B. burgdorferi levels in hearts did not significantly change the degree of inflammation or delay the resolution of carditis for B6 mice. Expression of the chemokines MIP-2 and MCP-1 was increased in CCR2–/– mice of both sensitive and resistant strains, suggesting that local chemokine levels in WT mice may be modulated in a feedback loop by infiltrating cells.

Surprisingly, we found no significant differences in the severity of cardiac pathology between WT and CCR2–/– mice on either a genetically resistant or a susceptible background, although histopathologic examination revealed differences between resistant and sensitive mouse strains. Inflammation was minimal in B6 mice (WT and CCR2–/–), and thus, few effects of the absence of CCR2 could be appreciated. However, for C3H mice, which have more-pronounced inflammation, the cellular makeup of the inflammatory infiltrate was changed in CCR2–/– animals. While the overall levels of inflammation remained similar for C3H WT and CCR2–/– animals, there was an increased presence of PMN in C3H CCR2–/– mice, suggesting that PMN recruitment is a compensatory mechanism in the absence of CCR2. The dramatic increase in the recruitment of PMN in CCR2–/– C3H mice was accompanied by an unexpected decrease in B. burgdorferi loads. Thus, infected C3H mice have more-efficient clearance of B. burgdorferi in the absence of macrophages (CCR2–/–) than in their presence (WT). This brings to light a possible natural defect in the recruitment or function of macrophages in WT C3H mice, which may contribute to the increased sensitivity of C3H animals to infection with B. burgdorferi.

Although a partial reduction in macrophage functions as a result of silica treatment did not significantly affect murine Lyme carditis as assessed by histology (4), other macrophage deficiencies do contribute to the pathology of infected hearts. Lyme carditis was more severe in the absence of ß2 integrins, which mediate the adhesion of leukocytes to the endothelium and thus entry into infected organs (17, 18). Increased carditis in ß2 integrin-deficient animals may be due to either an increased pathogen burden or increased expression of MCP-1, which has been shown to increase myocarditis (14, 22). Infection of MyD88-deficient mice, which have a defect in macrophage activation via toll-like receptors, results in significantly higher spirochete burdens in the heart but no increase in cardiac inflammatory responses (7, 25). These studies of inhibited or absent macrophages document that the presence of macrophages is critical for the resolution of Lyme carditis in vivo.

New insights into the role of macrophages in carditis are emerging from studies of CCR2–/– mice. Monocytes from CCR2–/– mice exhibit defects in both activation and recruitment to sites of infection (24), and CCR2–/– mice are more susceptible to infections with Listeria monocytogenes (23), Leishmania major (37), and Cryptococcus neoformans (39). CCR2 may act through mediating the release of monocytes from the bone marrow and not through their extravasation into sites of infection (38). Infection of CCR2–/– mice with Trypanosoma cruzi resulted in increased cardiac parasitism but no increase in cardiac inflammation (20). Taken together, these studies and the current results suggest that macrophages are more critical for the efficient control of pathogen burden than for the development of inflammation

In summary, we have demonstrated that the loss of CCR2 does not alter resistance or susceptibility to Lyme carditis, although it does have an effect on B. burgdorferi clearance by B6 animals and on the cellular makeup of the inflammatory infiltrate in C3H mice. The development of carditis by susceptible C3H CCR2–/– mice consists of an increased proportion of PMN in the cellular infiltrate and decreased cardiac B. burgdorferi loads compared with those for WT mice, highlighting a possible defect in macrophages of the C3H strain. Multiple factors, including tissue-specific components of the extracellular matrix and a mixture of cytokines and chemokines in the extracellular milieu, provide combinatorial signals for migrating leukocytes, which are augmented by chemokine production from newly recruited cells (11, 19, 40). B. burgdorferi disseminates through the bloodstream in vivo, where lipoprotein components interact with endothelial cells via CD14 and TLR2 to activate NF-B and stimulate the release of IL-8 (1, 10, 13, 16, 21, 43). IL-8 favors the recruitment of PMN, yet in Lyme carditis, macrophages dominate the inflammatory infiltrate (2, 5, 36). Understanding how infection with a single pathogen within a single host results in differential recruitment of phagocytes to infected organs will likely depend on organ-specific microenvironments in vivo and may uncover new avenues for manipulating cell recruitment in inflammatory diseases.
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Re: Lyme Disease and the heart

Post by Yvonne » Sun 16 May 2010 15:12

Clin Res Cardiol. 2010 May 13. [Epub ahead of print]

Complete AV block in Lyme carditis: an important differential diagnosis.

Semmler D, Blank R, Rupprecht HJ.

II. Medizinische Klinik, GPR-Klinikum, August-Bebel-Str. 59, 65428, Rüsselsheim, Germany, semmd@gmx.de.

Abstract
Lyme disease is a tick-borne spirochetal infection that may affect the heart. Cardiac manifestations include conduction disturbances and other pathologies of the heart. We report on a 37-year old male, who was admitted to the emergency department because of dizziness and generalized tiredness. Physical examination and the initial laboratory values revealed no abnormalities. The patient's electrocardiogram on admission revealed newly diagnosed bradycardia due to atrioventricular heart block. The ventricular heart rate was 35/min. The patient was admitted to the ICU. Lyme serology and Western blot were positive for Borrelia antibodies. After institution of antibiotic therapy with ceftriaxone, atrioventricular heart block resolved rapidly. We therefore have to assume that in this patient Lyme carditis was the cause of third-degree AV block.

PMID: 20464556
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Re: Lyme Disease and the heart

Post by Yvonne » Mon 12 Jul 2010 15:24

http://www.rcpe.ac.uk/journal/issue/jou ... charya.pdf

Lyme carditis: a reversible cause of complete atrioventricular block
Abstract

A 54-year-old American woman presented with an episode of syncope.
This had occurred against a background of several days of dizziness and
palpitations. Her medical history included Bell’s palsy, which had been diagnosed
three weeks earlier. On examination, she had a resting bradycardia of 31 beats
per minute and her electrocardiogram demonstrated third-degree atrioventricular
(AV) block. She was referred to cardiology for consideration of permanent
pacemaker implantation. Given her facial nerve palsy and AV block, a diagnosis of
Lyme borreliosis was suspected. Within 48 hours of initiation of ceftriaxone, she
reverted to sinus rhythm, albeit with a marked first-degree AV block. Subsequent
serology confirmed the diagnosis. Reversible causes of complete AV block should
always be considered and appropriate therapy may avoid the need for permanent
pacemaker insertion.
Case report
A 54-year-old American woman on vacation was admitted
to our hospital following an episode of syncope which had
occurred against a background of several days of dizziness
and palpitations. Three weeks previously she had developed
left-sided facial weakness, which was diagnosed as Bell’s
palsy, and had been treated with a three-day course of
prednisolone and acyclovir. The only feature of note in
her medical history was manic depression, for which she
was treated with lithium carbonate.
On examination, she was afebrile. There was no skin rash
or lymphadenopathy. She had a resting bradycardia of
31 beats per minute and a blood pressure of 97/38 mmHg.
There were no murmurs or signs of heart failure.
Neurological examination revealed a left lower motor
neurone seventh nerve palsy.
The patient’s initial laboratory data were unremarkable.
In particular, her electrolytes, cardiac enzymes and white
cell count with differential were all normal and lithium
levels were in the therapeutic range. Her chest X-ray
was normal. Her electrocardiogram demonstrated third-
degree atrioventricular (AV) block (Figure 1A). She was
referred to cardiology for consideration of permanent
pacemaker implantation.

However, given her facial palsy and heart block, a
diagnosis of Lyme borreliosis was suspected. Blood was
taken for Lyme serology. On closer questioning, the
patient also reported being a keen walker in the hills of
Massachusetts, but she could not recall any tick bites or
skin rash in the previous 30 days.

She was admitted to the coronary care unit, placed on
continuous monitoring and treated with intravenous
ceftriaxone, 2 g daily. Within 48 hours, she reverted to
sinus rhythm, albeit with marked first-degree AV block
(Figure 1B). Thereafter, her hospital stay was
uncomplicated and she remained in sinus rhythm with a
shortening P–R interval and her facial nerve palsy
resolving. Subsequently, Lyme borreliosis was confirmed
with positive serology and Western blot analysis. The
patient has since returned to the USA and has suffered
no long-term sequelae of her infection.
Discussion

Lyme borreliosis is a multisystem disease caused by
infection with the spirochaete Borrelia burgdorferi. It is
one of the most common tickborne infections in the
northern hemisphere and is considered endemic in the
highlands of Scotland. The clinical manifestations of Lyme
borreliosis are classically divided into three stages: early
localised, early disseminated and late disease. Early
localised disease generally occurs several days or up to
one month after the initial tick bite. An influenza-like
illness may occur and is often accompanied by the
erythema migrans rash. The early disseminated stage
occurs weeks or months after the erythema migrans rash
and is characterised by neurological symptoms and
musculoskeletal complaints. Isolated facial nerve palsy is a
common neurological manifestation. Finally, the late stage
occurs several months to years after the erythema
migrans rash and is characterised by a monoarthritis or
oligoarthritis and the development and progression of
neurological sequelae. The diagnosis is suspected
clinically and confirmed by the detection of antibodies to
the spirochaete. False positive tests may occur with
enzyme-linked immunoabsorbent assay, and Western blot
analysis should be used for confirmation.

Cardiac manifestations occur in about 10% of patients
with untreated Lyme borreliosis. Other systemic
features may also be present, as occurred in this case.
Varying degrees of AV block are the most common
feature of Lyme carditis. In addition, pericarditis,
endocarditis, myocarditis, pericardial effusion, myocardial
infarction, coronary artery aneurysm, QT interval
prolongation, tachyarrhythmias and congestive heart
failure have been reported. Myopericarditis is rare but
may lead to transient cardiomegaly or pericardial
effusion with non-specific ST and T wave changes on
the electrocardiogram.

The choice of antibiotic treatment for Lyme borreliosis
depends on the stage of the disease. Early disease can be
treated with oral doxycycline, 100 mg twice a day for 14
days. Extracutaneous involvement in stage two requires
more intensive treatment to eradicate infection and
prevent late complications. Intravenous ceftriaxone, 2 g
As in this case, it is often
daily, is given in these cases.
effective in leading to a rapid resolution of the heart
block associated with carditis.
The causes of AV block can be divided into congenital
and acquired, with some causes of the latter being
reversible (Table 1). In elderly patients, third-degree AV
block is most often due to degenerative disease of the
conducting system. In these patients, permanent
pacemaker implantation is usually indicated. However, in
younger patients, a reversible cause of AV block should
always be considered before submitting them to
pacemaker implantation. This case of Lyme borreliosis,
promptly treated with the appropriate antibiotic,
provides a clear illustration of this point.
Conclusion

Reversible causes of AV block should always be
considered prior to pacemaker insertion. This case
provides an unusual example of reversible AV block.
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Re: Lyme Disease and the heart

Post by Yvonne » Fri 16 Jul 2010 14:11

Cas Lek Cesk. 1996 Nov 20;135(22):729-31

Borrelia burgdorferi as a cause of sick sinus syndrome?

[Article in Czech]


Bartůnĕk P, Nĕmec J, Mrázek V, Gorican K, Zapletalová J.
IV. interní klinika 1. LF UK a VFN, Praha.

The authors describe the case of a 42 years old man, who was implanted a permanent pacemaker on the basis of the sick sinus syndrome, suspected to have been induced by the infection with Borrelia burgdorferi. The review of world literature has indicated that it is an exceptional indication of permanent cardiac stimulation.

PMID: 8998826
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Re: Lyme Disease and the heart

Post by Yvonne » Fri 16 Jul 2010 14:12

Z Kardiol. 2003 Dec;92(12):1029-32.

Lyme carditis and symptomatic sinus node dysfunction

[Article in German]

Franck H, Wollschläger H.

I. Medizinische Klinik, Klinikum St. Marien, Mariahilfbergweg 5-7, 92224 Amberg, Germany.

Abstract
Lyme carditis is typically associated with AV nodal conduction abnormalities. We describe the case of a 66 year old female patient, who experienced a series of syncopal attacks after several tick bites two weeks earlier. ECG monitoring revealed recurrent sinus arrest with a maximum pause duration of 8 seconds. After institution of antibiotic therapy for Lyme carditis, sinus node dysfunction resolved rapidly and the patient had no further syncopes. Pacemaker implantation was not necessary. We therefore have to assume that in this patient Lyme carditis was the cause of symptomatic sinus node dysfunction.

PMID: 14663614
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Re: Lyme Disease and the heart

Post by Yvonne » Tue 20 Jul 2010 15:36

http://www.cancernetwork.com/display/ar ... 0162/11011

Case in Point: Heart Block as the Presenting Symptom of Lyme Disease
A 16-year-old girl presented to the emergency department (ED) with a 24-hour history of feeling tired and weak. The patient reported that she awoke that morning with the "worst headache of her life" and "passed out" while sitting on the edge of her bed. She did not tell her friends or family.

The headache persisted in the frontal region and was unrelieved by acetaminophen. While at lunch with a group of friends, she slumped over in her chair and became unresponsive for 30 seconds. During this episode, the patient was not incontinent nor did she have any abnormal movements consistent with an overt seizure. After the event, she was awake and alert and was brought by ambulance to the ED.

The patient had been healthy before this episode and had no significant medical history. Her family history was noncontributory for any genetic components or illnesses. She lived with her parents and 2 healthy siblings in Rhode Island. Her activities included lifeguarding at a town beach and bike riding. She reported that the only medication she took was acetaminophen. A full adolescent HEADSS assessment (Home, Education, Activities, Drugs, Sexual history, Suicidality/depression) did not reveal any contributory findings to explain this patient's syncopal episodes. She denied any new symptoms other than fatigue and a constant frontal headache. There was no history of nausea, vomiting, neck stiffness, or photophobia, nor were there complaints of chest, abdominal, or joint pain. She did not remember any insect bites or rashes occurring during the past month.

In the ED, the patient was awake and alert with a frontal headache. Her vital signs were normal and stable. Heart rate, 62 beats per minute, respiratory rate, 18 breaths per minute; blood pressure, 126/74 mm Hg; and oxygen saturation, 98% on room air. She weighed 54 kg and was 157 cm tall with a normal body mass index of 21.9. Evaluation of the head, eyes, ears, nose, and throat revealed 5-mm bilateral pupils that reacted slowly to light. Extraocular muscle function was intact. Funduscopic findings were normal. Breath sounds were clear bilaterally. Chest assessment revealed an irregular heart rate and rhythm, with a mean of 60 beats per minute and no audible murmur. Abdominal examination findings were normal, with no hepatosplenomegaly. Extremities were warm, without bruises or rashes. The patient's skin was warm and her cheeks were flushed. Mucous membranes were pink and moist. Results of the neurologic examination were grossly normal. Muscle strength was 5+ and symmetric. Deep tendon reflexes were 2+ and symmetric with no focal findings

The complete blood cell count and levels of electrolytes, blood urea nitrogen, creatinine, glucose, calcium, magnesium, and phosphorus were all within normal limits, as were results of liver function tests. Results of a urinalysis, urine toxicology screen, urine pregnancy test, and a Monospot test were negative.

Given the patient's account of awaking with the worst headache of her life and the possibility of an intracranial process, serial transaxial CT images of the head were obtained from the foramen magnum to the skull vertex. There was no evidence of acute intracerebral hemorrhage, extra-axial fluid collection, midline shift, or mass effect. The ventricles were of normal size, shape, and configuration for the patient's age. The bony calvarium was intact and the paranasal sinuses were well aerated.

Because of the 2 syncopal episodes, an ECG was also obtained (Figure 1). The tracings showed complete heart block with an atrial rate of 100 beats per minute and a ventricular rate of 60 beats per minute. There were narrow QRS complexes and a pause of up to 3.5 seconds on the rhythm strip (Figure 2).

The pediatric cardiology service was consulted. An echocardiogram showed a structurally normal heart with good biventricular shortening function. There was mild mitral valve regurgitation and no pericardial effusion.

Additional laboratory tests were ordered, including those for Lyme disease and creatine phosphokinase. Because Lyme carditis was being considered in the differential diagnosis, intravenous ceftriaxone therapy was initiated. The patient was admitted to the electrophysiology service for monitoring and for possible insertion of a temporary pacemaker.

Test results confirmed the diagnosis of Lyme carditis. Western blot studies for Borrelia burgdorferi IgG antibodies were positive for bands 18, 23, 39, 41, 45, and 58. (IgG antibodies to any 5 of the following 10 significant bands is considered a positive result: 18, 23, 28, 30, 39, 41, 45, 58, 66, or 93kDa.) Western blot studies for IgM antibodies were positive on all 3 bands. (IgM antibodies to any 2 of the following 3 significant bands is considered a positive result: 23, 39, and 41kDa.) There were no Ehrlichia IgG or IgM antibodies or Babesia IgM antibodies.

The infectious disease service was consulted and a lumbar puncture was recommended to assess for neuroborreliosis. Results of polymerase chain reaction assays for Lyme disease in the cerebrospinal fluid were negative. Lyme total antibody test with reflex was positive at 3.52 immune status ratio (ISR). (A result of 1.10 ISR or greater is considered positive.) This panel is appropriate for Lyme disease testing 4 weeks after a diagnosis of erythema migrans or the onset of disease symptoms.

The patient was admitted to a general ward, where a high-grade atrioventricular (AV) block subsequently developed. She required transcutaneous pacing and a transvenous pacemaker, which remained in place for approximately 14 hours. Thereafter, the patient's rhythm became a 2:1 AV block and then a first-degree AV block. The transvenous pacemak-er was removed and the patient was closely monitored via telemetry. She had no further episodes of high-grade AV block.

The patient received 28 days of ceftriaxone therapy and was advised to follow up with her primary care provider and cardiologist.
Cardiovascular manifestations of untreated Lyme disease often occur within 21 days of exposure and include fluctuating degrees of AV block, acute myopericarditis or mild left ventricular dysfunction, and rarely, cardiomegaly or fatal pericarditis.2 Carditis occurs in approximately 4% to 10% of untreated adults--and in a much lower proportion of children in the United States.3 (In one prospective, longitudinal, community-based cohort study of 201 children [1 to 21 years old] with newly diagnosed Lyme disease, carditis developed in only 0.5%.4)Neurologic involvement, which can affect up to 15% of untreated patients, can include facial nerve palsy (Bell palsy) and aseptic meningitis; less commonly, cerebellar ataxia, radiculoneuritis, myeli-tis, and pseudotumor cerebri may develop.5

Timely diagnosis of Lyme carditis rests on including this disorder in the differential when an adolescent presents with a syncopal episode. In this patient's case, confounding factors such as severe headache made the diagnosis somewhat harder. Some patients have no history or findings that suggest Lyme disease. In some cases, for example, heart block is the first and only manifestation of Lyme disease.6

The diagnosis of Lyme carditis is confirmed by the association of clinical features with serologic testing, including enzyme-linked immunosorbent assay and/or Western blot analysis. However, Lyme carditis can occur early in the course of Lyme disease, before there has been a detectable antibody response (which typically occurs at 6 to 8 weeks). Thus, a negative test result does not rule out the diagnosis. However, if cardiac features have been present for more than 1 to 2 months, the patient should be seropositive and a negative test result should cast doubt on the diagnosis of Lyme carditis.3

No studies have specifically addressed the treatment of Lyme carditis. Although there is no evidence that antibiotic therapy hastens the resolution of cardiac abnormalities, such therapy is recommended for affected patients with this purpose in mind and to prevent later manifestations of Lyme disease.3 There are no comparative treatment trials in carditis, and there is no evidence to suggest that parenteral antibiotic therapy is more effective than oral antibiotic therapy (Table).7

For patients with Lyme carditis, the prognosis remains positive, and spontaneous resolution of heart block can be expected within a few days or weeks. There have been cases (like this one), in which temporary pacing is required.
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Re: Lyme Disease and the heart

Post by Yvonne » Sat 7 Aug 2010 19:48

http://www.amc.edu/amr/archives/200606/case1.html

Case Report - A 52-year-old Man with Increasing Fatigue and a Syncopal Episode
A 52-year-old male marathon runner with a past medical history significant for glaucoma presented to the emergency department with a two-week history of increasing fatigue after an episode of syncope.

He initially presented to his primary care doctor’s office complaining of flu like symptoms one week after running a marathon and three weeks prior to admission. He described fever, chills, night sweats, increasing fatigue and body aches. He was noted to be an avid runner who had finished within the top five to ten athletes in prior marathons. He stated that despite training intensely, he only finished in 50th place. During this visit, a chest x-ray was obtained which showed no evidence of pneumonia or other abnormalities. He was diagnosed with a minor viral upper respiratory tract infection and over the following week began to notice improvement of his symptoms.

He returned to the office two weeks after the initial visit with worsening fatigue and decreased exercise tolerance. He had become increasingly short of breath after running more than 2 milles. A serologic test for Lyme disease was performed to rule out Lyme carditis after an EKG showed first-degree heart block.

While awaiting the results of the serologic studies the patient had a syncopal episode lasting several seconds and was instructed to go immediately to the emergency department. On review of systems, he denied fever, chills, lightheadedness, chest pain, palpitations, shortness of breath, diaphoresis, nausea, vomiting, abdominal pain, rashes, arthralgias, myalgias or trauma. First-degree heart block was again noted on an EKG. The patient was discharged with an appointment to see cardiology as an outpatient. Two days later, the patient had a similar syncopal event during his cardiology appointment. An immediate EKG showed a 2:1 heart block and the patient was admitted to the coronary care unit for further observation and workup.

His past medical history was significant for glaucoma, for which he took xalatan eye drops. He denied any additional medications or drug allergies. His family history was significant for a father who died from chronic lymphocytic lymphoma.

PHYSICAL EXAM
Physical examination revealed a temperature of 99° F, blood pressure of 159/76 mm Hg, pulse range of 38 to 45 beats per minute, respiratory rate of 18 breaths per minute, oxygen saturation of 100% on room air, weight of 173 lbs and height of 6 feet. The patient was in no acute distress. His skin was warm and dry. The oral mucosa was moist and his throat was without erythema or lesions. His neck was supple without lymphadenopathy or nuchal rigidity. The lung fields were clear to auscultation bilaterally. Cardiac exam was significant for bradycardia without murmurs, rubs or gallops. The abdominal exam was unremarkable. Extremities revealed full range of motion, no pedal edema and good peripheral pulses. No deficits were noted on the neurologic exam

Differential Diagnosis

1.Lyme carditis
2.Ischemic cardiomyopathy
3.Viral myocarditis
4.Idiopathic cardiomyopathy
5.Cardiac valvular disease
6.Sick sinus syndrome

An electrocardiogram (EKG) showed sinus bradycardia at 37 beats per minute with a 2:1 Mobitz heart block. Chest X-ray showed no active disease.

Serologic studies done at the primary care physician’s office were negative for Lyme disease.
HOSPITAL COURSE

The patient was empirically treated with intravenous ceftriaxone for suspicion of Lyme disease-induced heart block. Outpatient Lyme serologies were negative. An enzyme-liked immunosorbent assay (ELISA) and Western Blot test for Lyme disease were resent due to the high false negative rate associated with Lyme serolgies performed early in the course of the illness. In addition, viral serologies for cytomegalovirus (CMV), Ebstein Barr virus (EBV), Coxsackie virus, and Parvovirus were also performed. An echocardiogram showed mild left atrial dilation, trace tricuspid regurgitation and a normal ejection fraction. The patient refused to complete an attempted stress echo secondary to emotional distress. A stress EKG showed first-degree heart block with intermittent 2:1 Mobitz heart block and a right bundle branch block. No ischemic changes were noted. A MRI of the heart showed mild dilation of the left atrium, similar to that seen on the echo.

Hematology consultation attributed the patient’s anemia to be a result of chronic disease due to an underlying inflammatory process. The patient’s iron studies, folate, vitamin B12, direct Coombs test, Parvovirus, EBV IgM, CMV IgM, erythropoietin level and peripheral smear were all within normal limits. The second set of Lyme ELISA and western blot tests were positive and the diagnosis of Lyme carditis was confirmed.
Lyme carditis is a complication of disseminated (stage 2) Lyme disease. Cardiac involvement may be manifested as an atrioventricular block, myopericarditis or cardiomegaly. An AV block, as seen in this case, is the most common manifestation of Lyme carditis. Hospitalization with continuous telemetry monitoring is recommended for patients who present with second or third degree AV block, or those who present with first degree AV block with the PR interval exceeding 0.30 seconds. Most patients with Lyme carditis treated early with appropriate IV antibiotics have an excellent prognosis. The antibiotic treatments include either 2 grams of ceftriaxone IV daily, 2 grams of cefotaxime IV three times daily or 5 million units of penicillin G four times daily.

Patients who do not respond to IV antibiotics and have persistent AV block may require permanent pacemaker placement. Lyme carditis is a rare cause of AV Block, but one with an excellent prognosis if the signs and symptoms are recognized early and the proper treatment is initiated without delay.
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Yvonne
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Re: Lyme Disease and the heart

Post by Yvonne » Sun 8 Aug 2010 10:20

http://www.nejm.org/doi/full/10.1056/NE ... 8173430716

Bradycardia
The differential diagnosis of bradycardia reviewed recently by Mangrum and DiMarco (March 9 issue)1 should include Lyme carditis.2-4 Here, we describe a patient with Lyme carditis.

A 42-year-old patient presented with acute first-to-third-degree atrioventricular block. He reported having been bitten by a tick (Ixodes ricinus) six weeks before admission to the hospital. He had not had fever but had had unspecific discomfort of the knee and elbow joints and a sudden decrease in physical energy during the four weeks before admission. He had not had a syncopal event but had had attacks of dizziness. At admission, the results of clinical, radiologic, and echocardiographic examinations were normal. The electrocardiogram at admission showed a prolonged PR interval of 0.38 second with a normal ventricular response. The 24-hour electrocardiogram showed first-degree atrioventricular block and intermittent third-degree atrioventricular block. The lowest heart rate was 37 beats per minute. Because of this history, we immediately started antibiotic therapy with ceftriaxone, which was given for 20 days (4 g per day initially and 2 g per day at the end of treatment), with no pacemaker but with continuous monitoring during the first days of treatment. The effect of treatment on atrioventricular conduction was a steady decline in the PR interval from greater than 0.4 second initially to under 0.2 second by day 13 — an effect that persisted on day 31

The results of microbiologic testing for Borrelia burgdorferi were as follows. The enzyme-linked immunosorbent assay for B. burgdorferi was positive for IgG antibodies (titer, 1:320) and negative for IgM antibodies. In the Western blot for IgG antibodies, the serum reacted with bands at 18, 60, and 88 kd. In the Western blot for IgM antibodies, reactions with bands at 41 kd and weak reactions with bands at 21 kd were noted. This pattern is characteristic of the postacute phase of the infection

In patients such as the one we describe, Lyme carditis should be considered. Although it is rare, this condition can be treated effectively with antibiotics
Listen to all,
plucking a feather from every passing goose,
but follow no one absolutely

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