CARDIOVASCULAR

MANIFESTATION OF
TUBERCULOSIS
OLEH:
DR. ERTA PRIADI WIRAWIJAYA, SPJP, FIHA
A good heart is one of the best assets possessed by
a patient suffering from pulmonary Tuberculosis.
F.M. Pottanger 1909
As the focus of infection grows larger the effect on the
heart becomes greater. The deleterius influances are
many and varied.
The position of the heart in the chest is altered, the
pulmonary circulation is embarrassed, changes occur in
the systemic arteries as well in the heart itself.
Blood pressure is altered, relative intensity of the heart
tones is changed, numerous murmurs appear at the
varius valve areas and numerable adventitious sound
are heard.
First changes that occurs as soon as the infection is of
sufficient grade to cause clinical symptoms is an
acceleration of the pulse. It maybe noted only after
exertion of itu may be marked and even show when the
patient is at rest.
 Mr. Ujang, a farmer. 65 y.o.
Treated for TB 10 years ago.
Complained dyspnea and
pedal edema. Currently
treated in RSKC for relapsing
TB + Severe Pulmonary
Hypertension with Cor
Pulmonale...
 POSSIBLE CARDIOVASCULAR
COMPLICATION OF TB
Tuberculous aortitis
Pericarditis & Constrictive Pericarditis
Pericardial Effusion & Tamponade
Myocarditis and Cardiomiopathy
Pulmonary Hypertension & Cor Pulmonale
Cardiac Arrythmia
TUBERCOLOUS
AORTITIS
Rare entity, indicative of
disseminated tuberculosis.
Associated with aneurysm
formation in half of cases.
Possible complication is
perforation of adjacent
structures.
Both abdominal and thoracic
aorta are involved with equal
frequency.
Fatal outcomes frequently
reported even after
antituberculosis chemotherapy
and surgical intervention.
PERICARDITIS TB
Found in approximately 1% of all autopsied
cases of TB and in 1% to 2% of instances of
pulmonary TB.
Most common cause of pericarditis in Africa
and other countries in which TB remains a
major public health problem.
South Africa 69.5% (162 of 233) of cases
referred for diagnostic pericardiocentesis.
Compared to only 4% of cases in developed
countries.
 INITIAL EVALUATION
PERICARDITIS TB
Chest radiograph suggestive for pulmonary TB in 30% of cases.
Echo: presence of a pericardial effusion with frond-like projections, and thick
porridge-like exudate is suggestive of an exudate (not specific for a TB
etiology)
Chest CT scan and/or MRI alternative imaging modalities where available
pericardial effusion and thickening (5 mm) and typical mediastinal and
tracheobronchial lymphadenopathy (10 mm, hypodense centers, matting),
with sparing of hilar lymph nodes.
Lymph node biopsy if pericardial fluid is not accessible and lymphadenopathy
is present.
Tuberculin skin test is not helpful regardless of the background prevalence of
tuberculosis.
- Sagrista-Sauleda J, Permanyer-Miralda G, Soler-Soler J. Tuberculous pericarditis: ten-year experience with a prospective protocol for diagnosis and
treatment. J Am Coll Cardiol. 1988;11:724 728.
- Ng TTC, Strang JIG, Wilkins EGL. Serodiagnosis of pericardial tuberculosis. Q J Med. 1995;88:317320.
 Diffuse pericarditis may involve a large
surface area of the heart, does not follow
the anatomical territory of a specific
coronary artery.
ST elevation in 90% of cases. Most
common pattern is ST elevation in V5 and
V6 (70%); more extensive involvement is
indicated by additional ST elevation in
leads aVL, aVF and V3-4.
ST elevation is concave or saddle shaped
Associated ST depression in aVR and V1 is
seen in 64% of cases
PR depression is another characteristic
ECG finding which can be seen in any lead
except aVR where PR elevation may occur.
This may occur without the ST elevation.
 CONSTRICTIVE
PERICARDITIS
One of the most serious sequelae of
pericarditis TB, occurring in 30% to
60% of patients, despite prompt
antituberculosis treatment and the
use of corticosteroids.
TB most frequent cause of
constrictive pericarditis in Africa and
Asia.
Clinical presentation highly variable : asymptomatic to severe constriction,
the diagnosis is often missed on cursory clinical examination.
Sign: The diastolic lift (pericardial knock) that coincides with a high-pitched
early diastolic sound and sudden inspiratory splitting of the second heart
sound are subtle but specific physical signs, found in 21%, 45%, and 36% of
patients with constrictive pericarditis, respectively. often missed
GAMBARAN RADIOLOGIS
 TUBERCULOUS
PERICARDIAL
EFFUSION
Common finding in clinical
practice either as incidental
finding or manifestation of a
systemic or cardiac disease.
Clinical spectrum ranges from
asymptomatic mild effusions
to cardiac tamponade.
Etiology differs between
developed vs. developing
country, where tuberculosis
is a leading cause of
pericardial disease.
 PERICARDIOCENTESIS
Therapeutic pericardiocentesis is indicated in the presence of
cardiac tamponade.
Diagnostic pericardiocentesis should be considered in all
patients with suspected tuberculous pericarditis, and the
following tests should be performed:
Direct inoculation of the pericardial fluid into double-strength liquid
Kirchner culture medium at the bedside and culture for M
tuberculosis.
Biochemical tests to distinguish between an exudate and a
transudate (fluid and serum protein; fluid and serum LDH).
Indirect tests for tuberculous infection: ADA, IFN-, or lysozyme assay.
*LDH indicates lactate dehydrogenase; IFN-, interferon-; and ADA, adenine deaminase.

Mayosi BM, Volmink JA, Commerford PJ. Pericardial disease: an evidence-based approach to diagnosis and treatment. In: Yusuf S, Cairns
3614 Circulation December 6, 2005 by guest on January 30, 2017 http://circ.ahajournals.org/ Downloaded from JA, Camm AJ, Fallen BJ, eds.
Evidence-Based Cardiology. 2nd ed. London: BMJ Books; 2003:735748.
PHYSICAL SIGN OF
PERICARDIAL EFFUSION
AND CONSTRICTIVE
PERICARDITIS
 CASE PERICARDIAL TAMPONADE
40 yo man, complained worsening dypnea after 1 month of TB therapy
and was refferred to Karisma Cimareme Hospital.
Patient was hypotensive with raised JVP(+) and dulled heart sound
 PERICARDIAL WINDOWS
Indication
Drainage of a purulent pericardial effusion
Early tuberculous pericarditis in which resection of
the pericardium is required to prevent future
pericardial constriction
Loculated effusions situated unilaterally or
posteriorly

PERICARDIAL BIOPSY
Therapeutic biopsy: as part of surgical drainage in patients with severe
tamponade relapsing after pericardiocentesis.
Diagnostic biopsy: in areas in which TB is endemic, a diagnostic biopsy is not
required before commencing empirical antituberculosis treatment. In areas in
which TB is not endemic, a diagnostic biopsy is recommended in patients with 3
weeks of illness and without etiologic diagnosis having been reached by other tests.
Mayosi BM, Volmink JA, Commerford PJ. Pericardial disease: an evidence-based approach to diagnosis and treatment. In: Yusuf S, Cairns 3614 Circulation
December 6, 2005 by guest on January 30, 2017 http://circ.ahajournals.org/ Downloaded from JA, Camm AJ, Fallen BJ, eds. Evidence-Based Cardiology.
2nd ed. London: BMJ Books; 2003:735748.
 TUBERCULOUS MYOCARDITIS
& CARDIOMIOPATHY
Rare cause of myocarditis.
Associated with a high mortality and is often diagnosed at post-mortem.
Prevalence in males is twice that in females.
Most of the reported cases of tuberculous myocarditis are predominantly in
immunocompetent patients.
Out of the reported fatalities (sudden cardiac deaths), eighty one percent
(81%) occur in the young patients (below 45 years). Antituberculosis drug
therapy does not appear to offer mortality benefit against sudden cardiac
deaths.
Tuberculosis related sudden deaths from 1966 and 2000 showed that most of
the cases were due to tuberculous bronchopneumonia (64%) and massive
haemoptysis (30%), with a minority of cases due to tuberculous myocarditis.
 CASE REPORT
25 y.o. Complained hemoptysis and weight loss, CXR 2 Patient had and improvement, but present with
month before showed right upper lobe consolidation worsened dypnea, DOE(+), OP (+), PND(+).
(cardiac silhouette is normal), AFB (+) Treated for TB
OTHER FINDINGS

ECG sinus tachycardia & non-

specific ST-T changes in the lateral
leads.
Echo global hypokinesia, enlarged
LA and LV, mild MR, severe left
ventricular systolic dysfunction with
an EF of 20%; RA and RV were
dilated with associated mild TR and
pulmonary artery systolic pressure of
47 mm Hg.
 CLINICAL COURSE
Patient experienced respiratory failure Intubated and treated in ICU
Frequent VES & Nonsustained VT, given amiodarone
Despite sufficient cardiopulmonary support patient died on second day of
admission because of VF.

Post-mortem cardiac biopsy revealed multi-focal areas of

caseous myocardial necrosis, Ziehl-Neelson stain for AFB
(+).
Post-mortem HIV serology postmortem nonreactive.
 PULMONARY HYPERTENSION &
COR PULMONALE
Pulmonary hypertension (PH) is a hemodynamic and pathophysiological
condition, defined as an increase in mean pulmonary arterial pressure >25
mm Hg at rest as assessed by right heart catheterization (RHC)
In TB Patient its caused by destruction of vascular bed due to parenchymal
abnormalities, vasculitis, and endarteritis, leading to reduced cross-sectional
area of the pulmonary vasculature.
Common presentation :
Dyspnea out of proportion to their radiological picture,
Desaturation at even mild exertion and sometimes as overt heart failure with
pedal edema,
Raised jugular venous pressure and
Tender hepatomegaly.
FUNCTIONAL CLASSIFICATION OF PH
ACCORDING TO WHO
 COR
PULMONALE
 PRIMARY THERAPY
Oxygen
Fundamental importance in all patients with arterial hypoxemia.
Diuretics
To treat fluid retention due to PH and to reduce hepatic congestion and
peripheral edema. Moreover, diuresis can prevent a distended right
ventricle from impending left ventricular filling. Diuretics are especially
useful in patients with groups 2 and 3 PH.
Anticoagulation
Patients with PH are at increased risk for intrapulmonary thrombosis and
thromboembolism, due to sluggish pulmonary blood flow, dilated right
heart chambers, venous stasis, and a sedentary lifestyle.
Exercise
Exercise training appears to be beneficial for patients with PH (Mereles
et al., 2006; de Man et al., 2009). A randomized controlled trial has
demonstrated an improvement in exercise capacity in patients with PAH
who took part in a training program (Mereles et al., 2006).
SECONDARY THERAPY
 CASE REPORT
Mrs. L, 50 yo, school teacher in cililin, complained of dyspnea,
stomach distension, and pedal edema. Shes was previously
being treated for relapsing TB in Cibabat hospital.
Vital signs:
BP 90/60 mmHg, HR 110-120 x/mnt, Pulse Rate: 90-
100x/mnt, pulsus deficit (+). RR: 30x/menit, O2 Sat: 85%
at rest
Physical exam:
Distended jugular vein, ascites(+), pedal edema,
cardiomegaly (+) with RV heave (+), P2>A2
ECG : AF, RVR, RAD, RVH with strain pattern.
ECHOCARDIOGRAPHY
 TREATMENT
O2 supplementation :
BNC 2-4 lt/mnt O2 Sat 88-90%,
Simple mask 4-6 lt/mnt O2 sat 92-95%
Bosentan (Dorner) 3x20 mcg
Sildenafil (Viagra) 3x20 mg symptoms improvement
Furosemide 2x80 mg 3x120 mg
Spironolactone 2x100 3x100 mg
Electrolyte supplemention
Abdominocentesis to relieve distanded stomach symptoms
improvement
TB medication
 CONCLUSION
Cardiovascular complication of TB is broad, symptoms
varies from mild to severe.
In certain cases treatment option is limited and expensive
resulting in poor life expextancy and poor quality of life.
Early detection and proper management of TB is
important.
Thank you...