Penyakit Jantung Tiroid

Pugud Samodro
Bag / SMF Ilmu Penyakit Dalam
FK Unsoed / RSUD Prof Margono Soekarjo
Purwokerto
Penyakit jantung tiroid
Hipertiroidisme
Hipotroidisme
TIROTOKSIKOSIS
Sindroma klinik akibat bahan tiroaktif beredar
dalam darah berlebihan, melebihi kebutuhan
jaringan.

HIPERTIROIDISME
Hiperaktifitas kelenjar tiroid
Conditions associated with
thyrotoxicosis
Diffuse toxic goiter (Graves disease)
Toxic adenoma (Plummers disease)
Toxic multinodular goiter
Subacute thyroiditis
Hyperthyroid phase of Hashimotos thyroiditis
Thyrotoxicosis factitia
Rare forms of thyrotoxicosis :
- ovarian struma
- metastatic carcinoma
- hydatiform mole
- hamburger thyrotoxicosis
- TSH-secreting pituitary tumor
- pituitary resistance to T3 and T4
EUTHYROID CIRCULATION
HYPERTHYROID
CARDIAC OUTPUT
19 L / min
CARDIAC OUTPUT
5 L / min
STROKE VOLUME
66 ml / beat
STROKE VOLUME
190 ml / beat
BLOOD PRESSURE
120 / 80
BLOOD PRESSURE
SYSTOLIC ^
DIASTOLIC +
BLOOD PRESSURE
NORMAL
BLOOD PRESSURE
EXPANDED
SYSTEMIC
VASCULAR
RESISTANCE
1636 (dyne-cm) sec
-5
SYSTEMIC
VASCULAR
RESISTANCE
717 (dyne-cm) sec-5
Comparison of the cardiovascular hemodynamic in euthyroid and
hyperthyroid at rest.
( Klein, 1990 )
T
4
T
3
T
4
T
3
Sites of action of Thyroid Hormone on the Heart and
Cardiovascular System
Tissue thermogenesis
Decreased systemic
vascular resistance
Decreased diastolic
blood pressure
Decreased afterload
Activation of
renin/angiotensin/aldosterone
system
Increased preload
Cardiac chronotropy
and inotropy
Increased cardiac
output
(Klein, 2005)
Cardiac output
Thyroid hormone Thyroid hormone
1 Heart rate
1 Heart rate
1 Myocardial
relaxation
Arterial to Venous
blood shift
1 Pulsatile
arterial load
4 SVR
4 Steady
arterial load
1 RAAS
1 SAP 4 DAP
1 Blood volume
1 Suction
phenomenon
1 Venous return
Mean AP
1 Pulse pressure
End-systolic
wall stress
/ 4 LVESV
1 / LVEDV 1 Stroke volume
Pathophysiological paradigm of the mechanisms by which at-rest cardiac output is
increased in human hyperthyroidism.
(Biondi et al, 2002)

Atrial Fibrillation in Hyperthyroidism

The prevalence among hyperthyroidism ranges
between 9 22%, compared with 2 3% in a
control population with normal thyroid function.
There was a stepwise increase in prevalence in
each decade.
Framingham cohort prevalence of AF after 10
years was 28% in patients with subclinical
hyperthyroidism compared with 11% in patients with
normal thyroid function with a relative risk of 3.1.

The treatment of Atrial Fibrillation in
hyperthyroidism

Control the heart rate with routine pharmacologic
therapy
Start antithyroid therapy
Cardioversion at approximately the 16
th
week
after normal thyroid function
Anticoagulant or antiplatelet
Embolic complications in about 15% of cases

ST
SVT
AF
Clinical Manifestations and Physical Examination
Congested Circulation
Rate related HF
CHF
Thyrotoxicosis cardiomyopathy
LVH
MR
Angina like chest pain
S
1
S
2
Apical impulse intensity 1
S
1
1 S
2
Palpitation
Exercise intolerance
Dyspneu deffort
SBP 1
DBP 1
Wide pulse
pressure
Hyperkinetic precordium

Heart failure in Hyperthyroidism

In one report of patients with hyperthyroidism,
there was a 6% frequency of CHF
Circulatory congestion state
Rate-related heart failure
Congestive heart failure
Thyrotoxic cardiomyopathy

The treatment of Heart Failure in
Hyperthyroidism


The goal is to slow the heart rate
BETABLOCKER
Conventional treatment of heart failure
Definitive / etiologic therapy

Hypothyroidism


The prevalence is estimated 3 4% for overt
disease and 7 10% for the milder forms of
disease.
Advancing age produces an increase in the
incidence of hypothyroidism and after age 60
years 12 15%
Rotterdam study Subclinical hypothyroidism is
a strong indicator of risk for aortic atherosclero-
sis and myocardial infarction in elderly women.

Clinical syndrome ~ TH deficiency
metabolic process
Accumulation of glycosaminoglycans
Myxedema (adult), cretin (new born)
Myxedema coma (severe)
INTRODUCTION
Hypothyroidism
Introduction
Hypothryoidism decreased oxygen and
substrate utilization
demands for cardiac output decrease
Alters cardiac function
Loss of the inotropic & chronotropic
Increased peripheral vascular resistance
Decreased blood volume

Pathophysiology
Major cardiovascular changes
decrease in cardiac contractility & mass
a reduction in heart rate, and
an increase in peripheral vascular
resistance

Effect of Thyroid Hormone on Hemodynamic and
Contractility of the Heart
Increased tissue
thermogenesis
Decreased systemic
vascular resistance
Triiodothyronine
Increased cardiac
inotropy and
chronotropy
Increased cardiac
output
Erythropoietin
Increased blood
volume
Increased renal
Na-reabsorption
Increased effective
arterial filling
volume
Increased
RAA system
Cardiovascular Effect of Hypothyroidism
Myocardial
contractility
Heart beats
Peripheral
vascular
resistance
Capillary
permeability
Stroke
volume
Cardiac
output
Blood
pressure
Pericardial
effusion
Total blood
volume
EUTHYROID CIRCULATION
HYPOTHYROID
CARDIAC OUTPUT
* 197 L/mm
CARDIAC OUTPUT
50 L/mm
STROKE VOLUME
- 66 ml/beat
STROKE VOLUME
- 190 ml/beat
BLOOD PRESSURE
- 120/80
BLOOD PRESSURE
SYSTOLIC ^
DIASTOLIC +
AVD
EXTRACTION
34 ml
AVD
EXTRACTION
-44 ml
BLOOD PRESSURE
NORMAL
BLOOD PRESSURE
EXPANDED
SYSTEMIC
VASCULAR
RESISTANCE
- 1636 dynes
SYSTEMIC
VASCULAR
RESISTANCE
717 dynes
Comparison of the cardiovascular hemodynamic in euthyroid and hyperthyroid at rest. The declines
in systemic vascular resistance and the increase in cardiac output, stroke volume, and heart rate
are similar to those observed in normal individuals with fistulas or pregnancy and with encrising.
Adapted from [25] and others [30,32 34]
LV
MASS
INCREASED
Cardiac Contractility
Reduction in cardiac output
Decreased ventricular diastolic relaxation
Impaired of compliance & diastolic filling
Multifactorial mechanisms
Increased after load
Changes in expression of the genes for
myocardial calcium regulatory proteins

Vascular Resistance
Thyroid hormone relaxes vascular smooth
muscle cells reducing peripheral
vascular (PV) resistance
Hypothyroidism increasing PV
resistance
Reduction in cardiac output
Reduction in tissue perfusion
Decreased tissue oxygen utilization
A-V oxygen extraction is not different
from that in normal subjects
CARDIOVASCULAR HEMODYNAMICS IN
HYPOTHYROIDISM
Systemic vascular
resistance
Cardiac output
Blood pressure
Systolic

Diastolic

Heart rate
Cardiac contractility


Cardiac mass


Blood volume
1

1

1 or normal

1 or normal

1 or normal
1


1


1
50%-60% higher

Decreased 30%-50%

Narrowed pulse-
pressure
20% prevalence of
diastolic hypertension

Systolic and diastolic
function both
subnormal
Pericardial effusion
may suggest
cardiomegaly
Findings Comments
(Klein & Ojama; 2001)
Clinical Manifestations and Physical Examination

Lack of energy
Exercise intolerance
Dyspneu deffort
SBP 1
DBP 1
Quiet precordium
ECG : - Low voltage
- SB
- Long QT
Hypertension
Chol 1 / LDL 1
CHD
Apical impulse diminished
Pericardial effusion
S
1
S
2
1
Clinical Manifestations
Exertional dyspnea and exercise
intolerance
Bradycardia; PVB; torsade de pointes
Hypertension: 20-40% cases, diastolic,
diminished pulse pressure
Cardiac dysfunction, with
poor contractility
dilatation or
pericardial effusion
Edema: periorbital; non-pitting
Seems as has
CHF
Severe primary hypothyroidism
A: A patient with unrecognised severe primary hypothyroidism who became severely obtunded after surgery
for fractured neck of femur. Marked myxoedema is evident. B: Several months later, after therapy including
thyroid hormone replacement.
COMMON SYMPTOMS ASSOCIATED WITH
HEART FAILURE AND HYPOTHYROIDISM
Weakness
Dyspnea
Edema
Dryness of skin
Personality
changes
Cold intolerance
+
+
+
+
+
+
+
+
+
+
+
+
Symptoms CHF Hypothyroidism
( Ascheim & Hryniewicz, 2002 )
Low T3 Syndrome
Heart failure adaptive compensatory
AMI Low T3 predictor of mortality
Post CABG 5 monodeiodination +

30% patients with CHF have a low serum T3

The fall of serum T3 is proportional to the severity of CHF (NYHA)
T3 Treatment in Low T3 Syndrome
Some beneficial effects of T3 treatment have
been observed in patients submitted to cardio-
surgery, heart failure and in animals after AMI.
The changes in thyroid hormone metabolism
contribute to impairment of cardiac function
remains to be determined
The demonstration of beneficial effects on
cardiovascular end points of long term T3
replacement in cardiac patients with low T3
syndrome can answer this fundamental issue.
THANK YOU
FOR YOUR ATTENTION
Pugud Samodro