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1. PRESENTER—
HABIBUR RAHAMAN
CHAIRPERSON—
DR.PIJUSH KANTI BISWAS,Assistant
Prof

2.  In systemic disease ,invovlement of multiple
organs is the general rule.Yet cardiac
involvement in many systemic diseses is not
well recognise ,as the dominant manifestation
frequently reside in other organ systems.Cardiac
involvement is very common with many
systemic disease and may account for serious
morbidity or mortality.Early recognisation of
cardiac involvement may impact upon patient
management and prognosis.

5. • Pericarditis -is the most commonly
recognized cardiac problem[30%].Pericardial
effusion
Myocarditis –common histologically but
seldom present as HF unless hypertensive.It
is parallel to disease activity.
Endocarditis—Fibrinous Libman Sacks
endocarditis,lesion may cause embolic
events or infected but rarely cause
haemodynamically important regurgitation.
Vascular –occlusive events as MI,CVA,TIA
increase(3 TO 10 fold).More common if
APLA.

6. • MI—due to primarily accelerated
atherosclerosis.
• Riskfactors for accelerated atherosclerosis
include old age,HTN,Dyslipidemia,Repeated
high score disease activity, diseaseduration,
high total or daily dose of
glucocorticoids,postmenopausal statusand
high homocysteine.
• Babies born to mothers with SLEand havean
increased incidence of congenital completeAV
block.

7. • Unexplained recurrent venous or arterial
thrombosis, or frequent secondor third trimester
miscarriages.
• Venous thrombosis –Superficial and DVT,cerebral
vein throbosis,pulmonary embolism& HTN,retinal vein
thrombosis.
• Arterial thrombosis—stroke,TIA,MI(10%).cardiac
valve involvement or dysfunction(14%),upper and
lower extremities leg ulcer ,digital gangrene and
many more
• Heart valve leaflet thickening, thrombotic masses
extendingfrom the valve ring or leaflets, or
vegetations.

8.  Cardiac involvement often silent in SSc
frequently detected when screened with
sensitive tools as TDE,cMRI,thalium screening.
Evident cardiac involvement –poor prognosis.
May involve all layer ,manifest as acute
pericarditis ,pericardial effusion, constrictive
pericarditis, heart block or arrthymia
,ventricular dysfunction to overt HF.

9. • Ventricular conduction abnormalities are
common and, along with a septal pseudo-infarct
pattern (q wave inversion in ecg mimic mi due to
elongation and partial stretching of cardiac nerve
fibres) , correlate with reduced myocardial
function with exercise
• Cardiac involve more in dcSSc than lcSSc
and generally develop within 3yrs of
onset of skin thickening

10. • Most common form of chronicinflammatory
polyarthritis.can involve any layers of
heart.
PERICARDIUM-Pericarditis-pericardial effusion(10-
40%),EXUDATIVE- Decrease Complement.
• MYOCARDIUM-Rare,CMPdueto
necrotising myocarditis.
• ENDOCARDIUM-Coronaryarteritis,intimal
inflammation present 20%,rarelymanifest.
• Valveinvolvement—duetogranuloma,mitral
andaorticvalve,MR

11.  Associated with pancarditis and proximal
AORTITIS.
 Aortic involvement mainly in aortic root but
may extent upto aortic and mitral
valve,ventricular myocardium.
 1/10 significant AR and 1/3 present with
conduction block (even CHB)
 AR may precedes onset of arthritis ,SO DX OF
SERONEGETIVE ARTHRITIS SHOULD BE
CONSIDERED IN YOUNG MALE WITH
ISOLATED AR

12. • Granulomatous inflammatory diseaseof
unknown cause.
• Pericarditis though uncommon –usually
clinically insignificant
• Granulomatous infiltrative diseaseof the
myocardium is often asymptomatic, but can
causearrhythmias, conduction diseaseand,
rarely, otherwise unexplained congestive
heart failure

13. • Pulmonary artery hypertension and cor
pulmonale canoccur in sarcoidosis,generally
asaresult of pulmonary fibrosis.
• Systemicvasculitis - anuncommon
complication of sarcoidosis.
• Sarcoidvasculitis canaffect small- to large-
caliber vessels,including the aorta.

15. CAD is the most common causeof death in
adults with DM.
• DM, is an independent risk factor for CAD
and accounts for 14–50% of new casesof
cardiovasculardisease.
• Pathogenesis-
• endothelial dysfunction
• increased lipoprotein peroxidation
• increased inflammation,
• aprothrombotic state,
• associated metabolic abnormalities.

17. Diabetic patients aremore likely to have
MI ,greater burden of CAD,
larger infarct size,
more post infarct complications( HF, shock,death).
•.“SILENT ISCHEMIA,”resulting from ANS
dysfunction, accounting for up to 90%of their
ischemic events.
•ATYPICALischemic symptoms-
nausea,dyspnea,arrthymias,pulmonaryedema,heart
block,syncope—ANGINALEquivalent

18. Patients with DM also may have
• Abnormal LV systolic anddiastolic function,
reflecting concomitant hypertension,
Coronary microvascular disease,
• Endothelial dysfunction,
• Ventricular hypertrophy,
• Autonomic dysfunction.
• Restrictive cardiomyopathy
• INSULIN THERAPY MAY DECREASE
OVERALL MYOCARDIAL DYSFUNCTION.

20.  Bp is altered across the entire spectrum thyroid
function.
 HYPERTHYROID ISM:-
Widened pulse pressure
arterial stiffness ISOLATED SYS HTN
low systemic VR
HYPOTHYROIDISM:-
Endothelial dysfunction
Impaired VSM relaxation Diastolic HTN

21.  INCREASES in
– heart rate
– cardiac contractility,
– systolic and mean pulmonary artery pressure,
– cardiac output, diastolic relaxation, and
– myocardial oxygen consumption
 REDUCTIONS in
– systemic vascular resistance and
– diastolic pressure

22. Tachycardia, at rest, during sleep, and
exaggerated
during exercise.
• Palpitations – tachy/forceful cardiac
contractility
• Hyperdynamic precordium.
• Systolic hypertension with widened pulse
pressure
• Exertional dyspnea, which is due to respiratory
and skeletal muscle weakness

23. • Uncommon heart murmur which occurs in
patients with hyperthyroidism.
• It is a mid-systolic scratching sound best heard
over the second left intercostal space at the end of
expiration.
• Results from the rubbing of
the pericardium against the pleura in the context
of hyperdynamic circulation and tachycardia,
• Mimic the sound of a pericardial rub.

25.  Major cardiovascular changes
– decrease in cardiac output
– decrease in cardiac contractility
– reduction in heart rate
– increase in peripheral vascular resistance.
 • Others
– Hypercholesterolemia ,
– diastolic hypertension,
carotid intimal media thickness

26. • Exertional dyspnea
• Cardiac dysfunction with poor contractility.
• Bradycardia.
Pericardial effusions, in approximately 25% of patients
and may be quite large.
•Increased systemic capillary permeability and
disturbances in electrolyte metabolism.
• characterized by a high protein and cholesterol content.

27.  – Hypercholesterolemia
 – Diastolic hypertension, and
 – Elevated homocysteine levels
 – Elevated C-reactive protein and
 – Endothelial dysfunction
• Patients with angina pectoris probably have
less symptoms as they are less active and
peripheral oxygen demands decrease.

28. • Exposureof the heart toexcessivegrowth hormone
may causeCHFasaresult of high cardiac output,
diastolic dysfunction owing to ventricular
hypertrophy global systolicdysfunction.
• Hypertension occurs in up to one-third of patients
with acromegaly and is characterized by
suppression of the renin-angiotensin-aldosterone
axisand increases in total-body sodium andplasma
volume.
• Some form of cardiac disease occurs in about one-
third of patients with acromegaly and is associated
with adoubling of the risk of cardiac death.

29. • In addition to causing labile or sustained
hypertension, the high circulating levels of
catecholamines resulting from a
pheochromocytoma may causedirect myocardial
injury.
• Focalmyocardial necrosis and inflammatory cell
infiltration are present in ~50%of patients whodie
with pheochromocytoma and may contribute to
clinically significant left ventricular failure and
pulmonary edema.
• Left ventricular dysfunction and CHFmay resolve
after removal of thetumor.

31.  The pulseless disease or occlusive
thromboaortopathy.
 Aneurysm most common and clinically
most significant in aortic root where
they can lead to valvular
regurgitation(aprox 20%)

32. • Causeof GCAremains unknown, the
inflammatory lesion begins in theadventitia.
• Most characteristic features of GCAare new
onset of atypical and often severe headaches,
scalp and temporal artery tenderness, acute
visual loss, polymyalgia rheumatica, and painin
the muscles of mastication.
• GCAmay produce clinically apparent aortitisin
~15%of casesand involve the primarybranches
of the aorta, especially thesubclavian arteries,

33. • Raresyndrome that includes ahistory of asthma,
eosinophilia, pulmonary infiltrates, upper airway
inflammation, and avariable frequency of renal,
neurological, cutaneous, and cardiac
involvement.
• Cardiacdiseasein CSSis the most commoncause
of death. It is reported in 15 to 55 percent of
casesand may include pericarditis, myocarditis,
and coronary arteritis. Congestive heart failure
occurs in 15 to 30 percent ofcases.

34. • Nongranulomatous disease of onlymedium-
sized arteries.
• Necrotizing changesseen, with weakening of
the vesselwall and aneurysm formation or
myointimal proliferation, causingstenosisand
occlusion.
• cardiac disease(10 to 30 percent; congestive
failure, angina, infarction, pericarditis)
hypertension (approximately 30 percent)

35. • Acute febrile systemic illness of childhood.
• Cardiacabnormalities - pericardial effusions (~30
%),myocarditis, mitral regurgitation (~ 30 %),
aortitis and aortic regurgitation (infrequent),
congestive heart failure, and atrial andventricular
arrhythmias.
• Deaths usually result from acute coronaryartery
thrombosis in aneurysms that form following
vasculitis.

37. • Thiamine deficiency hasbeen found in 20–90% of
patients with chronic heart failure. This deficiency
appears to result from both reduced dietary intake
and adiuretic-induced increase in the urinary
excretion ofthiamine.
• The acute administration of thiamine to these
patients increases the left ventricular ejection
fraction and the excretion of saltand water.
• The classic associated cardiovascular syndrome is
characterized by high-output heart failure,
tachycardia, and often elevated biventricular filling
pressures

38. • In patients whose intake of protein,calories,
or both is severely deficient, the heart may
become thin, pale, and hypokinetic with
myofibrillar atrophy and interstitial edema.
• Generalized edema is common and relates to
a variety of factors, including reduced serum
oncotic pressure and myocardialdysfunction.
• Open-heart surgery posesincreased risk in
malnourished patients.

39. • 50%of patients with carcinoid syndrome
havecardiac involvement, usually manifesting
asabnormalities of the tricuspid or pulmonic
valves.
• Carcinoid heart diseasemost often presents
as tricuspid regurgitation, pulmonic stenosis,
or both. In some cases,ahigh cardiac output
state may occur, presumably asaresult of a
decrease in systemic vascular resistance
resulting from vasoactive substancesreleased
by the tumor

40. • Obesity is associated with an increased
prevalence of hypertension, glucose
intolerance, atherosclerotic CAD,atrial
fibrillation, obstructive sleep apnea, and
pulmonary hypertension, and is associated
with increased cardiovascular morbidity and
mortality rates.
• In addition, obesepatients haveadistinct
hemodynamic profile characterized by
increased total and central bloodvolumes,
increased cardiac output, and elevatedleft
ventricular filling pressure

41. • In part asaresult of chronic volume overload,
eccentric cardiac hypertrophy with cardiac dilation
and ventricular diastolic and/or systolicdysfunction
may develop.
• In addition, altered levels of adipokines secretedby
adipose tissue may contribute to adverse
myocardial remodeling via direct effects on cardiac
myocytes and other cells.