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Systemic disease involving cardiovascular system
1. Systemic disease involving
cardiovascular system
Presented by
Dr. Md. Ahasanul Kabir
Resident, Phase B
Department of Cardiology, BSMMU
Chairperson:
Assoc. Prof. Dr. Mukhlesur
Rahman
UCC, BSMMU
3. Common Cardiovascular Manifestations
of Systemic Autoimmune Diseases
Disease Sex
Distributi
on
Cardiovascular
Manifestations
Rheumatoid
arthritis
F>M o Pericarditis
o Coronary artery disease
o Cardiomyopathy
o Congestive heart failure
Systemic lupus
erythematosus
F>M o Pericarditis
o Libman-Sacks endocarditis
o Coronary artery disease,
o Hypertension
Inflammatory
myopathies
F>M o Pericarditis
o Conduction system abnormalities
o Congestive heart failure
o Myocarditis
4. Common Cardiovascular Manifestations
of Systemic Autoimmune Diseases
Disease Sex
Distributi
on
Cardiovascular
Manifestations
Systemic sclerosis F>M o Pulmonary hypertension,
o Pericarditis
o Cardiomyopathy
o conduction system disease
Seronegative
spondyloarthropathy
M>F o Aortitis,
o Conduction system disease
5. Accelerated Atherosclerosis
in Rheumatic Diseases
īļ Association between inflammatory diseases and
accelerated atherogenesis â eg RA & SLE.
īļ Ankylosing spondylitis, psoriatic arthritis, TA, and
APS - associated with premature atherosclerosis.
6. Accelerated Atherosclerosis
in Rheumatic Diseases
īļ Should consider an underlying inflammatory disease in
young patients with otherwise unexplained angina,
myocardial infarction, or stroke.
īļ Pts with a rheumatic disease who suffer a myocardial
infarction have worse outcomes in terms of both heart
failure and mortality than does the age-matched
general population.
7. Endothelial Dysfunction and Vascular
Injury
īļ Prolonged systemic inflammation such as that
seen in RA and SLE may promote endothelial
injury, increased endothelial apoptosis, and
endothelial vasodilator dysfunction.
īļ Inflammation may exacerbate the effects of
classic risk factors
8. Endothelial Dysfunction and Vascular
Injury
īļ Compared with the general population, patients
with systemic inflammatory diseases more
commonly exhibit endothelial dysfunction and
increased aortic stiffness.
īļ Systemic inflammatory environment may
predispose to increased plaque instability and
rupture
9. Molecular mechanisms for atherosclerotic
disease and cardiovascular events.
īļ Proinflammatory cytokines â TNF-Îą, IL-1 & IL-6 effects on endothelial
activation, leukocyte adhesion, endothelial injury, and permeability.
īļ â endothelial cell apoptosis and â capacity for repair may contribute.
īļ Others:
īŧ Autoantibodies (e.g antiphospholipid antibodies)
īŧ CD4 + CD28â cytotoxic T cells
īŧ Th17/TREG imbalance
īŧ Complement deficiency or excessive activation
īŧ Genetic polymorphisms
īŧ Deleterious effects of drugs, including corticosteroids & cyclosporine
10. Rheumatoid Arthritis
īļ A variety of studies have shown subclinical arterial disease with
increased carotid intimal-medial thickness (IMT) and early
plaque development.
īļ A recent study of microvascular and macrovascular function in
RA has suggested that the classic cardiovascular risk factors may
influence endothelial function more than disease-related
inflammation does.
īļ The direct effect of chronic inflammation on vascular
endothelium may itself promote atherogenesis, in addition to
exacerbating the actions of traditional cardiovascular risk
factors.
11. Rheumatoid ArthritisâĻ
īļ Patients with RA have increased classic risk
factors for atherosclerosis.
īļ Tobacco smoking is associated with both
cardiovascular risk and the development of RA.
īļ Insulin resistance and the metabolic syndrome are
more common in RA.
12. Atherosclerotic Disease in Rheumatoid
Arthritis
īļ High TG levels and low levels HDL & LDL cholesterol
īļ Risk for MI in patients with RA similar to that in those with
DM and women with RA are twice as likely as age-matched
controls in the general population
īļ Patients with RA who suffer a MI are less likely to receive
acute reperfusion therapy and secondary preventive
measures and thus have worse outcomes.
14. Pericarditis
īļ The most common cardiovascular manifestation of
SLE is pericarditis,
īļ Up to 42% of pts in echo shows effusion.
īļ May be detected at any point in the disease and are
usually asymptomatic and small.
15. PericarditisâĻ
īļ Acute pericarditis may occur - 20% to 30% of
patients
īļ May be associated with cardiac tamponade;
īļ Chronic pericarditis may occasionally lead to
constriction
16. Systemic Lupus Erythematosus
īļ Studies suggested an â risk for MI and stroke in patients with
SLE(Between 2-fold and 10-fold and up to 50-fold greater than
general population)
īļ Young age of patients with SLE and CVS disease (67% of female
patients with SLE and a first cardiac event are typically
initially seen before 55 years of age) suggests that SLE
accelerates arterial disease.
īļ Worse outcomes following MI than the age-matched general
population with a higher risk of cardiac failure and increased
mortality.
17. Systemic Lupus Erythematosus
īļ HTN common in SLE - presence of renal disease and
the use of glucocorticoids
īļ Commonly have metabolic syndrome - associated
with renal impairment, higher corticosteroid doses,
and Korean or Hispanic ethnicity.
īļ Lipid abnormalities - including high levels of VLDL
and TG, elevated or normal LDL cholesterol, and
reduced HDL cholesterol.
20. Cardiovascular Disease in the
Systemic Vasculitides
Kawasaki disease 1. Coronary artery aneurysm
2. MI
3. Myocarditis
4. Pericarditis
5. Valvular dysfunction,
6. Cardiac failure
21. Cardiovascular Disease in the
Systemic Vasculitides
Medium-Vessel Vasculitis CARDIOVASCULAR COMPLICATIONS
Churg-Strauss syndrome o Myocarditis
o Pericarditis
o coronary arteritis,
o Cardiomyopathy
o cardiac fibrosis
o Valvular dysfunction
o MI
Polyarteritis nodosa o Myocarditis
o Pericarditis
o coronary arteritis,
o coronary aneurysm
o Hypertension
o cardiac failure
22. Cardiovascular Disease in the
Systemic Vasculitides
Medium-Vessel Vasculitis CARDIOVASCULAR COMPLICATIONS
Granulomatous polyangiitis o Myocarditis
o Pericarditis
o Coronary arteritis
o Valvular heart disease
o Cardiac failure
Microscopic polyangiitis o Pericarditis
o Coronary microaneurysm
o MI
23. Giant Cell Arteritis
īļ Severe cardiovascular complications - dissecting
thoracic aortic aneurysms.
īļ Imaging and autopsy studies - aortitis and aortic wall
thickening are frequent in GCA
īļ â FDG uptake in the thoracic aorta associated with an
â risk for aortic dilation.
īļ 17-fold increased risk for thoracic aortic aneurysms.
24. Giant Cell Arteritis
īļ Annual thoracic aortic screening for those with
FDG-PETâpositive thoracic aortic uptake or
magnetic resonance angiography (MRA) or
computed tomography angiography (CTA)
evidence of aortic wall thickening
īļ Every 2 to 3 years in the remainder of patients.
27. Takayasu Arteritis
īļ Cardiac complications:
o Aortic valve insufficiency
o Accelerated atherosclerosis,
o Cardiac ischemia,
o Myocardial infarction, and
o Heart failure.
28. Takayasu Arteritis
ī Neither MRA nor 18F-FDG-PET-CT reliably identifies
coronary arteritis.
ī Coronary disease is often asymptomatic
ī Silent myocardial injury in 27% of a cohort
ī â risk from secondary accelerated atherosclerosis.
29. Takayasu ArteritisâĻ
ī Thallium stress scintigraphy revealed myocardial
perfusion defects in 53%,
ī intra-arterial angiography has shown that up to
30% have coronary artery lesions typically
affecting the ostia and proximal segments, with the
left main coronary artery being most commonly
affected.
30. Takayasu Arteritis
ī Inflammation of the ascending aorta â coronary
artery involvement
ī Dilation of the aortic root â AR
ī LV dysfunction up to 20% and is due to
myocarditis, ischemic heart disease, and
hypertension
ī Common finding often associated with renal artery
stenosis in TA.
31. Kawasaki Disease
īą Cardiovascular complications:
ī Coronary artery aneurysm( 25% of untreated patient)
ī Sudden death â MI following acute coronary thrombosis or rupture of
a coronary artery aneurysm.
ī Pericarditis
ī Pericardial effusion
ī Myocarditis
ī Valvular dysfunction
ī Heart failure
ī Peripheral arterial involvement (limb, renal & visceral arteries) â less
common
32. Churg-Strauss Syndrome
ī Of all the vasculitides, CSS is the most likely to be
associated with severe cardiac disease
ī Cardiac involvement complicates up to 60% of
cases.
ī Cardiac complications:
o Pericarditis
o Myocarditis
o coronary arteritis
o myocardial infarction,
o cardiac fibrosis,
o arterial thrombosis, and
o valvular dysfunction.
33. Churg-Strauss Syndrome
ī Cardiac disease - prominent cause of death.
ī Cardiomyopathy - result of ischemia secondary to arteritis of
intramyocardial arteries or, less frequently, the epicardial
coronary arteries.
ī Myocarditis is associated with eosinophilic infiltration, fibrosis,
and occasionally, granulomatous infiltration.
ī Myocarditis can be life threatening and may result in the
development of restrictive, congestive, or dilated
cardiomyopathy.
34. Polyarteritis Nodosa
ī Cardiac involvement often subclinical and clinically
apparent in only 10% of patients.
ī CCF most commonly seen and consequence of a
specific myocarditis or coronary arteritis.
ī 5% of pts â Pericarditis, supraventricular tachycardia
and valvular disease.
ī CAG may reveal coronary artery microaneurysms,
coronary arteritis, or coronary spasm.
35. PERICARDITIS
īļ Pericarditis commonly complicates the
autoimmune connective tissue diseases,
particularly SLE, SSc, and RA.
īļ Clinically significant pericarditis develops in
fewer than 30% of patients.
īļ Diagnosed by echocardiography, which detects
pericardial thickening or small effusions in up to
50% of these patients.
36. PERICARDITIS
īļ CMR can also provide accurate definition of the extent
of pericardial involvement.
īļ In SLE - pericarditis is usually associated with a flare
of disease and often with polyserositis.
īļ Clinically significant pericarditis affects only 1% to 2%
of patients with RA, more commonly male,
seropositive patients.
37. MYOCARDITIS
īļ Myocarditis is a rare but recognized cause of
mortality in patients with autoimmune rheumatic
diseases and is most commonly seen in patients
with SLE, SSc, and polymyositis or
dermatomyositis.
īļ Myocarditis is also rarely associated with other
rheumatic diseases, including ankylosing
spondylitis, adult Still disease, GCA, and TA.
38. VALVULAR HEART DISEASE
īļ Clinically significant valvular disease can complicate
many rheumatic diseases.
īļ Mechanisms - direct damage to cardiac valve leaflets or
aortic valve regurgitation as a consequence of aortitis
affecting the ascending aorta.
39. VALVULAR HEART DISEASEâĻ.
īļ In SLE pt:
o Verrucous endocarditis (Libman-Sacks endocarditis) and
nonspecific valvular thickening are most commonly
detected.
o Valvulitis with rapid valvular dysfunction
o Libman-Sacks lesions typically affects both valve
surfaces, most commonly the mitral valve.
40. VALVULAR HEART DISEASE
īą Seronegative Spondyloarthropathies:
īļ Aortic valvulitis leads to aortic cusp thickening and
retraction and subsequently to symptomatic aortic
regurgitation, which may cause heart failure.
īļ Proximal aortitis affecting the ascending aorta leads to
aortic root thickening and subsequently to dilation and
aortic regurgitation, the prevalence of which is related
to disease duration.
41. VALVULAR HEART DISEASE
īą In RA pts:
īļValvular thickening is commonly associated
with RA in echo
īļEcho- shows mitral valve involvement, with
valve thickening, asymptomatic mitral
regurgitation, and prolapse being the
predominant findings.
42. VALVULAR HEART DISEASE
īą In TA:
o Cardiac valve dysfunction commonly complicates
TA
o Inflammation of the ascending aorta predisposes
to dilation of the aortic root with subsequent
aortic valve regurgitation.
43. CARDIAC CONDUCTION DISTURBANCES
īą IN SLE pt:
īļ Adult SLE seldom causes primary conduction abnormalities
or rhythm disturbance, which may instead result from
underlying ischemic heart disease or myocarditis.
44. īļ Female patients with SLE or SjÃļgren syndrome who test
positive for antibodies against the Ro and/ or La antigens
carry the risk of bearing a child with congenital heart
block, which may be complicated by myocarditis.
īļ These antibodies may cross the placenta and induce
myocardial inflammation and can target the conduction
system and lead to fibrosis
45. CARDIAC CONDUCTION DISTURBANCES
īą In SS pt:
īļ affects up to 50% of patients.
īļ Cause- patchy myocardial fibrosis â disruption
of the conduction pathways.
īļ Supraventricular arrhythmias are usually benign
and amenable to treatment.
46. īļ Ventricular conduction abnormalities also
frequently occur in SSc and may impair
myocardial function.
īļ In these patients ventricular ectopy is common
and closely associated with sudden death.
47. CARDIAC CONDUCTION DISTURBANCES
īą Spondyloarthropathies
īļ Frequently complicate the HLA-B27â related
spondyloarthropathies.
īļ In AS up to 30% of patients experience conduction
system disease,
īļ Cause - subaortic fibrosis extending into the septum
and affecting AV node.
īļ Atrioventricular conduction block occurs commonly
and may become complete.
48. CARDIAC CONDUCTIONâĻ.
īą Polymyositis and Dermatomyositis:
īļLeft anterior hemiblock and right bundle
branch block occur most frequently and
occasionally progress to complete heart
block.
īļCauses: Inflammation and fibrosis affect the
conduction pathways
49. CARDIAC CONDUCTIONâĻ.
īą RA patients:
īļECG screening studies - arrhythmias or
conducting system abnormalities in up to 50%
īļCause: myocarditis and amyloid deposition in
the heart can cause atrioventricular node
conduction block.
īļSimilarly, rheumatoid nodules may disrupt
the conduction system and cause all types of
conduction abnormality.
50. PULMONARY ARTERIAL HYPERTENSION
ī PAH can result from the connective tissue diseases
and is of concern to rheumatologists as a
significant cause of premature mortality.
ī Often manifested late or goes undiagnosed.
ī Frequently proves resistant to optimized
treatment of the underlying connective tissue
diseases.
51. Pulmonary Arterial Hypertension in
Rheumatic Diseases
RHEUMATIC
DISEASE
FEATURES OF PULMONARY ARTERIAL
HYPERTENSION
Systemic
sclerosis
Prevalence of 5-12%. More common in lSSc
PM/Scl overlap Annual screening recommended. Survival rate at 3 years of 47-
56%
Systemic lupus
erythematosus
Prevalence of 0.5-17.5%. Survival rate at 3 years of 74%.
Thrombotic arteriopathy is the most common underlying cause.
83% of patients have anticardiolipin antibodies. Patients with
severe Raynaud phenomenon, anticardiolipin
antibodies, and anti-U1RNP require screening
Rheumatoid
arthritis
Prevalence data limited; reported to be up to 20%. Clinically
significant disease rare, often secondary to COPD, chronic
thromboembolic disease, or interstitial lung disease. Improved.
RA treatment may result in a reduced incidence
52. SjÃļgren
syndrome
PAH a very rare complication of SjÃļgren
syndrome. Usually occurs late in the course of
disease. Prevalence unknown
Takayasu arteritis Pulmonary arteritis present in up to 50% of
patients. PAH prevalence of 12%
53. THROMBOSIS IN THE RHEUMATIC
DISEASES
īļ Thrombosis is an important pathologic process in many
rheumatic diseases and a cause of significant morbidity and
mortality.
īļ Large vessel thrombosis, both venous and arterial, can occur
in Behçet disease and APS.
54. THROMBOSISâĻ.
īļ Thrombosis in situ also occurs in small vessels, principally
as the end result of chronic vessel wall hyperplasia or
inflammation in diseases such as SSc, the vasculitides, and
PAH.
īļ Chronic thromboembolic PAH can complicate SLE and SSc.
58. Cushingâs syndrome
Cardiovascular manifestation:
o Secondary HTN
o Accelerated atherosclerosis â coronary artery disease
o Heart failure
o LVH & LV dysfunction
o DCM
o Increased coronary artery calcification and plaque volume
o Changes in PR & QT intervals ( abnormalities in voltage gated
Na & k channels)
o Carni complex (Cushing + cardiac myxoma + pigmented
dermal lesions)
59. Addison disease
Cardiac manifestations:
īļ Hypotension & tachycardia ( with loss of autonomic
tone & electrolyte imbalance) â cardiovascular
collapse and crisis
īļ Low diastolic BP & orthostatic hypotension
īļ ECG abnormalities of hyperkalaemia( low amplitude p
wave and tall peaked T wave)
īļ Cardiac atrophy (teardrop heart)
62. Hyperparathyroidism & Hypercalcaemia
īļ â cardiac contractility
īļ Shortening of the ventricular action potential duration,
primarily through changes in phase 2
īļ Blunting of the T wave and changes in the ST segment,
īļ Shortening of QT interval & occasionally decreases in
the PR interval.
īļ Treatment with digitalis glycosides appears to increase
sensitivity of the heart to hypercalcemia.
63. Hypocalcemia
īļ Low serum levels of total and ionized calcium directly
alter myocyte function.
īļ Hypocalcemia prolongs phase 2 of the action potential
duration and the QT interval.
īļ Severe hypocalcemia can impair cardiac contractility
68. Coronary Heart Disease
īļ Strongly associated with type 2 DM and leading
cause of death regardless of the duration of
disease.
īļ 2-4-fold increase relative risk ratio of
cardiovascular disease in type 2 DM
īļ Degree and duration of hyperglycemia are strong
risk factors for the development of microvascular
and macrovascular complications.
69. Coronary Heart Disease
īļ IGT increases cardiovascular risk.
īļ Hyperglycemia enhance the progression of
atherosclerosis in type 2 diabetes.
70. Acute Coronary Syndromes
īļ High-risk group for developing and surviving acute MI.
īļ Pts with type 1 DM have a worse outcome than patients with
type 2 DM
īļ Diabetic women have almost twice the risk of mortality of
diabetic men.
īļ In a meta-analysis of the major trials comparing thrombolytic
therapy to percutaneous coronary intervention (PCI), diabetic
patients had significantly higher 30-day mortality when
compared with nondiabetic patients
71. Chronic Coronary Artery Disease
īļ Diabetic patients often are unaware of myocardial
ischemic pain, and thus, silent MI and ischemia are
markedly increased
īļ Concern for the development of sudden cardiac
death in those with diabetes.
72. Diabetic Cardiomyopathy
īļ Diabetic cardiomyopathy is a term used by clinicians to
encompass the multifactorial etiologies of diabetes-related
left ventricular failure characterized by both systolic and
diastolic function
īļ The Framingham heart Study - showed that men with
diabetes are twice as likely to develop congestive heart
failure compared with their nondiabetic counterparts and
females with diabetes had a five-fold increase in the rate of
congestive heart failure.
īļ Diastolic dysfunction is exceedingly common (>50%
prevalence in some studies) and may be linked to diabetes
without the presence of concomitant hypertension.
73. Diabetic Cardiomyopathy
īļ The etiology of impaired left ventricular function may
involve any of the following mechanisms:
(1) Coronary atherosclerotic disease,
(2) Hypertension
(3) left ventricular hypertrophy
(4) Obesity
(5) Endothelial dysfunction
(6) Coronary microvasculature disease
(7) Autonomic dysfunction, and
(8) Metabolic abnormalities.
74. THE HEART AND KIDNEY DISEASE
ī CKD is associated withâ risk of heart disease and CVD
the most frequent cause of death in patients with
ESRD.
ī Cardiovascular mortality(In ESRD pts) - 10 to 30
times higher than in the general population a
ī Similar marked and graded increases in risk of all-
cause death, death due to CVD, and risk of
hospitalization with declining GFR have also been
reported for the general population
75. Impact of CKD on Cardiovascular Risks and
Outcomes According to the Severity of Kidney
Disease
Description Normal to Mild
Decrease in GFR
Moderate GFR Loss Severe
GFR Loss
CKD stage
eGFR mL/min/1.73 m2
1-2
âĨ60
3
30-59
4
15-29
Cardiovascular risk factors
Hypertension
Diabetes
C-reactive protein >0.21 mg/dL
Hemoglobin <13 g/dL15
40%
3.1%-6.5%
25%-30%
4%
55%
16.8%
48.7%
7%
77%
22.8%
57.7%
29%
Acute myocardial infarction
Prevalence among patients
Risk of 1-year mortality AMI
28.5%
2.3%
43.5%
9.4%
30%
24.2%
76. CORONARY HEART DISEASE
ī CAD highly prevalent among pts with CKD & a
major cause of morbidity and mortality
ī Presence of albuminuria and/or eGFR < 60
mL/min/1.73 m2, considered a major risk for
mortality after an acute coronary event
ī Pts with DM and CKD may present with evidence
of a previous âsilentâ myocardial infarction
77. CORONARY HEART DISEASEâĻ..
ī LVHâassociated ST-segment changes are common
among CKD patients, thus ST-segment depression on
a resting ECG is considered an unreliable marker of
coronary ischemia in dialysis patient
ī ESRD patients may experience changes in serum
potassium, serum calcium, and fluid volume that
affect the ECG, complicating its interpretation.
78. CONGESTIVE HEART FAILURE
ī Impaired renal function â risk for all-cause death,
cardiovascular death, and hospitalization for heart failure in
patients with CHF with both preserved as well as reduced
systolic function.
ī Albuminuria an independent baseline risk factor for the
development of CHF in patients with diabetes.
ī Echo in ESRD pts- HCM characterized by left ventricular
hypertrophy, ASH and/or impaired contractility, as well as DCM
ī High-output cardiac failure is a rare complication of a high-flow
AV fistula.
79. Pericarditis
ī Before dialysis was widely available - preterminal event in
uremic patients.
ī Incidence of clinically apparent pericarditis has decreased
from 50% to approximately 5% to 20% of uremic patients
requiring chronic dialysis.
ī Both uremic and dialysis pericarditis occur more frequently in
younger than in older persons and occur more commonly in
women than in men.
ī Pericardial effusion is even more frequent in dialysis patients
because it is linked to ECV expansion.
ī Cardiac tamponade is rare
80. CARDIAC ARRHYTHMIAS
ī the single largest cause of death : 58% of all cardiac
deaths (or 25% of all-cause mortality) among peritoneal
dialysis patients and 64% of all cardiac deaths (or 27% of
all-cause mortality) among HD patients are due to
âcardiac arrest/cause unknownâ or arrhythmia
ī â risk of ventricular arrhythmia in ESRD patients is likely
due to a combination of factors that include ischemic
heart disease, CHF, calcification of the conduction system
from secondary hyperparathyroidism, pericarditis,
dialysis-associated hypotension, dialysis-induced acidâbase
and electrolyte shifts, obstructive sleep apnea, and
hypoxemia
83. Pulmonary Hypertension
Def: PH is defined as a mean pulmonary arterial
hypertension at least 25 mm Hg at rest measured by
invasive monitoring.
84. Dana Point 2008 Classification
īļ The Dana Point 2008 4th World Symposium on
Pulmonary Hypertension is based on shared
pathologic, pathobiologic, and clinical features
īļ Type 3. Pulmonary hypertension due to lung diseases
and/or hypoxia
ī§ 3.1. Chronic obstructive pulmonary disease
ī§ 3.2. Interstitial lung disease
ī§ 3.3. Other pulmonary diseases with mixed restrictive and
obstructive pattern
ī§ 3.4. Sleep-disordered breathing
ī§ 3.5. Alveolar hypoventilation disorders
ī§ 3.6. Chronic exposure to high altitude
ī§ 3.7. Developmental abnormalities
85. Chronic Cor Pulmonale
īļ Chronic cor pulmonale is âhypertrophy of the
right ventricle resulting from diseases affecting
the function and/or structure of the lung, except
when these pulmonary alterations are the result
of diseases that primarily affect the left side of
the heart or congenital heart disease.â
86. Pathophysiologic Classification of Diseases of
the Lungs That Can Cause Cor Pulmonale
Principal Pathophysiologic
Mechanism
Disease Entity
Persistent vasoconstriction High-altitude dwellers
Hypoventilation syndromes
Chest deformities
? Idiopathic pulmonary hypertension
Loss of cross-sectional area
of the
vascular bed
Thromboembolic disease
Emphysema
Lung resection
Fibrotic lung diseases
Cystic fibrosis
91. Duchenne and Becker muscular
dystrophies
īą Cardiovascular manifestations:
īļ Cardiomyopathy: most common
âĸ 90% of DMD at the age of 18 yrs
âĸ BMD â more variable
īļ Arrythmia:
âĸ Sinus tachycardia
âĸ Atrial arrhythmia â AF & Atrial flutter
âĸ AV conduction defects â short or long PR interval
âĸ Ventricular arrhythmia (30% of pts) â PVC, complex ventricular
arrhythmia
92. Myotonic Dystrophies
īļ Cardiovascular manifestations: degeneration,
fibrosis, and fatty infiltration in conduction tissue
including the SA node, AV node, and His-Purkinje
system
īļ Arrythmia:
īŧ Symptomatic AV block â PPM
īŧ AF & Atrial flutter
īŧ VT
īŧ Sudden death
95. Spinal Muscular Atrophy
īą Cardiovascular manifestations:
īļ Complex congenital heart disease â ASD
īļ Cardiomyopathy, and
īļ Arrhythmias - AF & Atrial flutter & AV conduction defect
96. Guillain-BarrÊ Syndrome
īļ Cardiac involvement rela- autonomic nervous system
dysfunction (50% of pts)
īļ Cardiac manifestations include hypertension,
orthostatic hypotension, resting sinus tachycardia,
loss of heart rate variability, electrocardiographic ST
abnormalities, and both bradycardia and
tachycardias.
īļ Arrhythmias observed include asystole, symptomatic
bradycardia, rapid atrial fibrillation and ventricular
tachycardia or fibrillation.
98. ACUTE CEREBROVASCULAR DISEASE
īą Cardiovascular manifestations:
ī Most commonly found in SAH
ī ECG abnormalities: 70% pts with SAH
ī§ ST elevation and depression,
ī§ T wave inversion, and
ī§ pathologic Q waves
ī§ Peaked inverted T waves and
ī§ a prolonged QT interval
99. ACUTE CEREBROVASCULAR DISEASE
ī â Troponins
ī LV dysfunction (in Echo)
ī Pulmonary oedema
ī Life threatening arrhythmia: VT, VF, torsades De Pointes
ī Atrial arrhythmia â AF (most commonly acute
thromboembolic stroke)
ī Bradycardias including SA block, sinus arrest, and AV block
- 10% of patients with SAH