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Transient Cardiac Disease
Rachel Aubrey
Patient One
.
54yo man presents with chest pain
PmHx:


T2DM
CKD – stage IV- V kidney disease,
eGFR 15%, due to start peritoneal
dialysis
Medications:

Insulin

Inhibace plus

Metoprolol

HTN

Aspirin

Ex smoker

Calcium

High BMI

Alu-tabs

Neorecormon
NKDA
Patient One
.
54yo man presents with chest pain
HxPC:

Pain is sharp located in the anterior and central chest radiating to the
neck and shoulders. Onset 4 hours ago, took paracetamol at home
with nil effect. Ongoing so presents to ED.

Associated with dyspnoea, no nausea or diaphoresis.

Worse when laying flat, with inspiration and swallowing.

Chronic peripheral oedema unchanged.

No calf pain or swelling, prolonged immobility/surgery, haemoptysis,
history of malignancy, history of VTE.

Possible fevers at home.

No cough/cold/ coryza or gastrointestinal symptoms.

Longstanding history of poor exertional capacity with occasional
chest pain, normal ETT 3 years ago.
Patient One
.
54yo man presents with chest pain
O/E:
HS dual + added sounds
HR: 114bpm
JVP 4-5cm
RR: 24bpm
Peripheral oedema and pitting to
knees
SpO2: 96% o/a
BP: 145/82 (L) 147/88 (R)
Temp: 37.4
Chest: reduced AE bases and
few creps
Abdomen SNT
Patient One
.
54yo man presents with chest pain
Widespread concave ST elevation and PR depression is present throughout the
precordial (V2-6) and limb leads (I, II, aVL, aVF).
There is reciprocal ST depression and PR elevation in aVR
Patient One
.
54yo man presents with chest pain
Bloods:
FBC:
U&E:

Hb 106

Cr 500

WCC: 13.4

Urea 32

Neut: 8.6

Na 131

Plt: 268

K 5.9
Troponin T 62, (prev 45)
CRP 82
PA: No significant pulmonary venous congestion, Increased CTR, “globular” or
“flask shaped”
Lateral: Loss of retrosternal clear space, “Fat-pad” sign - “Oreo” sign,
Pleural effusion
Pericarditis


Acute inflammation of pericardium
Exudate in pericardial space, usually contains only 15-50mls
 Inflammatory cells -mainly PMN – leukocytes
 Fibrinous with adhesion formation
 Can be serous or haemorrhagic
~ 5- 8% of ED presentations
with CP without MI


M > F , adults > children

~80% are post-viral or idiopathic
Causes
Infectious:

Viral (HIV, CMV,
coxsackie*)

Bacterial (tuberculosis)

Fungal
Inflammatory:

SLE*

Scleroderma

ANCA-associated
vasculitis
Metabolic:

Hypothyroidism
Neoplastic:

Metastatic

Primary
Medications:

Hydralazine*

Methyldopa

Procainamide*

Minoxidil
Other:

Idiopathic (procedures)

Blunt or penetrating

Post-MI (Dressler’s
syndrome)*

Myocardial infarction

Uraemia *
* Common causes
Uraemic Pericarditis
Manifestations of pericarditis before RRT or within 8
weeks of starting (dialysis pericarditis affects those on
RRT for > 8 weeks)
 Common at autopsy 50% or uraemic patients have
pericarditis.
 More common in younger patients and in women.
 Higher incidence of haemorrhagic effusion
 Caused by accumulation of uraemic toxins.
 Good response from dialysis – 76% recover.

[ Dialysis – Due to inadequate dialysis, possibly
substrates of dialysis, poorer response to dialysis and
more likely to be subacute, more likely to be
complicated by adhesions]

Clinical Presentation
Symptoms:

Chest pain – most common, 40100% (sharp, dull, burning,
pressing, radiation -> trapezius
ridge, worse on inspiration,
lying flat and movement)

Cough, Dyspnoea

Malaise, fevers,

Assymptomatic in 8-30%
Investigations:


Physical Signs:

Pericardial Rub 35-85%

Tachypnoea

Tachycardia

Leukocytosis, Elevated
ESR/CRP, trop in ~30%
ECG:
 PR segment depression.
 Widespread concave
(‘saddle-shaped’) ST
elevation.
 Reciprocal ST depression
and PR elevation in aVR
and V1
 Absence of reciprocal ST
depression elsewhere
CXR: Cardiomegaly, pleural
effusions 50%
Pericarditis vs Benign Early
Repolarization:
Benign Early Repolarization:
Pericarditis:
ST elevation limited to the precordial
Leads

Generalised ST elevation

Presence of PR depression

Normal T wave amplitude

ST segment / T wave ratio > 0.25


Absence of PR depression

Prominent T waves

ST segment / T wave ratio < 0.25
Characteristic “fish-hook” appearance
in V4

ECG changes usually stable over time
(i.e non-progressive)



Absence of “fish hook” appearance
in V4
ECG changes evolve slowly over
time
Pericarditis
Benign Early Repolarization
4 Stages of ECG Changes

Stage 1, seen in the first hours to days.


Stage 2, typically seen in the first week.


Normalization of the ST and PR segments.
Stage 3,


Diffuse ST elevation (typically concave up) with reciprocal ST
depression in leads aVR and V1. There is also an atrial current of
injury, reflected by elevation of the PR segment in lead aVR and
depression of the PR segment in other limb leads and in the left
chest leads, primarily V5 and V6.
Development of diffuse T wave inversions, generally after the ST
segments have become isoelectric. However, this stage is not
seen in some patients.
Stage 4.

Normalization of the ECG or indefinite persistence of T wave
inversions ("chronic" pericarditis).
Diagnosis
Acute pericarditis is diagnosed by the presence of at least two of the
following criteria:
 Typical chest pain (sharp and pleuritic, improved by sitting up and
leaning forward)
 Pericardial friction rub (a superficial scratchy or squeaking sound best
heard with the diaphragm of the stethoscope over the left sternal
border) – may need repeat exams.
 Suggestive changes on the electrocardiogram (typically widespread
ST segment elevation)
 New or worsening pericardial effusion


Investigations: bloods inc CRP, ESR, Trop and cultures if febrile,
ECG – all
CXR – all
Echo – tamponade, purrulent infection, myocarditis
Management:


Rule out differential causes
Stable → Outpatient mx:




NSAIDs +/- colchicine


If persistent >1 week need
further investigation
Management of complications:
If tamponade is suspected →
Echo (gold std)

R/V meds – anti coagulants,
contributing meds
Admit if:


Effusion – large, tamponade

On warfarin

Traumatic

Trop rise – (myopericarditis)


Fever, leukocytosis,
immunocompromised
> 1 week, not responding to
NSAIDs


Tachycardia, tachypnoea,
hypotension, signs of hypoperfusion, distended neck
veins, muffled heart sounds,
pulsus paradoxus, 'Becks
triad'
Pericardiocentesis – subxiphoid if emergent.
Restrictive pericarditis requires
resection.
Persistent (>1 week) requires
further investigation.
Patient Two
60 year old woman presents with chest pain
HxPC:
60yr old woman was upstairs with her husband who is a patient on a
medical ward. During a family meeting she began to report central chest
pain and presents to ED immediately.
She looks unwell and is taken into monitored.
On arrival she reports:
- Ongoing retrosternal chest heaviness
- Non radiating
- Associated nausea and dyspnoea, nil other associated
symptoms
- Has been otherwise well.
PmHx:
Hypothyroidism on thyroxine, hyperlipidaemia,
No cardiac hx, HTN, T2DM, non smoker and no family hx of IHD
Patient Two
60 year old woman presents with chest pain
Patient Two
60 year old woman presents with chest pain
Management:

Moved to Resus and activate STEMI protocol
Quick bedside examination:
BP 140/90, HR 80, SpO2 98%,
HS dual non added, chest clear


IVL placed on the ward and bloods return with troponin T of 140,
.

Given aspirin, heparin bolus and ticagrelor

Transferred to Cath Lab
Patient Two
60 year old woman presents with chest pain

Troponin T – 140 → 480

Angiogram: no significant flow limiting lesion, mild coronary artery
disease.

Left ventriculography was performed which showed: akinesis of the
apical half of the left ventricle and apical ballooning. LVEF was
reduced at 35%
Apical Ballooning or
Takotsubo Cardiomyopathy




Transient systolic dysfunction of the apical
and/or mid segments of the left ventricle
that mimics myocardial infarction, but in the
absence of obstructive coronary artery disease
Contractile function of the mid and apical segments of the LV are
depressed, and there is hyperkinesis of the basal walls, producing a
balloon-like appearance of the distal ventricle with systole.
Frequently but not always triggered by an acute medical illness or by
intense emotional or physical stress
Pathogenesis unknown. ? catecholamine excess, coronary artery
spasm (though few have spasm with Ach provocation), microvascular
dysfunction or dynamic mid-cavity or LV outflow tract obstruction.

Mainly post-menopausal women, F >> M, Mean age 61 – 76yrs

~1-2% of troponin +ve ACS
Clinical Features

Presentation – same as AMI






CP, dyspnoea, ECG changes – often ST elevation and
usually in anterior pre-cordial leads 35-55%. Other changes
include: deep T wave inversion, QT prolongation, abnormal
Q waves, non-specific abnormalities or normal. (Can't
distinguish AMI)
Also syncope, arrhythmia, CHF, cardiogenic shock.
Acute HF is more likely in >70yrs, LVEF <40%, presence of
physical stressor.
Troponin elevated in 75-85%, usually out of proportion to
haemodynamic compromise.
Usually affect LV only.
Diagnosis made on Echo or ventriculography or cardiac MRI
– typical appearance. Absence of CAD on angiogram
Management:

Treat as ACS in ED

Primary PCI or fibrinolytic therapy

LV impairement treated as normal – ACEi, B-blockers.

If shock present → USS to look for LVOT obstruction


If present (~15%): NO inotropes, B-blockers, fluid resus

If absent: Cautious use of inotropes -dobutamine & DA
Most recover well over a period of weeks (with regain of normal
systolic function), increased risk of recurrance (figure unknown)
and long term adreno-receptor blockade may reduce risk of
this.
Patient Three
26yo woman presents with chest pain and febrile illness
HxPC:
Unwell 8 days with fevers, cough, coryza, myalgias and fatigue. Others
at home are unwell with the same – daughter currently admitted with
bronchiolitis.
Onset of chest pain 2/7 ago. The pain is anterior, central, sometimes
radiating to shoulders and worse with cough and deep inspiration.
Cough with green phlegm.
No palpitations.
SOB has noticed a reduced exertional capacity.
Has been sleeping on 3 pillows for the past 2 days.
No leg swelling.
Amoxycillin by GP 4/7 ago, not improving.
Previously fit and well
Patient Three
26yo woman presents with chest pain and febrile illness
O/E:
Looks unwell,
HS S1, S2 + S3
HR: 125bpm
Dry mucous membranes,
BP: 100/60
JVP 4cm.
RR: 25
Calves SNT, no pitting
Temp: 38.7
SpO2: 96% oa
Chest: bilateral exp wheeze,
few scattered creps
Abdomen: SNT
Patient Three
26yo woman presents with chest pain and febrile illness
Patient Three
26yo woman presents with chest pain and febrile illness
Bloods:
U&E:
Na 132
FBC:
K 3.4
Hb 120
Cr 80
WCC 18.6
Neut 11.2
LFTs:
Plt 540
ALT 180
AST 166
Troponin 230
Otherwise normal
CRP 113
*daughter's NPA - adenovirus
Myocarditis


Inflammatory infiltrate of the myocardium with necrosis and/or
degeneration of adjacent myocytes not typical of the ischemic
damage associated with coronary heart disease.
Incidence is unknown. One study suggested that myocarditis is the
cause of sudden cardiac death in 8.6% of cases and is identified in
up to 9% of routine post-mortem examinations

Multiple causes (see next slide)

Can be acute or chronic

Focal or diffuse (viral usually diffuse, more likely to cause CHF)

Spectrum of disease – assymptomatic → fulminant heart failure
(Children more likely to have fulminant, and men more likely to have
severe viral myocarditis, fulminant = better prognosis)
Causes

Infectious




Giant cell, SLE, sarcoidosis, IBD, Kawasaki, + many more
Drug – hypersenstitivity


Diptheria, fungal, parasitic and rickettsial
Immune mediated


Viral infection – most common cause, Coxsackie, adenovirus,
parvovirus B19, enterovirus. [less common EBV, Hep, CMV]
Clozapine, isoniazid, phenytoin, thiazides + many more
Toxic causes

Drugs: ethanol, cocaine, lithium,

Heavy metal poisoning: lead, copper, iron.

Others: arsenic, insect stings and bites, CO
Physical

Electrical injury, radiation
Clinical Features
Findings:
Presentation:

fever

chest pain

tachycardia

fatigue

S3 and S4

SOB

pericardial rub

palpitations

signs of biventricular failure

fever

cardiogenic shock

malaise


Arthralgias


Arrhyrthmia or sudden death

Elevated WCC, CRP, ESR,
LFTs
ECG: ST, ST elevation, Tw
changes – inversion
CXR: normal, cardiomegaly or
pulm oedema
Diagnosis


Requires high level of suspicion as variable presentation.
 Elevated troponin
 ECG suggesting myocardial injury or pericarditis
 Arrhythmia
 New or unexplained altered cardiac function
 Particularly in younger patients 20-50yrs
 +/- viral/infective history – many do not have
Initial testing:
 ECG
 Troponin/CK
 Routine labs – though non-specific
 BNP if uncertain whether CHF present.
Diagnosis

Differentials:

IHD, valvular heart disease, pulmonary disease

Echo, CMRI +/- angiogram can be useful in distinguishing



Echo: LV dilation, more spheroidal shape, RWMAs, usually global
systolic dysfunction, can be focal. +/- pericardial effusion.
CMRI – inflammation, hyperaemia, oedema, necrosis, scar,
systolic dysfunction
Definitive Diagnosis

Pathological diagnosis

Endomyocardial biopsy – histology “ Dallas Criteria”

Immunohistochemical stains, PCR for viral genomes
Management:

Treat as ACS if features are indistinguishable – troponin elevation,
ischaemic changes on ECG, risk factors for CAD or history of same.

Urgent Echo if large effusion or compromise

CHF




Usual therapies: diuresis, fluid and Na restriction, ACEi, Bblockers.
May require balloon pump
Arrhythmias

Need monitoring,

TachyC can precipitate CHF – amiodarone, cautious BB, CCB

BradyC pacing – usually only with temporary wire
Anticoagulation
Management:

Specific therapies:


Anti-virals: usually outside of treatment window – don't often see
early myocarditis.
Immunosuppressive agents: Inflammation exceeds infection,
effective in some animal studies but difficult to assess response in
people due to rapid spontaneous recovery. Corticosteroids,
cylcophosphamide, azathioprine – may exacerbate viral causes.

Immunoglobulin – may be useful

NOT NSAIDs

Cardiac transplant → chronic myocarditis with persistent CHF

Bed rest during acute phase – fevers and infective symptoms

Reduction in alcohol intake

Follow up 1-3 monthly with regular Echo
Prognosis

Mild cases unclear as only most unwell get EMB and diagnosis.

Dependent on cause


Fulminant myocarditis – much better prognosis, most return to
normal LV systolic function.
Idiopathic Giant cell myocarditis usually fatal

Usually inflammation is self limiting without long term sequelae

Poorer prognosis if:

ECG: BBB, high degree AV block, Q waves

LVEF < 40%

Pulmonary hypertension