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
HTN
Ex smoker
High BMI
Medications:
Insulin
Inhibace plus
Metoprolol
Aspirin
Calcium
Alu-tabs
Neorecormon
NKDA
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
Patient One .
54yo man presents with chest pain
O/E:
HR: 114bpm
RR: 24bpm
SpO2: 96% o/a
BP: 145/82 (L) 147/88 (R)
Temp: 37.4
HS dual + added sounds
JVP 4-5cm
Peripheral oedema and pitting to knees
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:
Hb 106
WCC: 13.4
Neut: 8.6
Plt: 268
U&E:
Cr 500
Urea 32
Na 131
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, 40-100% (sharp, dull, burning, pressing, radiation -> trapezius ridge, worse on inspiration, lying flat and movement)
Cough, Dyspnoea
Malaise, fevers,
Assymptomatic in 8-30%
Physical Signs:
Pericardial Rub 35-85%
Tachypnoea
Tachycardia
Investigations:
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: ST elevation limited to the precordialLeads
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)
Pericarditis:
Generalised ST elevation
Presence of PR depression
Normal T wave amplitude
ST segment / T wave ratio > 0.25
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.
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.
Stage 2, typically seen in the first week.
Normalization of the ST and PR segments. Stage 3,
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:
Management of complications:
If tamponade is suspected → Echo (gold std)
Tachycardia, tachypnoea, hypotension, signs of hypo-perfusion, distended neck veins, muffled heart sounds, pulsus paradoxus, 'Becks triad'
Pericardiocentesis – sub-xiphoid if emergent.
Restrictive pericarditis requires resection.
Persistent (>1 week) requires further investigation.
Rule out differential causes
Stable → Outpatient mx:
NSAIDs +/- colchicine
If persistent >1 week need further investigation
R/V meds – anti coagulants, contributing meds
Admit if:
Effusion – large, tamponade
Fever, leukocytosis, immunocompromised
On warfarin
Traumatic
Trop rise – (myopericarditis)
> 1 week, not responding to NSAIDs
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 Three26yo 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 Three26yo woman presents with chest pain and febrile illness
O/E:
HR: 125bpm
BP: 100/60
RR: 25
Temp: 38.7
SpO2: 96% oa
Looks unwell,
HS S1, S2 + S3
Dry mucous membranes,
JVP 4cm.
Calves SNT, no pitting
Chest: bilateral exp wheeze,
few scattered creps
Abdomen: SNT
Patient Three26yo woman presents with chest pain and febrile illness
Patient Three26yo woman presents with chest pain and febrile illness
Bloods:
FBC:
Hb 120
WCC 18.6
Neut 11.2
Plt 540
Troponin 230
CRP 113
U&E:
Na 132
K 3.4
Cr 80
LFTs:
ALT 180
AST 166
Otherwise normal
*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
Viral infection – most common cause, Coxsackie, adenovirus, parvovirus B19, enterovirus. [less common EBV, Hep, CMV]
Diptheria, fungal, parasitic and rickettsial Immune mediated
Giant cell, SLE, sarcoidosis, IBD, Kawasaki, + many more Drug – hypersenstitivity
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
Presentation:
chest pain
fatigue
SOB
palpitations
fever
malaise
Arthralgias
Arrhyrthmia or sudden death
Findings:
fever
tachycardia
S3 and S4
pericardial rub
signs of biventricular failure
cardiogenic shock 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, B-blockers.
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