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