Causes of HfrEF
Ischaemic CMP- 66%
=>Nonischaemic:
* Myocarditis
*Takotsubo/ Peripartum/ Septic CMP
* Drug induced- Alcohol, sympathomimetics
* Tachycardia induced-Atrial/ventricular
* valvular- regurgitant lesions
* Infilterative diseases- amyloid, haemachromatosis
* Nutritional deficiencies- thiamine, scurvy, Pellagra
* Neuromuscular- myotonic dystrophy, Neurofibromatosis,
* Idiopathic- Familial
* High output states- AV fistula,AV malformation
* Endocrine causes- Thy
Myocarditis causes
Saare Drugs Saale Heart ko Chedte hai
Sarcoid Drugs SLE Hlh Connective tissue dis
classification
Based on chronicity
->Acute myocarditis: <1 month between symptom onset and diagnosis.
Fulminant myocarditis:
Acute myocarditis requiring therapy with inotropes and/or mechanical support–>M/C with giant cell myocarditis or eosinophilic myocarditis.
->Subacute myocarditis: >1-3 months between symptom onset and diagnosis.
->Chronic inflammatory cardiomyopathy: symptoms persist for >1 month (this overlaps with subacute myocarditis)
Epidemiology
M/C in younger age group-<50yrs
M/C among males
Accounts for upto 7% cases of sudden death in younger individuals
Clinical Presentation of Myocarditis
Prodromal Phase (~50%)-often Viral-type illness preceding cardiac symptoms.
* Flu-like illness.
* Upper respiratory tract infection
* Gastrointestinal upset.
* Rash +/-
⸻
Symptoms
1). Chest Pain (~90%)
* Can mimic angina.
* Typically associated with ST–T changes
2). Dyspnea
* Due to congestive heart failure.
3). Syncope, palpitations, or arrhythmia
* SVT possible.
* VT:
- Polymorphic VT → active myocarditis.
- Monomorphic VT → chronic myocarditis.
* Bradycardia uncommon-> seen in sarcoidosis or systemic autoimmune disease
* Syncope presentation = high risk of death or transplant
4). Fever
Lupus & Connective Tissue Disease–Associated Myocarditis
aetiologies, clues, Tt
MCTD- Multisystem Connective Tissue Disease
Evaluation
=>History:
Infective symptoms - esp viral prodrome
vaccination
Travel history-
Medications
Exposure to sympathomimetics
Family H/O myocarditis
Investigations
Labs:
CBE–>infection, Eosinophilia, inflammatory markers
Cardiac evaluation->Troponins, BNP, ECG, Echocardiogram, cardiac MRI, Coronary angiogram to r/o AMI
Infection- Viral markers- PCR for Influenza, covid, community acquired respiratory viruses, CMV, HIV screen
TFTs, Urinary metanephrines as indicated
Protein electrophoresis for amyloidosis
Urinary drug screen
ANA
ANCA, MPO- if vasculitis suspected
Endocardial Bx
->Echo- WMA not corresponding to coronary territories, thickened myocardium due to oedema, rather than thinned out
->Cardiac MRI–> Late patchy Gadolenium enhancement.
May guide the optimal location and yield of endocardial Bx
Endomyocardial biopsy-
Indications
Complications
endomyocardial biopsy
=>Indications for biopsy:Suspicion of
* Fulminant myocarditis.
* Giant cell myocarditis
* eosinophilic myocarditis.
* Failure to respond to usual care within 1-2 weeks.
* Persistent release of troponin.
=>Lymphocytic myocarditis (~75%) m/c histological form.
->complications of endomyocardial biopsy:
* Supraventricular arrhythmias.
* Pericardial effusion/tamponade due to perforation (right-sided biopsy).
* Stroke or systemic embolism (left-sided biopsy).
* Transient heart block
Management Principles
=>Pts with HfrEF and Unstable haemodynamics-
Inotropes, vasopressors,Mechanical support as a bridge to recovery
=>Stable pts wiht HfrEF-
* HfrEF management
* Anticoagulation
* Immunosuppression
* EP interventions
* Colchicin for pts with pericardial inv.
* Followup with serial troponins and echos
Mx of Acute myocarditis
=> Reduced LVEF – Hemodynamic Status Guides Therapy
->Stable hemodynamics
* Treat as HFrEF:
* ACEi / ARB / ARNI.
* Beta-blocker.
* Mineralocorticoid receptor antagonist.
* SGLT2 inhibitor.
->Unstable hemodynamics
* Inotropes.
* Mechanical circulatory support (IABP, Impella, ECMO):
- as Bridge to recovery.
- If no recovery → bridge to transplant or durable LVAD.
=> Anticoagulation
* Indicated for apical aneurysm → prevent LV thrombus
=> Perimyocarditis * Colchicine recommended. * NSAIDs not recommended: ineffective, may worsen myocarditis in animal models
=> EP interventions:
transcatheter ablation of may be required in case of persistent ventricular arrhythmias that fail to resolve/ respond to less invasive measures(m/c in Giant cell arteritis / Sarcoidisis)
Immunosuppression
=>Indications for Immunosuppression
Follow up
With serial Troponins->sharp decline- favourable
Inflammatory Markers
Serial echos- LV function, Effusion/ Tamponade
Prognostic features
Higher risk of mortality if :
[1] LVEF <50%.
[2] Sustained ventricular arrhythmias.
[3] Hemodynamic instability (heart failure or cardiogenic shock).
[4] High-degree AV block
Other Prognostic features:
ECG:–>Interval prolongation:
Second or third-degree AV block.
QRS >120 ms.
Prolonged QT interval.
Ventricular arrhythmias.
–>Evidence of myocardial functional loss:
Low voltage (may correlate with diffuse myocardial edema in fulminant myocarditis)
Q-waves.
Very high troponin level is a marker of high risk.
Right ventricular dysfunction