HEART FAILURE FOLLOWING VIRAL MYOCARDITIS

 I have been given this case to solve in an attempt to understand the topic of "patient clinical data analysis" to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and come up with a diagnosis and treatment plan. 

You can find the details regarding this case in the link below

https://madhur116.blogspot.com/2020/05/on-1452020.html?m=1

ANALYSISPOSITIVE FINDINGS FROM HISTORY AND EXAMINATION

HISTORY

-High grade fever with chills -  1 month ago

-Shortness of breath since 2 weeks

-Pedal edema since 2 weeks.

-Generalized weakness since 2 weeks.

-Paroxysmal nocturnal dyspnea.

CLINICAL EXAMINATION

-Pitting type of pedal edema

-raised JVP

-Early inspiratory crepts on right side.

INVESTIGATIONS

-USG : Moderate pleural effusion on  Rt side

           Grade 1 fatty liver

           Mild ascites

-2D ECHO: EF-27 %

                  IVC dilated non collapsing

                  Mild Tricuspid regurgitation

                  Severe Mitral regurgitation 

                  Aortic regurgitation

                  All chambers dilated 

                  Global hypokinesia

                  Severe LV dysfunction

CAUSES EXCLUDED FROM THE ABOVE DATA

1.Respiratory causes : no any complaints of cough , cold, sore throat, wheeze .

2.Renal causes: no decreased urine output, facial puffiness, burning micturition.

3.Liver causes: as there is no tenderness in right upper quadrant , hepatomegaly, predominant ascites.

 THEREFORE ALL THE ABOVE POSITIVE FINDINGS POINT TOWARDS CARDIAC PROBLEM WITH REDUCED EJECTION FRACTION(LESSTHAN 40%) .

ETIOLOGY OF HEART FAILURE WITH REDUCED EJECTION FRACTION

As the patient had history of fever we can infer that etiology may be Viral myocarditis that caused heart failure.

PATHOPHYSIOLOGY

Viral myocarditis progresses chronologically in three distinct pathological phases 

FIRST PHASE- Direct destruction of cardiomyocytes occurs in viral mediated lysis causing degradation of cell structures which in turn facilitates entry of virus into cells with consequential myocyte injury and cardiac dilatation. Initial phase passes unnoticed as it is prevented by innate immune response.

SECOND PHASE- It developed as a result of immune response dysregulatio n triggered by initial cardiomyocyte injury. The initial cellular and humoral immune responses Amy improve the outcome during phase 1 conversely they are responsible for the harmful effect during phase 2 . This is in part induced by molecular mimicry which is caused by mimicked epitopes shared between viral and cardiac antigens.

THIRD PHASE- Typically picture of dilated cardiomyopathy developed as a result of extensive myocardial injury

.

 

Cardiotropic viruses that can cause myocarditis include Adenoviruses, Enterovirus, Parvovirus B19, CMV all of which are common cold viruses which individual may be attacked once in their life time but only a few developing cardiac problems shows role of GENETICS .

POSSIBLE TREATMENT OPTIONS 

NON PHARMACOLOGICAL OPTIONS

-Limitation of direct physical activity - as exercise during active viral infection may increase viral replication.

PHARMACOLOGICAL OPTIONS

It includes symptomatic and standard treatment for heart failure. Which includes

Diuretics 

Beta blockers

ACE inhibitors OR  ARB 

Careful monitoring for arrhythmias.

SPECIFIC THERAPY

Preventing direct viral damage using antiviral therapy is one possible option.

Immunomodulatory and or antiviral treatment along with the symptomatic treatment shown to be beneficial in some clinical trials.

REFRENCES

- Harrison principles of internal medicine 19 e 

- Davidson principles and practice of medicine

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2519249/

https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.113.001372

https://www.uwhealth.org/health/topic/special/heart-failure-with-reduced-ejection-fraction-systolic-heart-failure/tx4090abc.html