Myocarditis

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Myocarditis

ETP Cardiovascular System

ETP Cardiovascular System

Introduction to the cardiovascular system
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy clinical correlates: Heart
Anatomy of the superior mediastinum
Anatomy of the inferior mediastinum
Anatomy clinical correlates: Mediastinum
Development of the cardiovascular system
Fetal circulation
Cardiac muscle histology
Artery and vein histology
Arteriole, venule and capillary histology
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Coronary circulation
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Resistance to blood flow
Compliance of blood vessels
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Cardiac contractility
Frank-Starling relationship
Cardiac preload
Cardiac afterload
Law of Laplace
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac cycle
Cardiac work
Pressure-volume loops
Changes in pressure-volume loops
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Normal heart sounds
Abnormal heart sounds
Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Cardiac conduction system
Cardiac conduction velocity
ECG basics
ECG rate and rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG normal sinus rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
Arterial disease
Angina pectoris
Stable angina
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Myocardial infarction
Prinzmetal angina
Coronary steal syndrome
Peripheral artery disease
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Aneurysms
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Vasculitis
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Kawasaki disease
Hypertension
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Renal artery stenosis
Coarctation of the aorta
Cushing syndrome
Conn syndrome
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Deep vein thrombosis
Lymphedema
Lymphangioma
Shock
Vascular tumors
Human herpesvirus 8 (Kaposi sarcoma)
Angiosarcomas
Persistent truncus arteriosus
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Total anomalous pulmonary venous return
Tetralogy of Fallot
Hypoplastic left heart syndrome
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Ventricular septal defect
Atrial septal defect
Atrial flutter
Atrial fibrillation
Premature atrial contraction
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Ventricular tachycardia
Brugada syndrome
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
Atrioventricular block
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Pulmonary valve disease
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Dilated cardiomyopathy
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Hypertrophic cardiomyopathy
Heart failure
Cor pulmonale
Endocarditis
Myocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Deep vein thrombosis and pulmonary embolism: Pathology review
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Positive inotropic medications
Cardiomyopathies: Clinical
Congenital heart defects: Clinical
Valvular heart disease: Clinical
Infective endocarditis: Clinical
Pericardial disease: Clinical
Chest trauma: Clinical
Hypertension: Clinical
Aortic aneurysms and dissections: Clinical
Peripheral vascular disease: Clinical
Heart failure: Clinical
Coronary artery disease: Clinical
Pulmonary hypertension
Raynaud phenomenon
Fascia, vessels and nerves of the upper limb
Vessels and nerves of the forearm
Vessels and nerves of the hand
Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
Fascia, vessels and nerves of the lower limb
Vessels and nerves of the gluteal region and posterior thigh
Anatomy of the popliteal fossa
Ventilation
Ventilation-perfusion ratios and V/Q mismatch
Gas exchange in the lungs, blood and tissues
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Carbon dioxide transport in blood
Trypanosoma cruzi (Chagas disease)
Yellow fever virus
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Arteriovenous malformation
Cerebral circulation

Transcript

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With myocarditis, myo- means muscle, card- means heart, and -itis means inflammation. So, myocarditis is inflammation of the myocardium, which is the muscular middle layer of the heart wall, which contracts and relaxes so the heart can pump blood all around the body.

Inflammation in the myocardium layer causes swelling, which damages the heart muscle cells’ ability to contract. That means that less blood gets pumped out of the heart with each heartbeat. If myocarditis is severe enough, it can lead to heart failure, which is when the heart can’t keep up with the demands of the body. Once the inflammation resolves, the heart contraction typically returns to normal, but occasionally, when the inflammation is really severe, it can cause fibrosis, or scar tissue, in the myocardium. Scar tissue doesn’t contract normally, so if that happens, it can cause long term problems with heart contraction.

In North America, viral infections, specifically Coxsackievirus B infections, are the main cause of myocarditis. Viral infections can trigger lymphocytic myocarditis, which is when lymphocytes - the B and T cells of the immune system - and water make their way into the interstitial space - the space in between heart muscle cells. There are plenty of other infectious causes as well, though. One of these is trypanosoma cruzi, a single-cell protozoan that causes Chagas disease throughout South America. In Chagas disease, under a microscope, it’s possible to see groups of amastigotes within the heart muscle cells, which are trypanosomes that are in the intracellular stage. As a result, the heart muscle cells necrose or die. There’s also Trichinella, a roundworm that moves from the intestines into various parts of the body, causing a variety of problems, including myocarditis. Myocarditis can also be seen in Lyme disease which is caused by the bacteria Borrelia burgdorferi, which is spread by deer ticks. Finally, in immunocompromised individuals, there’s Toxoplasma gondii, a single-cell parasite harbored by cats, that can cause myocarditis.

Those were the infectious causes, but there are also non-infectious causes of myocarditis as well. These include systemic lupus erythematosus, also known as lupus, and polymyositis, a generalized inflammation of the muscles, where the immune system starts to attack the myocardial layer of the heart. There’s also drug-associated myocarditis, which means there’s an adverse drug reaction that inflames the heart. Drug reactions cause a hypersensitivity myocarditis, which is when eosinophils get into the blood vessels in the myocardium. Finally, there’s giant cell myocarditis, which causes inflammation in the heart, from an unknown cause. The key finding is that macrophages - immune cells that engulf foreign substances - start to fuse together to form a single giant cell, hence the name.

Individuals with myocarditis can have chest pain that is sometimes positional, meaning that it can get better or worse depending on the body’s position. It can also cause arrhythmias, or irregular heartbeats, because the inflammation affects the pacemaker cells traveling through the myocardium. There can also be more general symptoms like fatigue, fever and shortness of breath. In severe cases, where myocarditis starts to develop into heart failure, there can be additional symptoms like fluid retention in the feet and ankles.

Key Takeaways

Myocarditis is an inflammation of the heart muscle, also known as the myocardium. It can be caused by a variety of different infections, including viruses, bacteria, fungi, and parasites. It can also be caused by autoimmune diseases, such as lupus, or by drugs and toxins. Symptoms of myocarditis include chest pain, palpitations, shortness of breath, and fluid retention which might be an indication of heart failure. Treatment for myocarditis involves medications to reduce inflammation, and antibiotics to treat any underlying infections. In some cases, a heart transplant may be necessary.

Sources

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  2. "Myocarditis overview" Life in the Fastlane (2017)
  3. "Treatment and prognosis of myocarditis in adults" UpToDate (2017)
  4. "Robbins Basic Pathology (10 edition)" Elsevier (2017)
  5. "First Aid for the USMLE Step 1 2017 (27 edition)" McGraw-Hill Education / Medical (2017)
  6. "Beta blockers and heart failure." Trinity Student Medical Journal 2003 (2003)
  7. "Myocarditis" Texas Heart Institute (2017)
  8. "Myocarditis" Wikipedia.
  9. "Fundamentals of Pathology: Medical Course and Step 1 Review" Pathoma LLC (2017)
  10. "Myocarditis: practice essentials" Medscape (2016)
  11. "Myocarditis pathology" Medscape (2015)