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The signs and symptoms associated with myocarditis are varied, and relate either to the actual inflammation of the myocardium or to the weakness of the heart muscle that is secondary to the inflammation. Signs and symptoms of myocarditis include the following:
- Chest pain (often described as "stabbing" in character)
- Congestive heart failure (leading to swelling, shortness of breath and liver congestion)
- Palpitations (due to abnormal heart rhythms)
- Sudden death (in young adults, myocarditis causes up to 20% of all cases of sudden death)
- Fever (especially when infectious, e.g. in rheumatic fever)
- Symptoms in young children tend to be more nonspecific, with generalized malaise, poor appetite, abdominal pain, and chronic cough. Later stages of the illness will present with respiratory symptoms with increased work of breathing, and is often mistaken for asthma.
Since myocarditis is often due to a viral illness, many patients give a history of symptoms consistent with a recent viral infection, including fever, rash, diarrhea, joint pains, and easily becoming tired.
Myocarditis is often associated with pericarditis, and many people with myocarditis present with signs and symptoms that suggest myocarditis and pericarditis at the same time.
Dilated cardiomyopathy develops insidiously, and may not initially cause symptoms significant enough to impact on quality of life. Nevertheless, many people experience significant symptoms. These might include:
- Shortness of breath
- Syncope (fainting)
- Angina, but only in the presence of ischemic heart disease
A person suffering from dilated cardiomyopathy may have an enlarged heart, with pulmonary edema and an elevated jugular venous pressure and a low pulse pressure. Signs of mitral and tricuspid regurgitation may be present.
Dilated cardiomyopathy (DCM) is a condition in which the heart becomes enlarged and cannot pump blood effectively. Symptoms vary from none to feeling tired, leg swelling, and shortness of breath. It may also result in chest pain or fainting. Complications can include heart failure, heart valve disease, or an irregular heartbeat.
Causes include genetics, alcohol, cocaine, certain toxins, complications of pregnancy, and certain infections. Coronary artery disease and high blood pressure may play a role, but are not the primary cause. In many cases the cause remains unclear. It is a type of cardiomyopathy, a group of diseases that primarily affects the heart muscle. The diagnosis may be supported by an electrocardiogram, chest X-ray, or echocardiogram.
In those with heart failure treatment may include medications in the ACE inhibitor, beta blocker, and diuretic families. A low salt diet may also be helpful. In those with certain types of irregular heartbeat, blood thinners or an implantable cardioverter defibrillator may be recommended. If other measures are not effective a heart transplant may be an option in some.
About 1 per 2,500 people are affected. It occurs more frequently in men than women. Onset is most often in middle age. Five-year survival rate is about 50%. It can also occur in children and is the most common type of cardiomyopathy in this age group.
Myocarditis, also known as inflammatory cardiomyopathy, is inflammation of the heart muscle. Symptoms can include shortness of breath, chest pain, decreased ability to exercise, and an irregular heartbeat. The duration of problems can vary from hours to months. Complications may include heart failure due to dilated cardiomyopathy or cardiac arrest.
Myocarditis is most often due to a viral infection. Other causes include bacterial infections, certain medications, toxins, and autoimmune disorders. A diagnosis may be supported by an electrocardiogram (ECG), increased troponin, heart MRI, and occasionally a heart biopsy. An ultrasound of the heart is important to rule out other potential causes such as heart valve problems.
Treatment depends on both the severity and the cause. Medications such as ACE inhibitors, beta blockers, and diuretics are often used. A period of no exercise is typically recommended during recovery. Corticosteroids or intravenous immunoglobulin (IVIG) may be useful in certain cases. In severe cases an implantable cardiac defibrillator or heart transplant may be recommended.
In 2013, about 1.5 million cases of acute myocarditis occurred. While people of all ages are affected, the young are most often affected. It is slightly more common in males than females. Most cases are mild. In 2015 cardiomyopathy, including myocarditis, resulted in 354,000 deaths up from 294,000 in 1990. The initial descriptions of the condition are from the mid-1800s.
These depend on the amount of inflammation. These are covered in their relevant articles.
- Acute: Heart failure; pericardial effusion; etc.
- Chronic: Valve diseases as noted above; Reduced cardiac output; Exercise intolerance.
Autoimmune heart diseases are the effects of the body's own immune defense system mistaking cardiac antigens as foreign and attacking them leading to inflammation of the heart as a whole, or in parts. The commonest form of autoimmune heart disease is rheumatic heart disease or rheumatic fever.
The symptoms/signs of pulmonary heart disease (cor pulmonale) can be non-specific and depend on the stage of the disorder, and can include blood backing up into the systemic venous system, including the hepatic vein. As pulmonary heart disease progresses, most individuals will develop symptoms like:
Pulmonary heart disease, also known as cor pulmonale is the enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance (such as from pulmonic stenosis) or high blood pressure in the lungs.
Chronic pulmonary heart disease usually results in right ventricular hypertrophy (RVH), whereas acute pulmonary heart disease usually results in dilatation. Hypertrophy is an adaptive response to a long-term increase in pressure. Individual muscle cells grow larger (in thickness) and change to drive the increased contractile force required to move the blood against greater resistance. Dilatation is a stretching (in length) of the ventricle in response to acute increased pressure.
To be classified as pulmonary heart disease, the cause must originate in the pulmonary circulation system. Two causes are vascular changes as a result of tissue damage (e.g. disease, hypoxic injury), and chronic hypoxic pulmonary vasoconstriction. If left untreated, then death may result, RVH due to a defect is not classified as pulmonary heart disease. The heart and lungs are intricately related; whenever the heart is affected by a disease, the lungs risk following and vice versa.
Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as pneumonia), myocardial infarction (a heart attack), abnormal heart rhythms (such as atrial fibrillation), uncontrolled high blood pressure, or the person's failure to maintain a fluid restriction, diet, or medication. Other well recognized precipitating factors include anemia and hyperthyroidism which place additional strain on the heart muscle. Excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones, may also precipitate decompensation.
Acute myocardial infarction can precipitate acute decompensated heart failure and will necessitate emergent revascularization with thrombolytics, percutaneous coronary intervention, or coronary artery bypass graft.
Up to 80% of individuals with ARVD present have symptoms like syncope and dyspnea.The remainder frequently present with palpitations or other symptoms due to right ventricular outflow tract (RVOT) tachycardia (a type of monomorphic ventricular tachycardia).
Symptoms are usually exercise-related. In populations where hypertrophic cardiomyopathy is screened out prior to involvement in competitive athletics, it is a common cause of sudden cardiac death.
The first clinical signs of ARVD are usually during adolescence. However, signs of ARVD have been demonstrated in infants.
Difficulty breathing, a cardinal symptom of left ventricular failure, may manifest with progressively increasing severity as the following:
- Difficulty breathing with physical activity (exertional dyspnea)
- Difficulty breathing while lying flat (orthopnea)
- Episodes of waking up from sleep gasping for air (paroxysmal nocturnal dyspnea)
- Acute pulmonary edema
Other cardiac symptoms of heart failure include chest pain/pressure and palpitations. Common noncardiac signs and symptoms of heart failure include loss of appetite, nausea, weight loss, bloating, fatigue, weakness, low urine output, waking up at night to urinate, and cerebral symptoms of varying severity, ranging from anxiety to memory impairment and confusion.
Arrhythmogenic right ventricular dysplasia (ARVD) is an inherited heart disease.
ARVD is caused by genetic defects of the parts of heart muscle (also called "myocardium" or "cardiac muscle") known as desmosomes, areas on the surface of heart muscle cells which link the cells together. The desmosomes are composed of several proteins, and many of those proteins can have harmful mutations.
The disease is a type of nonischemic cardiomyopathy that involves primarily the right ventricle. It is characterized by hypokinetic areas involving the free wall of the right ventricle, with fibrofatty replacement of the right ventricular myocardium, with associated arrhythmias originating in the right ventricle.
ARVD can be found in association with diffuse palmoplantar keratoderma, and woolly hair, in an autosomal recessive condition called Naxos disease, because this genetic abnormality can also affect the integrity of the superficial layers of the skin most exposed to pressure stress.
ARVC/D is an important cause of ventricular arrhythmias in children and young adults. It is seen predominantly in males, and 30–50% of cases have a familial distribution.
Even though many types of sick sinus syndrome produce no symptoms, a person may present with one or more of the following signs and symptoms:
- Stokes-Adams attacks – fainting due to asystole or ventricular fibrillation
- Dizziness or light-headedness
- Palpitations
- Chest pain or angina
- Shortness of breath
- Fatigue
- Headache
- Nausea
Chest pain is one of the common symptoms of acute pericarditis. It is usually of sudden onset, occurring in the anterior chest and often has a sharp quality that worsens with breathing in or coughing, due to inflammation of the pleural surface at the same time. The pain may be reduced with sitting up and leaning forward while worsened with lying down, and also may radiate to the back, to one or both trapezius ridges. However, the pain can also be dull and steady, resembling the chest pain in an acute myocardial infarction. As with any chest pain, other causes must also be ruled out, such as GERD, pulmonary embolism, muscular pain, etc.
A pericardial friction rub is a very specific sign of acute pericarditis, meaning the presence of this sign invariably indicates presence of disease. However, absence of this sign does not rule out disease. This rub can be best heard by the diaphragm of the stethoscope at the left sternal border arising as a squeaky or scratching sound, resembling the sound of leather rubbing against each other. This sound should be distinguished from the sound of a murmur, which is similar but sounds more like a "swish" sound than a scratching sound. The pericardial rub is said to be generated from the friction generated by the two inflamed layers of the pericardium; however, even a large pericardial effusion does not necessarily present a rub. The rub is best heard during the maximal movement of the heart within the pericardial sac, namely, during atrial systole, ventricular systole, and the filling phase of early ventricular diastole.
Fever may be present since this is an inflammatory process.
The onset of FAC caused by aggregation of the V122I mutation and wild-type TTR, and senile systemic amyloidosis caused by the exclusive aggregation of wild-type TTR, typically occur after age 60. Greater than 40% of these patients present with carpal tunnel syndrome before developing ATTR-CM. Cardiac involvement is often identified with the presence of conduction system disease (sinus node or atrioventricular node dysfunction) and/or congestive heart failure, including shortness of breath, peripheral edema, syncope, exertional dyspnea, generalized fatigue, or heart block. Unfortunately, echocardiographic findings are indistinguishable from those seen in AL amyloidosis, and include thickened ventricular walls (concentric hypertrophy, both right and left) with a normal-to-small left ventricular cavity, increased myocardial echogenicity, normal or mildly reduced ejection fraction (often with evidence of diastolic dysfunction and severe impairment of contraction along the longitudinal axis), and bi-atrial dilation with impaired atrial contraction. Unlike the situation in AL amyloidosis, the ECG voltage is often normal, although low voltage may be seen (despite increased wall thickness on echocardiography). Marked axis deviation, bundle branch block, and AV block are common, as is atrial fibrillation.
Acute pericarditis is a type of pericarditis (inflammation of the sac surrounding the heart, the pericardium) usually lasting less than 6 weeks. It is by far the most common condition affecting the pericardium.
Cardiorenal syndrome (CRS) is an umbrella term used in the medical field that defines disorders of the heart and kidneys whereby “acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other”. The heart and the kidneys are involved in maintaining hemodynamic stability and organ perfusion through an intricate network. These two organs communicate with one another through a variety of pathways in an interdependent relationship. In a 2004 report from National Heart, Lung and Blood Institute, CRS was defined as a condition where treatment of congestive heart failure is limited by decline in kidney function. This definition has since been challenged repeatedly but there still remains little consensus over a universally accepted definition for CRS. At a consensus conference of the Acute Dialysis Quality Initiative (ADQI), the CRS was classified into five subtypes primarily based upon the organ that initiated the insult as well as the acuity of disease.
The symptoms associated with MI are dependent on which phase of the disease process the individual is in. Individuals with acute MI are typically severely symptomatic and will have the signs and symptoms of acute decompensated congestive heart failure (i.e. shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea), as well as symptoms of cardiogenic shock (i.e., shortness of breath at rest). Cardiovascular collapse with shock (cardiogenic shock) may be seen in individuals with acute MI due to papillary muscle rupture, rupture of a chorda tendinea or infective endocarditis of the mitral valve.
Individuals with chronic compensated MI may be asymptomatic for long periods of time, with a normal exercise tolerance and no evidence of heart failure. Over time, however, there may be decompensation and patients can develop volume overload (congestive heart failure). Symptoms of entry into a decompensated phase may include fatigue, shortness of breath particularly on exertion, and leg swelling. Also there may be development of an irregular heart rhythm known as atrial fibrillation.
Findings on clinical examination depend on the severity and duration of MI. The mitral component of the first heart sound is usually soft and with a laterally displaced apex beat, often with heave. The first heart sound is followed by a high-pitched holosystolic murmur at the apex, radiating to the back or clavicular area. Its duration is, as the name suggests, the whole of systole. The loudness of the murmur does not correlate well with the severity of regurgitation. It may be followed by a loud, palpable P, heard best when lying on the left side. A third heart sound is commonly heard.
In acute cases, the murmur and tachycardia may be the only distinctive signs.
Patients with mitral valve prolapse may have a holosystolic murmur or often a mid-to-late systolic click and a late systolic murmur. Cases with a late systolic regurgitant murmur may still be associated with significant hemodynamic consequences.
Tachycardia is often asymptomatic. If the heart rate is too high, cardiac output may fall due to the markedly reduced ventricular filling time. Rapid rates, though they may be compensating for ischemia elsewhere, increase myocardial oxygen demand and reduce coronary blood flow, thus precipitating an ischemic heart or valvular disease. Sinus tachycardia accompanying a myocardial infarction may be indicative of cardiogenic shock.
On an EKG, Junctional Tachycardia exhibits the following classic criteria:
- P-Waves: The p-wave may be inverted in leads II, III and V or not visible
- Narrow QRS complexes (which is consistent with non-ventricular rhythms)
It can coexist with other superventricular tachycardias due to the disassociation between the SA node and the AV node. Junctional Tachycardia can appear similar to atrioventricular nodal reentrant tachycardia.
One form is junctional ectopic tachycardia.
It can be associated with digitalis toxicity. It may be also be due to onset of acute coronary syndrome, heart failure, conduction system diseases with enhanced automaticity, or administration of theophylline.
The disease typically develops two to four weeks after a throat infection. Symptoms include: fever, painful joints with those joints affected changing with time, involuntary muscle movements, and occasionally a characteristic non-itchy rash known as erythema marginatum. The heart is involved in about half of cases. Damage to the heart valves usually occurs only after multiple attacks but may occasionally occur after a single case of RF. The damaged valves may result in heart failure and also increase the risk of atrial fibrillation and infection of the valves.
Sick sinus syndrome (SSS), also called sinus dysfunction, or sinoatrial node disease ("SND"), is a group of abnormal heart rhythms (arrhythmias) presumably caused by a malfunction of the sinus node, the heart's primary pacemaker. Tachycardia-bradycardia syndrome is a variant of sick sinus syndrome in which the arrhythmia alternates between slow and fast heart rates. Tachycardia-bradycardia syndrome is often associated with ischemic heart disease and heart valve disease.
Mitral insufficiency (MI), mitral regurgitation or mitral incompetence is a disorder of the heart in which the mitral valve does not close properly when the heart pumps out blood. It is the abnormal leaking of blood backwards from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts, i.e. there is regurgitation of blood back into the left atrium. MI is the most common form of valvular heart disease.
Sinus tachycardia (also colloquially known as sinus tach or sinus tachy) is a sinus rhythm with an elevated rate of impulses, defined as a rate greater than 100 beats/min (bpm) in an average adult. The normal resting heart rate in the average male adult ranges from 60–100 bpm and women 60-90bpm. Note that the normal heart rate varies with age, with infants having normal heart rate of 110–150 bpm, in contrast to the elderly, who have slower normals.