Cardiac troponin I (cTnI) is the most specific indicator of myocardial infarction.
Continuous monitoring is essential because the first 24 hours after the onset of symptoms is the time of highest risk for sudden death.
Cardiac transplantation.
Most cardiomyopathies are the result of remodeling caused by the effect of neurohumoral responses to ischemic heart disease or hypertension on the heart muscle.
Idiopathic dilated cardiomyopathy often has a familial origin with associated alterations in genes coding for contractile proteins, mitochondrial dysfunction, and immune defects.
Hypoxemia may accompany heart failure.
To prevent pulmonary and systemic embolism.
cTnI has a sensitivity of more than 95% and a negative predictive value of 99% for the diagnosis of acute myocardial infarction.
Extra heart sounds and cardiac murmurs.
Hypertrophic obstructive cardiomyopathy.
Extra heart sounds and murmurs.
Myocardial infarction can be described as anterior, inferior, posterior, lateral, subendocardial, or transmural depending on its location and extent of tissue damage.
cTnI should be obtained on admission to the emergency department.
Non-STEMI is treated in the same way as unstable angina including antithrombotics and anticoagulation.
The use of cardiac stem cells.
Angina, syncope, palpitations, and symptoms of MI and left heart failure.
Pulmonary congestion is expected in dilated cardiomyopathy, although fulminant pulmonary edema is uncommon.
The wall is weakened and tension stretches the noncontracting infarcted heart muscle, producing infarct expansion or aneurysm formation
Dysrhythmias, particularly ventricular fibrillation
A characteristic Q wave often develops on ECG in STEMI some hours later.
Pain is treated with morphine sulfate.
Myocardial pacemakers (pacing).
When heart rate is increased and intravascular volume is decreased.
Impaired systolic function leads to increases in intracardiac volume, ventricular dilation, and systolic heart failure.
The morbidity and mortality rates for peripartum cardiomyopathy are high at 5% to 32%.
Thinning of the wall, poor collateral flow, shearing effect of muscular contraction against the stiffened necrotic area, marked necrosis at the terminal end of the blood supply, and aging of the myocardium with laceration of the myocardial microstructure
Debris and clots that collect inside dilated aneurysmal sacs or from the infarcted endocardium
Twelve-lead ECGs help localize the affected area through identification of changes in ST segments and T waves.
Other biomarkers released by myocardial cells include CPK-MB and LDH.
Echocardiography and MRI.
Through autosomal dominant inheritance.
Many cases of cardiomyopathy are idiopathic.
Serious ventricular arrhythmias and sudden death.
Alcohol and many drugs such as some chemotherapeutic, inotropic, and antidysrhythmic agents can be directly toxic to the myocardium.
Organic brain syndrome
Rupture
Acute inflammation of the pericardium
It can occur both with myocardial infarction (MI) and in individuals who suffer ischemia during cardiovascular procedures such as cardiac surgery.
Hibernating myocardium refers to tissue that is persistently ischemic and undergoes metabolic adaptation to prolong myocyte survival until perfusion can be restored.
Aggressive fluid resuscitation, inotropic drugs, and possible emergent invasive procedures.
Implantable cardioverter-defibrillators (ICDs).
Pain, fever, friction rub, pleural effusion, and arthralgias.
Because of estrogen deficiency–mediated effects on the microvasculature.
Blood should be drawn for troponin and isoenzyme determinations as soon as possible after the onset of symptoms.
Thickening of the septal wall, which may cause outflow obstruction to the left ventricle outflow tract.
Valvular heart disease causes cardiac chamber volume and pressure overload that can result in long-term myocardial dysfunction.
Transient ischemic attacks or an outright cerebrovascular accident
Ventricular tachydysrhythmias
Myocardial remodeling is mediated by angiotensin II, aldosterone, catecholamines, adenosine, oxidative stress, and inflammatory cytokines.
Approximately 1% to 2%.
Anterior chest pain that worsens with respiratory effort.
A delayed form of acute pericarditis that can occur from 1 week to several months after acute MI.
Earthquakes, lightning strikes, noncardiac surgery, seizures, trauma, anesthesia, and alcohol withdrawal.
Adjacent to the zone of hypoxic injury is a zone of reversible ischemia.
The individual should be placed on supplemental oxygen and given an aspirin immediately (clopidogrel or prasugrel if intolerant to aspirin).
Corticosteroids and immunosuppressants.
Cardiomyopathies are a diverse group of diseases that affect the myocardium.
Echocardiography and cardiac catheterization.
Beta-blockers or verapamil to slow the heart rate, surgical resection of the hypertrophied myocardium, septal ablation, and prophylactic placement of an ICD in high-risk individuals.
Dilated cardiomyopathies may be the late autoimmune consequences of previous viral infections resulting in myocarditis and subsequent decreases in contractility.
Audible, harsh cardiac murmurs; increased LVEDP; and decreased systemic blood pressure
Early mobilization and prophylactic anticoagulation therapy
In the anterior chest, although it may radiate to the back
Repair consists of degradation of damaged cells, proliferation of fibroblasts, and synthesis of scar tissue.
Radiation to the neck, jaw, back, shoulder, or left arm is common.
Cardiac murmurs may indicate acute valvular insufficiency.
Elevations of cardiac biomarkers above the 99th percentile URL are indicative of periprocedural myocardial necrosis.
Acute onset of chest pain, ST elevation, elevated troponins, and BNP after emotional stress.
Corticosteroids.
The 'broken heart syndrome'.
A social worker, pastor, and mental health care providers.
Additional analgesics.
Pericardial inflammation.
Chyle leaking from the thoracic duct entering the pericardium.
Decreased ventricular filling, decreased stroke volume, and reduced cardiac output.
The arterial blood pressure during expiration exceeds arterial pressure during inspiration by more than 10 mmHg.
cTnI elevation is detectable 2 to 4 hours after the onset of symptoms.
Blood pressure.
Two major categories of thickening of the myocardium: hypertrophic obstructive cardiomyopathy and hypertensive or valvular hypertrophic cardiomyopathy.
Yes, an individual may display characteristics of more than one type of cardiomyopathy.
Systemic and pulmonary emboli are common complications of dilated cardiomyopathy.
It becomes more fibrotic but continues to bulge with systole
Immediate intervention and careful monitoring
A temporary loss of contractile function that persists for hours to days after perfusion has been restored.
Stunning is less severe in individuals who have experienced ischemic preconditioning.
After 6 weeks, the necrotic area is completely replaced by scar tissue, which is strong but unable to contract and relax like healthy myocardial tissue.
Various cardiovascular changes are found on physical examination, including increased heart rate and blood pressure, abnormal extra heart sounds, cardiac murmurs, pulmonary congestion, and peripheral vasoconstriction.
Nearly half of MIs are not preceded by any previous angina symptoms.
Elevations of cardiac biomarkers above the 99th percentile URL are indicative of periprocedural myocardial necrosis.
Bed rest followed by gradual return to activities of daily living.
Decreased cardiac contractility with abnormal wall motion, altered left ventricular compliance, decreased stroke volume, decreased ejection fraction, increased left ventricular end-diastolic pressure (LVEDP), and SA or AV node malfunction.
Cardiogenic shock.
Transient dyskinesis of the left ventricle in the absence of acute coronary artery disease, acute head trauma, myocarditis, or other forms of cardiomyopathy.
Rest.
Distention of the jugular veins, edema, hepatomegaly.
A 'water-bottle' configuration of the cardiac silhouette.
The infarcted myocardium is surrounded by a zone of hypoxic injury, which may progress to necrosis or return to normal.
The individual's blood sugar is usually elevated and the glucose tolerance level may remain abnormal for several weeks.
Salt restriction and the careful use of vasodilators, diuretics, and inotropic agents.
A hyperdynamic state, especially with exercise.
Dilated cardiomyopathy is characterized by diminished myocardial contractility, which is reflected in diminished systolic performance of the heart.
Peripartum cardiomyopathy occurs in previously healthy women in the final month of pregnancy and up to 5 months after delivery.
Rupture of these muscles or of the chordae tendineae
Thromboembolism
Acute pericarditis
It causes myocyte hypertrophy, scarring, and loss of contractile function in the areas of the heart distant from the site of infarction.
Detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value above the 99th percentile of the upper reference limit (URL) together with evidence of myocardial ischemia with at least one of the following: symptoms of ischemia, electrocardiographic changes indicative of new ischemia, development of pathologic Q waves in the electrocardiogram, imaging evidence of new loss of viable myocardium or new regional wall motion abnormality, sudden unexpected cardiac death involving cardiac arrest, or pathologic findings of an acute myocardial infarction.
DVT prophylaxis as long as their activity is significantly limited.
Chest pain, dyspnea, ST-segment elevation, and moderately elevated cardiac biomarkers.
Relieving symptoms.
In all forms of pericarditis.
Tuberculosis, neoplasm, uremia, or radiation.
The pericardium can stretch to accommodate large quantities of fluid without compressing the heart.
Dyspnea, tachycardia, jugular venous distention, cardiomegaly, and pulsus paradoxus.
An effusion as small as 20 ml.
Pericardial biopsy.
Additional measurements are recommended within 6 to 9 hours and again at 12 to 24 hours if clinical suspicion is high and previous samples were negative.
Progressive decreases in contractility.
Asymmetric septal hypertrophic cardiomyopathy or subaortic stenosis.
Cardiomyopathies can be secondary to inherited disorders, infectious disease, exposure to toxins, systemic connective tissue disease, infiltrative and proliferative disorders, or nutritional deficiencies.
Ischemic cardiomyopathy is the most common type.
Palpitations and associated dysrhythmias may cause dizziness (syncope).
An increase in the radius of the ventricle, leading to increased pressure and tension over time
Widespread knowledge of cardiopulmonary resuscitation
Another disorder, such as infection, trauma, surgery, neoplasm, or a metabolic, immunologic, or vascular disorder
A pericardial friction rub—a short, scratchy, grating sound
It is at this time in the recovery period (10 to 14 days after infarction) that individuals feel more capable of increasing activities and thus may stress the newly formed scar tissue.
Nausea and vomiting may occur because of reflex stimulation of vomiting centers by pain fibers.
The diagnosis of acute MI is made on the basis of history, physical examination, ECG, and serial cardiac biomarker alterations.
With insulin.
The hemodynamic consequences.
Inflammation of the pericardium (pericarditis).
They cause coronary artery spasm, coronary microvascular abnormalities, direct myocardial damage, and neurogenic myocardial stunning.
Diffuse ST-segment elevation that is concaved upward without Q waves.
The accumulation of fluid in the pericardial cavity.
A transudate, such as serous effusion.
Distant or muffled heart sounds, poorly palpable apical pulse, dyspnea on exertion, and dull chest pain.
Removal of the pericardial fluid.
Prominent pulmonary vessels and calcification of the pericardium.
Leukocytosis and elevated CRP may indicate inflammation.
Careful evaluation for potentially reversible underlying causes.
Abnormalities of collagen deposition and altered contractile proteins in the myocytes.
Cardiomyopathies are categorized as dilated, hypertrophic, or restrictive depending on their tissue characteristics, genomics, and hemodynamic effects.
Nutritional deficiencies including niacin, vitamin D, and selenium can cause cardiomyopathy.
Rupture of heart structures
Months or years after the acute event
Idiopathic or viral infection by coxsackievirus, influenza, hepatitis, measles, mumps, or varicella viruses
Restoring adequate perfusion to the myocardium with revascularization therapies can improve myocardial function.
The pain associated with MI tends to be more severe and prolonged compared to angina.
Severe myocardial damage may cause hypotension despite elevated catecholamine activity.
The term 'myocardial infarction' should be used when there is evidence of myocardial necrosis in a clinical setting with myocardial ischemia.
To eliminate the need for straining, which can precipitate bradycardia and cause possible cardiac overload.
Episodes of extreme mental stress, like the loss of a loved one.
Targeted emotional support and standard psychological counseling.
Combined nonsteroidals and colchicine.
Aneurysms, trauma, or coagulation defects.
Restrictive pericarditis (chronic pericarditis).
A pericardial knock (early diastolic sound).
Diastolic relaxation and ventricular compliance.
Common causes include ischemic heart disease, valvular disease, diabetes, renal failure, hyperthyroidism, alcohol or drug toxicity, peripartum complications, genetic disorder, or infection.
Hyperthyroidism may present with atrial fibrillation and dilated cardiomyopathy, which may be reversible with treatment of the thyroid disorder.
Septal rupture
The breaking loose of deep venous thrombi of the legs in individuals who are confined to bed
Several days of fever, myalgias, and malaise followed by the sudden onset of severe chest pain that worsens with respiratory movements and with lying down
MI causes a severe inflammatory response that ends with wound repair.
It may be described as heavy and crushing, such as an 'elephant sitting on my chest.'
Thrombolytics.
The atria, ventricles, nodal regions, or conduction tissues.
An immunologic (antigen-antibody) response to the necrotic myocardium.
Weakening and ballooning.
No, friction rubs are not always present and may be intermittently heard.
The right atrium and ventricle.
To identify the cause of the effusion.
Idiopathic causes, radiation exposure, rheumatoid arthritis, uremia, or CABG.
Exercise intolerance, dyspnea on exertion, fatigue, and anorexia.
Ischemic cardiomyopathy can occur as the direct result of myocardial infarction or from repetitive ischemic insults in those with poorly controlled angina.
Chest pain in dilated cardiomyopathy may be present but it is usually nonspecific and unlike anginal pain.
Impaired pump function
Acute pericarditis, pericardial effusion, or constrictive pericarditis
They become inflamed and roughened, and a pericardial effusion may develop
New therapies are being explored that can simulate ischemic preconditioning prior to cardiovascular procedures or that can be used after ischemic events to reduce the effects of stunning (post-conditioning).
The first symptom of acute MI is usually sudden, severe chest pain.
The sympathetic nervous system (SNS) is reflexively activated to compensate, resulting in a temporary increase in heart rate and blood pressure.
Up to one-third of MI cases present with STEMI as the first symptomatic manifestation of coronary disease.
ACE inhibitors, beta-blockers, and statins.
No, they do not improve mortality.
Inflammation without necrosis.
A pericardial effusion.
Acute pericarditis, heart surgery, some chemotherapeutic agents, infections, and autoimmune disorders.
Rapid accumulation of fluid, even in small amounts (50 to 100 ml).
Right atrial filling during diastole.
Life-threatening circulatory collapse may occur.
Chemotherapeutic agents.
No, it never develops suddenly.
Weight loss, edema, jugular vein distention, and hepatic congestion.
CT, MRI, and transesophageal echocardiography.
Diabetes and uremia are associated with decreased myocardial contractility and dilated cardiomyopathy.
The most common symptoms of dilated cardiomyopathy are dyspnea and fatigue.
Ventricular aneurysm formation
Dysphagia, restlessness, irritability, anxiety, and weakness
Within 24 hours, leukocytes infiltrate the necrotic area and proteolytic enzymes from scavenger neutrophils degrade necrotic tissue.
Some individuals, especially older adults or those with diabetes, experience no pain, thereby having a 'silent' infarction.
Pulmonary findings of congestion, including dullness to percussion and inspiratory crackles at the lung bases, can occur if the individual develops heart failure.
Increases of biomarkers greater than 5 × 99th percentile URL plus either new pathologic Q waves or new LBBB, or angiographically documented new graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium have been designated as defining CABG-related myocardial infarction.
Dysrhythmias (arrhythmias).
Steroids.
Aspirin, beta-blockers, angiotensin-converting enzyme inhibitors, and statins.
Salicylates and nonsteroidal anti-inflammatory drugs (NSAIDs).
CT scan.
T-wave inversions and atrial fibrillation.
Degree of left ventricular dysfunction, degree of left ventricular ischemia, potential for ventricular dysrhythmias, and the individual’s age
MI, trauma, neoplasm, surgery, uremia, bacterial infection, connective tissue disease, or radiation therapy
Recurrent pericarditis, pericardial constriction, and cardiac tamponade
Stunning is caused by alterations in electrolyte pumps, calcium homeostasis, and the release of toxic oxygen radicals.
These changes can be limited and even reversed through rapid restoration of coronary flow and the use of ACE inhibitors, beta-blockers, statins, sequential pacemakers, and ventricular assist devices after MI.
Abnormal extra heart sounds reflect left ventricular dysfunction.
Education on diet, caffeine, smoking cessation, exercise, and other aspects of risk factor reduction.
In Japan in 1991.
The rub caused by the roughened pericardial membranes rubbing against each other.
To determine the appropriate treatment and management.
With analgesics, anti-inflammatory medications, or steroids.
Low-grade fever and sinus tachycardia
It is characterized by decreased contraction and conduction and can contribute to heart failure, shock, and dysrhythmias.
A collagen matrix is deposited and is initially weak, mushy, and vulnerable to reinjury.
Infarction often simulates a sensation of unrelenting indigestion.
Peripheral vasoconstriction may cause the skin to become cool and clammy.
Increases of biomarkers greater than 3 × 99th percentile URL have been designated as defining PCI-related myocardial infarction.
Emergent PCI and antithrombotics.
Ischemia, hypoxia, autonomic nervous system imbalances, lactic acidosis, electrolyte abnormalities, alterations of impulse conduction pathways or conduction defects, drug toxicity, or hemodynamic abnormalities.
Pulmonary congestion, reduced myocardial contractility, and abnormal heart wall motion.
Anterior infarction.
Postmenopausal women at times of acute stress.
The roughened pericardial membranes rubbing against each other.
Aspirating the excessive fluid.
Whether the fluid creates sufficient pressure to cause cardiac compression, known as tamponade.
It eventually equals diastolic pressure within the heart chambers, preventing chamber filling.
The presence of a large pericardial effusion or tamponade.
Echocardiogram.
Tuberculosis.
Surgical excision of the restrictive pericardium.
The ECG may remain abnormal for days or even weeks.
No, it is not necessarily clinically significant except that it indicates an underlying disorder.
Impairment of diastolic filling of the left ventricle plus reduction of blood volume within all four cardiac chambers.
If the underlying cause of tamponade is trauma or aneurysm.
Fibrous scarring with occasional calcification of the pericardium.
It compresses the heart and eventually reduces cardiac output.
It is both diagnostic and therapeutic.
Tuberculosis.
Pericardiocentesis (aspiration of excessive pericardial fluid).
They encase the heart in a rigid shell.
A pericardial 'window' can be created or the individual may require pericardectomy.
Dietary sodium restriction, digitalis glycosides, and diuretics to improve cardiac output.
