Takotsubo Cardiomyopathy
Cardiomyopathies
Cardiomyopathy, Dilated
Electrocardiography
Torsades de Pointes
Ventricular Dysfunction, Left
Cardiomyopathy, Hypertrophic
Echocardiography
Coronary Angiography
Atrioventricular Block
Long QT Syndrome
Cardiovascular Agents
Ventricular Function, Left
Syncope
Ventricular Dysfunction, Right
Heart Ventricles
Cardiomyopathy, Restrictive
Cardiac Catheterization
Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms. (1/196)
Tako-tsubo-like left ventricular dysfunction phenomenon (TTP) has primarily been described in Japan and is characterized by transient left ventricular apical ballooning in the absence of coronary artery disease, associated with chest symptoms, electrocardiographic changes and minimal cardiac enzymes release. Aim of the present review is to summarize the current knowledge about TTP. TTP has been described predominantly in females. TTP occurs also outside Japan. Clinical symptoms comprise anginal chest pain, dyspnea and syncope. TTP occurs frequently after acute emotional or physical stress. Electrocardiographic ST- elevations may be present only for several hours. Then, normalization of the ST-segment occurs, followed by negative T waves, which persist for months. Arterial hypertension in TTP is found in up to 76%, hyperlipidaemia in up to 57%, diabetes mellitus in up to 12% and smoking in up to 18% of the patients. Several pathomechanisms have been proposed: myocardial stunning due to increased catecholamine levels, coronary vasospasm, atherosclerotic plaques rupture, myocarditis, catecholamine-induced hyperkinesis of the basal left ventricular segments and genetic. Patients with TTP should be monitored like patients with myocardial infarction. Care should be taken in the application of catecholamines and nitrates. Betablockers should be given in the acute and chronic phase, and possibly indefinitely to prevent recurrences. The prognosis of TTP is assumed to be good, but in the acute phase there are deaths due to multisystem organ failure, cardiogenic shock, ventricular fibrillation and ventricular rupture. The long term prognosis of TTP patients is largely unknown. (+info)An unusual presentation of "tako-tsubo cardiomyopathy". (2/196)
We report a case of tako-tsubo cardiomyopathy, complicated by left ventricular apical thrombus. (+info)Subaortic dynamic obstruction: a contributing factor to haemodynamic instability in tako-tsubo syndrome? (3/196)
We present a case of transient apical ballooning with haemodynamic instability in a female patient with normal coronaries and a history of poorly controlled systemic arterial hypertension. There was dynamic obstruction of the outflow tract and moderate secondary mitral regurgitation at presentation. These were due to systolic anterior motion of the mitral valve, which normalised gradually with the recovery of left ventricular function, and to a 'sigmoid' septum. Mid-cavity obstruction is potentially an important contributory factor to the haemodynamic instability sometimes encountered in this syndrome. (+info)Apical ballooning syndrome complicated by acute severe mitral regurgitation with left ventricular outflow obstruction--case report. (4/196)
BACKGROUND: Apical ballooning syndrome (or Takotsubo cardiomyopathy) is a syndrome of transient left ventricular apical ballooning. Although first described in Japanese patients, it is now well reported in the Caucasian population. The syndrome mimicks an acute myocardial infarction but is characterised by the absence of obstructive coronary disease. We describe a serious and poorly understood complication of Takotsubo cardiomyopathy. CASE PRESENTATION: We present the case of a 65 year-old lady referred to us from a rural hospital where she was treated with thrombolytic therapy for a presumed acute anterior myocardial infarction. Four hours after thrombolysis she developed acute pulmonary oedema and a new systolic murmur. It was presumed she had acute mitral regurgitation secondary to a ruptured papillary muscle, ischaemic dysfunction or an acute ventricular septal defect. Echocardiogram revealed severe mitral regurgitation, left ventricular apical ballooning, and systolic anterior motion of the mitral valve with significant left ventricular outflow tract gradient (60-70 mmHg). Coronary angiography revealed no obstructive coronary lesions.She had an intra-aortic balloon pump inserted with no improvement in her parlous haemodynamic state. We elected to replace her mitral valve to correct the outflow tract gradient and mitral regurgitation. Intra-operatively the mitral valve was mildly myxomatous but there were no structural abnormalities. She had a mechanical mitral valve replacement with a 29 mm St Jude valve. Post-operatively, her left ventricular outflow obstruction resolved and ventricular function returned to normal over the subsequent 10 days. She recovered well. CONCLUSION: This case represents a serious and poorly understood association of Takotsubo cardiomyopathy with acute pulmonary oedema, severe mitral regurgitation and systolic anterior motion of the mitral valve with significant left ventricular outflow tract obstruction. The sequence of our patient's presentation suggests that the apical ballooning caused geometric alterations in her left ventricle that in turn led to acute and severe mitral regurgitation, systolic anterior motion of the mitral valve and left ventricular outflow tract obstruction. The left ventricular outflow tract obstruction and mitral regurgitation were corrected by mechanical mitral valve replacement. We describe a variant of Takotsubo cardiomyopathy with acute mitral regurgitation, systolic anterior motion of the mitral valve leaflet and left ventricular outflow tract obstruction of a dynamic nature. (+info)Assessment of coronary flow reserve by transthoracic Doppler echocardiography in left apical ballooning syndrome. (5/196)
We present the time course of transthoracic coronary flow reserve in the left anterior descending artery in a patient who suffered a transient left apical ballooning syndrome. (+info)Tako-Tsubo cardiomyopathy: intraindividual structural analysis in the acute phase and after functional recovery. (6/196)
AIMS: To gain more insight into the phenomenon of Tako-Tsubo cardiomyopathy (TTC), the purpose of the present study was to investigate the myocardial structure in the acute phase of TTC and after functional recovery. METHODS AND RESULTS: We studied eight patients presenting with TTC diagnosed by coronary angiography, ventriculography, magnetic resonance imaging, and echocardiography. Serial myocardial biopsies were taken during the phase of severely impaired left ventricular function and after functional recovery. Specimens were examined by light and electron microscope as well as immunohistochemistry. Additionally, specific methods detecting different types of cell death and measurements of virus titer were performed. All patients showed the typical contractile pattern of TTC and complete functional recovery within 12 +/- 3 days. In 'acute' biopsies, many vacuoles of different size were found contributing to cellular hypertrophy. PAS staining revealed intracellular accumulation of glycogen. Additionally, structural deteriorations characterized by disorganization of contractile and cytoskeletal proteins could be detected. The extracellular matrix proteins were increased. Signs of oncotic and apoptotic cell death were absent. After functional recovery, all described alterations showed a nearly complete reversibility. CONCLUSION: TTC is accompanied by severe morphological alterations potentially resulting from catecholamine excess followed by microcirculatory dysfunction and direct cardiotoxicity. However, the affected myocardium represents a high potential of structural reconstitution which correlates with the rapid functional recovery. (+info)The role of cardiovascular magnetic resonance in patients presenting with chest pain, raised troponin, and unobstructed coronary arteries. (7/196)
AIMS: Troponin measurement is used in the assessment and risk stratification of patients presenting acutely with chest pain when the main cause of elevation is coronary artery disease. However, some patients have no coronary obstruction on angiography, leading to diagnostic uncertainty. We evaluated the incremental diagnostic value of cardiovascular magnetic resonance (CMR) in these patients. METHODS AND RESULTS: Sixty consecutive patients (mean age 44 years, 72% male) with a troponin-positive episode of chest pain and unobstructed coronary arteries were recruited within 3 months of initial presentation. All patients underwent CMR with cine imaging, T2-weighted imaging for detection of inflammation, and late gadolinium enhancement imaging for detection of infarction/fibrosis. An identifiable basis for troponin elevation was established in 65% of patients. The commonest underlying cause was myocarditis (50%), followed by myocardial infarction (11.6%) and cardiomyopathy (3.4%). In the 35% of patients where no clear diagnosis was identified by CMR, significant myocardial infarction/fibrosis was excluded. CONCLUSION: CMR is a valuable adjunct to conventional investigations in a diagnostically challenging and important group of patients with troponin-positive chest pain and unobstructed coronary arteries. (+info)Left ventricular apical rupture caused by takotsubo cardiomyopathy--comprehensive pathological heart investigation. (8/196)
An 81-year-old woman with emotionally-induced takotsubo cardiomyopathy developed a fatal left ventricular (LV) apical rupture. During the hospitalization persistent ST-segment elevation with no electrocardiographic time evolution was observed on the ECG, characteristic for takotsubo cardiomyopathy. Histopathologically, transmural myocardial necrosis with hemorrhage was found at the rupture site, but there were foci of coagulation and contraction band necrosis with mononuclear lymphocyte infiltrations in other heart regions, and the intensity and distribution of these pathological changes corresponded to the distribution of the LV contraction abnormalities seen on ventriculography. The article concludes that: the LV functional disorder in takotsubo cardiomyopathy may be caused by distracted foci of coagulation and contraction band necrosis in the myocardium; contraction band necrosis (a sign of catecholamine cardiotoxicity) may reflect the sympathetic hyperactivity in this disease; persistent myocardial damage expressed by persistent ST-segment elevation without an electrocardiographic time evolution should be carefully observed with sequential echocardiographic examinations because of the possibility of cardiac rupture. (+info)Takotsubo cardiomyopathy, also known as Takotsubo syndrome or stress-induced cardiomyopathy, is a temporary heart condition usually triggered by emotional or physical stress. It's named after the Japanese word for "octopus pot" because of the shape of the left ventricle during the contraction phase, which resembles this pot.
In Takotsubo cardiomyopathy, a part of the heart muscle becomes weakened and doesn't pump well, often following a surge of stress hormones. The condition can be misdiagnosed as a heart attack because it has similar symptoms and test results. However, unlike a heart attack, there's no evidence of blocked heart arteries in Takotsubo cardiomyopathy.
The symptoms of Takotsubo cardiomyopathy include chest pain, shortness of breath, irregular heartbeat, and sometimes fluid retention. Treatment typically includes medication to manage symptoms and support the heart while it recovers. Most people with Takotsubo cardiomyopathy make a full recovery within a few weeks. However, in rare cases, complications such as heart failure or arrhythmias can occur.
Cardiomyopathies are a group of diseases that affect the heart muscle, leading to mechanical and/or electrical dysfunction. The American Heart Association (AHA) defines cardiomyopathies as "a heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that usually (but not always) exhibit inappropriate ventricular hypertrophy or dilatation and frequently lead to heart failure."
There are several types of cardiomyopathies, including:
1. Dilated cardiomyopathy (DCM): This is the most common type of cardiomyopathy, characterized by an enlarged left ventricle and impaired systolic function, leading to heart failure.
2. Hypertrophic cardiomyopathy (HCM): In this type, there is abnormal thickening of the heart muscle, particularly in the septum between the two ventricles, which can obstruct blood flow and increase the risk of arrhythmias.
3. Restrictive cardiomyopathy (RCM): This is a rare form of cardiomyopathy characterized by stiffness of the heart muscle, impaired relaxation, and diastolic dysfunction, leading to reduced filling of the ventricles and heart failure.
4. Arrhythmogenic right ventricular cardiomyopathy (ARVC): In this type, there is replacement of the normal heart muscle with fatty or fibrous tissue, primarily affecting the right ventricle, which can lead to arrhythmias and sudden cardiac death.
5. Unclassified cardiomyopathies: These are conditions that do not fit into any of the above categories but still significantly affect the heart muscle and function.
Cardiomyopathies can be caused by genetic factors, acquired conditions (e.g., infections, toxins, or autoimmune disorders), or a combination of both. The diagnosis typically involves a comprehensive evaluation, including medical history, physical examination, electrocardiogram (ECG), echocardiography, cardiac magnetic resonance imaging (MRI), and sometimes genetic testing. Treatment depends on the type and severity of the condition but may include medications, lifestyle modifications, implantable devices, or even heart transplantation in severe cases.
Dilated cardiomyopathy (DCM) is a type of cardiomyopathy characterized by the enlargement and weakened contraction of the heart's main pumping chamber (the left ventricle). This enlargement and weakness can lead to symptoms such as shortness of breath, fatigue, and fluid retention. DCM can be caused by various factors including genetics, viral infections, alcohol and drug abuse, and other medical conditions like high blood pressure and diabetes. It is important to note that this condition can lead to heart failure if left untreated.
Electrocardiography (ECG or EKG) is a medical procedure that records the electrical activity of the heart. It provides a graphic representation of the electrical changes that occur during each heartbeat. The resulting tracing, called an electrocardiogram, can reveal information about the heart's rate and rhythm, as well as any damage to its cells or abnormalities in its conduction system.
During an ECG, small electrodes are placed on the skin of the chest, arms, and legs. These electrodes detect the electrical signals produced by the heart and transmit them to a machine that amplifies and records them. The procedure is non-invasive, painless, and quick, usually taking only a few minutes.
ECGs are commonly used to diagnose and monitor various heart conditions, including arrhythmias, coronary artery disease, heart attacks, and electrolyte imbalances. They can also be used to evaluate the effectiveness of certain medications or treatments.
Torsades de Pointes is a type of polymorphic ventricular tachycardia, characterized by a distinct pattern on the electrocardiogram (ECG) where the QRS complexes appear to twist around the isoelectric line. This condition is often associated with a prolonged QT interval, which can be congenital or acquired due to various factors such as medications, electrolyte imbalances, or heart diseases. Torsades de Pointes can degenerate into ventricular fibrillation, leading to sudden cardiac death if not promptly treated.
Left ventricular dysfunction (LVD) is a condition characterized by the impaired ability of the left ventricle of the heart to pump blood efficiently during contraction. The left ventricle is one of the four chambers of the heart and is responsible for pumping oxygenated blood to the rest of the body.
LVD can be caused by various underlying conditions, such as coronary artery disease, cardiomyopathy, valvular heart disease, or hypertension. These conditions can lead to structural changes in the left ventricle, including remodeling, hypertrophy, and dilation, which ultimately impair its contractile function.
The severity of LVD is often assessed by measuring the ejection fraction (EF), which is the percentage of blood that is pumped out of the left ventricle during each contraction. A normal EF ranges from 55% to 70%, while an EF below 40% is indicative of LVD.
LVD can lead to various symptoms, such as shortness of breath, fatigue, fluid retention, and decreased exercise tolerance. It can also increase the risk of complications, such as heart failure, arrhythmias, and cardiac arrest. Treatment for LVD typically involves managing the underlying cause, along with medications to improve contractility, reduce fluid buildup, and control heart rate. In severe cases, devices such as implantable cardioverter-defibrillators (ICDs) or left ventricular assist devices (LVADs) may be required.
Hypertrophic cardiomyopathy (HCM) is a genetic disorder characterized by the thickening of the heart muscle, specifically the ventricles (the lower chambers of the heart that pump blood out to the body). This thickening can make it harder for the heart to pump blood effectively, which can lead to symptoms such as shortness of breath, chest pain, and fatigue. In some cases, HCM can also cause abnormal heart rhythms (arrhythmias) and may increase the risk of sudden cardiac death.
The thickening of the heart muscle in HCM is caused by an overgrowth of the cells that make up the heart muscle, known as cardiomyocytes. This overgrowth can be caused by mutations in any one of several genes that encode proteins involved in the structure and function of the heart muscle. These genetic mutations are usually inherited from a parent, but they can also occur spontaneously in an individual with no family history of the disorder.
HCM is typically diagnosed using echocardiography (a type of ultrasound that uses sound waves to create images of the heart) and other diagnostic tests such as electrocardiogram (ECG) and cardiac magnetic resonance imaging (MRI). Treatment for HCM may include medications to help manage symptoms, lifestyle modifications, and in some cases, surgical procedures or implantable devices to help prevent or treat arrhythmias.
Echocardiography is a medical procedure that uses sound waves to produce detailed images of the heart's structure, function, and motion. It is a non-invasive test that can help diagnose various heart conditions, such as valve problems, heart muscle damage, blood clots, and congenital heart defects.
During an echocardiogram, a transducer (a device that sends and receives sound waves) is placed on the chest or passed through the esophagus to obtain images of the heart. The sound waves produced by the transducer bounce off the heart structures and return to the transducer, which then converts them into electrical signals that are processed to create images of the heart.
There are several types of echocardiograms, including:
* Transthoracic echocardiography (TTE): This is the most common type of echocardiogram and involves placing the transducer on the chest.
* Transesophageal echocardiography (TEE): This type of echocardiogram involves passing a specialized transducer through the esophagus to obtain images of the heart from a closer proximity.
* Stress echocardiography: This type of echocardiogram is performed during exercise or medication-induced stress to assess how the heart functions under stress.
* Doppler echocardiography: This type of echocardiogram uses sound waves to measure blood flow and velocity in the heart and blood vessels.
Echocardiography is a valuable tool for diagnosing and managing various heart conditions, as it provides detailed information about the structure and function of the heart. It is generally safe, non-invasive, and painless, making it a popular choice for doctors and patients alike.
Chest pain is a discomfort or pain that you feel in the chest area. The pain can be sharp, dull, burning, crushing, heaviness, or tightness. It may be accompanied by other symptoms such as shortness of breath, sweating, nausea, dizziness, or pain that radiates to the arm, neck, jaw, or back.
Chest pain can have many possible causes, including heart-related conditions such as angina or a heart attack, lung conditions such as pneumonia or pleurisy, gastrointestinal problems such as acid reflux or gastritis, musculoskeletal issues such as costochondritis or muscle strain, and anxiety or panic attacks.
It is important to seek immediate medical attention if you experience chest pain that is severe, persistent, or accompanied by other concerning symptoms, as it may be a sign of a serious medical condition. A healthcare professional can evaluate your symptoms, perform tests, and provide appropriate treatment.
Coronary angiography is a medical procedure that uses X-ray imaging to visualize the coronary arteries, which supply blood to the heart muscle. During the procedure, a thin, flexible catheter is inserted into an artery in the arm or groin and threaded through the blood vessels to the heart. A contrast dye is then injected through the catheter, and X-ray images are taken as the dye flows through the coronary arteries. These images can help doctors diagnose and treat various heart conditions, such as blockages or narrowing of the arteries, that can lead to chest pain or heart attacks. It is also known as coronary arteriography or cardiac catheterization.
Atrioventricular (AV) block is a disorder of the electrical conduction system of the heart that causes a delay or interruption in the transmission of electrical signals from the atria (the upper chambers of the heart) to the ventricles (the lower chambers of the heart). This results in an abnormal heart rhythm, also known as an arrhythmia.
There are three degrees of AV block:
1. First-degree AV block: In this type of AV block, there is a delay in the conduction of electrical signals from the atria to the ventricles, but all signals are eventually conducted. This condition may not cause any symptoms and is often discovered during a routine electrocardiogram (ECG).
2. Second-degree AV block: In this type of AV block, some electrical signals from the atria are not conducted to the ventricles. There are two types of second-degree AV block: Mobitz type I and Mobitz type II. Mobitz type I is characterized by a progressive prolongation of the PR interval (the time between the electrical activation of the atria and ventricles) until a QRS complex (which represents the electrical activation of the ventricles) is dropped. Mobitz type II is characterized by a constant PR interval with occasional non-conducted P waves.
3. Third-degree AV block: In this type of AV block, no electrical signals are conducted from the atria to the ventricles. The atria and ventricles beat independently of each other, resulting in a slow heart rate (bradycardia) and an irregular rhythm. This condition can be life-threatening if not treated promptly.
The causes of AV block include aging, heart disease, medications, and certain medical conditions such as hypothyroidism and Lyme disease. Treatment depends on the severity of the condition and may include medication, a pacemaker, or surgery.
Long QT syndrome (LQTS) is a cardiac electrical disorder characterized by a prolonged QT interval on the electrocardiogram (ECG), which can potentially trigger rapid, chaotic heartbeats known as ventricular tachyarrhythmias, such as torsades de pointes. These arrhythmias can be life-threatening and lead to syncope (fainting) or sudden cardiac death. LQTS is often congenital but may also be acquired due to certain medications, medical conditions, or electrolyte imbalances. It's essential to identify and manage LQTS promptly to reduce the risk of severe complications.
Cardiovascular agents are a class of medications that are used to treat various conditions related to the cardiovascular system, which includes the heart and blood vessels. These agents can be further divided into several subcategories based on their specific mechanisms of action and therapeutic effects. Here are some examples:
1. Antiarrhythmics: These drugs are used to treat abnormal heart rhythms or arrhythmias. They work by stabilizing the electrical activity of the heart and preventing irregular impulses from spreading through the heart muscle.
2. Antihypertensives: These medications are used to lower high blood pressure, also known as hypertension. There are several classes of antihypertensive drugs, including diuretics, beta-blockers, calcium channel blockers, and angiotensin-converting enzyme (ACE) inhibitors.
3. Anticoagulants: These drugs are used to prevent blood clots from forming or growing larger. They work by interfering with the coagulation cascade, which is a series of chemical reactions that lead to the formation of a blood clot.
4. Antiplatelet agents: These medications are used to prevent platelets in the blood from sticking together and forming clots. They work by inhibiting the aggregation of platelets, which are small cells in the blood that help form clots.
5. Lipid-lowering agents: These drugs are used to lower cholesterol and other fats in the blood. They work by reducing the production or absorption of cholesterol in the body or increasing the removal of cholesterol from the bloodstream. Examples include statins, bile acid sequestrants, and PCSK9 inhibitors.
6. Vasodilators: These medications are used to widen blood vessels and improve blood flow. They work by relaxing the smooth muscle in the walls of blood vessels, causing them to dilate or widen. Examples include nitrates, calcium channel blockers, and ACE inhibitors.
7. Inotropes: These drugs are used to increase the force of heart contractions. They work by increasing the sensitivity of heart muscle cells to calcium ions, which are necessary for muscle contraction.
These are just a few examples of cardiovascular medications that are used to treat various conditions related to the heart and blood vessels. It is important to note that these medications can have side effects and should be taken under the guidance of a healthcare provider.
Left ventricular function refers to the ability of the left ventricle (the heart's lower-left chamber) to contract and relax, thereby filling with and ejecting blood. The left ventricle is responsible for pumping oxygenated blood to the rest of the body. Its function is evaluated by measuring several parameters, including:
1. Ejection fraction (EF): This is the percentage of blood that is pumped out of the left ventricle with each heartbeat. A normal ejection fraction ranges from 55% to 70%.
2. Stroke volume (SV): The amount of blood pumped by the left ventricle in one contraction. A typical SV is about 70 mL/beat.
3. Cardiac output (CO): The total volume of blood that the left ventricle pumps per minute, calculated as the product of stroke volume and heart rate. Normal CO ranges from 4 to 8 L/minute.
Assessment of left ventricular function is crucial in diagnosing and monitoring various cardiovascular conditions such as heart failure, coronary artery disease, valvular heart diseases, and cardiomyopathies.
Syncope is a medical term defined as a transient, temporary loss of consciousness and postural tone due to reduced blood flow to the brain. It's often caused by a drop in blood pressure, which can be brought on by various factors such as dehydration, emotional stress, prolonged standing, or certain medical conditions like heart diseases, arrhythmias, or neurological disorders.
During a syncope episode, an individual may experience warning signs such as lightheadedness, dizziness, blurred vision, or nausea before losing consciousness. These episodes usually last only a few minutes and are followed by a rapid, full recovery. However, if left untreated or undiagnosed, recurrent syncope can lead to severe injuries from falls or even life-threatening conditions related to the underlying cause.
Right ventricular dysfunction is a condition characterized by the impaired ability of the right ventricle (one of the two pumping chambers in the heart) to fill with blood during the diastolic phase or eject blood during the systolic phase. This results in reduced cardiac output from the right ventricle, which can lead to various complications such as fluid accumulation in the body, particularly in the abdomen and lower extremities, and ultimately congestive heart failure if left untreated.
Right ventricular dysfunction can be caused by various factors, including damage to the heart muscle due to a heart attack, high blood pressure in the lungs (pulmonary hypertension), chronic lung diseases, congenital heart defects, viral infections, and certain medications. Symptoms of right ventricular dysfunction may include shortness of breath, fatigue, swelling in the legs, ankles, or abdomen, and a decreased tolerance for physical activity.
Diagnosis of right ventricular dysfunction typically involves a combination of medical history, physical examination, imaging tests such as echocardiography, cardiac MRI, or CT scan, and other diagnostic procedures such as electrocardiogram (ECG) or cardiac catheterization. Treatment options depend on the underlying cause but may include medications to reduce fluid buildup, improve heart function, and manage symptoms, as well as lifestyle modifications such as reducing salt intake and increasing physical activity levels. In severe cases, more invasive treatments such as surgery or implantable devices like pacemakers or ventricular assist devices may be necessary.
The heart ventricles are the two lower chambers of the heart that receive blood from the atria and pump it to the lungs or the rest of the body. The right ventricle pumps deoxygenated blood to the lungs, while the left ventricle pumps oxygenated blood to the rest of the body. Both ventricles have thick, muscular walls to generate the pressure necessary to pump blood through the circulatory system.
Restrictive cardiomyopathy (RCM) is a type of heart muscle disorder characterized by impaired relaxation and filling of the lower chambers of the heart (the ventricles), leading to reduced pump function. This is caused by stiffening or rigidity of the heart muscle, often due to fibrosis or scarring. The stiffness prevents the ventricles from filling properly with blood during the diastolic phase, which can result in symptoms such as shortness of breath, fatigue, and fluid retention.
RCM is a less common form of cardiomyopathy compared to dilated or hypertrophic cardiomyopathies. It can be idiopathic (no known cause) or secondary to other conditions like amyloidosis, sarcoidosis, or storage diseases. Diagnosis typically involves a combination of medical history, physical examination, echocardiography, and sometimes cardiac MRI or biopsy. Treatment is focused on managing symptoms and addressing underlying causes when possible.
Cardiac catheterization is a medical procedure used to diagnose and treat cardiovascular conditions. In this procedure, a thin, flexible tube called a catheter is inserted into a blood vessel in the arm or leg and threaded up to the heart. The catheter can be used to perform various diagnostic tests, such as measuring the pressure inside the heart chambers and assessing the function of the heart valves.
Cardiac catheterization can also be used to treat certain cardiovascular conditions, such as narrowed or blocked arteries. In these cases, a balloon or stent may be inserted through the catheter to open up the blood vessel and improve blood flow. This procedure is known as angioplasty or percutaneous coronary intervention (PCI).
Cardiac catheterization is typically performed in a hospital cardiac catheterization laboratory by a team of healthcare professionals, including cardiologists, radiologists, and nurses. The procedure may be done under local anesthesia with sedation or general anesthesia, depending on the individual patient's needs and preferences.
Overall, cardiac catheterization is a valuable tool in the diagnosis and treatment of various heart conditions, and it can help improve symptoms, reduce complications, and prolong life for many patients.
Stroke volume is a term used in cardiovascular physiology and medicine. It refers to the amount of blood that is pumped out of the left ventricle of the heart during each contraction (systole). Specifically, it is the difference between the volume of blood in the left ventricle at the end of diastole (when the ventricle is filled with blood) and the volume at the end of systole (when the ventricle has contracted and ejected its contents into the aorta).
Stroke volume is an important measure of heart function, as it reflects the ability of the heart to pump blood effectively to the rest of the body. A low stroke volume may indicate that the heart is not pumping efficiently, while a high stroke volume may suggest that the heart is working too hard. Stroke volume can be affected by various factors, including heart disease, high blood pressure, and physical fitness level.
The formula for calculating stroke volume is:
Stroke Volume = End-Diastolic Volume - End-Systolic Volume
Where end-diastolic volume (EDV) is the volume of blood in the left ventricle at the end of diastole, and end-systolic volume (ESV) is the volume of blood in the left ventricle at the end of systole.