Anterior Wall Myocardial Infarction
Inferior Wall Myocardial Infarction
Ventricular Function, Left
Heart Rupture, Post-Infarction
Angioplasty, Balloon, Coronary
Ventricular Dysfunction, Left
Predictive Value of Tests
Coronary Care Units
Coronary Artery Bypass
Tomography, Emission-Computed, Single-Photon
Platelet Aggregation Inhibitors
Percutaneous Coronary Intervention
Coronary Artery Disease
Tomography, X-Ray Computed
Myocardial Reperfusion Injury
Usefulness of the index of microcirculatory resistance for invasively assessing myocardial viability immediately after primary angioplasty for anterior myocardial infarction. (1/56)(+info)
Dual left anterior descending artery distribution. (2/56)(+info)
Low adiponectin blood concentration predicts left ventricular remodeling after ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention. (3/56)BACKGROUND: Left ventricular remodeling (LVR), an increase in left ventricular end-diastolic volume index > or = 20%, is an adverse consequence of myocardial infarction. The aim of this study was to assess the association between LVR and adiponectin, which has been shown to protect against myocardial ischemia-reperfusion injury. METHODS: In 75 patients echocardiographic examination was performed one year after ST-segment elevation myocardial infarction, successfully treated with primary percutaneous coronary intervention (pPCI). Two groups of patients were analyzed: those with LVR (n = 15) and those without LVR (n = 60). RESULTS: The predictors of LVR were: anterior myocardial infarction, glucose at admission, baseline C-reactive protein, adiponectin, and echocardiographic parameters: left ventricular end-diastolic and end-systolic volume indices, ejection fraction < 40% and left ventricular wall motion score index (WMSI) at discharge. On multivariable regression analysis, lower adiponectin level (OR = 0.67, 95% CI 0.49-0.91, p < 0.05) and higher WMSI (OR = 20.14, 95% CI 2.62-154.82, p < 0.01) were the only independent negative predictors of LVR. The optimal cut-off for adiponectin for predicting LVR was < or = 4.7 mg/mL (sensitivity: 73%, specificity: 85%) and this level increased the risk of LVR 15-fold (95% CI 4.05-59.87, p = 0.0001). CONCLUSIONS: Baseline low blood adiponectin concentration, along with WMSI, can be considered as a predictor of the LVR in male patients one year after myocardial infarction and pPCI. (+info)
Dor procedure for dyskinetic anteroapical myocardial infarction fails to improve contractility in the border zone. (4/56)(+info)
Right ventricular involvement in anterior myocardial infarction: a translational approach. (5/56)(+info)
Retrograde approach to a totally occluded right coronary artery via a septal perforator artery: the tale of a long and winding wire. (6/56)Retrograde recannalization of chronic total occlusions has developed as a viable alternative to restore coronary patency. Techniques continue to evolve and complications described. We present a new complication related to equipment developed to improve outcomes via a retrograde approach. (+info)
Complete atrioventricular block complicating acute anterior myocardial infarction can be reversed with acute coronary angioplasty. (7/56)INTRODUCTION: A retrospective case series of acute anterior myocardial infarction (MI) patients complicated by complete atrioventricular block (AVB) treated with acute percutaneous transluminal coronary angioplasty (PTCA). CLINICAL PICTURE: Eight patients with anterior MI and complete AVB underwent acute PTCA between 2000 and 2005. Mean onset of complete AVB was 16.6 +/- 16.9 hours from chest pain onset. TREATMENT: All patients underwent successful PTCA to the left anterior descending artery. OUTCOME: Complete AVB resolved with PTCA in 88%; mean time of resolution was 89 +/- 144 minutes after revascularisation. One patient had permanent pacemaker implanted at Day 12 after developing an 8-second ventricular standstill during hospitalisation but not pacing-dependent on follow-up. The rhythm on discharge for the other surviving patients was normal sinus rhythm. CONCLUSION: This case series suggests that complete AVB complicating anterior MI is reversible with acute PTCA and survivors are not at increased risk of recurrent AVB. Nevertheless, this condition is associated with extensive myocardial damage and high mortality during the acute hospitalisation was not improved with correction of AVB with temporary pacing. (+info)
Coronary flow velocity pattern and recovery of regional left ventricular function: the relationship observed in patients with reperfused acute myocardial infarction. (8/56)Coronary flow velocity pattern (CFVP) recorded within 3 days of percutaneous coronary intervention (PCI) has been reported to be useful in predicting left ventricular (LV) function. The aim of this prospective study was to investigate, via transthoracic Doppler echocardiography, whether the relationship between CFVP and recovery of LV function persists. Our study group comprised 37 patients with 1st anterior-wall acute myocardial infarction who underwent successful PCI for lesions in the left anterior descending coronary artery (LAD). The CFVP in the LAD was recorded at 24-48 hours, 7 days, and 4 weeks after PCI. Myocardial contrast echocardiography was performed at 24-48 hours after PCI. The diastolic deceleration time (DDT) at each stage correlated significantly with the regional LV wall-motion score index at 6-month follow-up (r=-0.58 at 24-48 hr, -0.57 at day 7, and -0.50 at week 4; P <0.01 for all). The mean DDT increased over time. Optimal cutoff values for DDT to predict regional LV wall-motion score indices of <2.0 were 327 ms at 24-48 hours (sensitivity, 0.78; specificity, 0.64), 495 ms at day 7 (sensitivity, 0.75; specificity, 0.69), and 525 ms at week 4 (sensitivity, 0.83; specificity, 0.69). The DDT at 24-48 hours significantly correlated, better than the peak creatine kinase value, with reperfusion (r=0.68, P <0.01) as defined by myocardial contrast echocardiography. In conclusion, CFVP in the LAD can be used, within 4 weeks after PCI, to predict the recovery of regional LV function in patients with reperfused anterior-wall acute myocardial infarction. (+info)
1. The patient was diagnosed with an anterior wall myocardial infarction after experiencing chest pain and shortness of breath.
2. The anterior wall myocardial infarction was caused by a blockage in the left anterior descending coronary artery, which supplies blood to the front wall of the heart.
3. The patient underwent urgent angioplasty to open up the blocked artery and restore blood flow to the affected area, reducing the risk of further damage to the heart muscle.
Symptoms of Inferior Wall Myocardial Infarction:
* Chest pain or discomfort that may radiate to the arm, neck, jaw, or back
* Shortness of breath
* Lightheadedness or dizziness
Diagnosis of Inferior Wall Myocardial Infarction:
* Electrocardiogram (ECG) to detect abnormal heart rhythms and determine the location of the infarction
* Blood tests to check for cardiac enzymes, such as troponin, which are released when the heart muscle is damaged
* Echocardiogram or cardiac magnetic resonance imaging (MRI) to visualize the heart and detect any damage to the heart muscle
Treatment of Inferior Wall Myocardial Infarction:
* Medications to dissolve blood clots, reduce inflammation, and manage pain
* Angiography or angioplasty to open up the blocked coronary artery
* Cardiac rehabilitation to improve cardiovascular health and prevent future heart problems.
There are different types of myocardial infarctions, including:
1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.
Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.
Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.
Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.
Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.
The risk of post-infarction heart rupture is highest in individuals who have had a large heart attack, particularly if it involves the left ventricle, which is the main pumping chamber of the heart. Other risk factors include older age, diabetes, high blood pressure, and prior history of heart disease.
Symptoms of post-infarction heart rupture can include chest pain, shortness of breath, fatigue, and swelling of the legs. In some cases, there may be no symptoms at all, and the condition is diagnosed incidentally on a medical imaging test.
Post-infarction heart rupture is typically diagnosed using echocardiography, a non-invasive imaging test that uses sound waves to visualize the heart. Other diagnostic tests that may be used include electrocardiogram (ECG), chest X-ray, and cardiac magnetic resonance imaging (MRI).
Treatment of post-infarction heart rupture usually involves supportive care, such as oxygen therapy, pain management, and medication to manage symptoms. In some cases, surgery may be necessary to repair the damaged heart tissue or to insert a device to help the heart pump more effectively.
Overall, post-infarction heart rupture is a serious complication of heart attacks that can have significant morbidity and mortality. Prompt recognition and treatment are essential to improve outcomes for patients with this condition.
The term "infarction" is derived from the Latin words "in" meaning "into" and "farcire" meaning "to stuff", which refers to the idea that the tissue becomes "stuffed" with blood, leading to cell death and necrosis.
Infarction can be caused by a variety of factors, including atherosclerosis (the buildup of plaque in the blood vessels), embolism (a blood clot or other foreign material that blocks the flow of blood), and vasospasm (constriction of the blood vessels).
The symptoms of infarction vary depending on the location and severity of the blockage, but can include chest pain or discomfort, shortness of breath, numbness or weakness in the affected limbs, and confusion or difficulty speaking or understanding speech.
Diagnosis of infarction typically involves imaging tests such as electrocardiograms (ECGs), echocardiograms, or computerized tomography (CT) scans to confirm the presence of a blockage and assess the extent of the damage. Treatment options for infarction include medications to dissolve blood clots, surgery to restore blood flow, and other interventions to manage symptoms and prevent complications.
Prevention of infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, and obesity, as well as maintaining a healthy diet and exercise routine. Early detection and treatment of blockages can help reduce the risk of infarction and minimize the damage to affected tissues.
Cerebral infarction can result in a range of symptoms, including sudden weakness or numbness in the face, arm, or leg on one side of the body, difficulty speaking or understanding speech, sudden vision loss, dizziness, and confusion. Depending on the location and severity of the infarction, it can lead to long-term disability or even death.
There are several types of cerebral infarction, including:
1. Ischemic stroke: This is the most common type of cerebral infarction, accounting for around 87% of all cases. It occurs when a blood clot blocks the flow of blood to the brain, leading to cell death and tissue damage.
2. Hemorrhagic stroke: This type of cerebral infarction occurs when a blood vessel in the brain ruptures, leading to bleeding and cell death.
3. Lacunar infarction: This type of cerebral infarction affects the deep structures of the brain, particularly the basal ganglia, and is often caused by small blockages or stenosis (narrowing) in the blood vessels.
4. Territorial infarction: This type of cerebral infarction occurs when there is a complete blockage of a blood vessel that supplies a specific area of the brain, leading to cell death and tissue damage in that area.
Diagnosis of cerebral infarction typically involves a combination of physical examination, medical history, and imaging tests such as CT or MRI scans. Treatment options vary depending on the cause and location of the infarction, but may include medication to dissolve blood clots, surgery to remove blockages, or supportive care to manage symptoms and prevent complications.
During ventricular remodeling, the heart muscle becomes thicker and less flexible, leading to a decrease in the heart's ability to fill with blood and pump it out to the body. This can lead to shortness of breath, fatigue, and swelling in the legs and feet.
Ventricular remodeling is a natural response to injury, but it can also be exacerbated by factors such as high blood pressure, diabetes, and obesity. Treatment for ventricular remodeling typically involves medications and lifestyle changes, such as exercise and a healthy diet, to help manage symptoms and slow the progression of the condition. In some cases, surgery or other procedures may be necessary to repair or replace damaged heart tissue.
The process of ventricular remodeling is complex and involves multiple cellular and molecular mechanisms. It is thought to be driven by a variety of factors, including changes in gene expression, inflammation, and the activity of various signaling pathways.
Overall, ventricular remodeling is an important condition that can have significant consequences for patients with heart disease. Understanding its causes and mechanisms is crucial for developing effective treatments and improving outcomes for those affected by this condition.
Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.
The symptoms of coronary disease can vary depending on the severity of the condition, but may include:
* Chest pain or discomfort (angina)
* Shortness of breath
* Swelling of the legs and feet
* Pain in the arms and back
Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.
Preventative measures for coronary disease include:
* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.
There are several potential causes of LVD, including:
1. Coronary artery disease: The buildup of plaque in the coronary arteries can lead to a heart attack, which can damage the left ventricle and impair its ability to function properly.
2. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, it can lead to LVD.
3. Cardiomyopathy: This is a condition where the heart muscle becomes weakened or enlarged, leading to impaired function of the left ventricle.
4. Heart valve disease: Problems with the heart valves can disrupt the normal flow of blood and cause LVD.
5. Hypertension: High blood pressure can cause damage to the heart muscle and lead to LVD.
6. Genetic factors: Some people may be born with genetic mutations that predispose them to developing LVD.
7. Viral infections: Certain viral infections, such as myocarditis, can inflame and damage the heart muscle, leading to LVD.
8. Alcohol or drug abuse: Substance abuse can damage the heart muscle and lead to LVD.
9. Nutritional deficiencies: A diet lacking essential nutrients can lead to damage to the heart muscle and increase the risk of LVD.
Diagnosis of LVD typically involves a physical exam, medical history, and results of diagnostic tests such as electrocardiograms (ECGs), echocardiograms, and stress tests. Treatment options for LVD depend on the underlying cause, but may include medications to improve cardiac function, lifestyle changes, and in severe cases, surgery or other procedures.
Preventing LVD involves taking steps to maintain a healthy heart and reducing risk factors such as high blood pressure, smoking, and obesity. This can be achieved through a balanced diet, regular exercise, stress management, and avoiding substance abuse. Early detection and treatment of underlying conditions that increase the risk of LVD can also help prevent the condition from developing.
Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.
There are several types of myocardial ischemia, including:
1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.
Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.
Symptoms of cystocele may include:
* A bulge in the vagina that may be felt through the skin
* Pain or discomfort during sexual activity
* Difficulty starting a stream of urine
* Frequent urination
* Increased urgency to urinate
* Leaking of urine
Diagnosis of cystocele is typically made through a physical exam and may also involve imaging tests such as ultrasound or MRI. Treatment for cystocele depends on the severity of the condition and may include:
* Kegel exercises to strengthen the muscles that support the bladder
* A pessary, which is a device inserted into the vagina to support the bladder
* Surgery to repair or remove the damaged tissue
It's important for individuals experiencing symptoms of cystocele to consult with a healthcare provider for proper diagnosis and treatment.
Angina pectoris is a medical condition that is characterized by recurring chest pain or discomfort due to reduced blood flow and oxygen supply to the heart muscle, specifically the myocardium. It is also known as stable angina or effort angina. The symptoms of angina pectoris typically occur during physical activity or emotional stress and are relieved by rest.
The term "angina" comes from the Latin word for "strangulation," which refers to the feeling of tightness or constriction in the chest that is associated with the condition. Angina pectoris can be caused by atherosclerosis, or the buildup of plaque in the coronary arteries, which supply blood to the heart muscle. This buildup can lead to the formation of atherosclerotic plaques that can narrow the coronary arteries and reduce blood flow to the heart muscle, causing chest pain.
There are several types of angina pectoris, including:
1. Stable angina: This is the most common type of angina and is characterized by predictable and reproducible symptoms that occur during specific situations or activities, such as exercise or emotional stress.
2. Unstable angina: This type of angina is characterized by unpredictable and changing symptoms that can occur at rest or with minimal exertion. It is often a sign of a more severe underlying condition, such as a heart attack.
3. Variant angina: This type of angina occurs during physical activity, but the symptoms are not relieved by rest.
4. Prinzmetal's angina: This is a rare type of angina that occurs at rest and is characterized by a feeling of tightness or constriction in the chest.
The diagnosis of angina pectoris is typically made based on a combination of physical examination, medical history, and diagnostic tests such as electrocardiogram (ECG), stress test, and imaging studies. Treatment for angina pectoris usually involves lifestyle modifications, such as regular exercise, a healthy diet, and stress management, as well as medications to relieve symptoms and reduce the risk of complications. In some cases, surgery or other procedures may be necessary to treat the underlying condition causing the angina.
Word origin: Greek "anginos" meaning "pain in the neck".
Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.
In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.
Coronary Thrombosis can cause a range of symptoms including chest pain, shortness of breath, lightheadedness and fatigue. The severity of the symptoms depends on the location and size of the clot. In some cases, the condition may be asymptomatic and diagnosed incidentally during a medical examination or imaging test.
Diagnosis of Coronary Thrombosis is typically made using electrocardiogram (ECG), blood tests and imaging studies such as angiography or echocardiography. Treatment options include medications to dissolve the clot, surgery to open or bypass the blocked artery or other interventional procedures such as angioplasty or stenting.
Prevention of Coronary Thrombosis includes managing risk factors such as high blood pressure, high cholesterol levels, smoking and diabetes through lifestyle changes and medications. Early detection and treatment can help reduce the risk of complications and improve outcomes for patients with this condition.
The buildup of plaque in the coronary arteries is often caused by high levels of low-density lipoprotein (LDL) cholesterol, smoking, high blood pressure, diabetes, and a family history of heart disease. The plaque can also rupture, causing a blood clot to form, which can completely block the flow of blood to the heart muscle, leading to a heart attack.
CAD is the most common type of heart disease and is often asymptomatic until a serious event occurs. Risk factors for CAD include:
* Age (men over 45 and women over 55)
* Gender (men are at greater risk than women, but women are more likely to die from CAD)
* Family history of heart disease
* High blood pressure
* High cholesterol
* Lack of exercise
Diagnosis of CAD typically involves a physical exam, medical history, and results of diagnostic tests such as:
* Electrocardiogram (ECG or EKG)
* Stress test
* Coronary angiography
Treatment for CAD may include lifestyle changes such as a healthy diet, regular exercise, stress management, and quitting smoking. Medications such as beta blockers, ACE inhibitors, and statins may also be prescribed to manage symptoms and slow the progression of the disease. In severe cases, surgical intervention such as coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) may be necessary.
Prevention of CAD includes managing risk factors such as high blood pressure, high cholesterol, and diabetes, quitting smoking, maintaining a healthy weight, and getting regular exercise. Early detection and treatment of CAD can help to reduce the risk of complications and improve quality of life for those affected by the disease.
Signs and symptoms of cardiogenic shock may include:
* Shortness of breath
* Chest pain or discomfort
* Confusion or altered mental status
* Cool, clammy skin
* Weak or absent pulse in the arms and legs
* Rapid or irregular heartbeat
* Low blood pressure
Treatment of cardiogenic shock typically involves supportive care to help the heart pump more effectively, as well as medications to help improve blood flow and reduce inflammation. In some cases, a procedure called extracorporeal membrane oxygenation (ECMO) may be used to take over the work of the heart and lungs.
Cardiogenic shock can be caused by a variety of factors, including:
* Heart attack or myocardial infarction
* Heart failure or ventricular dysfunction
* Cardiac tamponade or fluid accumulation in the space around the heart
* Myocarditis or inflammation of the heart muscle
* Coronary artery disease or blockages in the blood vessels that supply the heart
* Other conditions that can cause damage to the heart, such as aortic dissection or endocarditis.
Treatment options for uterine prolapse include lifestyle changes such as exercise, weight loss, and pelvic floor exercises, as well as surgical procedures such as hysterectomy or vaginal repair. The choice of treatment depends on the severity of the condition and the individual's overall health status.
It is important to seek medical advice if symptoms persist or worsen over time, as uterine prolapse can lead to complications such as urinary incontinence, kidney damage, and bowel problems if left untreated. Early diagnosis and treatment can help prevent these complications and improve quality of life for individuals affected by the condition.
MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.
The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.
The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.
The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.
Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.
In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.
Examples of acute diseases include:
1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.
Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.
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Ischemia of the heart - what forms can manifest
- ST segment elevation of the ECG is often used in determining the treatment protocol (see also ST Elevation Myocardial Infarction ). (nih.gov)
- ST segment elevation in the ECG is often used in determining the treatment protocol (see also NON-ST ELEVATION MYOCARDIAL INFARCTION ). (nih.gov)
- Fothergill RT, Watson LR, Virdi GK, Moore FP, Whitbread M. Survival of resuscitated cardiac arrest patients with st-elevation myocardial infarction (STEMI) conveyed directly to a heart attack centre by ambulance clinicians. (smw.ch)
- ESC guidelines for the management of acute myocardial infarction in patients presenting with st-segment elevation. (smw.ch)
- 2013 ACCF/AHA guideline for the management of st-elevation myocardial infarction: A report of the american college of cardiology foundation/american heart association task force on practice guidelines. (smw.ch)
- 1. Circulating Endothelial Cells and Endothelial Function Predict Major Adverse Cardiac Events and Early Adverse Left Ventricular Remodeling in Patients With ST-Segment Elevation Myocardial Infarction. (nih.gov)
- 2. Prognosis-based definition of left ventricular remodeling after ST-elevation myocardial infarction. (nih.gov)
- 3. Combined assessment of left ventricular end-diastolic pressure and ejection fraction by left ventriculography predicts long-term outcomes of patients with ST-segment elevation myocardial infarction. (nih.gov)
- 5. Adverse diastolic remodeling after reperfused ST-elevation myocardial infarction: An important prognostic indicator. (nih.gov)
- 7. Prognostic value of left ventricular global function index in patients after ST-segment elevation myocardial infarction. (nih.gov)
- 9. Relation of plasma brain natriuretic peptide levels on admission for ST-elevation myocardial infarction to left ventricular end-diastolic volume six months later measured by both echocardiography and cardiac magnetic resonance. (nih.gov)
- 10. Plasma angiopoietin-1 level, left ventricular ejection fraction, and multivessel disease predict development of 1-year major adverse cardiovascular events in patients with acute ST elevation myocardial infarction - a pilot study. (nih.gov)
- 11. Sustained endothelial dysfunction in the infarct-related coronary artery is associated with left ventricular adverse remodeling in survivors of ST-segment elevation myocardial infarction. (nih.gov)
- 14. Left ventricular global function index assessed by cardiovascular magnetic resonance for the prediction of cardiovascular events in ST-elevation myocardial infarction. (nih.gov)
- 15. Intracoronary administration of bone marrow-derived progenitor cells improves left ventricular function in patients at risk for adverse remodeling after acute ST-segment elevation myocardial infarction: results of the Reinfusion of Enriched Progenitor cells And Infarct Remodeling in Acute Myocardial Infarction study (REPAIR-AMI) cardiac magnetic resonance imaging substudy. (nih.gov)
- Cases with Inferior ST elevation Myocardial Infarction. (scirp.org)
- Andersen, H.R., Nielsen, D. and Falk, E. (1989) Right Ventricular Infarction: Diagnostic Value of ST Elevation in Lead III Exceeding That of Lead II during Inferior/Posterior Infarction and Comparison with Right-Chest Leads V3R to V7R. (scirp.org)
- 2000) Usefulness of ST Elevation II/III Ratio and ST Deviation in Lead I for Identifying the Culprit Artery in Inferior Wall Acute Myocardial Infarction. (scirp.org)
- 2010) ST-Segment Depression in aVR as a Predictor of Culprit Artery and Infarct size in Acute Inferior Wall ST-Segment Elevation Myocardial Infarction. (scirp.org)
- 2009) Predicting the Culprit Artery in Acute ST-Elevation Myocardial Infarction and Introducing a New Algorithm to Predict Infarct-Related Artery in Inferior ST-Elevation Myocardial Infarction: Correlation with Coronary Anatomy in the HAAMU Trial. (scirp.org)
- This was initially unrecognised by the emergency department as unstable coronary syndrome and she subsequently progressed to an anterior non-ST elevation MI (NSTEMI). (bmj.com)
- The diagnosis is atrial tachycardia , ST elevation myocardial infarction (STEMI) of the anterior wall, QRS (electrical) alternans, and T-wave alternans. (medscape.com)
- ST segment elevation is seen in leads V3-V5 (↓), consistent with an acute anterior wall STEMI. (medscape.com)
- Electrocardiographic ST-segment elevation in lead aVR was previously described in association with left main, left anterior descending, and triple-vessel coronary artery disease as well as Takotsubo cardiomyopathy. (radcliffecardiology.com)
- is large enough, it can produce ST elevation in the posterior leads (not performed in this case), and ST depression in the anterior leads, especially V1, V2, and V3. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- Patients with inferior ST elevation myocardial infarction (STEMI), associated with right ventricular infarction, are thought to be at higher risk of developing hypotension when administered nitroglycerin (NTG). (xn--22c0bihcbb7dg4lnac3am9zla.com)
- However, current basic life support (BLS) protocols do not differentiate location of STEM … ST elevation, developing Q waves and T wave inversion may all be present depending on the timing of the ECG relative to the onset of myocardial infarction. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- The ST depression in V2 suggests posterior wall injury, and would normally be seen in V1 as well, unless something else is causing ST elevation in V1 at the same time. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- IMSEAR at SEARO: Multivessel Percutaneous Coronary Intervention in Patients with Acute ST-segment Elevation Myocardial Infarction in Same Sitting. (who.int)
- Conclusion: In the current prospective non randomized study, we found that the multivessel primary PCI for ST elevation myocardial infarction with non-culprit vessel are suitable for PCI at the same sitting with better in-hospital and 1 yr survival outcome. (who.int)
- Nomograms referenced by cardiac magnetic resonance in the prediction of cardiac injuries in patients with ST-elevation myocardial infarction. (amedeo.com)
- Reply to Machine learning-based prediction of infarct size in patients with ST-segment elevation myocardial infarction: Misinterpretation. (amedeo.com)
- Disparities in the management of non-ST-segment elevation myocardial infarction in the United States. (amedeo.com)
- Speckle-tracking echocardiography has emerged as a unique technique for accurately evaluating myocardial function by analyzing the motion of speckles identified. (who.int)
- Dobutamine stress echocardiography was performed 4 days post-infarction accompanied with automated functional imaging analysis of left ventricle during rest and then during low dose stress. (who.int)
- Her echocardiography showed anterior wall hypokinesia with moderate left ventricular dysfunction. (heartviews.org)
- 6. Extent of RV dysfunction and myocardial infarction assessed by CMR are independent outcome predictors early after STEMI treated with primary angioplasty. (nih.gov)
- The aim of the current study was to evaluate stress speckle tracking to detect myocardial viability in comparison to cardiac MRI in post-STEMI patients. (who.int)
- Strain rate obtained from speckle tracking during stress is a novel method of detecting myocardial viability after STEMI. (who.int)
- 2002) Impact of Normalized Myocardial Perfusion after Successful Angioplasty in Acute Myocardial Infarction. (scirp.org)
- Echocardiographic findings in cardiogenic shock due to acute myocardial infarction versus heart failure. (amedeo.com)
- Inferior, posterior and lateral wall myocardial infarction Inferior, posterior and lateral wall myocardial infarction. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- This prospective study included a total of 74 revascularization using M4S probe in left lateral myocardial infarction patients diagnosed with ST position. (who.int)
- These conditions are (1) spinal cord injury, (2) diabetes, (3) acute myocardial infarction (AMI), and (4) macular degeneration (namely Stargardt macular dystrophy and age-related macular degeneration). (nature.com)
- The knowledge of the incidence of LVT may therefore be of importance to guide antiplatelet and antithrombotic therapy after acute myocardial infarction (AMI). (smw.ch)
- Jugdutt BI, Sivaram CA. Prospective two-dimensional echocardiographic evaluation of left ventricular thrombus and embolism after acute myocardial infarction. (smw.ch)
- Left ventricular thrombus formation after acute myocardial infarction as assessed by cardiovascular magnetic resonance imaging. (smw.ch)
- Left ventricular mural thrombi complicating acute myocardial infarction. (smw.ch)
- 13. Effect of intensive vs standard statin therapy on endothelial progenitor cells and left ventricular function in patients with acute myocardial infarction: Statins for regeneration after acute myocardial infarction and PCI (STRAP) trial. (nih.gov)
- Sclarovsky, S. (1999) Electrocardiography of Acute Myocardial Ischaemic Syndromes. (scirp.org)
- Zimetbaum, P.J. and Josephson, M.E. (2003) Use of the Electrocardiogram in Acute Myocardial Infarction. (scirp.org)
- The death certificate listed "acute myocardial infarction" due to "atherosclerotic coronary artery disease" as the immediate cause of death. (cdc.gov)
- The autopsy listed "coronary atherosclerosis" followed by "stenosis, thrombosis, chronic myocardial infarct, subacute myocardial infarcts, acute myocardial infarct, and acute ischemic change" as the cause(s) of death. (cdc.gov)
- Pericardial Effusion (PE) is a complication after acute myocardial infarction (AMI), the objectives of this study was to determine the frequency and severity of PE after AMI and its association with other AMI complications. (innspub.net)
- Pericardial effusion in acute myocardial infarction: frequency and in-hospital course. (innspub.net)
- Pericardial Effusion Early in Acute Myocardial Infarction. (innspub.net)
- 1985. Review Plaque fissuring-the cause of acute myocardial infarction, sudden ischaemic death, and crescendo angina. (innspub.net)
- 1976. Pathology of acute myocardial infarction with particular reference to occlusive coronary thrombi. (innspub.net)
- Pericardial Effusion as a Consequence of Acute Myocardial Infarction. (innspub.net)
- Myocardial infarction (MI) or acute myocardial infarction (AMI) is the death of heart muscle from the sudden blockage of a coronary artery by a blood clot. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- Myocardial infarction 0 Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack 0 Typical symptoms of … Critical Cases in Electrocardiography. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- RESULTS: We found 72 cases of acute myocardial rupture with a mortality rate of 98.6% and 24 cases of sub-acute myocardial rupture with 41.6% of deaths. (bjcvs.org)
- YOSHIDA, K. - Ventricular free wall rupture following acute myocardial infarction: a two dimensional echocar-diographic assessment. (bjcvs.org)
Associated with acute1
- Acute inferior MI Leads II, III and aVF reflect electrocardiogram changes associated with acute infarction of the inferior aspect of the heart. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- On recording the right-sided ECG for those patients, there was ST … Electrocardiography in suspected myocardial infarction has the main purpose of detecting ischemia or acute coronary injury in emergency department populations coming for symptoms of myocardial infarction (MI). (xn--22c0bihcbb7dg4lnac3am9zla.com)
- Objectives: The aim of the study was to assess the role of ST segment depression in the limb leads aVR and aVL for the diagnosis of acute posterior wall infarction and the identification of infarct related artery (IRA) in patients with acute inferior wall MI. (scirp.org)
- Further work has shown that CMR can recently emerged as a quantitative ultrasound technique differentiate between the densely bright infarct core and for accurately evaluating myocardial function by the adjacent peri-infarct zone, which appears with lower analyzing the motion of speckles identified on routine signal intensity because of the admixture of infarct and 2-dimensional sonograms (2, 3, 4). (who.int)
- From these patients 1.05% had cardiac rupture as an ischaemic complication of the myocardium infarction. (bjcvs.org)
- MYOCARDIAL INFARCTION in which the inferior wall of the heart is involved. (nih.gov)
- ST segment depression in limb leads aVR and aVL with avR ≥ aVL helps to diagnose left circumflex artery as a culprit IRA in an acute inferior wall MI. (scirp.org)
- ventricular MI (RVMI) is typically a conse-quent of large inferior wall MI and is pre- account for 40% to 55% of cases of MI. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- Right Ventricular AMIs Right Ventricular Infarcts (RVI) are most often due to an occlusion of the RCA and almost always occur in conjunction with an inferior wall MI (Kinch & Ryan 1994). (xn--22c0bihcbb7dg4lnac3am9zla.com)
- Up to 40% of inferior wall Myocardial infarctions have associated right ventricular involvement. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- An inferior myocardial infarction is a problem with the heart where cells along the inferior wall of the heart die in response to oxygen deprivation. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- Inferior wall MI (IWMI) patients remain quite common and. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- 1. To compare ivabradine with metoprolol in acute inferior wall MI in terms of feasibility, tolerability, and efficacy. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- Heart attack or myocardial infarction (MI) is broadly of 2 types: anterior wall and inferior wall, depending on the wall of heart involved. (stackexchange.com)
- Those showing reciprocal changes had higher (65% vs. 15.5%) incidence of complications such as dysrhythmias, conduction defects, hypotension, left ventricular failure which was more conspicuous in inferior infarction. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- Asinger RW, Mikell FL, Elsperger J, Hodges M. Incidence of left-ventricular thrombosis after acute transmural myocardial infarction. (smw.ch)
- Furthermore, a clear inverse relationship was found between the segmental strain and the transmural extent of infarction in each segment. (who.int)
- Meanwhile it provided 81.82% sensitivity and 82.6% specificity to detect transmural from non-transmural infarction at a cut-off value of -10.15. (who.int)
- Twelve pts who were treated with streptokinase (SK) within 6 hours of MI were given L 9 g/day IV for 5 days followed by 3 g/day orally for 3 months (group A). Eighteen pts treated with SK received no LC (group B). Wall motion indices (WMI) and LV diastolic volume indices (DVI) were echocardiographically determined at 5th and 10th days, and 1st and 3rd months. (archivestsc.com)
- The aim of this study was to investigate the effect of sacubitril/ valsartan (Sal/Val) on left ventricular (LV) remodeling in patients with LV systolic dysfunction following acute anterior wall myocardial infarction (AAMI). (bvsalud.org)
- The current status of stem cell therapies for patients with myocardial infarction is discussed from a bioengineering and biomaterial perspective in this review. (nature.com)
- We describe (a) the current status of clinical trials of human pluripotent stem cells (hPSCs) compared with clinical trials of human adult or fetal stem cells, (b) the gap between fundamental research and application of human stem cells, (c) the use of biomaterials in clinical and pre-clinical studies of stem cells, and finally (d) trends in bioengineering to promote stem cell therapies for patients with myocardial infarction. (nature.com)
- Here, we have described the current status of stem cell therapies using hPSCs for patients with myocardial infarction (MI), focusing on the bioengineering aspects of these therapies. (nature.com)
- METHODS: In 177 patients with large, mainly anterior AMI, standard cardiac magnetic resonance imaging (CMR) including cine and late gadolinium enhancement (LGE) imaging was performed shortly after AMI as per protocol. (smw.ch)
- Background: Aim of the study was to evaluate the primary procedural success of Multivessel Percutaneous coronary intervention in patients with acute ST-segment elevated myocardial infarction at the same sitting. (who.int)
- We examined the effect of l-carnitine (LC) on left ventricular (LV) function in patients (pts) with a first acute anterior myocardial infarction (AMI) treated with trombolytic agents. (archivestsc.com)
- Effects of sacubitril/valsartan on ventricular remodeling in patents with left ventricular systolic dysfunction following acute anterior wall myocardial infarction. (bvsalud.org)
- 354). Dr. Stanley S. Josef, of Central Arkansas Cardiovascular Institute (CACI), reported that Plaintiff had a history of angina, status post PTCA (percutaneous transluminal coronary angioplasty), and stenting of the LAD (left anterior descending) in 2003, and the risk factors included hypertension and hyperlipidemia.2 He stated that plaintiff also suffered from paroxysmal atrial fibrillation3 and was on Coumadin and Rythmol therapy. (justia.com)
- Association of anxiety or depression with risk of recurrent cardiovascular events and death after myocardial infarction: A nationwide registry study. (amedeo.com)
- Cardiovascular Diseases: Increased risk of myocardial infarction, sudden cardiac death and stroke has been reported in association with use of GnRH analogs in men. (nih.gov)
- A myocardial infarction that does not produce elevations in the ST segments of the ELECTROCARDIOGRAM. (nih.gov)
- 2008) Value of the 12-Lead Electrocardiogram to Define the Level of Obstruction in Acute Anterior Wall Myocardial Infarction: Correlation to Coronary Angiography and Clinical Outcome in the DANAMI-2 Trial. (scirp.org)
- inferior myocardial infarction: infarction in which the inferior or diaphragmatic wall of the heart is involved, producing indicative changes in leads II, III, and aVF in the electrocardiogram. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- Pulmonary: pulmonary oedema, pulmonary infarction, and haemoptysis. (bmj.com)
- As shown in the examples below, myocardial infarction diagnosis in right bundle branch block is not very different from normal MI diagnosis. (xn--22c0bihcbb7dg4lnac3am9zla.com)
- As emergency angioplasty and stent placement of his left anterior descending coronary artery was started, the FF had an arrhythmia and cardiac arrest. (cdc.gov)
Conventional risk factors1
- A 32 years old female without any conventional risk factors except obesity presented with acute anterior wall myocardial infarction (MI). (heartviews.org)
- Wellens' syndrome refers to specific ECG abnormalities in the precordial T-wave segment, which are associated with critical stenosis of the proximal left anterior descending (LAD) coronary artery culminating in an acute anterior wall myocardial infarction (MI) if the patient is not urgently revascularised. (bmj.com)
- Anterior wall myocardial infarction is often caused by occlusion of the left anterior descending coronary artery. (nih.gov)
- Myocardial infarction in the absence of obstructive coronary artery disease. (nih.gov)
- The death certificate (completed by the coroner) listed "cardiac arrest with electromechanical dissociation" due to "acute anterior wall myocardial infarction" due to "coronary artery disease" (CAD) as the cause of death. (cdc.gov)
- Angiography showed tight stenosis of the proximal left anterior descending (LAD) and borderline lesion in left circumflex coronary artery (LCX). (heartviews.org)
- 1. Anterior descending coronary artery flow. (nih.gov)
- Pericardial effusion in the course of myocardial infarction: incidence, natural history, and clinical relevance. (innspub.net)
- Myocardial blood flow (MBF) is the critical determinant of cardiac function. (snmjournals.org)
- Moreover, it carries a promising role in post-myocardial infarction risk stratification with a reasonable prediction of reversible cardiac-related hospital re-admission. (who.int)
- Polygenic risk scores point toward potential genetic mechanisms of type 2 myocardial infarction in people with HIV. (amedeo.com)
- Symptoms develop from lesions in the CORPUS CALLOSUM or medial frontal cortex, stroke, infarction, and neurodegenerative diseases (e.g. (nih.gov)
- Investigating strain rate obtained with stress speckle tracking after revascularization predicted the extent of myocardial scar, determined by contrast-enhanced magnetic resonance imaging. (who.int)