Left ventricular noncompaction (LVNC) is a heart muscle disorder characterized by excessive trabeculations and deep recesses in the left ventricle. It is diagnosed using echocardiography or cardiac MRI based on specific criteria. Symptoms vary and include heart failure, arrhythmias, and thromboembolic events like stroke. The cause involves abnormal heart muscle development during fetal life. Genetic factors are involved in some cases. Treatment focuses on managing symptoms and complications. Prognosis depends on the severity of symptoms and complications.
ARVD (Arrythmogenic right ventricular cardiomyopathy) - updated task force cr...Imran Ahmed
This document discusses arrythmogenic right ventricular cardiomyopathy (ARVC). It begins by explaining the genetics of ARVC, noting that mutations can be either dominant or recessive. It then describes the natural history, clinical presentation, diagnosis, and criteria used to diagnose ARVC based on the revised Task Force Criteria. This includes major and minor criteria in categories such as imaging, electrocardiography findings, biopsy results, and family history. The document concludes by discussing management strategies for ARVC including ICD therapy, antiarrhythmic drugs, ablation, heart failure treatment, and transplantation.
Left ventricular non compaction is rare congenital cardiomyopathy with gaining interest due to advancement in imaging modalities for diagnosis and assessment of undulating phenotype
LVNC is a rare genetic cardiomyopathy characterized by a spongy appearance of the myocardium due to incomplete compaction of the embryonic myocardium. It can present with heart failure, arrhythmias, or thromboembolism. Echocardiography and cardiac MRI are used to diagnose LVNC based on identifying a two-layered myocardium. Management involves treating heart failure and preventing thromboembolism with anticoagulation in high-risk patients. While the cause of LVNC is thought to be due to an arrest in normal myocardial compaction during embryonic development, the pathophysiology is not fully understood.
ARVC is a heritable heart muscle disorder that predominantly affects the right ventricle. It is caused by genetic defects in cardiac desmosomes, which are important for cell-to-cell adhesion. This leads to progressive loss of right ventricular myocardium and replacement by fibrofatty tissue. ARVC can cause dangerous ventricular arrhythmias and is a leading cause of sudden cardiac death in young people. Diagnosis involves imaging tests and electrocardiography to detect right ventricular structural abnormalities and arrhythmias.
Vein of Galen malformations are rare congenital vascular anomalies that develop between weeks 6-11 of fetal development. They present as an aneurysmally dilated midline deep venous structure fed by abnormal arteriovenous communications. In neonates, they can cause high-output cardiac failure. Older children and adults may present with hydrocephalus, neurological deficits, or seizures. Diagnosis is made through imaging like CT, MRI, and angiography. Treatment involves endovascular embolization of the arteriovenous shunts to reduce cardiac overload and improve neurological outcomes. With advances in interventional neuroradiology, vein of Galen malformations can now be successfully treated with low complication rates.
This document summarizes the history and criteria for diagnosing left ventricular noncompaction (LVNC) via echocardiography. It describes the original 1990 criteria using X/Y ratios between trabeculations and recesses. Second 1999 criteria used a noncompacted to compacted myocardium ratio over 2.3. Later studies refined understanding. The latest 2014 criteria require all 4 criteria be met regarding prominent trabeculations, synchronous movement, two-layer structure, and perfusion of intertrabecular spaces. Echocardiography looks for a noncompaction to compaction ratio over 2 and more than 3 recesses communicating to the left ventricle in diastole. MRI diagnoses if noncompaction mass is
CARDIOPULMONARY BYPASS AND PRETERM NEONATES Adhi Arya
This document discusses the surgical options and risks for a 3 day old premature infant born with transposition of the great arteries, coarctation of the aorta, and hypoplastic right ventricle. It notes the risks of surgery in preterm infants include complications from immature organ systems, effects of cardiopulmonary bypass like coagulation abnormalities, and the underlying heart defects. The document advocates for strategies like limiting bypass and cross-clamp times, minimizing hemodilution, steroid administration, and close postoperative management to optimize outcomes for these high-risk patients.
The patient presented with altered sensorium, decreased movement in their right side, and deviation of their mouth to the left. Imaging showed a non-hemorrhagic infarct in the left fronto-parietal region consistent with a stroke. An echocardiogram found left ventricular non-compaction (LVNC), a mobile clot attached to the left ventricle, and normal systolic function. The final diagnosis was LVNC, stroke, hyperhomocysteinemia, and hyperlipidemia. LVNC is a rare heart condition where the left ventricle fails to compact during development, leaving prominent trabeculations. It can cause heart failure, arrhythmias, and thromboemb
ARVD (Arrythmogenic right ventricular cardiomyopathy) - updated task force cr...Imran Ahmed
This document discusses arrythmogenic right ventricular cardiomyopathy (ARVC). It begins by explaining the genetics of ARVC, noting that mutations can be either dominant or recessive. It then describes the natural history, clinical presentation, diagnosis, and criteria used to diagnose ARVC based on the revised Task Force Criteria. This includes major and minor criteria in categories such as imaging, electrocardiography findings, biopsy results, and family history. The document concludes by discussing management strategies for ARVC including ICD therapy, antiarrhythmic drugs, ablation, heart failure treatment, and transplantation.
Left ventricular non compaction is rare congenital cardiomyopathy with gaining interest due to advancement in imaging modalities for diagnosis and assessment of undulating phenotype
LVNC is a rare genetic cardiomyopathy characterized by a spongy appearance of the myocardium due to incomplete compaction of the embryonic myocardium. It can present with heart failure, arrhythmias, or thromboembolism. Echocardiography and cardiac MRI are used to diagnose LVNC based on identifying a two-layered myocardium. Management involves treating heart failure and preventing thromboembolism with anticoagulation in high-risk patients. While the cause of LVNC is thought to be due to an arrest in normal myocardial compaction during embryonic development, the pathophysiology is not fully understood.
ARVC is a heritable heart muscle disorder that predominantly affects the right ventricle. It is caused by genetic defects in cardiac desmosomes, which are important for cell-to-cell adhesion. This leads to progressive loss of right ventricular myocardium and replacement by fibrofatty tissue. ARVC can cause dangerous ventricular arrhythmias and is a leading cause of sudden cardiac death in young people. Diagnosis involves imaging tests and electrocardiography to detect right ventricular structural abnormalities and arrhythmias.
Vein of Galen malformations are rare congenital vascular anomalies that develop between weeks 6-11 of fetal development. They present as an aneurysmally dilated midline deep venous structure fed by abnormal arteriovenous communications. In neonates, they can cause high-output cardiac failure. Older children and adults may present with hydrocephalus, neurological deficits, or seizures. Diagnosis is made through imaging like CT, MRI, and angiography. Treatment involves endovascular embolization of the arteriovenous shunts to reduce cardiac overload and improve neurological outcomes. With advances in interventional neuroradiology, vein of Galen malformations can now be successfully treated with low complication rates.
This document summarizes the history and criteria for diagnosing left ventricular noncompaction (LVNC) via echocardiography. It describes the original 1990 criteria using X/Y ratios between trabeculations and recesses. Second 1999 criteria used a noncompacted to compacted myocardium ratio over 2.3. Later studies refined understanding. The latest 2014 criteria require all 4 criteria be met regarding prominent trabeculations, synchronous movement, two-layer structure, and perfusion of intertrabecular spaces. Echocardiography looks for a noncompaction to compaction ratio over 2 and more than 3 recesses communicating to the left ventricle in diastole. MRI diagnoses if noncompaction mass is
CARDIOPULMONARY BYPASS AND PRETERM NEONATES Adhi Arya
This document discusses the surgical options and risks for a 3 day old premature infant born with transposition of the great arteries, coarctation of the aorta, and hypoplastic right ventricle. It notes the risks of surgery in preterm infants include complications from immature organ systems, effects of cardiopulmonary bypass like coagulation abnormalities, and the underlying heart defects. The document advocates for strategies like limiting bypass and cross-clamp times, minimizing hemodilution, steroid administration, and close postoperative management to optimize outcomes for these high-risk patients.
The patient presented with altered sensorium, decreased movement in their right side, and deviation of their mouth to the left. Imaging showed a non-hemorrhagic infarct in the left fronto-parietal region consistent with a stroke. An echocardiogram found left ventricular non-compaction (LVNC), a mobile clot attached to the left ventricle, and normal systolic function. The final diagnosis was LVNC, stroke, hyperhomocysteinemia, and hyperlipidemia. LVNC is a rare heart condition where the left ventricle fails to compact during development, leaving prominent trabeculations. It can cause heart failure, arrhythmias, and thromboemb
Noncompaction cardiomyopathy is a rare congenital heart condition caused by the failure of the heart muscle to develop and thicken normally during fetal development. It results in a thickened heart muscle with prominent trabeculations and deep recesses.
The diagnosis is challenging due to a lack of consensus on diagnostic criteria and the inability to clearly differentiate between normal trabeculations and pathological noncompaction using imaging modalities like echocardiography and MRI. Current echocardiographic criteria may be too sensitive, leading to overdiagnosis.
The condition can cause heart failure, arrhythmias and blood clots. Treatment involves medications and lifestyle changes to manage symptoms. The long term prognosis depends on the extent of involvement
Left ventricular noncompaction (LVNC) is a rare cardiomyopathy characterized by prominent trabeculations and deep recesses in the left ventricular wall. It results from the failure of embryonic myocardial compaction. LVNC can be isolated or associated with other conditions. The diagnosis is made using echocardiography or cardiac MRI based on specific criteria. Management involves treating any heart failure, arrhythmias, or thromboembolic risks present. While genetic causes have been identified in some families, the underlying pathogenesis remains incompletely understood and LVNC remains a diagnostic and management challenge.
This document discusses a case of an 8-hour-old male infant presenting with breathlessness, abdominal distension, and swelling in the lower limbs and sacral area, who was diagnosed with a vein of Galen malformation. Vein of Galen malformations are congenital abnormalities that develop during weeks 6-11 of fetal development. They can cause congestive heart failure, hydrocephalus, and developmental delays. Investigation with cranial ultrasound, MRI/CT, and angiography are used for diagnosis. Treatment involves a multidisciplinary team and endovascular embolization of the abnormal vessels, though care must be taken with neonates. Prognosis has improved with advances in minimally invasive treatments.
This document discusses Uhl's anomaly and arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). It presents a case study of a 50-year-old man with palpitations and ventricular ectopic beats. Key differences between Uhl's anomaly and ARVD/C are described. Uhl's anomaly is a rare congenital disorder characterized by a thin-walled right ventricle, while ARVD/C is an inherited cardiomyopathy characterized by structural abnormalities and fatty infiltration of the right ventricle myocardium. Diagnostic criteria for ARVD/C include family history, electrocardiogram abnormalities, arrhythmias on monitoring, and structural changes seen on imaging like echocard
Arrhythmogenic right ventricular dysplasiaDomina Petric
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an inherited heart muscle disease characterized by structural abnormalities and fatty replacement of the right ventricle muscle leading to ventricular arrhythmias. It is an important cause of sudden cardiac death in young adults. The disease results from genetic mutations that cause programmed cell death and fibrosis of the right ventricle muscle. Diagnosis is based on ECG findings like inverted T-waves in the right ventricle leads and epsilon waves, along with imaging showing right ventricle structural changes. Treatment involves medications like beta-blockers and implantable defibrillators to prevent arrhythmias.
Arrhythmogenic right ventricular dysplasia (ARVD) is a genetic heart condition characterized by replacement of right ventricular myocardium with fat and fibrous tissue. This causes ventricular arrhythmias which can lead to sudden cardiac death. ARVD is diagnosed based on criteria involving cardiac imaging, biopsy, electrocardiogram findings and genetic testing. A combination of major and minor criteria must be met, including ventricular dysfunction, aneurysms, conduction abnormalities and evidence of fibrofatty tissue replacement on biopsy. ARVD has an autosomal dominant inheritance pattern and is a leading cause of sudden cardiac death in young people.
A 33-year-old female patient presented with severe heart failure for one year and was previously diagnosed with dilated cardiomyopathy. She underwent cardiac imaging tests including echocardiography, ECG, and MSCT to rule out coronary artery disease. The echocardiography and MSCT revealed prominent trabeculations and a spongiform appearance of the left ventricle consistent with noncompaction cardiomyopathy. Noncompaction cardiomyopathy is a rare genetic heart condition characterized by excessive trabeculations and deep intratrabecular recesses in the left ventricle.
1) Cerebrovascular malformations are classified based on their histopathologic features, including arteriovenous malformations (AVMs), venous angiomas, cavernous malformations, and capillary telangiectasias.
2) AVMs are vascular abnormalities consisting of direct connections between arteries and veins without an intervening capillary bed. They typically present with hemorrhage, seizures, or focal neurological deficits.
3) Treatment options for AVMs include observation, endovascular surgery, stereotactic radiosurgery, and microsurgery, with the appropriate treatment depending on factors like the AVM's size, location, and whether it has already hemorrhaged.
The document summarizes arrhythmogenic right ventricular dysplasia (ARVD), a condition where the right ventricle of the heart is replaced by fat and fibrous tissue. It affects mostly young males and can cause sudden cardiac death. Genetic factors are involved in many cases. The condition starts with fatty infiltration of the right ventricle and progresses to include fibrosis, thinning of the ventricular wall, and later involvement of the left ventricle. Diagnosis involves criteria related to structural changes, electrocardiogram abnormalities, arrhythmias, and family history.
A 25-year-old male presented with painless vision loss in the right eye for 2 months. Examination found vision loss and retinal abnormalities in the right eye and an opaque cornea in the left eye. Imaging found brain and retinal lesions. Based on clinical and family history, the patient was diagnosed with Von Hippel-Lindau disease with cerebellar and retinal hemangioblastomas. The patient underwent eye and brain surgeries. Long-term screening of family members is important for early detection and treatment of VHL manifestations.
Mitral valve prolapse (MVP) is a common heart valve abnormality where the mitral valve leaflets bulge into the left atrium during contraction. MVP affects around 2-3% of the population and can cause a range of symptoms from none to chest pain and palpitations. Diagnosis is made through auscultation of mid-systolic clicks and murmurs as well as echocardiography showing billowing of the mitral valve leaflets. While most cases are mild and asymptomatic, some patients develop complications like atrial fibrillation or worsening mitral regurgitation over time that may require surgery.
Tetralogy of Fallot (TOF) is a congenital heart defect characterized by four anatomical features - ventricular septal defect, right ventricular outflow tract obstruction, overriding aorta, and right ventricular hypertrophy. It is the most common cyanotic heart defect in children beyond infancy. Patients typically present with cyanosis in infancy which worsens with activity due to right-to-left shunting through the ventricular septal defect. On examination, a systolic murmur may be heard due to the outflow tract obstruction. Without surgical repair, long-term outcomes are poor.
arrhythmogenic right ventricular dysplasia/CardiomyopathyAnthony Kaviratne
This case discusses arrhythmogenic right ventricular cardiomyopathy (ARVC) in a 19-year-old female whose sister recently passed away from the condition. ARVC is characterized by replacement of the RV myocardium with fibrofatty tissue and electrical instability. The patient's sister's autopsy confirmed ARVC. The doctor discusses the pathology, diagnosis, treatment including ICDs and screening of relatives of ARVC to help inform the patient of her risk.
ARVD is one of important coardiomyopathy in our clinical practice,early diagnosis, risk stratification and early diagnosis of CHF, management of VT will make big difference in patient life
1. World Health Organization (WHO) grade 1 and 2 gliomas account for 60% of pediatric supratentorial tumors, with pilocytic astrocytomas being the most common, making up 1/3 of pediatric gliomas. Pilocytic astrocytomas have an excellent prognosis with 95% 10-year survival.
2. Diffuse astrocytomas are less common low-grade tumors in children. High-grade gliomas including anaplastic gliomas and glioblastomas are rare in children but have a poor prognosis, though survival is better than in adults.
3. Subependymal giant cell tumors are slow-growing tumors seen in children with tuberous s
This document presents a case of a 37-year-old male who experienced a sudden and severe headache while having sex. Imaging revealed a subarachnoid hemorrhage localized to the perimesencephalic cisterns. The document then discusses perimesencephalic subarachnoid hemorrhage, defining it as a benign and non-aneurysmal form of subarachnoid hemorrhage centered around the midbrain. It reviews the epidemiology, proposed etiologies involving venous anomalies, clinical features and good prognosis of perimesencephalic subarachnoid hemorrhage.
This document discusses left ventricular noncompaction cardiomyopathy (LVNC), a rare genetic heart condition where the heart muscle does not compact properly during fetal development. It begins by defining LVNC and describing its increasing recognition due to advances in diagnostic imaging. The document then discusses the embryological development of the heart and how a disruption in the normal compaction process can lead to LVNC. It outlines the characteristic features of LVNC seen on imaging studies and potential genetic associations. The document concludes by discussing the challenges in diagnosing and managing LVNC.
1) ARVD is a genetic cardiomyopathy characterized by replacement of RV myocardium by fat and fibrosis. It is diagnosed using criteria in 5 categories: RV structure/function by echo/CMR, RV biopsy, ECG repolarization/depolarization abnormalities, arrhythmias, and family history.
2) Major diagnostic criteria include RV akinesia/aneurysm by echo/CMR, >500 ventricular extrasystoles per 24 hours by Holter, nonsustained or sustained VT of left bundle branch block morphology, and epsilon waves on ECG. Meeting criteria in different categories is needed for a definite diagnosis.
3) Exercise commonly provokes ventricular arrhythmias in ARVD patients, likely due
A rare case of cardiac amyloidosis diagnosed by MRIPrasunDas31
This document presents a case report of a rare case of cardiac amyloidosis diagnosed by MRI. A 73-year-old man presented with dyspnea and was found to have hypertrophied ventricles and diastolic dysfunction on echocardiogram. CMR revealed increased wall thickness, dilated atria, reduced ejection fraction, and global subendocardial late gadolinium enhancement of the ventricles and atria, consistent with cardiac amyloidosis which was later confirmed by biopsy. The case report demonstrates how CMR can help diagnose cardiac amyloidosis in a non-invasive manner by detecting characteristic amyloid infiltration patterns earlier than other imaging modalities.
Rasopathies are a group of genetic conditions caused by mutations in the Ras-MAP Kinase signaling pathway. This document discusses several Rasopathies including Noonan syndrome, which is one of the most common genetic syndromes associated with congenital heart disease. Noonan syndrome is characterized by short stature, congenital heart defects such as pulmonary stenosis, and distinctive facial features. Cardiac manifestations also include hypertrophic cardiomyopathy. Treatment for cardiac issues in Noonan syndrome follows guidelines for non-syndromic cases, but bleeding risks must be considered.
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/ARVC) is a genetic heart condition characterized by structural abnormalities and fatty infiltration of the right ventricle, leading to ventricular arrhythmias and sudden cardiac death. It is a common cause of sudden cardiac death in young athletes. Clinical features include palpitations, syncope, chest pain, and dyspnea. Diagnosis relies on a combination of ECG findings, echocardiogram abnormalities of the right ventricle, and genetic testing.
Noncompaction cardiomyopathy is a rare congenital heart condition caused by the failure of the heart muscle to develop and thicken normally during fetal development. It results in a thickened heart muscle with prominent trabeculations and deep recesses.
The diagnosis is challenging due to a lack of consensus on diagnostic criteria and the inability to clearly differentiate between normal trabeculations and pathological noncompaction using imaging modalities like echocardiography and MRI. Current echocardiographic criteria may be too sensitive, leading to overdiagnosis.
The condition can cause heart failure, arrhythmias and blood clots. Treatment involves medications and lifestyle changes to manage symptoms. The long term prognosis depends on the extent of involvement
Left ventricular noncompaction (LVNC) is a rare cardiomyopathy characterized by prominent trabeculations and deep recesses in the left ventricular wall. It results from the failure of embryonic myocardial compaction. LVNC can be isolated or associated with other conditions. The diagnosis is made using echocardiography or cardiac MRI based on specific criteria. Management involves treating any heart failure, arrhythmias, or thromboembolic risks present. While genetic causes have been identified in some families, the underlying pathogenesis remains incompletely understood and LVNC remains a diagnostic and management challenge.
This document discusses a case of an 8-hour-old male infant presenting with breathlessness, abdominal distension, and swelling in the lower limbs and sacral area, who was diagnosed with a vein of Galen malformation. Vein of Galen malformations are congenital abnormalities that develop during weeks 6-11 of fetal development. They can cause congestive heart failure, hydrocephalus, and developmental delays. Investigation with cranial ultrasound, MRI/CT, and angiography are used for diagnosis. Treatment involves a multidisciplinary team and endovascular embolization of the abnormal vessels, though care must be taken with neonates. Prognosis has improved with advances in minimally invasive treatments.
This document discusses Uhl's anomaly and arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). It presents a case study of a 50-year-old man with palpitations and ventricular ectopic beats. Key differences between Uhl's anomaly and ARVD/C are described. Uhl's anomaly is a rare congenital disorder characterized by a thin-walled right ventricle, while ARVD/C is an inherited cardiomyopathy characterized by structural abnormalities and fatty infiltration of the right ventricle myocardium. Diagnostic criteria for ARVD/C include family history, electrocardiogram abnormalities, arrhythmias on monitoring, and structural changes seen on imaging like echocard
Arrhythmogenic right ventricular dysplasiaDomina Petric
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an inherited heart muscle disease characterized by structural abnormalities and fatty replacement of the right ventricle muscle leading to ventricular arrhythmias. It is an important cause of sudden cardiac death in young adults. The disease results from genetic mutations that cause programmed cell death and fibrosis of the right ventricle muscle. Diagnosis is based on ECG findings like inverted T-waves in the right ventricle leads and epsilon waves, along with imaging showing right ventricle structural changes. Treatment involves medications like beta-blockers and implantable defibrillators to prevent arrhythmias.
Arrhythmogenic right ventricular dysplasia (ARVD) is a genetic heart condition characterized by replacement of right ventricular myocardium with fat and fibrous tissue. This causes ventricular arrhythmias which can lead to sudden cardiac death. ARVD is diagnosed based on criteria involving cardiac imaging, biopsy, electrocardiogram findings and genetic testing. A combination of major and minor criteria must be met, including ventricular dysfunction, aneurysms, conduction abnormalities and evidence of fibrofatty tissue replacement on biopsy. ARVD has an autosomal dominant inheritance pattern and is a leading cause of sudden cardiac death in young people.
A 33-year-old female patient presented with severe heart failure for one year and was previously diagnosed with dilated cardiomyopathy. She underwent cardiac imaging tests including echocardiography, ECG, and MSCT to rule out coronary artery disease. The echocardiography and MSCT revealed prominent trabeculations and a spongiform appearance of the left ventricle consistent with noncompaction cardiomyopathy. Noncompaction cardiomyopathy is a rare genetic heart condition characterized by excessive trabeculations and deep intratrabecular recesses in the left ventricle.
1) Cerebrovascular malformations are classified based on their histopathologic features, including arteriovenous malformations (AVMs), venous angiomas, cavernous malformations, and capillary telangiectasias.
2) AVMs are vascular abnormalities consisting of direct connections between arteries and veins without an intervening capillary bed. They typically present with hemorrhage, seizures, or focal neurological deficits.
3) Treatment options for AVMs include observation, endovascular surgery, stereotactic radiosurgery, and microsurgery, with the appropriate treatment depending on factors like the AVM's size, location, and whether it has already hemorrhaged.
The document summarizes arrhythmogenic right ventricular dysplasia (ARVD), a condition where the right ventricle of the heart is replaced by fat and fibrous tissue. It affects mostly young males and can cause sudden cardiac death. Genetic factors are involved in many cases. The condition starts with fatty infiltration of the right ventricle and progresses to include fibrosis, thinning of the ventricular wall, and later involvement of the left ventricle. Diagnosis involves criteria related to structural changes, electrocardiogram abnormalities, arrhythmias, and family history.
A 25-year-old male presented with painless vision loss in the right eye for 2 months. Examination found vision loss and retinal abnormalities in the right eye and an opaque cornea in the left eye. Imaging found brain and retinal lesions. Based on clinical and family history, the patient was diagnosed with Von Hippel-Lindau disease with cerebellar and retinal hemangioblastomas. The patient underwent eye and brain surgeries. Long-term screening of family members is important for early detection and treatment of VHL manifestations.
Mitral valve prolapse (MVP) is a common heart valve abnormality where the mitral valve leaflets bulge into the left atrium during contraction. MVP affects around 2-3% of the population and can cause a range of symptoms from none to chest pain and palpitations. Diagnosis is made through auscultation of mid-systolic clicks and murmurs as well as echocardiography showing billowing of the mitral valve leaflets. While most cases are mild and asymptomatic, some patients develop complications like atrial fibrillation or worsening mitral regurgitation over time that may require surgery.
Tetralogy of Fallot (TOF) is a congenital heart defect characterized by four anatomical features - ventricular septal defect, right ventricular outflow tract obstruction, overriding aorta, and right ventricular hypertrophy. It is the most common cyanotic heart defect in children beyond infancy. Patients typically present with cyanosis in infancy which worsens with activity due to right-to-left shunting through the ventricular septal defect. On examination, a systolic murmur may be heard due to the outflow tract obstruction. Without surgical repair, long-term outcomes are poor.
arrhythmogenic right ventricular dysplasia/CardiomyopathyAnthony Kaviratne
This case discusses arrhythmogenic right ventricular cardiomyopathy (ARVC) in a 19-year-old female whose sister recently passed away from the condition. ARVC is characterized by replacement of the RV myocardium with fibrofatty tissue and electrical instability. The patient's sister's autopsy confirmed ARVC. The doctor discusses the pathology, diagnosis, treatment including ICDs and screening of relatives of ARVC to help inform the patient of her risk.
ARVD is one of important coardiomyopathy in our clinical practice,early diagnosis, risk stratification and early diagnosis of CHF, management of VT will make big difference in patient life
1. World Health Organization (WHO) grade 1 and 2 gliomas account for 60% of pediatric supratentorial tumors, with pilocytic astrocytomas being the most common, making up 1/3 of pediatric gliomas. Pilocytic astrocytomas have an excellent prognosis with 95% 10-year survival.
2. Diffuse astrocytomas are less common low-grade tumors in children. High-grade gliomas including anaplastic gliomas and glioblastomas are rare in children but have a poor prognosis, though survival is better than in adults.
3. Subependymal giant cell tumors are slow-growing tumors seen in children with tuberous s
This document presents a case of a 37-year-old male who experienced a sudden and severe headache while having sex. Imaging revealed a subarachnoid hemorrhage localized to the perimesencephalic cisterns. The document then discusses perimesencephalic subarachnoid hemorrhage, defining it as a benign and non-aneurysmal form of subarachnoid hemorrhage centered around the midbrain. It reviews the epidemiology, proposed etiologies involving venous anomalies, clinical features and good prognosis of perimesencephalic subarachnoid hemorrhage.
This document discusses left ventricular noncompaction cardiomyopathy (LVNC), a rare genetic heart condition where the heart muscle does not compact properly during fetal development. It begins by defining LVNC and describing its increasing recognition due to advances in diagnostic imaging. The document then discusses the embryological development of the heart and how a disruption in the normal compaction process can lead to LVNC. It outlines the characteristic features of LVNC seen on imaging studies and potential genetic associations. The document concludes by discussing the challenges in diagnosing and managing LVNC.
1) ARVD is a genetic cardiomyopathy characterized by replacement of RV myocardium by fat and fibrosis. It is diagnosed using criteria in 5 categories: RV structure/function by echo/CMR, RV biopsy, ECG repolarization/depolarization abnormalities, arrhythmias, and family history.
2) Major diagnostic criteria include RV akinesia/aneurysm by echo/CMR, >500 ventricular extrasystoles per 24 hours by Holter, nonsustained or sustained VT of left bundle branch block morphology, and epsilon waves on ECG. Meeting criteria in different categories is needed for a definite diagnosis.
3) Exercise commonly provokes ventricular arrhythmias in ARVD patients, likely due
A rare case of cardiac amyloidosis diagnosed by MRIPrasunDas31
This document presents a case report of a rare case of cardiac amyloidosis diagnosed by MRI. A 73-year-old man presented with dyspnea and was found to have hypertrophied ventricles and diastolic dysfunction on echocardiogram. CMR revealed increased wall thickness, dilated atria, reduced ejection fraction, and global subendocardial late gadolinium enhancement of the ventricles and atria, consistent with cardiac amyloidosis which was later confirmed by biopsy. The case report demonstrates how CMR can help diagnose cardiac amyloidosis in a non-invasive manner by detecting characteristic amyloid infiltration patterns earlier than other imaging modalities.
Rasopathies are a group of genetic conditions caused by mutations in the Ras-MAP Kinase signaling pathway. This document discusses several Rasopathies including Noonan syndrome, which is one of the most common genetic syndromes associated with congenital heart disease. Noonan syndrome is characterized by short stature, congenital heart defects such as pulmonary stenosis, and distinctive facial features. Cardiac manifestations also include hypertrophic cardiomyopathy. Treatment for cardiac issues in Noonan syndrome follows guidelines for non-syndromic cases, but bleeding risks must be considered.
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/ARVC) is a genetic heart condition characterized by structural abnormalities and fatty infiltration of the right ventricle, leading to ventricular arrhythmias and sudden cardiac death. It is a common cause of sudden cardiac death in young athletes. Clinical features include palpitations, syncope, chest pain, and dyspnea. Diagnosis relies on a combination of ECG findings, echocardiogram abnormalities of the right ventricle, and genetic testing.
This document discusses the use of electrocardiograms (ECGs) in diagnosing congenital heart disease (CHD) and other cardiac conditions in infants, children, and young adults. It notes that while ECGs are not very sensitive for CHD diagnosis, they can provide clues to underlying issues like left or right ventricular hypertrophy. It also discusses how ECG findings of arrhythmias, conduction abnormalities, ischemia, and other issues can indicate certain CHDs or complications from surgical repairs. The document concludes that interpreting pediatric ECGs requires understanding how the heart and ECG change through development, in order to distinguish normal variants from abnormalities requiring further evaluation.
This document provides information on hypertrophic cardiomyopathy (HCM), including its definition, history, etiology, pathophysiology, diagnosis, and clinical presentation. HCM is a genetic heart condition characterized by thickened heart muscle not caused by other conditions like high blood pressure. It affects around 1 in 500 people and can cause chest pain, dizziness, and heart failure. The pathophysiology involves left ventricular outflow tract obstruction, diastolic dysfunction, myocardial ischemia, and mitral regurgitation. Diagnosis involves imaging of the thickened heart muscle. Most patients are asymptomatic but may develop limiting symptoms like shortness of breath or chest pain in their 40s-60s as obstruction develops.
Isolated monomorphic premature ventricular complexes (PVCs) without
structural heart disease are generally benign.
► Frequent PVCs can cause reversible cardiomyopathy or aggravate an existing
cardiomyopathy.
► Short coupled PVCs can trigger sustained ventricular fibrillation. These are
often from the Purkinje tissue or rarely the outflow tract.
► Beta blockers are considered first-line therapy but have low efficacy.
Catheter ablation and AADs are reasonable to suppress PVCs in appropriate
patients.
► Ablation is often curative and success depends on location and accessibility
of PVCs.
► Implantable defibrillators are reasonable in patients at higher risk of sudden
cardiac death.
Hypertrophic cardiomyopathy (HCM) is a genetic heart condition characterized by thickened heart muscle. It is defined as thickening of the left ventricle in the absence of another cause like hypertension. The thickening can occur in any part of the left ventricle but commonly involves the septum. HCM is diagnosed based on echocardiogram findings showing thickened heart muscle of 15mm or more. Management involves preventing sudden cardiac death through ICD implantation in high risk patients and treating heart failure symptoms with medications like beta blockers.
This document discusses cardiovascular involvement in various collagen vascular disorders, including systemic lupus erythematosus (SLE). It notes that up to 70% of SLE patients show cardiovascular involvement upon autopsy or echocardiography. Common manifestations include pericardial disease, valvular disease, coronary artery disease, and myocardial disease. Pericarditis is the most common cardiovascular manifestation in SLE, occurring in 22-54% of patients. Valvular abnormalities like thickening and regurgitation are also common. The document further discusses cardiovascular involvement in other disorders like antiphospholipid antibody syndrome, systemic sclerosis, and drug-induced lupus.
This document discusses congenital heart disease in adults. It notes that 1 million adults in the US have congenital heart disease, with 20,000 more reaching adulthood each year due to increased survival of children with CHD. Common adult presentations of CHD include effort dyspnea, atrial fibrillation, and right heart failure. The document reviews the pathophysiology, clinical features, diagnostic evaluation, and management of various CHD lesions that may present in adulthood, such as atrial septal defects, ventricular septal defects, patent ductus arteriosus, tetralogy of Fallot, Ebstein's anomaly, and coarctation of the aorta. Surgical and percutaneous interventions are discussed
HCM is a common genetic heart disease reported in populations globally
Inherited in an autosomal dominant pattern
The distribution of HCM is equal by sex, although women are diagnosed less commonly than men
The prevalence of unexplained asymptomatic hypertrophy in young adults has been reported to range from 1:200 to 1:500
The document provides information on inferior wall myocardial infarction (MI), including:
1. Definitions, epidemiology, etiology, clinical features, diagnosis, treatment and complications of inferior wall MI are discussed. Worldwide over 7 million people experience STEMIs or NSTEMIs annually.
2. Diagnosis involves ECG, cardiac imaging, cardiac biomarkers like troponin and CK-MB. Reperfusion therapy within 6 hours includes PCI or thrombolysis. General treatment measures include aspirin, clopidogrel, anticoagulants, analgesics, beta-blockers, nitrates and oxygen.
3. The history of pioneers in cardiology and development of techniques like echocardi
Tricuspid atresia is a congenital heart defect where the tricuspid valve is absent or not formed, preventing communication between the right atrium and right ventricle. It occurs in approximately 0.06 per 1000 live births with no gender predominance. The condition ranges in severity from complete absence of the tricuspid valve to stenosis. Early presentation includes severe cyanosis, hypoxemia, and acidosis in infants with low pulmonary blood flow, while those with higher flow present with heart failure symptoms later in infancy. Echocardiography can identify the absent tricuspid valve and associated defects. Without surgical intervention, few infants survive beyond 6 months, but current treatments including shunts and the
This document discusses the definition, terminology, epidemiology, etiology, and prognosis of heart failure with reduced ejection fraction (HFrEF). It defines HFrEF as HF with a left ventricular ejection fraction (LVEF) of less than 40%. It also discusses the categories of HF with mid-range ejection fraction (HFmrEF) between 40-49% and HF with preserved ejection fraction (HFpEF) of 50% or greater. The document outlines the various terminology used to describe the different stages and types of HF and reviews the epidemiology including risk factors, prevalence, and etiologies of HFrEF.
PVCs are common, occurring in 40-75% of the general population on Holter monitoring. While traditionally thought to be benign without structural heart disease, they represent an increased risk of sudden death in patients with conditions like ischemic heart disease. The frequency and complexity of PVCs is associated with increased mortality in these patients. Implantable cardioverter defibrillators are indicated for those with nonsustained ventricular tachycardia due to prior myocardial infarction and left ventricular ejection fraction ≤40% who are inducible for sustained ventricular arrhythmias on electrophysiological study. However, for patients with congestive heart failure, PVCs do not provide significant prognostic value beyond clinical variables. The concept of PVC-induced
Left Ventricular Noncompaction Cardiomyopathy (LVNC) with Left Ventricular Ap...M A Hasnat
This case report describes a 60-year-old man diagnosed with left ventricular non-compaction cardiomyopathy (LVNC) presenting with congestive heart failure. Echocardiography revealed prominent trabeculations in the left ventricle with blood flow in the intertrabecular recesses, and a ratio of non-compacted to compacted myocardium greater than 2:1, consistent with LVNC. A small thrombus was also present. The patient was treated medically and showed improvement. LVNC is a rare congenital heart condition characterized by excessive trabeculations in the left ventricle that can cause heart failure, arrhythmias, or thromboembolic events. Echocardiography is
This case report describes a 60-year-old man diagnosed with left ventricular non-compaction cardiomyopathy (LVNC) presenting with congestive heart failure. Echocardiography revealed prominent trabeculations in the left ventricle with blood flow in the intertrabecular recesses, and a ratio of non-compacted to compacted myocardium greater than 2:1, consistent with LVNC. A small thrombus was also present. The patient was treated medically and showed improvement. LVNC is a rare congenital heart condition characterized by excessive trabeculations in the left ventricle that can cause heart failure, arrhythmias, or thromboembolism. Echocardiography is
This document discusses venous thromboembolic disease (VTE), which includes deep vein thrombosis (DVT) and pulmonary embolism (PE). Some key points:
- PE is a common cause of death and VTE can result in long-term disability. Risk factors include hospitalization, surgery, trauma, and reduced mobility.
- VTE has variable and non-specific symptoms, making it difficult to diagnose. Imaging tests like ultrasound, CT, and pulmonary angiography are used to confirm diagnosis.
- Treatment involves anticoagulation to prevent clot extension and recurrence. Therapy is typically divided into acute, maintenance, and long-term phases. Anticoagulation is effective but carries
Contemporary Perspectives on the Diagnosis and Management of Hypertrophic Car...asclepiuspdfs
Hypertrophic cardiomyopathy (HCM) is a cardiovascular disorder with genetic predisposition. The number of treatment modalities has grown in the contemporary era, with use of pharmacotherapy, device therapy, and surgical intervention, though with the relative paucity of data derived from randomized trials. Its clinical course and prognosis are relatively good. The ongoing quest is to establish the optimal treatment strategy in patients with HCM. This is of direct relevance in reducing the mortality burden associated with sudden cardiac death primarily secondary to dysrhythmias. This review summarizes the clinical features, course, and management of HCM. In particular, we highlight advances in cardiac magnetic resonance imaging assessment of HCM and how risk stratification criteria for suitability of implantable cardioverter defibrillators differ between continents.
Dr. Walinjom Joshua presented on persistent truncus arteriosus, a congenital heart defect where a single arterial trunk arises from the heart, supplying the systemic circulation, pulmonary circulation, and coronary arteries. The key features are a large ventricular septal defect below the arterial trunk and a commonly incompetent truncal valve with two to four leaflets. Patients typically present within the first two weeks of life with cyanosis and congestive heart failure. Diagnosis is made using echocardiography, chest x-ray and electrocardiogram. Surgical repair is usually performed within the first month of life to separate the pulmonary and systemic circulations.
This document discusses a case of multiple endocrine neoplasia type 1 (MEN1) in a 46-year-old female patient and her brother. The patient presented with symptoms of hypoglycemia and was found to have hyperparathyroidism, a pituitary adenoma, and insulinomas. Genetic testing confirmed a MEN1 gene mutation. Her brother also had features of MEN1 including acromegaly, hyperparathyroidism, and insulinomas. MEN1 is a rare genetic disorder characterized by tumors of the parathyroid glands, anterior pituitary, and pancreatic islet cells. Early detection of MEN1-associated tumors through genetic screening and biochemical monitoring of at-risk family members
This document provides guidelines for the treatment of dyslipidemia to reduce cardiovascular risk. It defines dyslipidemia as abnormal lipid levels measured in a blood sample. The guidelines classify risk based on LDL cholesterol, total cholesterol, and HDL cholesterol levels. They recommend screening adults over certain ages for lipid levels and cardiovascular risk. Risk is assessed using tools like the Framingham Risk Score. Treatment involves starting statin therapy, with the intensity based on a patient's risk category. Lifestyle changes and other medications may also be used. The guidelines aim to identify those who will benefit most from treatment to lower lipid levels and cardiovascular risk.
This document discusses drug-induced liver injury (DILI). It begins by stating that multiple drugs can cause hepatotoxicity through various mechanisms. It then discusses the epidemiology of DILI, noting that its worldwide annual incidence is estimated between 1.3 to 19.1 per 100,000 exposed individuals. The document outlines the pathogenesis, clinical presentation, diagnosis, classification, histology, and management of DILI. Regarding histology, it describes various patterns of injury that can be seen such as hepatocellular necrosis, cholestasis, steatosis, and sinusoidal obstruction syndrome. The primary treatment for DILI is withdrawal of the causative drug, with specific therapies for certain cases like
1) Aortic stenosis is a narrowing of the aortic valve that obstructs blood flow from the left ventricle to the aorta.
2) The most common presenting symptoms are dyspnea on exertion, exertional dizziness, and exertional angina, reflecting the stiff left ventricle's inability to increase cardiac output during exercise.
3) On examination, the carotid pulse is weak and slow rising, and a crescendo-decrescendo murmur is best heard at the right upper sternal border when leaning forward.
This document discusses drug overdoses, including definitions, common drugs involved, risk factors, evaluation and treatment. It notes that overdoses can be intentional or accidental and are a major cause of morbidity and mortality worldwide. The most common drugs involved in overdoses are opioid analgesics and benzodiazepines. Men ages 45-49 have the highest death rates. Evaluation involves assessing vital signs and mental status while treatment focuses on stabilization, supportive care, prevention of further exposure, and administration of antidotes if available.
Scorpion stings, especially from the Indian red scorpion, are a major public health problem in tropical countries. The venom causes an autonomic storm that can lead to hypertension, pulmonary edema, hypotension and shock. Early symptoms include local pain, vomiting, sweating and priapism. Delayed treatment can result in high morbidity and mortality. Management involves fluid resuscitation, prazosin to block alpha receptors, vasodilators, antivenom and intensive care as needed for pulmonary edema or hypotension. Prevention focuses on reducing places scorpions may hide and using pesticides in endemic areas.
This document discusses acute HIV infection and CDC criteria for diagnosis. It defines acute HIV infection as occurring within approximately six months of infection. Symptoms may include fever, lymphadenopathy, sore throat, rash, and others nonspecific symptoms. Diagnosis is made by detecting HIV RNA during the window period before antibodies develop or with a positive combination antigen/antibody test and negative antibody-only test. Early diagnosis is important for individual treatment and reducing transmission.
head ache dizziness and sphincter disturbance s.pptxSruthi Meenaxshi
This document discusses several topics related to sensory disturbances:
1) It describes the anatomy of the sensory system and how sensations are transmitted from receptors to the central nervous system.
2) It defines different types of sensory loss or disturbances like hypoesthesia, anesthesia, hypalgesia, and hyperpathia.
3) It outlines how to perform a sensory examination to localize lesions, including testing touch, proprioception, vibration, temperature, and pain. Higher cortical sensations can also be examined.
Inflammatory Bowel Disease (IBD) represents a spectrum of chronic inflammatory conditions of the digestive tract including Ulcerative Colitis and Crohn's Disease. IBD is caused by an inappropriate immune response to intestinal bacteria in genetically predisposed individuals. Symptoms include diarrhea, abdominal pain, and weight loss. Treatment involves medications to reduce inflammation like aminosalicylates, corticosteroids, immunosuppressants, and biologics that target tumor necrosis factor-alpha. The goals of treatment are to induce and maintain remission of symptoms and prevent disease complications.
1. Premature ventricular contractions are early occurring, widened QRS complexes originating from the left or right ventricle that have a distinct morphology different from the normal sinus rhythm.
2. Ventricular tachycardia is defined as three or more successive ventricular complexes at a rate greater than 100 beats per minute and shows atrioventricular dissociation.
3. Ventricular fibrillation is identified by the complete absence of properly formed QRS complexes and P waves, with irregular ventricular activation above 300 beats per minute leading to cardiac arrest.
Digoxin toxicity can cause various arrhythmias due to its effects on intracellular calcium levels and vagal tone. Life-threatening arrhythmias may occur at plasma digoxin levels above 2.0 ng/mL. Hypokalemia and age over 65 increase toxicity risk. Symptoms include ectopic atrial tachycardia with block, various forms of AV block, and junctional rhythms. Distinguishing features between arrhythmias is important for appropriate treatment.
Vector borne diseases recent concepts in management and elimination targets...Sruthi Meenaxshi
This document discusses vector-borne diseases and strategies for their management and elimination. It begins by stating that vector-borne diseases account for 17% of infectious diseases globally, with malaria being the main contributor. Vectors transmit diseases between humans or animals. Vector management aims to optimize control and reduce incidence. Mosquitoes transmit diseases like malaria, dengue, chikungunya, Japanese encephalitis, and lymphatic filariasis. The National Vector Borne Disease Control Program integrates control of these diseases. Malaria elimination targets aim for transmission interruption in certain states by 2020 and nationwide by 2030. Integrated vector control includes insecticide spraying, bed nets, and source reduction.
This document discusses atrial septal defect (ASD) closure procedures. It describes that ASDs are often asymptomatic until adulthood but can lead to complications if left untreated. Preprocedural assessment includes echocardiography and additional imaging if needed. Surgical closure is preferred for primum, sinus venosus, and coronary sinus defects. Percutaneous closure is an alternative to surgery for secundum ASDs of appropriate size and anatomy. Percutaneous closure has comparable efficacy to surgery but shorter hospital stays and fewer complications. Complications of percutaneous closure include device embolization, arrhythmias, and erosion.
Echocardiography is the main tool for evaluating prosthetic heart valves. Transthoracic echocardiography (TTE) is generally used to assess normal valve function and identify dysfunction like stenosis or regurgitation. Transesophageal echocardiography (TEE) provides better imaging of valve structure and is helpful for evaluating regurgitation and complications like endocarditis. Echocardiograms establish a baseline after valve implantation and monitor for issues like pannus, thrombus, infection or degeneration over time. TTE and TEE are complementary, with TEE used when TTE is inadequate or clinical suspicion remains after a TTE.
Ventricular septal defects (VSDs) are openings in the wall separating the ventricles of the heart. There are four main types classified by location: membranous, muscular, supracristal, and inlet VSDs. Echocardiography is useful for diagnosing VSDs and assessing their characteristics like location, size, and impact on cardiac function. VSDs range from small and asymptomatic to large defects causing heart failure or pulmonary hypertension. Surgical or catheter-based closure may be required for large VSDs.
A 45 year old woman presented with shortness of breath on exertion. Echocardiography showed an atrial septal defect (ASD). ASDs are congenital heart defects where the wall separating the left and right atria is incomplete. The most common type is secundum ASD, which accounts for 70-75% of cases. ASDs allow blood to shunt from the left to the right atrium, overloading the right heart and lungs over time if not repaired. Echocardiography is the primary test to diagnose ASDs.
Echocardiography plays a key role in the diagnosis and management of infective endocarditis. It can identify valvular vegetations, abscesses, fistulas and other complications. The presence of an oscillating intracardiac mass or abscess on valves or endocardial surfaces are major echocardiographic criteria for the diagnosis. Transesophageal echocardiography is recommended if transthoracic is nondiagnostic or for complications. Follow up echos are important to monitor vegetation size with treatment and check for complications. Differentiating infective vegetations from other intracardiac masses or artifacts is important.
This document discusses different types of atrioventricular (AV) block and their classification. It describes:
- First, second, and third degree AV blocks, as well as high-grade block. Second degree block is further divided into Mobitz type I (Wenckebach) and type II.
- Etiologies of AV block.
- Class I indications for pacemaker placement, which include complete AV block and various types of symptomatic second degree block.
- Examples of ECGs demonstrating Wenckebach phenomenon, Mobitz type II block, complete heart block with and without myocardial infarction. Causes like muscular dystrophy are also discussed.
The document discusses the conduction system of the heart and bundle branch blocks. It notes that a bundle branch block is diagnosed when the QRS duration is over 120ms, there is a dominant S wave in V1, and a broad R wave in lateral leads. It lists causes of bundle branch blocks as conditions like aortic stenosis, dilated cardiomyopathy, and hypertension. The document explains that in left bundle branch block, conduction delay means the left ventricle is activated later via the septum, producing tall R waves in lateral leads and deep S waves in precordial leads, with an extended QRS duration. It also discusses right bundle branch block and criteria for diagnosing a myocardial infarction in the setting of left bundle branch block
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
One health condition that is becoming more common day by day is diabetes.
According to research conducted by the National Family Health Survey of India, diabetic cases show a projection which might increase to 10.4% by 2030.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd...Donc Test
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Study Guide Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Course Hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Answers Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Course hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Study Guide Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Ebook Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Questions Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Stuvia
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
2. Left ventricular noncompaction (LVNC) is a distinct phenotype characterized by prominent LV
trabeculae and deep intertrabecular recesses .
LVNC was previously also called spongy myocardium or hypertrabeculation syndrome but these
terms should not be used interchangeably with LVNC .
This review will focus on clinical manifestations and diagnosis of LVNC as an isolated disorder
distinct from other clinical settings in which non-compacted myocardium may be seen in
association with other cardiac and noncardiac abnormalities.
3. By definition, isolated LVNC occurs in the absence of other cardiac or noncardiac congenital abnormalities. (
Although LVNC has been categorized as an "unclassified" cardiomyopathy mounting evidence now points to
reclassification of LVNC as a distinct but not always pathological phenotype.
The presence of noncompacted myocardium by itself does not seem to cause disease. LVNC is a condition
resulting from genetics interacting with environment that is best labeled as a phenotype
LVNC is characterized by the following features:
●An altered myocardial wall with prominent trabeculae and deep intertrabecular recesses, resulting in thickened
myocardium with two layers consisting of noncompacted myocardium and a thin compacted layer of myocardium .
●Continuity between the LV cavity and the deep intertrabecular recesses, which are filled with blood from the
ventricular cavity without evidence of communication to the epicardial coronary artery system.
As discussed below, criteria for the extent of noncompaction have been developed to help distinguish the
trabeculation seen in LVNC from that seen in other forms of heart disease and in healthy individuals.
However, criteria are evolving and there may be morphologic overlap between LVNC and other types of
cardiomyopathy and other pathologic and nonpathologic phenotypes.
4.
5. LVNC is characterized by the following features:
●An altered myocardial wall with prominent trabeculae and deep intertrabecular recesses,
resulting in thickened myocardium with two layers consisting of noncompacted myocardium and
a thin compacted layer of myocardium .
●Continuity between the LV cavity and the deep intertrabecular recesses, which are filled with
blood from the ventricular cavity without evidence of communication to the epicardial coronary
artery system.
6. ◦ As discussed below, criteria for the extent of noncompaction have been
developed to help distinguish the trabeculation seen in LVNC from that seen in
other forms of heart disease and in healthy individuals.
◦ However, criteria are evolving and there may be morphologic overlap between
LVNC and other types of cardiomyopathy and other pathologic and
nonpathologic phenotypes
7. The prevalence of LVNC in the general population is not known, but its prevalence among patients undergoing
echocardiography is estimated at 0.014 to 1.3 percent .
A review from Switzerland identified 34 cases within 15 years, which represented 0.014 percent of
echocardiograms performed.
However, this may be an underestimate, since improved echocardiographic image quality, increased detection of
the entity on non-echo imaging, and increasing awareness of LVNC will likely lead to enhanced recognition of this
echocardiographic phenotype. Among patients with heart failure (HF), the prevalence of LVNC has been reported
as 3 to 4 percent .
Among patients with HF, criteria for LVNC are more frequently met among black patients than among white
patients .
One difficulty in ascertaining the prevalence of LVNC is that a variety of morphologic criteria for LVNC have been
applied; criteria for LVNC are evolving and likely have varying specificity in different populations.
As examples, most studies have not included wall thickness <8.1 mm as a criterion, and the morphology of
papillary muscles has seldom been addressed.
8. PATHOGENESIS
It has been suggested that LVNC may be due to intrauterine arrest of compaction of the loose
interwoven meshwork that makes up the fetal myocardial primordium.
However, the term "noncompaction" may be a misnomer: some authors have suggested that
noncompaction of the ventricular myocardium results from abnormal persistence of the trabecular
layer, rather than from noncompaction of the ventricular wall .
Pronounced hypertrabeculation may be the result of altered regulation in cell proliferation,
differentiation, and maturation during ventricular wall formation .
Trabeculations of the LV may be unique for each individual, like fingerprints .
Prominent trabeculations as seen in LVNC may develop during adult life.
Remodeling in response to LV loading conditions may explain the phenotypic characteristics of LVNC
seen in some athletes and in some individuals who are hypertensive, pregnant, or have heart failure
or hematologic disorders (eg, β-thalassemia) .
Additionally, LVNC can occur as a transient phenomenon in patients with other disorders, such as
myocarditis.
9. GENETICS
LVNC can be either sporadic or familial. In various reports, 12 to 50 percent of those with LVNC
had a family history of LVNC .
Other affected individuals can be detected by screening asymptomatic relatives of affected
patients .
Autosomal dominant inheritance is more common than X-linked inheritance or autosomal
recessive inheritance .
Differentiation of genotypes is not possible on the basis of current phenotypic data. The yield of
genetic testing in patients with LVNC is around 40 to 50 percent .
10. ◦ There is increasing recognition of considerable overlap in the genetic loci implicated in the major cardiomyopathies.
◦ Shared molecular etiology has been found for different cardiomyopathic phenotypes, including overlapping phenotypes between LVNC
and hypertrophic cardiomyopathy (HCM) and between LVNC and apical HCM .
◦ Despite the genetic overlap between LVNC and HCMs, LVNC co-occurs more commonly than HCM in patients with congenital heart
disease or Wolff-Parkinson-White syndrome.
11. CLINICAL MANIFESTATIONS
Clinical manifestations of LVNC are variable and may include dyspnea, chest pain, palpitations, syncope, or an abnormal electrocardiogram (ECG) or echocardiogram .
Cardiac symptoms and signs may not be present. The major complications of LVNC are HF, atrial and ventricular arrhythmias, sudden cardiac arrest, and thromboembolic
events, including stroke .
Symptoms and signs — The frequency of these manifestations at presentation is dependent on the population studied.
The following report is illustrative. In a systematic review including five studies with a total of 241 adult patients, 56 percent of patients were referred for HF, 27 percent were
referred for suspected LVNC based on prior clinical evaluation, and 11 percent were identified by screening . Baseline characteristics included the following:
•Dyspnea – 60 percent
•Chest pain − 15 percent
•Palpitations − 18 percent
•Syncope or presyncope − 9 percent
•Prior stroke – 3 percent
•New York Heart Association (NYHA) functional class III or IV HF – 31 percent
An increasing number of patients with isolated LVNC are initially diagnosed during childhood, however, criteria for diagnosis in children have not been established in large
studies . Initial diagnosis by prenatal ultrasound has been reported [47]. Similar presenting symptoms and signs have been reported in children
12. Complications — Complications of LVNC include HF, thromboembolism, and arrhythmias.
Heart failure — As noted above, among patients with LVNC, symptoms and signs of HF are
common at presentation, and hospitalization for HF is common .
Patients with LVNC can present as HF with reduced ejection fraction (HFrEF; LV ejection fraction
[LVEF] ≤40 percent), or less commonly, HF with preserved ejection fraction (HFpEF: LVEF ≥50
percent) or HF with mid-range ejection fraction (HFmrEF; LVEF 41 to 49 percent).
13. Thromboembolism — The risk of thromboembolism in patients with LVNC has not been
established. Given the available data, it is not clear whether the thromboembolic rate in patients
with LVNC differs from the rate generally observed in patients with HF.
. Patients with stroke or embolism had higher rates of hypertension and higher CHADS2 and
CHA2DS2-VASc scores than patients without stroke or embolism. LV fractional shortening was
similar in patients with and without a stroke or embolism event.
Atrial fibrillation was nominally more frequent in patients with stroke or embolic event but there
was no significant difference compared to patients without an event.
14. Arrhythmias — Ventricular and atrial arrhythmias occur commonly in patients with LVNC. In a
systematic review, 33 percent of patients had nonsustained ventricular tachycardia and 5
percent had sustained ventricular tachycardia .
Atrial fibrillation was documented in 10 percent of patients. There are no data on the sudden
cardiac death (SCD) risk of athletes with LVNC. LVNC has not been described in autopsy studies
of athletes with SCD; however, LVNC could have been missed at autopsy or described as HCM.
Initial testing — An ECG is commonly obtained in patients with suspected LVNC. The ECG is
usually abnormal (32 of 34 patients in the above report), but findings are nonspecific.
The abnormalities that may be seen include left or right bundle branch block, fascicular block,
atrial fibrillation, and ventricular tachycardia. Sinus bradycardia or Wolff-Parkinson-White
syndrome has been described in up to 18 percent of pediatric patients with LVNC .
The role of echocardiography and other cardiac imaging in the diagnosis of LVNC is described
below.
15.
16. Echocardiography
Echocardiography criteria — Echocardiography is the test most commonly used both to
establish the diagnosis of LVNC and as an aid during follow-up .For diagnosis of LVNC using
echocardiography, we use the Jenni criteria, which are the most widely accepted validated
criteria.
Alternatively, some clinicians use the Chin or Stöllberger criteria, which have also been
validated.
●The Jenni criteria were developed based upon echocardiographic appearance with pathologic
confirmation in seven patients with LVNC; the criteria were validated in a second population .
The criteria are assessed in the parasternal short-axis view at base, mid, and apical levels.
17. The presence of all four of the following echocardiographic criteria are required for diagnosis:
•A thickened LV wall consisting of two layers: a thin compacted epicardial layer and a markedly
thickened endocardial layer with numerous prominent trabeculations and deep recesses with a
maximum ratio of noncompacted to compacted myocardium >2:1 at end-systole in the parasternal
short-axis view .
•Color Doppler evidence of flow within the deep intertrabecular recesses.
•Prominent trabecular meshwork in the LV apex or midventricular segments of the inferior and lateral
wall.
•Compacted wall thickness ≤8.1 mm. The criterion of maximal systolic compacta thickness of ≤8.1 mm
was found to be very specific for myocardial thickening in LVNC compared to normal controls or
patients with aortic stenosis
In addition, hypokinesis of noncompacted segments and possibly other adjoining segments may be
present.
18.
19.
20.
21.
22. The Chin criterion is based upon observations
from eight patients :
The presence of X/Y ≤0.5, where X is the distance from the epicardial surface to the trough of
the trabecular recess and Y is the distance from the epicardial surface to peak of trabeculation.
This criterion is applied to trabeculae at the LV apex on subxiphoid or apical four-chamber views
at end-diastole.
23. Stöllberger criteria emphasize
hypertrabeculation :
●More than three trabeculations protruding from the LV wall, apically to the papillary muscles,
visible in a single image plane.
• Intertrabecular spaces perfused from the ventricular cavity, visualized on color Doppler
imaging.
The role for contrast echocardiography has been incompletely evaluated in LVNC; in our
practice, we routinely use contrast echocardiography for diagnosis of LVNC in patients with
suboptimal image quality to help differentiate LVNC from apical HCM, eosinophilic
endomyocardial disease, and from apical thrombi.
A role for three-dimensional echocardiography in LVNC has not been established.
A three-dimensional echocardiographic study found significantly higher trabeculated LV volume
and trabeculated LV volume normalized by LV end-diastolic volume in patients with LVNC
compared to healthy controls and athletes
24.
25.
26. Other echocardiographic findings —
Nonspecific findings that may be seen on echocardiography include reduced global LV systolic
function, diastolic dysfunction, LV thrombi, and abnormal papillary muscle structure .
Absence of well-defined papillary muscles is a very typical finding of LVNC .
Tissue Doppler imaging has been used to assess patients with LVNC. The diagnostic benefit of
strain and strain rate imaging and speckle tracking in LVNC has yet to be determined.
As noted above, the echocardiographic appearance of isolated LVNC is heterogenous, including
dilated forms, hypertrophic variant, and restrictive types
27. Cardiovascular magnetic resonance imaging — CMR is generally used to aid in the diagnosis of
LVNC when echocardiographic findings are inconclusive.
In addition, since CMR provides morphologic information (including identification of fibrosis by
late gadolinium enhancement (LGE) which may have prognostic implications) that differs from
that provided by echocardiography, we perform it once in most patients to confirm the diagnosis
of LVNC and repeat it as indicated during follow-up as a component of the evaluation for
evolving clinical symptoms and complications.
28.
29. Various CMR criteria have differing sensitivity and specificity for LVNC. In a study comparing four
different CMR criteria for LVNC, 3 to 39 percent of patients referred for CMR fulfilled LVNC
criteria .
The Stöllberger echocardiographic criteria for LVNC may be insensitive when applied to CMR .
In a series of 19 LVNC patients diagnosed by echocardiography using the Stöllberger criteria,
only nine met these criteria on CMR (obtained in short- and long-axis views).
However, the overall CMR morphologic appearance in all cases confirmed the diagnosis of
LVNC.
30. CMR may be superior to standard echocardiography in assessing the extent of noncompaction
as suggested by a small study comparing CMR with echocardiography in 16 patients with LVNC .
All 17 left ventricular segments could be analyzed by CMR whereas 88 percent of segments
could be analyzed by echocardiography at end-diastole and 87 percent of segments could be
analyzed by echocardiography at end-systole.
A two-layer structure was identified in more segments by CMR than by the echocardiographic
methods. There was no significant difference between the maximum ratio of
noncompacted/compacted layers by CMR and echocardiography at end-diastole.
Echocardiography at end systole underestimated the ratio of noncompacted/compacted layers
compared to CMR.
31. Late gadolinium enhancement — Myocardial fibrosis or scar detected by late gadolinium
enhancement (LGE, also known as delayed hyperenhancement) of trabeculae has been
observed in some patients with LVNC and may have prognostic value .
LGE distribution in patients fulfilling LVNC criteria can be very heterogeneous, which suggests
that there are several distinct cardiomyopathic processes responsible for LVNC .
A study in patients with LVNC found that diffuse fibrosis reflected by T1 mapping on CMR was
associated with ventricular arrhythmias and myocardial dysfunction .
The potential prognostic value of LGE is discussed separately.
32. RV involvement
The presence of noncompaction of the right ventricular (RV) myocardium is often difficult to
confirm by imaging.
A CMR study found that LVNC is associated with increased trabeculations of the RV apex and that
RV dysfunction in an LVNC population is associated with adverse clinical events .
The same impact on prognosis of LVNC in patients with RV involvement was shown by
echocardiography