BackgroundTakotsubo cardiomyopathy is characterized by transient systolic dysfunction of the apical and mid segments of the left ventricle in the absence of obstructive coronary artery disease. Intraventricular thrombus formation is a rare complication of Takotsubo cardiomyopathy and current data almost exclusively consists of isolated case reports and a few case series. Here we describe a case of Takotsubo cardiomyopathy with formation of an apical thrombus within 24 h of symptom onset, which has been reported in the literature only once previously, to the best of our knowledge. We have reviewed the available literature that may aid clinicians in their approach to the condition, since no published guidelines are available.Case presentationA 68-year-old Sri Lankan female presented to a local hospital with chest pain. Electrocardiogram (ECG) showed ST elevation, and antiplatelets, intravenous streptokinase and a high dose statin were administered. Despite this ST elevation persisted; however the coronary angiogram was negative for obstructive coronary artery disease. Echocardiogram revealed hypokinesia of the mid and apical segments of the left ventricle with typical apical ballooning and a sizable apical thrombus. She had recently had a viral infection and was also emotionally distressed as her sister was recently diagnosed with a terminal cancer. A diagnosis of Takotsubo cardiomyopathy was made and anticoagulation was started with heparin and warfarin. The follow up echocardiogram performed 1 week later revealed a small persistent thrombus, which had completely resolved at 3 weeks.ConclusionThough severe systolic dysfunction is observed in almost all the patients with Takotsubo cardiomyopathy, intraventricular thrombus formation on the first day of the illness is rare. The possibility of underdiagnosis of thrombus can be prevented by early echocardiogram in Takotsubo cardiomyopathy. The majority of reports found in the literature review were of cases that had formed an intraventriclar thrombus within the first 2 weeks, emphasizing the importance of follow up echocardiography at least 2 weeks later. The management of a left ventricular thrombus in Takotsubo cardiomyopathy is controversial and in most cases warfarin and heparin were used for a short duration.

BackgroundAnaphylaxis is an acute, potentially fatal medical emergency. Myocardial injury or infarction in the setting of an anaphylaxis can be due the anaphylaxis itself, when it is known as Kounis syndrome or it can also be due to the effect of epinephrine treatment. Epinephrine is considered as the cornerstone in management of anaphylaxis. Myocardial infarction secondary to therapeutic doses of adrenaline is a rare occurrence and only a few cases have been reported in literature. The mechanism of myocardial injury was considered to be due to coronary vasospasm secondary to epinephrine as the coronary angiograms were normal on these occasions.Case presentationA 21-year- old previously healthy male got admitted to the local hospital with an urticarial rash and difficulty in breathing, one hour after ingestion of prawns for which he was known to be allergic. He was treated with 0.5 ml of intramuscular adrenaline (1:1000) which was administered to the lateral side of the thigh, following which he developed palpitations and tightening type central chest pain. Electrocardiogram showed ST segment depressions in leads III, aVF and V1 to V5 and he was transferred to a tertiary care hospital. The second electrocardiogram, done 2 h later, showed resolution of ST segment depressions but new T inversions in leads I and aVL. Troponin I was elevated with a titer of 2.15 ng/ml. He was treated with sublingual GTN in the emergency treatment unit and the symptoms resolved. Transthoracic 2D echocardiogram and stress testing with treadmill was normal and CT coronary angiogram revealed normal coronary arteries.ConclusionHere we present a case of a young healthy adult with no significant risk factors for coronary artery disease who developed myocardial infarction following intramuscular administration of therapeutic dose of adrenalin for an anaphylactic reaction. The postulated mechanism is most likely an alpha receptor mediated coronary vascular spasm. However the use of adrenaline in the setting of life threatening anaphylaxis is life saving and the benefits far outweigh the risks of adverse effects. Therefore the purpose of reporting this case is not to discourage the use of adrenaline in anaphylaxis but to make aware of this potential adverse effect which can occur in the acute setting.

BackgroundTakayasu arteritis is a rare, chronic large vessel vasculitis involving the aorta and its primary branches. As the disease progresses, the active inflammation of large vessels leads to dilation, narrowing and occlusion of the arteries. Arterial dissection is due to separation of the layers of the arterial wall resulting in a false lumen, where blood seeps into the vessel wall. Neurological sequelae of intracranial arterial dissection results from cerebral ischemia due to thromboembolism and hypo perfusion. Internal carotid artery dissection in Takayasu arteritis is very rare and complete ophthalmoplegia due to internal carotid artery dissection is also rare. This is the first case report of Takayasu arteritis presenting as complete ophthalmoplegia due to internal carotid artery dissection.Case presentationA 38-year-old Sri Lankan female presented with sudden onset severe headache, fixed dilated pupil, complete ptosis and ophthalmoplegia on the right side. On imaging, dissection and dilatation was evident in the right internal carotid artery from the origin up to the cavernous segment. She also had stenosis and aneurysmal dilatation of right subclavian artery. Takayasu arteritis was diagnosed subsequently. She was started on aspirin and high dose steroids.ConclusionsInternal carotid artery dissection within the cavernous sinus can lead to third, fourth and sixth nerve palsy due to compression, stretching and ischemia from occlusion of the nutritional arteries. This case report illustrates that internal carotid artery dissection should be a differential diagnosis in palsies of the third, fourth, or sixth cranial nerves, especially when associated with headache. In cases of internal carotid artery dissection, vasculitis such as Takayasu arteritis should also be considered.

BackgroundAnaphylaxis is an acute, potentially fatal medical emergency. Myocardial injury or infarction in the setting of an anaphylaxis can be due the anaphylaxis itself, when it is known as Kounis syndrome or it can also be due to the effect of epinephrine treatment. Epinephrine is considered as the cornerstone in management of anaphylaxis. Myocardial infarction secondary to therapeutic doses of adrenaline is a rare occurrence and only a few cases have been reported in literature. The mechanism of myocardial injury was considered to be due to coronary vasospasm secondary to epinephrine as the coronary angiograms were normal on these occasions.Case presentationA 21-year- old previously healthy male got admitted to the local hospital with an urticarial rash and difficulty in breathing, one hour after ingestion of prawns for which he was known to be allergic. He was treated with 0.5 ml of intramuscular adrenaline (1:1000) which was administered to the lateral side of the thigh, following which he developed palpitations and tightening type central chest pain. Electrocardiogram showed ST segment depressions in leads III, aVF and V1 to V5 and he was transferred to a tertiary care hospital. The second electrocardiogram, done 2 h later, showed resolution of ST segment depressions but new T inversions in leads I and aVL. Troponin I was elevated with a titer of 2.15 ng/ml. He was treated with sublingual GTN in the emergency treatment unit and the symptoms resolved. Transthoracic 2D echocardiogram and stress testing with treadmill was normal and CT coronary angiogram revealed normal coronary arteries.ConclusionHere we present a case of a young healthy adult with no significant risk factors for coronary artery disease who developed myocardial infarction following intramuscular administration of therapeutic dose of adrenalin for an anaphylactic reaction. The postulated mechanism is most likely an alpha receptor mediated coronary vascular spasm. However the use of adrenaline in the setting of life threatening anaphylaxis is life saving and the benefits far outweigh the risks of adverse effects. Therefore the purpose of reporting this case is not to discourage the use of adrenaline in anaphylaxis but to make aware of this potential adverse effect which can occur in the acute setting.

BackgroundTakotsubo cardiomyopathy is characterized by transient systolic dysfunction of the apical and mid segments of the left ventricle in the absence of obstructive coronary artery disease. Intraventricular thrombus formation is a rare complication of Takotsubo cardiomyopathy and current data almost exclusively consists of isolated case reports and a few case series. Here we describe a case of Takotsubo cardiomyopathy with formation of an apical thrombus within 24 h of symptom onset, which has been reported in the literature only once previously, to the best of our knowledge. We have reviewed the available literature that may aid clinicians in their approach to the condition, since no published guidelines are available.Case presentationA 68-year-old Sri Lankan female presented to a local hospital with chest pain. Electrocardiogram (ECG) showed ST elevation, and antiplatelets, intravenous streptokinase and a high dose statin were administered. Despite this ST elevation persisted; however the coronary angiogram was negative for obstructive coronary artery disease. Echocardiogram revealed hypokinesia of the mid and apical segments of the left ventricle with typical apical ballooning and a sizable apical thrombus. She had recently had a viral infection and was also emotionally distressed as her sister was recently diagnosed with a terminal cancer. A diagnosis of Takotsubo cardiomyopathy was made and anticoagulation was started with heparin and warfarin. The follow up echocardiogram performed 1 week later revealed a small persistent thrombus, which had completely resolved at 3 weeks.ConclusionThough severe systolic dysfunction is observed in almost all the patients with Takotsubo cardiomyopathy, intraventricular thrombus formation on the first day of the illness is rare. The possibility of underdiagnosis of thrombus can be prevented by early echocardiogram in Takotsubo cardiomyopathy. The majority of reports found in the literature review were of cases that had formed an intraventriclar thrombus within the first 2 weeks, emphasizing the importance of follow up echocardiography at least 2 weeks later. The management of a left ventricular thrombus in Takotsubo cardiomyopathy is controversial and in most cases warfarin and heparin were used for a short duration.

BackgroundTakayasu arteritis is a rare, chronic large vessel vasculitis involving the aorta and its primary branches. As the disease progresses, the active inflammation of large vessels leads to dilation, narrowing and occlusion of the arteries. Arterial dissection is due to separation of the layers of the arterial wall resulting in a false lumen, where blood seeps into the vessel wall. Neurological sequelae of intracranial arterial dissection results from cerebral ischemia due to thromboembolism and hypo perfusion. Internal carotid artery dissection in Takayasu arteritis is very rare and complete ophthalmoplegia due to internal carotid artery dissection is also rare. This is the first case report of Takayasu arteritis presenting as complete ophthalmoplegia due to internal carotid artery dissection.Case presentationA 38-year-old Sri Lankan female presented with sudden onset severe headache, fixed dilated pupil, complete ptosis and ophthalmoplegia on the right side. On imaging, dissection and dilatation was evident in the right internal carotid artery from the origin up to the cavernous segment. She also had stenosis and aneurysmal dilatation of right subclavian artery. Takayasu arteritis was diagnosed subsequently. She was started on aspirin and high dose steroids.ConclusionsInternal carotid artery dissection within the cavernous sinus can lead to third, fourth and sixth nerve palsy due to compression, stretching and ischemia from occlusion of the nutritional arteries. This case report illustrates that internal carotid artery dissection should be a differential diagnosis in palsies of the third, fourth, or sixth cranial nerves, especially when associated with headache. In cases of internal carotid artery dissection, vasculitis such as Takayasu arteritis should also be considered.