Averycleveland1070

The incidence of the post-infarct ventricular septal defect (VSD) is 0.17%. Surgical repair is the definitive treatment and percutaneous closure is an alternative in high-risk patients. We report a case of post-myocardial infarction inferior wall aneurysm associated with a large ventricular septal rupture, with a communication between the aneurysm and right ventricle. Successful percutaneous closure of both the aneurysm and the post-infarct (VSD) was performed using two Amplatzer septal occluder devices.

A 76-year-old man was referred to the clinic 2 weeks after an inferior wall myocardial infarction. A harsh, pansystolic murmur was appreciated on his left parasternal area and across the pericardium. An echocardiogram demonstrated a large, true aneurysm in the mid-cavity inferior wall. The inferior septum was ruptured and dissected, with a large, left-to-right shunt. The patient's coronary angiography revealed a multi-vessel disease. The patient was considered as high surgical risk and thus transcatheter vourable to device placement.

Acute pericarditis is frequently encountered in clinical practice; however, pericarditis as the first presentation of Graves' disease is rare and mainly limited to case reports in the literature. We hereby report a case in which a young patient presented with pericarditis as the first manifestation of Graves' disease.

A 24-year-old male was admitted to hospital with presenting complaint of left-sided chest pain, gradual in onset, 6/10 in intensity, sharp in character, increased by deep breathing and improved by leaning forward. Patient also gave a history of insomnia, unintentional weight loss despite a good appetite, heat intolerance, and anxiety. On clinical examination, the patient had features of thyrotoxicosis, i.e., tachycardia, high volume pulse, and sweaty palms with fine tremors. There was no associated pericardial rub. Neck examination shows diffuse, non-tender goitre. Electrocardiogram findings were consistent with acute pericarditis. His thyroid function tests demonstrated hyperthyroidism and -pericarditis is a rare entity, and limited literature is available regarding this combination. BAY-61-3606 chemical structure The exact aetiology of Graves associated pericarditis is unknown. There is a possibility of interaction of autoantibodies with receptors on pericardium. Diagnosis is based on a detailed history, clinical examination, supplemented by relevant investigations (elevated free T4 and thyroid receptor antibodies, suppressed thyroid stimulating hormone (TSH) and Imaging via ultrasound). Mainstay of treatment includes non-steroidal anti-inflammatory drugs, beta-blockers, and anti-thyroidal medications.

Aortic aneurysms are known to cause compression of adjacent structures including the tracheobronchial tree, oesophagus, and recurrent laryngeal nerve. Extremely rarely, they can lead to compression of the tricuspid valve (TV) annulus. We describe a case where aortic aneurysm caused TV annulus compression and persistent right-to-left shunt through a patent foramen ovale (PFO).

A 75-year-old female was admitted with headache and dizziness. On examination, she had persistent arterial desaturation with oxygen levels reduced to 69% at rest whilst breathing ambient air. Complete blood count demonstrated polycythaemia (Hb 174 g/L). Right to left cardiac shunt was suspected after significant lung and haematologic pathology was excluded. Transoesophageal echocardiography demonstrated a trileaflet aortic valve with an ascending aorta aneurysm and a stretched PFO with persistent right to left shunt across it. The ascending aortic aneurysm was observed coursing superior to and compressing the TV annulus. Invasive haemodynamic data demonstrated prominent 'a' waves in the right atrium, low RV (12/1 mmHg), and pulmonary artery pressures (14/6 mmHg), reduced cardiac output and significant right to left shunt with QpQs 0.6. Computed tomography (CT) angiogram demonstrated a 5 cm fusiform ascending aorta aneurysm that coursed anteriorly causing TV annulus compression.

Tricuspid valve inflow obstruction associated with a right to left shunt across PFO can be an extremely rare complication of aortic aneurysm. This may result in persistent arterial hypoxaemia and secondary polycythaemia.

Tricuspid valve inflow obstruction associated with a right to left shunt across PFO can be an extremely rare complication of aortic aneurysm. This may result in persistent arterial hypoxaemia and secondary polycythaemia.

Accelerated idioventricular rhythm (AIVR) is known as reperfusion arrhythmia in the setting of acute myocardial infarction (AMI). In healthy individuals, it is usually considered to be benign. Alternating bundle branch block (ABBB) often progresses to complete atrioventricular block requiring permanent pacemaker implantation. We report a case of delayed appearance of AIVR following myocardial infarction (MI) in combination with ABBB as precursor of sudden cardiac arrest due to ventricular fibrillation (VF).

A 62-year-old male with pre-existing left bundle branch block (LBBB) was admitted with an acute non-ST segment elevation MI. He underwent successful percutaneous coronary intervention (PCI) of a subtotal proximal left anterior descending artery (LAD) stenosis. Before and after PCI the electrocardiogram (ECG) demonstrated sinus rhythm with LBBB. The patient was discharged 5 days after PCI, left ventricular function at this time was moderately reduced (ejection fraction of 40%). After another 5 days, the patient was admitted for elective cardiac rehabilitation. At this time, the ECG demonstrated an AIVR with right bundle branch block morphology. Due to ABBB, the patient was scheduled for permanent pacemaker implantation. Before pacemaker implantation could take place, the patient developed a sudden cardiac arrest due to VF and was successfully resuscitated. A follow-up coronary angiography revealed no novel lesions. A cardiac resynchronization therapy defibrillator was implanted for secondary prevention of sudden cardiac death.

Delayed occurrence of AIVR in combination with ABBB following AMI could be a predictor of sudden cardiac death. These patients are probably at high risk for malignant ventricular arrhythmias.

Delayed occurrence of AIVR in combination with ABBB following AMI could be a predictor of sudden cardiac death. These patients are probably at high risk for malignant ventricular arrhythmias.