A combined approach to correct posterior left ventricular aneurysm, aortic stenosis and coronary artery disease.

Ischaemic heart disease and aortic stenosis are potentially life-threatening conditions. A post-infarct left ventricular aneurysm, when combined with the above, is particularly hazardous. We present a case where all three conditions occurred simultaneously and describe the surgical approach undertaken to attempt correction. The patient underwent aneurysmectomy together with aortic valve replacement and two-vessel coronary artery bypass grafting. The aneurysm was excised with direct linear closure of the walls using a Teflon-buttressed interrupted mattress suture technique. Post-operatively, ventricular systolic function was good (LVEF 40%) together with a well-seated aortic valve showing no paravalvular leaks. This case highlights the importance of meticulous removal of thrombus from the aneurysm and everting the edges thereby eliminating a thrombogenic surface and the risk of embolic stroke. The restorative procedure itself serves to underline the importance of ventricular shape in the effective functioning of the myocardium for sustaining an adequate stroke volume with normalized physiology.

Delayed presentation of a traumatic descending thoracic aorta aneurysm as an aorto-oesophageal fistula.

Aorto-oesophageal fistula is a rarely described but life-threatening complication presenting with upper gastrointestinal haemorrhage. We present a case of a 58-year-old gentleman who presented to a peripheral hospital with a short duration of haematemesis and melaena and recent onset symptoms of dysphagia. This gentleman had a past medical history of alcohol excess and a history of trauma following a road traffic accident 38 years ago. Initial computer tomography scan demonstrated a large saccular aneurysm arising from the descending thoracic aorta adjacent to the oesophagus. The patient underwent radiological stenting of the large aneurysm with thoracic endovascular aortic replacement procedure. Follow-up computerized tomography (CT) angiography demonstrated satisfactory appearances of the thoracic aortic stent graft with no evidence of endo-leak. The triad of dysphagia, occult gastrointestinal blood loss and CT findings of a large aneurysm should prompt diagnosis or aorto-oesophageal fistula until proven otherwise.

Single stage repair for aortic root aneurysm in a patient with coexisting coarctation incorporating the Cabrol technique: a case report.

BACKGROUND: A 44 year old man who presented with a history of chest pain and dyspnoea was found to have an aneurysm of the aortic root, aortic valve insufficiency, and coarctation of the aorta. CASE PRESENTATION: The patient underwent a single stage procedure to treat the aortic root, valve and coarctation with a composite valved conduit and extra-anatomic bypass of the coarctation. The modified Cabrol technique was necessary to attach the coronary buttons due to grossly abnormal anatomy. The patient made a remarkable recovery and was discharged on the 8th post-operative day. CONCLUSION: This case report highlights the feasibility and efficacy of performing a single stage procedure on complex coarctation with associated cardiac defects. To the best of our knowledge, this is the first report of the modified Cabrol technique being used in this particular setting.

Etiology and management of spontaneous haemothorax.

Spontaneous haemothorax (SH) is a subcategory of haemothorax that involves the accumulation of blood within the pleural space in the abscence of trauma or other causes. The clinical presentation is variable and includes a rapid progression of symptoms of chest pain and dyspnea that can be life threatening when hemodynamic instability and hypovolemic shock occurs. Despite haemothorax, SH is much less common with data limited to case reports and case series. A literature review has been performed to identify and summarise all potentials causes leading to this clinical entity.

Obesity, inflammation and brachial artery flow-mediated dilatation: therapeutic targets in patients with microvascular angina (cardiac syndrome X).

BACKGROUND: The pathophysiology of microvascular angina (cardiac syndrome X, CSX), (effort-induced angina, a positive response to exercise stress testing and angiographically normal coronary arteries) has not been fully elucidated. Various pathogenic mechanisms have been proposed, amongst which coronary microvascular dysfunction features prominently. Management of patients with microvascular angina is often challenging as a substantial number of patients does not respond to conventional anti-anginal therapy. In this study, we sought to assess the association between brachial artery FMD, high-sensitive C-reactive protein (hs-CRP) and cardiovascular risk factors including obesity in patients with cardiac syndrome X. METHODS AND RESULTS: Thirty-four consecutive CSX patients (29 female, mean age 60 ± 9 years) were recruited from a specialised CSX clinic. Twelve asymptomatic subjects (10 female, mean age 51 ± 12 years) with comparable cardiovascular risk factor profile served as controls. All participants underwent standardized computer-assisted FMD measurements and assessment of hs-CRP concentrations at study entry. Body mass index (BMI), used as a general measure of obesity was calculated as weight (kilograms) divided by height (meters squared). Compared to controls, CSX patients had significantly higher hs-CRP concentrations (p = 0.003) and impaired FMD (p < 0.01). Moreover, among the CSX patients, a correlation between FMD and hs-CRP (r = -0.66, p < 0.01), FMD and BMI (r = 0.377, p = 0.028), and hs-CRP and BMI (r = -0.372, p = 0.030) was found. CONCLUSION: Impaired brachial artery FMD is significantly associated with elevated hs-CRP concentrations and BMI in patients with CSX. The results support the concept that low-grade inflammation and obesity may promote vascular dysfunction in these patients representing therapeutic targets for future research investigations.

Managing unstable angina and non-ST elevation MI.

Acute coronary syndrome (ACS), encompassing unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI), is often the result of an acute thrombotic occlusion of the coronary vessels, associated with atheromatous plaque rupture or erosion. ACS is associated with a severely impaired prognosis and requires prompt and efficient specialist treatment. The clinical presentation may be identical across all three components of ACS. Establishing an accurate diagnosis without delay is of paramount importance to start treatment promptly. Patients with suspected ACS need to be referred immediately to A&E. Prehospital treatment, which includes aspirin, nitrates, morphine and oxygen (if hypoxic), should be initiated rapidly. Important features pointing towards a diagnosis of ACS include: typical characteristics of chest pain, presence of risk factors, and ECG changes suggestive of myocardial ischaemia. Chest discomfort in patients with ACS typically occurs at rest, is anginal in character and can range from mild tightness to central crushing chest pain. It may be associated with nausea, dyspnoea or diaphoresis. The chest pain may radiate to the arms, back or jaw and is often >20 minutes in duration. An accurate clinical history and a detailed examination are vital. Initial investigations are the same for all ACS events, with the need for urgent serial ECGs and the measurement of cardiac troponin levels, to assess myocardial damage. In NSTEMI, ECG changes suggestive of ischaemia are often present and associated with elevated cardiac troponin. In UA, there is a considerable reduction in myocardial perfusion leading to symptoms; but there is no rise in cardiac troponin. Risk stratification is imperative in assessment of ACS to allow efficient delivery of specialist care. Treatment includes: antiplatelets; antithrombotic agents; angina drugs; analgesia, and PCI.