Large Left Ventricular Outflow Tract Pseudoaneurysm Closed Percutaneously From a Novel Apical Approach.

An incidental finding of a large left ventricular outflow tract pseudoaneurysm in a 74-year-old man, with high surgical risk, was managed with a novel, fully percutaneous, left ventricular apical approach. The pseudoaneurysm defect and the apical puncture site were successfully closed with Amplatzer septal occluders with successful positioning, as demonstrated on cardiac computed tomography at 6 weeks follow-up. ().

Myocardial infarction following sclerotherapy in a patient with a patent foramen ovale.

A case is reported of myocardial infarction occurring following sclerotherapy for varicose veins in a patient with a patent foramen ovale (PFO). It is believed that microemboli crossed the PFO as a result of the procedure and caused coronary artery embolisation, resulting in the symptoms, electrocardiographic and biochemical evidence of myocardial infarction.

Percutaneous closure of post-myocardial infarction ventricular septal defects: a single centre experience.

Background: Ventricular septal defect (VSD) is a serious complication of myocardial infarction (MI), occurring in about 0.2% of cases. Untreated, mortality in high and early surgical repair is difficult because of friable necrotic tissue.

Percutaneous closure of left ventricular free wall rupture with associated false aneurysm to prevent cardioembolic stroke.

Left ventricular (LV) false aneurysm is an uncommon complication of myocardial infarction. Conventional treatment mandates surgical repair but is associated with significant perioperative risk. We present a case of successful percutaneous closure of a LV false aneurysm in a patient at high operative risk who suffered cardioembolic stroke related to thrombus within the aneurysm.

Angina pectoris prior to myocardial infarction protects against subsequent left ventricular remodeling.

Objectives: To investigate the hypothesis that prior angina pectoris confers protection from remodeling occurring after myocardial infarction (MI), we analyzed echocardiograms from the Healing and Early Afterload Reducing Therapy (HEART) trial.

Background: Ischemia occurring before MI has been shown to reduce infarct size in experimental models and to improve outcomes in patients. The extent to which ischemia occurring before MI influences subsequent changes in ventricular size and function is unclear.

Associations between plasma natriuretic peptide levels, symptoms, and left ventricular function in patients with chronic aortic regurgitation.

In 40 patients with chronic moderate to severe aortic regurgitation, brain natriuretic peptide, N-brain natriuretic peptide, and atrial natriuretic peptide were higher in symptomatic patients compared with asymptomatic patients after adjustment for age, gender, and ejection fraction, but each natriuretic peptide correlated weakly with echocardiographic measures of left ventricular size and function. In patients with chronic aortic regurgitation, measurement of natriuretic peptide levels may provide information on left ventricular function in addition to echocardiography.

Value of the electrocardiogram in predicting left ventricular enlargement and dysfunction after myocardial infarction.

To identify electrocardiographic predictors of left ventricular enlargement or persistent dysfunction following a myocardial infarction. Baseline and predischarge 12-lead electrocardiograms (ECGs) from 272 patients with anterior myocardial infarction who were enrolled in the Healing and Early Afterload Reducing Therapy trial were evaluated and related to echocardiographic data obtained at baseline and day 90. ST-segment elevation, QRS score, and number of negative T waves were assessed at both time points.

Entrapment of mitral chordal apparatus causing early postoperative dysfunction of a St. Jude mitral prosthesis.

Preservation of subvalvular apparatus is increasingly performed during mitral valve replacement. We describe a case of early postoperative St. Jude mitral valve dysfunction as a result of chordal entrapment.