Retrograde percutaneous closure of a ventricular septal defect after myectomy for hypertrophic obstructive cardiomyopathy.

In patients with hypertrophic obstructive cardiomyopathy, hemodynamically significant ventricular septal defect after septal myectomy is a rare sequela that warrants closure. Percutaneous closure provides a safer alternative to repeated sternotomy, which is associated with significant morbidity and mortality rates. We report a possibly unique case of successful retrograde percutaneous closure, with an AMPLATZER Muscular VSD Occluder, of an iatrogenic ventricular septal defect consequent to surgical therapy for hypertrophic obstructive cardiomyopathy.

Underweight and overweight men have greater exercise-induced dyspnoea than normal weight men.

INTRODUCTION: Persons with high or low body mass index (BMI), involved in clinical or mechanistic trials involving exercise testing, might estimate dyspnoea differently from persons with a normal BMI. AIMS: Our objective was to investigate the relationship between BMI and dyspnoea during exercise in normal subjects with varying BMI. MATERIAL AND METHODS: A total of 37 subjects undertook progressive exercise testing. Subjects were divided into three groups: underweight (UW), normal weight (NW), and overweight (OW). Dyspnoea was estimated using the visual analogue scale (VAS). Spirometry, maximum voluntary ventilation (MVV), and respiratory muscle strength (RMS) were measured. RESULTS AND DISCUSSION: The intercept of the VAS/ventilation relationship was significantly higher in NW subjects compared to UW (P = 0.029) and OW subjects (P = 0.040). Relative to the OW group, FVC (P = 0.020), FEV(1) (P = 0.024), MVV (P = 0.019), and RMS (P = 0.003) were significantly decreased in the UW group. The greater levels of dyspnoea in UW subjects could possibly be due to decreased RMS. Healthy persons should aim to achieve an optimum BMI range to have the lowest exercise-induced dyspnoea.

Isolated nonspecific ST-segment and T-wave abnormalities in a cross-sectional United States population and Mortality (from NHANES III).

Most clinicians regard isolated, minor, or nonspecific ST-segment and T-wave (NS-STT) abnormalities to be incidental, often transient, and benign findings in asymptomatic patients. We sought to evaluate whether isolated NS-STT abnormalities on routine electrocardiograms (ECGs) are associated with increased risk of cardiovascular mortality (CM) and all-cause mortality (AM) in a cross-sectional United States population without known coronary artery disease. We included all adults 40 to 90 years of age without known coronary artery disease or risk equivalent based on history and laboratory values, enrolled in the NHANES III from 1988 to 1994, with electrocardiographic data available, and a total follow-up period of 59,781.75 patient-years. NS-STT abnormalities were defined by Minnesota Coding. Subjects were excluded if their mortality data were missing or if they had major electrocardiographic abnormalities, heart rate >120 beats/min, nonsinus rhythm, cardiac infarction/injury score ≥ 20 on ECG, left ventricular hypertrophy by Minnesota Codes 3.1 and 3.3, or patient-reported history coronary artery disease, congestive heart failure, stroke, diabetes, or peripheral arterial disease. The remaining 4,426 subjects were stratified by presence or absence of NS-STT abnormalities. Mortality was judged based on International Classification of Diseases, Tenth Revision coding linked to the National Death Index. Cox proportional hazard ratio was used for multivariate analysis, showing that CM (hazards ratio 1.71, 95% confidence interval 1.04 to 2.83, p = 0.04) and AM (hazards ratio 1.37, 95% confidence interval 1.03 to 1.81, p = 0.02) were significantly higher in the isolated NS-STT abnormalities group. In conclusion, isolated NS-STT abnormalities on ECG were associated with a higher incidence of CM and AM in this large nationally representative cross-sectional cohort without known coronary artery disease or coronary artery disease risk equivalents.

A tale of two pressures: a case of pseudo-prosthetic mitral valve stenosis.

We present a case of an 83-year-old female with past medical history of rheumatic fever associated mitral stenosis for which she underwent mitral commissurotomy 25 years prior to presentation. Subsequently, she underwent coronary artery bypass grafting and mitral valve replacement with a bio-prosthetic valve 8 years prior to presentation. Presently, she started experiencing worsening dyspnea and heart failure symptoms. Echocardiography showed mildly reduced left ventricular ejection fraction with severe aortic stenosis and pulmonary hypertension. The bioprosthetic mitral valve was functioning normally. We performed right and left heart catheterization for evaluation. Peak aortic gradient was 50 mm Hg with a mean gradient of 39 mm Hg. Aortic valve area was calculated to be 0.31 cm(2). However, simultaneous measurement of left ventricular and wedge pressures showed a significant gradient of 11 mm Hg across the mitral valve with a calculated mitral valve area of 0.4 cm(2). Because of discordant information between echocardiographic and hemodynamic data, we proceeded with trans-septal puncture to directly measure left atrial pressures. Simultaneous left atrial and left ventricular pressure measurement demonstrated a mean gradient of 4 mm Hg across the mitral valve with an area calculated at 1.9 cm(2). We review the tracings in detail and discuss the pitfalls of using pulmonary capillary wedge pressure as a surrogate for left atrial pressure.

Orthodeoxia platypnea syndrome in a patient with lipomatous hypertrophy of the interatrial septum due to long-term steroid use.

We describe an unusual case of orthodeoxia platypnea syndrome exacerbated by right ventricular inflow obstruction due to iatrogenic steroid-induced adipose deposition in cardiac tissues. A 68-year-old man on long-term prednisone therapy for eosinophilic pneumonia presented with progressive dyspnea worsened by bending forward. By using pulse oximetry, he was noted to have positional hypoxemia. Transthoracic echocardiogram demonstrated normal right-sided pressures but severe right to left shunting through a patent foramen ovale. Transesophageal echocardiogram showed a large patent foramen ovale, severe lipomatous hypertrophy of the interatrial septum, and massive adipose deposition in the pericardium causing compression of the right ventricular inflow tract. The patient underwent percutaneous closure of the patent foramen ovale, which resulted in the resolution of symptoms and hypoxemia. This case is unique because long-term steroid use resulted in reverse Lutembacher physiology and clinical orthodeoxia platypnea syndrome by inducing lipomatous hypertrophy of the interatrial septum and compression of the right atrium.