Normally functioning quadricuspid aortic valve mistaken for bicuspid valve in a septuagenarian.

A 70-year-old male underwent transthoracic (TTE) and transesophageal (TEE) echocardiography for a stroke. A bicuspid aortic valve was suspected by TTE, but TEE revealed a normally functioning quadricuspid aortic valve. A quadricuspid aortic valve may be more common than generally thought, as it may not be readily diagnosed by TTE, and may remain functionally normal.

Grade I diastolic dysfunction and elevated left ventricular end-diastolic pressure: Mitral Doppler inflow, pulmonary vein atrial reversal, and the M-mode mitral B-bump.

Grade I diastolic dysfunction (DD) is generally associated with a normal mean left atrial pressure (LAP) and normal left ventricular end-diastolic pressure (LVEDP). The first hemodynamic alteration seen in DD, however, is the development of an elevated LVEDP with a persistent normal LAP. This is manifested by echocardiography as a continued mitral pulsed wave (PW) E/A <0.8 (Grade I DD), but with evidence of an elevated LVEDP. Such findings include alterations in PV flow, mitral PW inflow response to Valsalva maneuver, and also the presence of a B-bump on the mitral M-mode tracing. When assessing diastolic function, it may be clinically helpful to assess for this early hemodynamic manifestation of DD.

Angiotensin-converting enzyme 2 over-expression in the central nervous system reduces angiotensin-II-mediated cardiac hypertrophy.

Angiotensin-converting enzyme type 2 (ACE2) has been shown to be an important member of the renin angiotensin system. Previously, we observed that central ACE2 reduces the development of hypertension following chronic angiotensin II (Ang-II) infusion in syn-hACE2 transgenic (SA) mice, in which the human ACE2 transgene is selectively targeted to neurons. To study the physiological consequences of central ACE2 over-expression on cardiac function and cardiac hypertrophy, SA and non-transgenic (NT) mice were infused with Ang-II (600 ng/kg/min, sc) for 14 days, and cardiac function was assessed by echocardiography. Blood pressure (BP), hemodynamic parameters, left ventricle (LV) mass/tibia length, relative ventricle wall thickness (2PW/LVD), cardiomyocyte diameters and collagen deposition were similar (P>0.05) between NT and SA mice during saline infusion. After a 2-week infusion, BP was elevated in NT but not in SA mice. Although ejection fraction and fractional shortening were not altered, Ang-II infusion increased 2PW/LVD compared to saline infusion in NT mice. Interestingly, the 2PW/LVD and LV mass/tibia ratios were significantly lower in SA compared to NT mice at the end of infusion. Moreover, Ang-II infusion significantly increased arterial collagen deposition and cardiomyocytes diameter in NT mice but not in transgenic animals (P<0.05). More importantly, ACE2 over expression significantly reduced the Ang-II-mediated increase in urine norepinephrine levels in SA compared to NT mice. The protective effect of ACE2 appears to involve reductions in Ang-II-mediated hypertension and sympathetic nerve activity.

Obesity and left ventricular dilatation in young adulthood: the Bogalusa Heart Study.

BACKGROUND: Cardiac enlargement is an important predictor of adverse cardiovascular (CV) events. Left ventricular (LV) dilatation is a precursor both of LV dysfunction and clinical heart failure. The present study examines risk factors for LV dilatation among 832 young adults (341 male, 491 female) who participated in the Bogalusa Heart Study. HYPOTHESIS: A unique set of risk factors predicts LV dilatation among young adults. METHODS: Standard ventricular dimensions were determined by M-mode echocardiography and indexed to height using a standard method. LV dilatation was considered as the top 20th percentile of LV end-diastolic dimension indexed to height. Logistic regression models were used, stratified by race and sex, to assess the relationship of CV risk factors with quintile of LV end-diastolic dimension indexed to height. RESULTS: The mean age (standard deviation) of men and women in the population was 36.4 years (3.9 years) and 35.9 years (4.6 years), respectively. In sex-specific models adjusted for age, race, systolic and diastolic blood pressure, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, and glycosylated hemoglobin, body mass index (BMI) was a significant predictor of LV dilatation in both men and women. The odds ratio (95% confidence interval) for a 1-unit change in BMI was 1.12 (1.02-1.19) in men and 1.09 (1.05-1.13) in women. Among men, triglyceride level was also significantly associated with LV dilatation (P=0.03), whereas among women there was no such association. CONCLUSIONS: Our findings indicate that obesity is the most consistent predictor of LV dilatation in both men and women, whereas triglyceride level was a significant predictor among men only.