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.

Ecstasy produces left ventricular dysfunction and oxidative stress in rats.

AIMS: Our aim was to determine whether the repeated, binge administration of 3,4-methylenedioxymethamphetamine (ecstasy; MDMA) produces structural and/or functional changes in the myocardium that are associated with oxidative stress. METHODS AND RESULTS: Echocardiography and pressure-volume conductance catheters were used to assess left ventricular (LV) structure and function in rats subjected to four ecstasy binges (9 mg/kg i.v. for 4 days, separated by a 10 day drug-free period). Hearts from treated and control rats were used for either biochemical and proteomic analysis or the isolation of adult LV myocytes. After the fourth binge, treated hearts showed eccentric LV dilation and diastolic dysfunction. Systolic function was not altered in vivo; however, the magnitude of the contractile responses to electrical stimulation was significantly smaller in myocytes from rats treated in vivo with ecstasy compared with myocytes from control rats. The magnitude of the peak increase in intracellular calcium (measured by Fura-2) was also significantly smaller in myocytes from ecstasy-treated vs. control rats. The relaxation kinetics of the intracellular calcium transients were significantly longer in myocytes from ecstasy-treated rats. Ecstasy significantly increased nitrotyrosine content in the left ventricle. Proteomic analysis revealed increased nitration of contractile proteins (troponin-T, tropomyosin alpha-1 chain, myosin light polypeptide, and myosin regulatory light chain), mitochondrial proteins (Ub-cytochrome-c reductase and ATP synthase), and sarcoplasmic reticulum calcium ATPase. CONCLUSION: The repeated binge administration of ecstasy produces eccentric LV dilation and dysfunction that is accompanied by oxidative stress. These functional responses may result from the redox modification of proteins involved in excitation-contraction coupling and/or mitochondrial energy production. Together, these results indicate that ecstasy has the potential to produce serious cardiac toxicity and ventricular dysfunction.

An Unusual Case of Embolic Stroke: A Permanent Ventricular Pacemaker Lead Entirely Within the Arterial System Documented by Transthoracic and Transesophageal Echocardiography.

A pacemaker lead in the left ventricle is a rare complication of implantation. Recognition of this complication is important because thromboembolic events are associated. We report the first case, to our knowledge, of a patient who had a permanent pacemaker implanted via the left subclavian artery to the left ventricle, which is documented by electrocardiography, chest radiography, thoracic echocardiography, and transesophageal echocardiography.

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.

Oxidative stress contributes to methamphetamine-induced left ventricular dysfunction.

AIMS: Our aim was to test the hypothesis that the repeated, binge administration of methamphetamine would produce oxidative stress in the myocardium leading to structural remodeling and impaired left ventricular function. METHODS AND RESULTS: Echocardiography and Millar pressure-volume catheters were used to monitor left ventricular structure and function in rats subjected to four methamphetamine binges (3 mg/kg, iv for 4 days, separated by a 10-day drug-free period). Hearts from treated and control rats were used for histological or proteomic analysis. When compared with saline treatment, four methamphetamine binges produced eccentric left ventricular hypertrophy. The drug also significantly impaired systolic function (decreased fractional shortening, ejection fraction, and adjusted maximal power) and produced significant diastolic dysfunction (increased -dP/dt and tau). Dihydroethedium staining showed that methamphetamine significantly increased (285%) the levels of reactive oxygen species in the left ventricle. Treatment with methamphetamine also resulted in the tyrosine nitration of myofilament (desmin, myosin light chain) and mitochondrial (ATP synthase, NADH dehydrogenase, cytochrome c oxidase, prohibitin) proteins. Treatment with the superoxide dismutase mimetic, tempol in the drinking water prevented methamphetamine-induced left ventricular dilation and systolic dysfunction; however, tempol (2.5 mM) did not prevent the diastolic dysfunction. Tempol significantly reduced, but did not eliminate dihydroethedium staining in the left ventricle, nor did it prevent the tyrosine nitration of mitochondrial and contractile proteins. CONCLUSION: This study shows that oxidative stress plays a significant role in mediating methamphetamine-induced eccentric left ventricular dilation and systolic dysfunction.