Haotian Gu

Cardiac valve disease and low-dose dopamine agonist therapy: an artefact of reporting bias?

Introduction  Chronic low‐dose cabergoline treatment for microprolactinoma may cause cardiac valve pathology, but the evidence is contradictory. We investigated whether the expectation of the echocardiographer could influence the report.

Reduced First-Phase Ejection Fraction and Sustained Myocardial Wall Stress in Hypertensive Patients with Diastolic Dysfunction: A Manifestation of Impaired Shortening Deactivation That Links Systolic to Diastolic Dysfunction and Preserves Systolic Ejection Fraction

Impaired shortening deactivation of cardiac myocytes could sustain myocardial contraction, preserving ejection fraction at the expense of diastolic dysfunction. We examined the relationship between first-phase ejection fraction (EF1), the fraction of left ventricular volume ejected from the start of systole to the time of the first peak in left ventricular pressure (corresponding to the time of maximal ventricular shortening) to the duration of myocardial contraction and diastolic function in patients with hypertension (n=163), and varying degrees of diastolic dysfunction. Left ventricular systolic pressure was estimated by carotid tonometry; time-resolved left ventricular cavity and wall volume were obtained by echocardiography with speckle wall tracking. Measurements were repeated after nitroglycerin, a drug known to influence ventricular dynamics, in a subsample (n=18) of patients. EF1 and time of onset of ventricular relaxation (as determined from the temporal pattern of myocardial wall stress) were independently correlated with diastolic relaxation as measured by tissue Doppler early diastolic mitral annular velocity (E′, standardized regression coefficients 0.48 and −0.34 for EF1 and time of onset of ventricular relaxation, respectively, each P<0.001, irrespective of adjustment for age, sex, antihypertensive treatment, measures of afterload, and ventricular geometry) and with diastolic function measured by the ratio of transmitral Doppler early filling velocity (E) to E′ (E/E′, regression coefficients −0.34 and 0.34, respectively, each P<0.001). Nitroglycerin increased EF1, decreased time of onset of ventricular relaxation, and improved diastolic function (each P<0.05). Hypertensive patients with diastolic dysfunction exhibit reduced EF1 which may sustain myocardial contraction, preserving systolic ejection fraction at the expense of impaired diastolic function.

Myocardial Deformation Measured by 3-Dimensional Speckle Tracking in Children and Adolescents With Systemic Arterial HypertensionNovelty and Significance

Systemic arterial hypertension predisposes children to cardiovascular risk in childhood and adult life. Despite extensive study of left ventricular (LV) hypertrophy, detailed 3-dimensional strain analysis of cardiac function in hypertensive children has not been reported. The aim of this study was to evaluate LV mechanics (strain, twist, and torsion) in young patients with hypertension compared with a healthy control group and assess factors associated with functional measurements. Sixty-three patients (26 hypertension and 37 normotensive) were enrolled (mean age, 14.3 and 11.4 years; 54% men and 41% men, respectively). All children underwent clinical evaluation and echocardiographic examination, including 3-dimensional strain. There was no difference in LV volumes and ejection fraction between the groups. Myocardial deformation was significantly reduced in those with hypertension compared with controls. For hypertensive and normotensive groups, respectively, global longitudinal strain was −15.1±2.3 versus −18.5±1.9 (P<0.0001), global circumferential strain −15.2±3 versus −19.9±3.1 (<0.0001), global radial strain +44.0±11.3 versus 63.4±10.5 (P<0.0001), and global 3-dimensional strain −26.1±3.8 versus −31.5±3.8 (P<0.0001). Basal clockwise rotation, apical counterclockwise rotation, twist, and torsion were not significantly different. After multivariate regression analyses blood pressure, body mass index and LV mass maintained a significant relationship with measures of LV strain. Similar ventricular volumes and ejection fraction were observed in hypertensive and normotensive children, but children with hypertension had significantly lower strain indices. Whether reduced strain might predict future cardiovascular risk merits further longitudinal study.

Forward and Backward Pressure Waveform Morphology in Hypertension

We tested the hypothesis that increased pulse wave reflection and altered backward waveform morphology contribute to increased pulse pressure in subjects with higher pulse pressure compared with lower pulse pressure and to actions of vasoactive drugs to increase pulse pressure. We examined the relationship of backward to forward wave morphology in 158 subjects who were evaluated for hypertension (including some normotensive subjects) divided into 3 groups by central pulse pressure: group 1, 33±6.5 mm Hg; group 2, 45±4.1 mm Hg; and group 3, 64±12.9 mm Hg (means±SD) and in healthy normotensive subjects during administration of inotropic and vasomotor drugs. Aortic pressure and flow in the aortic root were estimated by carotid tonometry and Doppler sonography, respectively. Morphology of the backward wave relative to the forward wave was similar in subjects in the lowest and highest tertiles of pulse pressure. Similar results were seen with the inotropic, vasopressor and vasodilator drugs, dobutamine, norepinephrine, and phentolamine, with the backward wave maintaining a constant ratio to the forward wave. However, nitroglycerin, a drug with a specific action to dilate muscular conduit arteries, reduced the amplitude of the backward wave relative to the forward wave from 0.26±0.018 at baseline to 0.19±0.019 during nitroglycerin 30 &mgr;g/min IV (P<0.01). These results are best explained by an approximately constant amount of reflection of the forward wave from the peripheral vasculature. The amount of reflection can be modified by dilation of peripheral muscular conduit arteries but contributes little to increased pulse pressure in hypertension.

Elevated Ejection-Phase Myocardial Wall Stress in Children With Chronic Kidney Disease

Myocardial wall stress (MWS) is thought to be the mechanical stimulus to ventricular hypertrophy. The objective of this study was to examine whether MWS is elevated in children with chronic kidney disease (CKD) who are at high risk of developing adverse cardiovascular events related to left ventricular (LV) hypertrophy. MWS, a function of left ventricular pressure, myocardial wall volume, and cavity volume, was obtained using carotid tonometry to estimate ventricular pressure and 2-dimensional transthoracic echocardiographic wall-tracking to obtain LV cavity and wall volumes. Ninety-two children (50 boys) aged 11.2±3.2 (mean±SD) years, including healthy controls (n=16), and those with CKD disease divided into 3 groups according to estimated glomerular filtration rate (mL/min per 1.73 m2) >90 (CKD 1, n=26), 60 to 90 (CKD 2, n=23), and <60 (CKD≥3, n=27) were studied. There was no significant difference in age, height, weight, central or peripheral blood pressure, LV mass, or mass index in the 4 study groups. By contrast, peak, mean, and end-systolic MWS were higher in children with CKD and increased across stages of CKD (peak MWS, 338.8±18.5 and 397.5±14.3 s/cm2 in controls and CKD≥3, respectively; P=0.01). Higher systolic MWS was explained by a form of LV dysfunction whereby dynamic values of the ratio of wall volume/cavity size during systole were lower in children with CKD than in those without (P=0.001). Children with CKD exhibit blood pressure–independent LV dysfunction which results in increased systolic MWS and which may predispose to LV hypertrophy in later life.

Elevated Myocardial Wall Stress in Children with Chronic Kidney Disease

Myocardial wall stress (MWS) is thought to be the mechanical stimulus to ventricular hypertrophy. The objective of this study was to examine whether MWS is elevated in children with chronic kidney disease (CKD) who are at high risk of developing adverse cardiovascular events related to left ventricular (LV) hypertrophy. MWS, a function of left ventricular pressure, myocardial wall volume, and cavity volume, was obtained using carotid tonometry to estimate ventricular pressure and 2-dimensional transthoracic echocardiographic wall-tracking to obtain LV cavity and wall volumes. Ninety-two children (50 boys) aged 11.2±3.2 (mean±SD) years, including healthy controls (n=16), and those with CKD disease divided into 3 groups according to estimated glomerular filtration rate (mL/min per 1.73 m2) >90 (CKD 1, n=26), 60 to 90 (CKD 2, n=23), and <60 (CKD≥3, n=27) were studied. There was no significant difference in age, height, weight, central or peripheral blood pressure, LV mass, or mass index in the 4 study groups. By contrast, peak, mean, and end-systolic MWS were higher in children with CKD and increased across stages of CKD (peak MWS, 338.8±18.5 and 397.5±14.3 s/cm2 in controls and CKD≥3, respectively; P=0.01). Higher systolic MWS was explained by a form of LV dysfunction whereby dynamic values of the ratio of wall volume/cavity size during systole were lower in children with CKD than in those without (P=0.001). Children with CKD exhibit blood pressure–independent LV dysfunction which results in increased systolic MWS and which may predispose to LV hypertrophy in later life.

Echocardiography Predicts Major Adverse Cardiovascular Events after Renal Transplantation

Introduction: Cardiovascular disease is a leading cause of morbidity and mortality after renal transplantation. We analysed whether pre-transplant transthoracic echocardiograms (TTE) predicted major adverse cardiovascular events (MACE) after transplant. Methods: We retrospectively analysed clinical and TTE data from patients having renal transplantation at a single centre between 1 January 2000 and 31 December 2010. The TTE were classified as: group A - normal; group B - mild abnormalities expected in renal failure; group C - moderate to severe abnormalities likely to change management. They were also scored based on four independent risk factors [age ≥50, left ventricular (LV) end systolic diameter ≥3.5 cm, LV wall thickness ≥1.4 cm and mitral annulus calcification]. Post-transplantation clinical notes were examined for MACE (death, stroke, myocardial infarction, and surgical or percutaneous revascularisation). Results: There were 343 patients, mean age 47 (range 21-83) years, 210 of whom were male. MACE occurred in 29 (8.5%) at a mean of 3.6 (SD 3.3) years after transplantation. They were older (p ≤ 0.001), had larger LV mass (p = 0.02), LV wall thickness (p = 0.008) and left atrial size (p = 0.001) than those without MACE. The MACE rate for groups A, B and C were 1.8, 13.6 and 16.4% (p ≤ 0.001), respectively. Using the score, the risk of MACE was 4.7, 10.7, 9.2 and 40% for scores 0, 1, 2 and 3 (p = 0.023), respectively. Conclusion: Preoperative transthoracic echocardiography identifies patients at risk of death or non-fatal cardiovascular events even late after renal transplantation. This suggests that echocardiography might be useful to identify patients requiring more aggressive long-term treatment of modifiable vascular risk factors.