Left ventricular adaptation to high altitude: speckle tracking echocardiography in lowlanders, healthy highlanders and highlanders with chronic mountain sickness.

Hypoxic exposure depresses myocardial contractility in vitro, but has been associated with indices of increased cardiac performance in intact animals and in humans, possibly related to sympathetic nervous system activation. We explored left ventricular (LV) function using speckle tracking echocardiography and sympathetic tone by spectral analysis of heart rate variability (HRV) in recently acclimatized lowlanders versus adapted or maladapted highlanders at high altitude. Twenty-six recently acclimatized lowlanders, 14 healthy highlanders and 12 highlanders with chronic mountain sickness (CMS) were studied. Control measurements at sea level were also obtained in the lowlanders. Altitude exposure in the lowlanders was associated with slightly increased blood pressure, decreased LV volumes and decreased longitudinal strain with a trend to increased prevalence of post-systolic shortening (p = 0.06), whereas the low frequency/high frequency (LF/HF) ratio increased (1.62 ± 0.81 vs. 5.08 ± 4.13, p < 0.05) indicating sympathetic activation. Highlanders had a similarly raised LF/HF ratio, but no alteration in LV deformation. Highlanders with CMS had no change in LV deformation, no significant increase in LF/HF, but decreased global HRV still suggestive of increased sympathetic tone, and lower mitral E/A ratio compared to healthy highlanders. Short-term altitude exposure in lowlanders alters indices of LV systolic function and increases sympathetic nervous system tone. Life-long altitude exposure in highlanders is associated with similar sympathetic hyperactivity, but preserved parameters of LV function, whereas diastolic function may be altered in those with CMS. Altered LV systolic function in recently acclimatized lowlanders may be explained by combined effects of hypoxia and changes in loading conditions.

Quantification of low-gradient severe aortic stenosis using a hybrid approach combining Doppler echocardiography and thermodilution.

BACKGROUND AND AIM OF THE STUDY: Estimation of stroke volume in the left ventricular outflow tract (LVOT) is a main limitation to aortic valve area (AVA) calculation by echocardiography when using the continuity equation. In this study, the hypothesis was tested that a hybrid method using thermodilution-derived cardiac output measurement and simultaneous Doppler estimation of the systolic ejection period and transvalvular aortic velocities could be used to accurately assess AVA in patients with low-gradient severe aortic stenosis (AS). METHODS: Eighteen patients with low mean gradient (< 40 mmHg) and nine patients with conventionally defined (> or = 40 mmHg) severe AS (< 1 cm2), as assessed by the echocardiographic continuity equation (baseline echocardiography), underwent catheterization and simultaneous Doppler recording of trans-aortic velocities. RESULTS: The mean pressure gradient was slightly lower by Doppler in the catheterization laboratory (35.8 +/-15.7 mmHg) compared to baseline echocardiography (37.4 +/- 15.2 mmHg) and invasive (38.5 +/- 16.6 mmHg) measurements (both p < 0.05). The AVA values were 0.72 +/- 0.12 cm2 during baseline echocardiography, 0.74 +/- 0.14 cm2 by catheterization, and 0.71 +/- 0.14 cm2 by the hybrid method (bias -0.01 +/- 0.11 cm2 and -0.02 +/- 0.08 cm2, versus echocardiography and catheterization, respectively; both p = NS). CONCLUSION: The hybrid method is reasonably accurate in assessing AVA in patients with low-gradient severe AS. Although the continuity equation should be used in routine clinical practice in most patients, this method could serve as an alternative when the LVOT diameter and/or velocities seem questionable.

Looking at the frame after the picture: "retrocardiac echocardiography".

We report three cases of mediastinal structures encroaching on the left atrium without haemodynamic compromise. These cases emphasize the potential role of echocardiography for the diagnosis and the management of several extracardiac mediastinal abnormalities.

Left ventricular adaptation to acute hypoxia: a speckle-tracking echocardiography study.

BACKGROUND: Hypoxia depresses myocardial contractility in vitro but does not affect or may even improve indices of myocardial performance in vivo, possibly through associated changes in autonomic nervous system tone. The aim of this study was to explore the effects of hypoxic breathing on speckle-tracking echocardiographic indices of left ventricular function, with and without ß1-adrenergic inhibition. METHODS: Speckle-tracking echocardiography was performed in 21 healthy volunteers in normoxia and after 30 min of hypoxic breathing (fraction of inspired oxygen, 0.12). Measurements were also obtained after the administration of atropine in normoxia (n = 21) and after bisoprolol intake in normoxia (n = 6) and in hypoxia (n = 10). RESULTS: Hypoxia increased heart rate (from 68 ± 11 to 74 ± 9 beats/min, P = .001), without changing mean blood pressure (P = NS), and decreased total peripheral resistance (P = .003). Myocardial deformation magnitude increased (circumferential strain, -19.6 ± 1.9% vs -21.2 ± 2.5%; radial strain, 19.2 ± 3.7% vs 22.6 ± 4.1%, P < .05; longitudinal and circumferential strain rate, -0.88 ± 0.11 vs -0.99 ± 0.15 sec(-1) and -1.03 ± 0.16 vs -1.18 ± 0.18 sec(-1), respectively, P < .05 for both; peak twist, 8.98 ± 3.2° vs 11.1 ± 2.9°, P < .05). Except for peak twist, these deformation parameters were correlated with total peripheral resistance (P < .05). Atropine increased only longitudinal strain rate magnitude (-0.88 ± 0.11 vs -0.97 ± 0.14 sec(-1), P < .05). The increased magnitude of myocardial deformation persisted in hypoxia under bisoprolol (P < .05). In normoxia, bisoprolol decreased heart rate (73 ± 10 vs 54 ± 7 beats/min, P = .0005), mean blood pressure (88 ± 7 vs 81 ± 4 mm Hg, P = .0027), without altering deformation. CONCLUSIONS: Hypoxic breathing increases left ventricular deformation magnitude in normal subjects, and this effect may not be attributed to hypoxia-induced tachycardia or ß1-adrenergic pathway changes but to hypoxia-induced systemic vasodilation.

Pulmonary hypertension and the right ventricle in hypoxia.

Hypoxia causes pulmonary vasoconstriction. Regional hypoxic vasoconstriction improves the matching of perfusion to alveolar ventilation. Global hypoxic vasoconstriction increases right ventricular afterload. The hypoxic pulmonary pressor response is universal in mammals and in birds, but with considerable interspecies and interindividual variability. Chronic hypoxia induces pulmonary hypertension in proportion to initial vasoconstriction. Prolonged hypoxic exposure is also associated with an increase in red blood cell mass, which aggravates pulmonary hypertension by an increase in blood viscosity. Hypoxic pulmonary hypertension in humans is usually mild to moderate, but pulmonary vascular pressure-flow relationships are steep, which corresponds to a substantial afterload on the right ventricle during exercise. A partial recovery of 10-25% of the hypoxia-induced decrease in maximal oxygen uptake has been reported with intake-specific pulmonary vasodilating interventions. Hypoxia has been reported to decrease myocardial fibre contractility in vitro. However, the acutely hypoxic right ventricle remains able to preserve the coupling of its contractility to increased afterload in intact animals. Echocardiographic studies of the right ventricle in healthy hypoxic human subjects show altered diastolic function, but systolic function that is preserved or even increased acutely and slightly depressed chronically. These findings are more pronounced in patients with chronic mountain sickness. Their clinical significance remains incompletely understood. Almost no imaging studies of right ventricular function have been reported in a minority of subjects who develop severe pulmonary hypertension and clinical right ventricular failure in hypoxia. No imaging studies of right ventricular function during hypoxic exercise in normal subjects are yet available. Thus, while it is plausible that the right ventricle limits exercise capacity in hypoxia, this still needs to be firmly established.

Infective endocarditis presenting as an isolated aneurysm of the posterior mitral leaflet.

We describe the case of a 64-year-old woman in whom an aneurysm located on the posterior mitral leaflet was detected. Blood cultures grew methicillin-sensitive Staphylococcus epidermidis, and histologic examination of the operative specimen showed polymorphonuclear neutrophilic infiltration of the valve wall associated with fibrin and necrosis, consistent with a diagnosis of endocarditis. The posterior mitral location of the aneurysm and the absence of vegetation are exceptionally rare in this setting. This case demonstrates that a mitral aneurysm may be the sole cardiac presentation of infective endocarditis.

Ischemic mitral regurgitation: not only a bystander.

Ischemic mitral regurgitation (MR) is a common complication of left ventricular (LV) dysfunction related to chronic coronary artery disease. This complex multifactorial disease involves global and regional LV remodeling, as well as dysfunction and distortion of the components of the mitral valve including the chordae, the annulus, and the leaflets. Its occurrence is associated with a poor prognosis. The suboptimal results obtained with the most commonly used surgical strategy, involving mitral valve annuloplasty with coronary bypass grafting, emphasize the need to develop alternative surgical techniques targeting the causal mechanisms of the disease. A comprehensive preoperative assessment of mitral valve configuration and LV geometry and function and an accurate quantification of MR severity at rest and during exercise may contribute to improve risk stratification and to tailor the surgical strategy according to the individual characteristics of the patient.

Normal left ventricular ejection fraction and mass but subclinical myocardial dysfunction in patients with Friedreich's ataxia.

AIMS: Myocardial involvement in Friedreich's ataxia (FRDA) is characterized by iron deposits, diffuse fibrosis, and focal necrosis. We hypothesized that subclinical left ventricular (LV) dysfunction may occur in 'FRDA patients who have normal LV ejection fraction (LVEF) and mass. METHODS AND RESULTS: Twenty patients homozygous for the GAA expansion in the frataxin gene (mean age: 35 ± 16 years) and twenty age- and sex-matched controls (mean age: 34 ± 15 years) were studied using conventional echocardiography and speckle-tracking imaging. The two groups did not differ in terms of the LVEF (68 ± 6 vs. 67 ± 6%, in patients and controls, respectively) or LV mass (91 ± 20 vs. 82 ± 17 g/m(2)). Global systolic longitudinal (-15.3 ± 2.1 vs. -17.5 ± 1.6%, P = 0.001) and circumferential (-19.5 ± 2.9 vs. -21.4 ± 2.6%, P = 0.034) strain, and peak LV twist (9.2 ± 3.3 vs. 11.7 ± 2.3°, P = 0.008) were significantly reduced in patients compared with controls. Indexed stroke volume was also significantly lower in patients (36 ± 5 vs. 43 ± 8 mL/m(2), P = 0.0012) and this decreased LV pump performance was associated with a concentric remodelling pattern (relative wall thickness: 0.47 ± 0.08 vs. 0.35 ± 0.05, P < 0.001). CONCLUSION: There is evidence of morphological and functional abnormalities in FRDA patients with normal LVEF and mass.

Management of multiple valve disease.

Multivalvular heart disease is not an uncommon situation, but the paucity of data for each specific situation does not allow the proposal of a standardised, evidence-based management strategy. This paper aims at reviewing the available evidence on the management of multivalvular disease, taking into account the interactions between different valve lesions, the diagnostic pitfalls and the strategies that should be considered in the presence of multiple valvular disease.

Myocardial homing and coronary endothelial function after autologous blood CD34+ progenitor cells intracoronary injection in the chronic phase of myocardial infarction.

Transcoronary transplantation of progenitor cells has been proposed as a novel therapy for ischemic heart failure. The primary aims were to assess the feasibility of obtaining CD34+ cells from blood without mobilization in chronic conditions and to compare homing with results reported in acute conditions. We also evaluated the effect of CD34+ on endothelial function. In 7 patients with a history of an anterior myocardial infarction (20 +/- 2 months), a large amount of CD34 (18.2 +/- 3.0 x 10(6)) were obtained and an intracoronary infusion into the left anterior descending artery via an over-the-wire balloon catheter was performed. Myocardial homing involved 3.2% +/- 0.6% of injected cells. Endothelial function studied with increasing doses of bradykinin was not significantly modified after 3 months. In the treated group, compared with 5 nonrandomized control patients with a similar clinical history, the only echocardiographic significant change (2-way analysis of variance) was a decrease in end-systolic volume (P < 0.03). In conclusion, large amounts of CD34+ cells can be obtained from blood, without mobilization, in the chronic phase of myocardial infarction. As reported in the acute situation 1 hour after treatment, intracoronary infusion of CD34+ cells results in myocardial homing of a few percents of the cells. In this small group of patients, no effect of this therapy is detected on the endothelial function and only marginal changes are observed on echocardiographic parameters.

C-reactive protein increase in acute myocardial infarction.

OBJECTIVE: Considering acute myocardial infarctions (AMI), data demonstrate that C-reactive protein (CRP) levels reflect the severity of myocardial damage and that high CRP level is associated with a worse outcome. This study evaluates the prognostic value of CRP and the determinants of its increase during AMI. METHODS AND RESULTS: A retrospective observational study of 126 patients with a ST-segment elevation myocardial infarction (STEMI); 101 patients had reperfusion therapy (93 thrombolysis, 8 PTCA). Peak CRP (median: 3.5 mg/dl) was achieved the third day. A correlation existed between this peak and age (r = 0.1838; p = 0.0408). Diabetic patients not requiring insulin showed peaks double those of other patients (10.4 versus 6.1 mg/dl; p = 0.0165). The peak was higher in anterior infarctions (anterior: 8.4, lateral: 6.9, inferior: 6.4, posterior: 3.9 mg/dl; p = 0.0206) and for those showing a Q-wave (7.5 versus 3.9 mg/dl; p = 0.0020). It was correlated with the CK (r = 0.246; p = 0.0188) and troponin Ic (r = 0.242; p = 0.0224) peaks among thrombolysed patients. There was an increasing relationship between the occurrence of cardiac failure and the magnitude of the CRP peak. An inverse linear relationship existed between the ejection fraction of the left ventricle and the CRP peak (r = -0.4187; p = 0.0000). CRP peak was lower with statins (3.8 versus 7.0 mg/dl; p = 0.0446). Fibrates were only associated with lower CRP levels at admission (0.6 versus 0.9 mg/dl; p = 0.0010). CONCLUSIONS: CRP is an indicator of the severity of STEMI. It is also an indicator for the occurrence of complications during hospitalization. The effect of statins and fibrates on CRP levels in AMI should be studied further.