Left ventricular function during exercise after aortic valve replacement.

Rationale: Exercise intolerance is common among military veterans with prior Southwest Asia (SWA) deployment and exposure to inhalational hazards (e.g. burn pits, desert dust, diesel). While a spectrum of airways pathology has been identified among individuals with deployment-related respiratory disease (DRRD), the role of cardiovascular abnormalities in contributing to exercise intolerance is poorly understood. Moreover, while exercise training including high-intensity interval training (HIIT) improves cardiovascular function in other populations, whether it modifies cardiovascular function in DRRD is unknown. Objective: In this exploratory analysis, our objective was to characterize left ventricular abnormalities among a cohort of veterans with DRRD and evaluate their response to HIIT. Methods: Veterans deployed to SWA for >30 days after September 2001 with DRRD and exercise intolerance underwent cardiopulmonary exercise testing (CPET) and stress transthoracic echocardiography (TTE). Participants then underwent a 12-week HIIT intervention including 3x/week HIIT sessions consisting of 40 minutes of upright bicycle exercise with 4, 4-minute intervals (reaching 90-95% maximum heart rate in the final minute) separated by 3-minute active recovery intervals. Following the intervention, CPET and TTE were repeated. Data were analyzed by paired t-test or two-way ANOVA with repeated measures. Results: Twelve participants enrolled (mean age 45.5 ± standard deviation 10.7 years, 12 males, FEV1 97±17% predicted and FEV1/FVC 80±4%). Eleven participants completed the HIIT intervention, while one dropped out of the study due to schedule constraints. All 11 completed pre- and post-HIIT CPET and 9 completed pre- and post-HIIT TTE. CPET and TTE parameters are presented in Table 1. Following HIIT, weight and BMI decreased by 1.0% and 0.8%, respectively. Blood pressure and resting heart rate did not significantly change. Maximum workload increased by 19% and VO2max increased by 10%. Ventilatory threshold increased by 24% and peak oxygen pulse increased by 8.7%. Left ventricular ejection fraction was normal pre- and post-HIIT. Left ventricular end-diastolic volume decreased less from rest to exercise following HIIT (pre-HIIT: 153±33 to 116 ±27, post-HIIT: 145±17 to 138±19, p=0.002, p-interaction=0.02). The change in stroke volume from rest to exercise increased following HIIT (pre-HIIT: 95±5 to 82±7, post-HIIT: 86±5 to 94±5, p=0.12, p-interaction=0.04). Conclusion: In a cohort of veterans with DRRD, a 12-week HIIT intervention resulted in weight loss and improved exercise capacity. HIIT was associated with an increase in exercise left ventricular end-diastolic volume and stroke volume, suggesting improved diastolic filling. The effects of HIIT on left ventricular diastolic function in veterans with DRRD merit further study.

Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging.

Absence of left ventricular volume loading in infants with coarctation of the aorta and a large ventricular septal defect

Effect of pericardiocentesis on right and left ventricular function and volumes in pericardial effusion

ObjectiveThis study aims to explore the feasibility of HeartModel A.I. (HM) three-dimensional echocardiography (3DE) to assess left ventricular function and discover suitable border parameter settings.MethodsA total of 113 patients that underwent echocardiography in our hospital were eligible for inclusion. The HM 3DE (HM method) and conventional 3DE (3D method) were used to analyze echocardiography images. The HM was set to different border settings (end-diastolic [ED] and end-systolic [ES] settings) to assess different left ventricular systolic function parameters including left ventricular end diastolic volume (LVEDV), left ventricular end systolic volume (LVESV), and left ventricular ejection fraction (LVEF), and left ventricular diastolic function parameters including maximal left atrium volume (LAVMAX). All of these parameters were evaluated using the HM method and then compared with the 3D method.ResultsThe differences in LVEDV, LVESV, and LVEF measured with different HM border settings were statistically significant (P<0.05) and were strongly correlated with the 3D method. For LVEF, the reading using the HM method with ED and ES = 70 and 30 showed the best agreement with the 3D method, and the difference in the readings was not statistically significant (P > 0.05). For LVEDV and LVESV, the reading using the HM method with ED and ES = 40 and 20 showed the best agreement with the 3D method, but the difference in the readings was statistically significant (P < 0.05). The measurements taken using the HM method were more reproducible than those taken using the 3D method (P<0.05). The measurement time when using the HM method was significantly less than the 3D method (P<0.05). In terms of LAVMAX, the correlation between the HM and 3D methods was strong, but the requirements for agreement were not satisfied.ConclusionEvaluation of the left ventricular function using HM 3DE is feasible, saves time, and is reproducible. To assess the left ventricular function, the border parameter setting of ED and ES = 70 and 30 provided the best fit for the Chinese population.

Cardiac magnetic resonance (CMR) has been recognized as the gold standard for the evaluation of left ventricular (LV) function. Cardiac gated PET allows the simultaneous assessment of LV function with the evaluation of myocardial perfusion and metabolism. But the correlations between PET and CMR remain controversial. We conducted a systematic electronic search of PubMed, Embase and the Cochrane Library . Forest plot, spearman correlation analysis and Bland-Altman analysis were used to evaluate the correlations between PET and CMR. Pooled analysis of 13 studies showed that PET underestimated left ventricular end-diastolic volumes (LVEDV) [mean difference (MD), -15.30; 95% confidence interval (CI), -23.10 to -7.50; P < 0.001] and left ventricular end-systolic volumes (LVESV) (MD, -6.20; 95% CI, -12.58 to 0.17; P = 0.06) but not left ventricular ejection fraction (LVEF) (MD, -0.35; 95% CI, -1.75 to 1.06; P = 0.63). Overall, there were very good correlations between PET and CMR measurements for LVEDV ( r , 0.897), LVESV ( r , 0.924) and LVEF ( r , 0.898). Subgroup analysis indicated that LVEDV ≥180 ml and LVEF <40% reduced the accuracy of PET, especially the measurement of LVEF ( r , LVEDV ≥180 vs . r , LVEDV < 180 : 0.821 vs. 0.944; r , LVEF < 40% vs . r , LVEF ≥40% : 0.784 vs. 0.901). Correlations between PET and CMR measurements of LVEDV, LVESV and LVEF were excellent, but these two methods could not be used interchangeably for accurate measurements of LV volume and LVEF in patients with significantly increased LV volume and decreased LVEF.

Immediate and long-term effect of mitral balloon valvotomy on left ventricular volume and systolic function in severe mitral stenosis

Objective: To compare the short-term effects of different hormone replacement therapy (HRT) regimens on left ventricular structure and function in healthy postmenopausal women. Methods: Forty-two apparently healthy postmenopausal women were evaluated prospectively in this controlled study. Subjects were divided into 4 groups. Ten subjects, who did not accept HRT or any other treatments, formed the control group. The remaining subjects were assigned to receive oral estradiol (2 mg/day) + norethisterone acetate (1 mg/day) (n = 11), transdermal estradiol (0.05 mg) + norethisterone acetate (0.25 mg) (n = 11) or tibolone (2.5 mg/day) (n = 10) therapy during 12 weeks. Echocardiography and Doppler techniques were used to assess the cardiac effects of different HRT regimens. Results: After 12 weeks of treatment, there were significant increases in left ventricular ejection fraction (transdermal group: p = 0.008, oral group: p = 0.003, tibolone group: p = 0.005) and cardiac output (transdermal group: p = 0.003, oral group: p = 0.003, tibolone group: p = 0.021) in all treatment groups. In addition, in the transdermal group, a slight increase in left ventricular end-diastolic volume was significant (p = 0.046). Conclusion: These data suggest that oral and transdermal HRT regimens and tibolone may contribute to the improvement in left ventricular systolic function without having an effect on left ventricular structure after short-term administration in healthy postmenopausal women.

The effect of oral propranolol on left ventricular ejection fraction, left ventricular volumes, cardiac output, and segmental wall motion was assessed with multigated blood pool imaging both at rest and during supine exercise in 15 patients with angina pectoris. Propranolol had no effect on resting left ventricular ejection fractions. Before propranolol, they did not change during exercise, whereas after propranolol the ejection fractions increased slightly. Exercise left ventricular ejection fractions increased with propranolol in three patients with resting left ventricular ejection fractions of less than 40 per cent. More specifically, left ventricular end-diastolic volume index, end-systolic volume index, stroke volume index, and cardiac index were not altered significantly at rest or during exercise by propranolol. Exercise left ventricular ejection fractions were increased in five and unchanged in eight patients by propranolol. Those patients with increases in left ventricular ejection fractions had a greater change in left ventricular end-diastolic volume indices and a greater change in left ventricular end-systolic volume indices during exercise while on propranolol. Left ventricular segmental wall motion was not altered significantly during exercise by propranolol. We conclude that: (1) Left ventricular functional responses to propranolol during exercise are heterogeneous and not easily predicted; (2) propranolol causes no consistent deterioration in exercise left ventricular ejection fraction even in patients with resting ventricular ejection fractions less than 40 per cent; (3) increased exercise left ventricular ejection fraction with propranolol is contributed to by significant increases in end-diastolic volume during exercise; and (4) gated blood pool imaging is a useful method for characterising rest and exercise left ventricular ejection fractions and left ventricular volumes during propranolol therapy.

Case presentation: A 66-year-old man is referred to a cardiologist for the evaluation of a heart murmur. The patient claims to be entirely asymptomatic, although his wife notes that he has decreased his physical activity over the past two years because he is “getting old.” At physical examination, his blood pressure was 120/70 mm Hg; pulse, 80 bpm; respiration, 13 breaths per minute; and temperature, 99.0°F. Cardiovascular examination revealed normal central venous pressure. His carotid upstrokes were reduced in volume and delayed in upstroke. Cardiac examination revealed a forceful sustained apical impulse in its normal position. There was a 3/6 late-peaking systolic ejection murmur heard at the right upper sternal border radiating to the neck. The rest of the physical examination was unremarkable. Echo-Doppler evaluation revealed an ejection fraction of 0.60, a left ventricular free wall thickness of 1.3 cm, and a peak transaortic flow velocity of 4.5 m/s. How should this patient be managed? Should he undergo aortic valve replacement now? Should he undergo longitudinal follow-up to monitor progression of his aortic stenosis? Over the past 40 years, diagnostic techniques, substitute cardiac valves, and valve implantation surgery have undergone continued improvement, reducing the risk of the valve replacement and enhancing its benefits. Thus, the risk-benefit analysis of valve surgery has tilted in favor of increasingly early intervention for valve disease. The following is a summary incorporating this concept into the current strategy for managing patients with aortic stenosis such as the one described above. The patient with severe aortic stenosis who presents with symptoms represents the most straightforward management strategy for the disease. Survival is nearly normal until the classic symptoms of angina, syncope, or dyspnea develop.1 However, only 50% of patients who present with angina survive 5 years, whereas 50% survival is 3 years for patients who …

To evaluate early and dynamic changes of the left ventricular systolic function of patients with septic shock by two-dimensional speckle tracking imaging (2D-STI), and to provide guidance for treatment and prognosis. Fifty-eight septic shock patients admitted to intensive care unit (ICU) of Subei People's Hospital from January 2016 to April 2017 were enrolled. The septic shock patients were given early fluid resuscitation. The left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), early diastolic mitral flow velocity/early diastolic mitral annular peak velocity (E/Em) were obtained by conventional echocardiography, and the left ventricular global longitudinal strain (GLS), global circumferential strain (GCS), global radial strain (GRS) were obtained by 2D-STI before fluid resuscitation and 1, 3, 7, 14 days after fluid resuscitation. According to the 28-day survival, the septic shock patients were divided into survival group (38 cases) and death group (20 cases). Thirty normal subjects with age and sex matched were selected as control group. (1) Compared with control group, heart rate (HR) and LVESV were increased [HR (bpm): 92.71±12.51 vs. 73.07±5.52, LVESV (mL): 42.50±7.89 vs. 38.73±4.23, both P < 0.05], while LVEF, GLS, GCS were decreased [LVEF: 0.57±0.06 vs. 0.61±0.03, GLS: (-17.72±1.35)% vs. (-22.07±1.95)%, GCS: (-17.08±1.49)% vs. (-22.98±1.97)%] in septic shock group (all P < 0.01). (2) Compared with the data before fluid resuscitation, heart rate was declined (bpm: 87.83±11.50 vs. 92.71±12.51, P < 0.01), while LVEDV and LVEF were increased [LVEDV (mL): 102.32±9.23 vs. 99.24±8.86, LVEF: 0.59±0.05 vs. 0.56±0.06] in patients of the septic shock after fluid resuscitation (all P < 0.01). (3) With the extension of treatment time, HR, LVEDV, LVESV, E/Em were increased gradually, and LVEF, GLS, GCS, GRS were decreased gradually in dead patients. In septic shock patients, compared with survival group, GCS was significantly different on day 1 [(-15.98±1.41)% vs. (-17.66±1.22)%, P < 0.05], HR, LVEDV, LVESV, GLS were significantly different on the 3rd day [HR (bpm): 104.60±10.94 vs. 88.71±5.06, LVEDV (mL): 109.69±10.00 vs. 103.99±5.74, LVESV (mL): 47.78±7.21 vs. 42.29±5.13, GLS: (-14.44±0.92)% vs. (-16.36±1.00)%, all P < 0.05], LVEF, GRS were significantly different on the 7th day [LVEF: 0.47±0.07 vs. 0.58±0.04, GRS: (28.27±3.23)% vs. (31.48±3.12)%, both P < 0.05], and E/Em was significantly different on the 14th day (12.81±1.56 vs. 10.61±1.27) in dead group (P < 0.05). Our study demonstrates myocardial dysfunction at the early phase in septic shock patients, and 2D-STI GCS can be more sensitive than the conventional echocardiography to determine prognosis. 2D-STI GCS, GLS, GRS were not volume-load dependent parameter. Low levels of GLS, GCS might suggest a poor prognosis.

Baroreflex dysfunction is common in chronic heart failure and contributes to the associated sympathoexcitation. Baroreceptor activity normally decreases during volume unloading, causing an increase in sympathetic outflow and resulting in forearm vasoconstriction. Some heart failure patients develop attenuated vasoconstriction or paradoxical vasodilation. The mechanism for this is unknown. We have recently demonstrated diastolic ventricular interaction in some patients with chronic heart failure as evidenced by increases in left ventricular (LV) end-diastolic volume in association with decreases in right ventricular (RV) volume during volume unloading. We reasoned that such an increase in LV volume, by increasing LV mechanoreceptor activity, would decrease sympathetic outflow and could therefore explain the abnormal vascular responses seen in such patients. We assessed changes in forearm vascular resistance (FVR) during application of -20 and -30 mm Hg lower-body negative pressure (LBNP) in 24 patients with chronic heart failure and 16 control subjects. Changes in LV and RV end-diastolic volumes were assessed during -30 mm Hg LBNP in all heart failure patients. Diastolic ventricular interaction was demonstrated in 12 patients as evidenced by increases in LV end-diastolic volume in association with decreases in RV end-diastolic volume during LBNP. Changes in FVR during LBNP (-20 and -30 mm Hg) were markedly attenuated in these 12 patients (-1.6+/-11.2 and -0.9+/-12.5 U) compared with both the remaining patients (11.9+/-10.0 and 17.0+/-12.3 U) and the control subjects (16.5+/-9.5 and 23.1+/-13.9 U) (P<.01 for both comparisons at each level of LBNP). FVR decreased in 5 of these 12 patients during -30 mm Hg LBNP, a response seen in none of the remaining patients (P=.01). Diastolic ventricular interaction in patients with chronic heart failure is associated with attenuated forearm vasoconstriction or paradoxical vasodilation during LBNP. This may explain the apparent derangement in baroreflex control of sympathetic outflow during acute volume unloading in heart failure.

OBJECTIVETo assess left ventricular function in adult Fallot patients with residual pulmonary regurgitation.SETTINGThe radiology department of a tertiary referral centre.PATIENTS14 patients with chronic pulmonary regurgitation and right ventricular volume overload...

Inflammatory pathways, particularly those involving vascular cell adhesion molecule-1 (VCAM-1), play a central role in post-ischemic myocardial remodeling. However, its relationship with left ventricle (LV) performance or volumetric changes has not been systematically examined. This study aimed to investigate the association between circulating VCAM-1 levels, LV volumes, and LV ejection fraction (LVEF), quantified using three-dimensional echocardiography (3-DE), in patients with acute coronary syndrome (ACS). All patients underwent comprehensive clinical evaluation and 3-DE assessment within the first 24 hours of hospital admission. Concurrently, a full panel of locally available laboratory tests was performed, including serum sampling for VCAM-1 analysis. A follow-up evaluation, comprising repeated biological and echocardiographic measurements, was conducted two months after the index event. A total of 90 patients with ACS (mean age 54 ± 9 years; 75 males) were included in the analysis. Among these, 30 patients (33.3%) had a ≥10% increase in left ventricular end-diastolic volume (LVEDV) at follow-up, indicative of adverse left ventricular remodeling. Baseline VCAM-1 levels were significantly correlated with subsequent changes in LVEDV and LVEF from admission to follow-up (r = -0.42, P < 0.05, and r = -0.43, P < 0.05, respectively). Furthermore, the dynamic changes in VCAM-1 between assessments also showed significant correlations with changes in LVEDV and LVEF (r = 0.41, P < 0.05; r = -0.46, P < 0.05). This study suggests that VCAM-1, an inflammatory biomarker, may be a prognostic indicator of LV remodeling and dysfunction in patients with acute coronary syndromes. The findings support further exploration of VCAM-1 for risk stratification and therapy.

Differing responses in right and left ventricular filling, loading and volumes during positive end-expiratory pressure