Prevalence of risk factors for atrial fibrillation and stroke among 1210 patients with sleep disordered breathing

Aims

This study sought to identify the prevalence of risk factors for atrial fibrillation and stroke in a sleep apnea population.

Methods

Study participants included 1210 consecutive adults who were referred with suspicion of sleep apnea. Statistical analysis was used to determine the relationship between sleep apnea syndrome and risk factors for atrial fibrillation and stroke.

Results

Among 1210 enrolled patients, 65.8% had severe sleep apnea (Apnea/hypopnea Index — AHI > 30), 25.2% had mild to moderate sleep apnea (AHI 5 to 30), and 8.8% had no sleep apnea (AHI < 5). At baseline, the mean apnea–hypopnea index in patients with sleep apnea syndrome was 35. Compared to patients with an AHI < 5, those with an AHI > 30 were older (47.3 ± 11.4 vs. 52.74 ± 12.4, p < 0.001) and had a higher body mass index (BMI) (30.7 ± 7.3 vs. 33.83 ± 10.1, p < 0.001), a higher prevalence of hypertension (38 vs. 16%, p < 0.001), and a higher CHADS₂ (congestive heart failure, hypertension, age, diabetes and prior stroke) score (0.59 ± 0.8 vs. 0.28 ± 0.64, p < 0.001).

Conclusions

Patients with severe sleep apnea have a higher prevalence of risk factors for atrial fibrillation and stroke when compared with subjects without sleep apnea.     

Impaired left ventricular systolic function reserve limits cardiac output and exercise capacity in HFpEF patients due to systemic hypertension

Objectives

Heart failure (HF) patients with preserved left ventricular (LV) ejection fraction (EF) (HFpEF) due to systemic hypertension (SHT) are known to have limited exercise tolerance. Despite having normal EF at rest, we hypothesize that these patients have abnormal systolic function reserve limiting their exercise capacity.

Methods

Seventeen patients with SHT (mean age 68 ± 9 years) but no valve disease and 14 healthy individuals (mean age of 65 ± 10 years) underwent resting and peak exercise echocardiography using conventional, tissue Doppler and speckle tracking techniques. The differences between resting and peak exercise values were also analyzed (Δ). Exercise capacity was determined as the workload divided by body surface area.

Results

Resting values for left atrial (LA) volume/BSA (r = − 0.66, p < 0.001) and global longitudinal strain rate (GLSR) in early (e) and late (a) diastole (r = 0.47 and 0.46, p < 0.05 for both) correlated with exercise capacity. LVEF increased during exercise in normals (mean Δ EF = 10 ± 8%) but failed to do so in patients (mean Δ EF = 0.6 ± 9%, p < 0.001 between groups). LV GLSR during systole (s) also failed to increase with exercise in patients, to the same extent as it did in normals (0.2 ± 0.2 vs. 0.6 ± 0.3 1/s, p < 0.001). The difference between rest and exercise (Δ) in LV lateral wall systolic velocity from tissue Doppler (s′) (0.71, p < 0.001), Δ in cardiac output (r = 0.60, p < 0.001) and Δ GLSRs (r = 0.48, p < 0.05) all correlated with exercise capacity independent of changes in heart rate.

Conclusion

HFpEF patients with hypertensive LV disease have significantly limited exercise capacity which is related to left atrial enlargement as well as compromised LV systolic function at the time of the symptoms. The limited myocardial systolic function reserve seems to be underlying important explanation for their limited exercise capacity.     

Impact of global hemodynamic load on exercise capacity in aortic stenosis

Background

The determinants of maximal exercise capacity (MEC) in aortic stenosis (AS) are, in large part, unknown. We hypothesized that the left ventricular (LV) global hemodynamic load – as assessed by the valvulo-arterial impedance (Zva) – is one of the main determinants of MEC and we sought to evaluate the factors associated with reduced MEC in AS.

Method and results

Asymptomatic patients with moderate or severe AS (n = 62, aortic valve area < 1.5 cm², 65 ± 13 years, 68% men) and preserved LV systolic function (ejection fraction > 50%) were prospectively referred for comprehensive resting echocardiography and cardiopulmonary exercise test. Absolute peak VO₂ was 19.5 ± 5.7 mL/kg/min (median 19.6 mL/kg/min; range 7.2–33.1 mL/kg/min). There were significant correlations between peak VO₂ and: age, body mass index, LV stroke volumes, cardiac output, mean flow rate, mitral annulus s′ and e′ wave velocities, E/e′ ratio and left atrial diameter (all p < 0.05). Indexed mean flow rate and Zva were the strongest univariable echocardiographic determinants of peak VO₂ (r = 0.44, p < 0.001 and r = − 0.39, p = 0.002, respectively). In addition, patients with reduced MEC (peak VO₂ < median) had higher Zva than those with preserved MEC (4.24 ± 1.18 vs. 3.71 ± 0.68 mm Hg/mL/m², p = 0.036). In multivariable analysis, age (p < 0.001) and Zva (p = 0.048) were the only independent predictors (r² = 0.40) of peak VO₂.

Conclusion

In asymptomatic patients with moderate to severe AS, MEC varies widely among patients, and is often lower than expected. Global LV hemodynamic load is the main echocardiographic determinant of reduced MEC in these patients, suggesting its usefulness for their clinical evaluation and management.     

Ascending aorta elasticity in children with isolated bicuspid aortic valve

Background

Aortic dilation is common in children with bicuspid aortic valve (BAV) but aortic complications are infrequent. The aim of this study was to investigate elastic properties of the ascending aorta (AAo) and its relation to AAo size in children with isolated BAV without significant valve dysfunction.

Methods

24 children with isolated BAV and 24 healthy controls with tricuspid aortic valve (TAV) matched by gender, age and body surface area (BSA) were studied. Aortic strain (AS), aortic distensibility (DIS) and aortic stiffness index (SI) were derived from M-mode echocardiography at the AAo together with cuff blood pressure recordings. BAV children with dilated AAo (z score ≥ 2) and non dilated (z score < 2) were compared.

Results

BAV children had larger aortas than controls at the sinuses of Valsalva, sinotubular junction and AAo (p < 0.05). AS was lower in BAV than in controls (10.15 ± 4.93 vs 16.93 ± 5.17 p = 0.000), DIS was lower in BAV than in controls (8.51 ± 3.90 vs 14.37 ± 4.20 p = 0.000) and SI was higher in BAV than in controls (7.19 ± 4.45 vs 4.05 ± 2.33 p = 0.04). There were no significant differences in AS, DIS and SI between children with dilated and non-dilated AAo. AS, DIS and SI were not related to BSA, age or AAo size.

Conclusions

AAo elasticity assessed by transthoracic echocardiography is impaired in BAV children without significant valve dysfunction compared to TAV children. Impaired elasticity seems to be independent from aortic dilation. Measuring aortic elasticity may help to identify children at greater risk for complications as adults.     

Quantification of left ventricular performance in different heart failure phenotypes by comprehensive ergometry stress echocardiography

Background

We evaluated the left ventricular (LV) performance in patients with heart failure and preserved ejection fraction (HFPEF) during exercise as compared to those with heart failure and reduced ejection fraction (HFREF) and healthy subjects.

Methods

All subjects received echocardiographic (Vivid7, GE Healthcare) examination with symptom-limited exercise testing on a semi-recumbent and tilting bicycle ergometer (Lode BV, Netherlands). The exercise images for 2-dimensional (2D) speckle tracking were acquired with heart rate of 90–100 bpm, while exercise images for tissue Doppler imaging (TDI) and M-mode echocardiography were stored with attainment of > 85% of maximal age-predicted heart rate.

Results

Stress echocardiographic examinations were performed in 40 HFPEF (aged 65 ± 9 years; 53% male), 40 HFREF (aged 62 ± 9 years; 90% male) and 30 normal controls (aged 56 ± 5 years; 33% male). Trends of progressive decline in 2D global longitudinal, circumferential and radial strains (GLS, GCS and GRS); TDI septal s′ and Sm; and M-mode mitral annular plane systolic excursion (MAPSE) were observed from control, HFPEF to HFREF groups (p < 0.05 for all). LV twist was preserved in HFPEF but reduced in HFREF patients as compared to normal controls (p < 0.05). Diastolic function measured by TDI septal e′, Em and septal E/e′ progressively decreased from controls, HFPEF to HFREF patients (all p < 0.05). Stroke volumes and cardiac indices (LVSI & LVCI) were preserved in HFPEF but deteriorated in HFREF than controls.

Conclusions

This study provides the reference values of LV performance during exercise in HFPEF and knowledge about these changes provide important insights for future clinical studies.     

Aerobic training in adults after atrial switch procedure for transposition of the great arteries improves exercise capacity without impairing systemic right ventricular function

Background

Exercise training safely and efficiently improves symptoms in patients with heart failure due to left ventricular dysfunction. However, studies in congenital heart disease with systemic right ventricle are scarce and results are controversial. In a randomised controlled study we investigated the effect of aerobic exercise training on exercise capacity and systemic right ventricular function in adults with d-transposition of the great arteries after atrial redirection surgery (28.2 ± 3.0 years after Mustard procedure).

Methods

48 patients (31 male, age 29.3 ± 3.4 years) were randomly allocated to 24 weeks of structured exercise training or usual care. Primary endpoint was the change in maximum oxygen uptake (peak VO₂). Secondary endpoints were systemic right ventricular diameters determined by cardiac magnetic resonance imaging (CMR). Data were analysed per intention to treat analysis.

Results

At baseline peak VO₂ was 25.5 ± 4.7 ml/kg/min in control and 24.0 ± 5 ml/kg/min in the training group (p = 0.3). Training significantly improved exercise capacity (treatment effect for peak VO₂ 3.8 ml/kg/min, 95% CI: 1.8 to 5.7; p = 0.001), work load (p = 0.002), maximum exercise time (p = 0.002), and NYHA class (p = 0.046). Systemic ventricular function and volumes determined by CMR remained unchanged. None of the patients developed signs of cardiac decompensation or arrhythmias while on exercise training.

Conclusions

Aerobic exercise training did not detrimentally affect systemic right ventricular function, but significantly improved exercise capacity and heart failure symptoms. Aerobic exercise training can be recommended for patients following atrial redirection surgery to improve exercise capacity and to lessen or prevent heart failure symptoms. (Clinical Trial Registration: ClinicalTrials.gov #NCT00837603)     

The contribution of stem cell therapy to skeletal muscle remodeling in heart failure

Background

The aim of our study was to investigate whether stem cell (SC) therapy with human amniotic fluid stem cells (hAFS, fetal stem cells) and rat adipose tissue stromal vascular fraction cells–GFP positive cells (rSVC-GFP) was able to produce favorable effects on skeletal muscle (SM) remodeling in a well-established rat model of right heart failure (RHF).

Methods

RHF was induced by monocrotaline (MCT) in Sprague–Dawley rats. Three weeks later, four millions of hAFS or rSVC-GFP cells were injected via tail vein. SM remodeling was assessed by Soleus muscle fiber cross sectional area (CSA), myocyte apoptosis, myosin heavy chain (MHC) composition, satellite cells pattern, and SC immunohistochemistry.

Results

hAFS and rSVC-GFP injection produced significant SC homing in Soleus (0.68 ± 1.0 and 0.67 ± 0.75% respectively), with a 50% differentiation toward smooth muscle and endothelial cells. Pro-inflammatory cytokines were down regulated to levels similar to those of controls.SC-treated (SCT) rats showed increased CSA (p < 0.004 vs MCT) similarly to controls with a reshift toward the slow MHC1 isoform. Apoptosis was significantly decreased (11.12. ± 8.8 cells/mm³ hAFS and 13.1 + 7.6 rSVC-GFP) (p < 0.001 vs MCT) and similar to controls (5.38 ± 3.0 cells/mm³).RHF rats showed a dramatic reduction of satellite cells(MCT 0.2 ± 0.06% Pax7 native vs controls 2.60 ± 2.46%, p < 0.001), while SCT induced a repopulation of both native and SC derived satellite cells (p < 0.005).

Conclusions

SC treatment led to SM remodeling with satellite cell repopulation, decreased atrophy and apoptosis. Modulation of the cytokine milieu might play a crucial pathophysiological role with a possible scenario for autologous transplantation of SC in pts with CHF myopathy.     

Hemodynamic causes of exercise intolerance in Fontan patients

Background

Exercise intolerance is frequent among Fontan patients and an important determinant for quality of life. This study investigated the hemodynamic causes of impaired exercise capacity in Fontan patients with particular focus on the influence of stroke volume index (SVI) and heart rate (HR).

Methods and results

In 38 Fontan patients, peak oxygen consumption (VO₂), SVI and HR were recorded during incremental load exercise test and compared with 19 age and gender matched controls.SVI (ml/m²) was lower in patients than controls during warm-up (28[26–31] vs. 35[30–39], p = 0.0093), at submaximal (40[37–43] vs. 55[51–59], p < 0.0001) and at maximal exercise (38[35–40] vs. 54[51–58], p < 0.0001). Similarly, HR (% of expected maximum) was lower in patients at warm-up (45[43–48]% vs. 64[57–64]%, p < 0.0001), submaximal (71[68–75]% vs 85[82–88]%, p < 0.0001) and maximal exercise (84[80–88]% vs. 97[95–99]%, p < 0.0001). Furthermore, SVI dropped 14% (from 44[41–48] to 38[35–40] ml/m²) in Fontan patients from the peak plateau to maximal exercise vs. 5% (from 57[53–61] to 54[51–58] ml/m²) in controls, p < 0.0001. The low SVI and HR explained 67% and 20% of the difference in peak VO₂ between Fontan patients and controls respectively.

Conclusion

SVI decreased significantly in Fontan patients near the end of maximal effort exercise. The low SVI at maximal exercise was the most important hemodynamic factor limiting exercise capacity in Fontan patients, whereas chronotropic impairment had a smaller impact. The low SVI and HR at maximal exercise accounted for the difference in peak VO₂ between Fontan patients and controls in this study.

Clinical trial registration

http://www.cvk.sum.dk/CVK/Home/English.aspx (protocol nr: H-3-2010-045).     

A six-month exercise intervention in subclinical diabetic heart disease: Effects on exercise capacity,autonomic and myocardial function

Objective

Autonomic dysfunction may contribute to the etiology and exercise intolerance of subclinical diabetic heart disease. This study sought the efficacy of exercise training for improvement of peak oxygen uptake (VO_2peak) and cardiac autonomic function in type 2 diabetic patients with non-ischemic subclinical left-ventricular (LV) dysfunction.

Materials/Methods

Forty-nine type 2 diabetic patients with early diastolic tissue Doppler velocity > 1 standard deviation below the age-based mean entered an exercise intervention (n = 24) or usual care (n = 25) for 6-months (controlled, pre-/post- design). Co-primary endpoints were treadmill VO_2peak and 5-min heart-rate variability (by the coefficient of variation of normal RR intervals [CVNN]). Autonomic function was additionally assessed by resting heart-rate (for sympathovagal balance estimation), baroreflex sensitivity, cardiac reflexes, and exercise/recovery heart-rate profiles. Echocardiography was performed for LV function (systolic/diastolic tissue velocities, myocardial deformation) and myocardial fibrosis (calibrated integrated backscatter).

Results

VO_2peak increased by 11% during the exercise intervention (p = 0.001 vs. − 1% in controls), but CVNN did not change (p = 0.23). Reduction of resting heart-rate in the intervention group (p < 0.05) was associated with an improvement in the secondary endpoint of heart-rate variability total spectral power (p < 0.05). However, baroreflex sensitivity, cardiac reflexes, and exercise/recovery heart-rate profiles showed no significant benefit. No effects on LV function were observed despite favorable reduction of calibrated integrated backscatter in the intervention group (p < 0.05).

Conclusions

The exercise intolerance of subclinical diabetic heart disease was amenable to improvement by exercise training. Despite a reduction in resting heart-rate and potential attenuation of myocardial fibrosis, no other cardiac autonomic or LV functional adaptations were detected.     

Benefits of combined aerobic/resistance/inspiratory training in patients with chronic heart failure. A complete exercise model? A prospective randomised study

Background

We hypothesised that combined aerobic training (AT) with resistance training (RT) and inspiratory muscle training (IMT) could result in additional benefits over AT alone in patients with chronic heart failure (CHF).

Methods

Twenty-seven patients, age 58 ± 9 years, NYHA II/III and LVEF 29 ± 7% were randomly assigned to a 12-week AT (n = 14) or a combined AT/RT/IMT (ARIS) (n = 13) exercise program. AT consisted of bike exercise at 70–80% of max heart rate. ARIS training consisted of AT with RT of the quadriceps at 50% of 1 repetition maximum (1RM) and upper limb exercises using dumbbells of 1–2 kg as well as IMT at 60% of sustained maximal inspiratory pressure (SPI_max). At baseline and after intervention patients underwent cardiopulmonary exercise testing, echocardiography, evaluation of dyspnea, muscle function and quality of life (QoL) scores.

Results

The ARIS program as compared to AT alone, resulted in additional improvement in quadriceps muscle strength (1RM, p = 0.005) and endurance (50%1RM × number of max repetitions, p = 0.01), SPI_max (p < 0.001), exercise time (p = 0.01), circulatory power (peak oxygen consumption × peak systolic blood pressure, p = 0.05), dyspnea (p = 0.03) and QoL (p = 0.03).

Conclusions

ARIS training was safe and resulted in incremental benefits in both peripheral and respiratory muscle weakness, cardiopulmonary function and QoL compared to that of AT. The present findings may add a new prospective to cardiac rehabilitation programs of heart failure patients whilst the clinical significance of these outcomes need to be addressed in larger randomised studies.     

Congenital valvular aortic stenosis in young adults: Predictors for rate of progression of stenosis and aortic dilatation

Background

Congenital aortic stenosis (AS) is the most common obstructive left-sided cardiac lesion in young adults, however little is known about the progression in adults. Therefore, we aimed to evaluate the progression rate of AS and aortic dilatation in a large multicenter retrospective cohort of asymptomatic young adults with congenital valvular AS.

Methods

Data were obtained from chart abstraction. Linear mixed-effects models were used to evaluate the progression of AS and aortic dilatation over time. A joint model combining longitudinal echocardiographic and survival data was used for survival analysis.

Results

A total of 414 patients (age 29 ± 10 years, 68% male) were included. Median follow-up duration was 4.1 (2.5–5.1) years (1587 patient-years). Peak aortic velocity was 3.4 ± 0.7 m/s at baseline and did not change over time in the total patient population (− 0.01 ± 0.03 m/s/year). Increased left ventricular mass was significantly associated with faster AS progression (p < 0.001). Aortic dilatation was present in 34% at baseline and 48% at follow-up (p < 0.001). The aortic diameter linearly increased over time with a rate of 0.7 ± 0.2 mm/year. Rate of aortic dissection was 0.06% per patient-year. Seventy patients required an aortic valve intervention (4.4% per patient-year), with AS progression rate as most powerful predictor (HR 5.11 (95% CI 3.47–7.53)).

Conclusions

In the majority of patients with mild-to-moderate congenital AS, AS severity does not progress over time. However patients with left ventricular hypertrophy are at risk for faster progression and should be monitored carefully. Although aortic dissections rarely occur, aortic dilatation is common and steadily progresses over time, warranting serial aortic imaging.     

Resistance training improves cardiac output,exercise capacity and tolerance to positive airway pressure in Fontan physiology

Background

Subjects with Fontan-type circulation have no sub-pulmonary ventricle and thus depend exquisitely on the respiratory bellows and peripheral muscle pump for cardiac filling. We hypothesised that resistance training to augment the peripheral muscle pump might improve cardiac filling, reduce inspiratory-dependence of IVC return to the heart and thus improve exercise capacity and cardiac output on constant positive airway pressure (CPAP).

Methods

Eleven Fontan subjects (32 +/− 2 years, mean +/− SEM) had cardiac magnetic resonance imaging (MRI) and exercise testing (CPET); six underwent 20 weeks of high-intensity resistance training; others were non-exercising controls. After training, CPET was repeated. Four trainers had MRI with real-time flow measurement at rest, exercise and on CPAP in the trained state and following a 12-month detrain.

Results

In the trained state, muscle strength increased by 43% (p = 0.002), as did total muscle mass (by 1.94 kg, p = 0.003) and peak VO₂ (by 183 ml/min, p = 0.02). After detraining, calf muscle mass and peak workload had fallen significantly (p < 0.03 for both) as did peak VO₂ (2.72 vs. 2.18 l/min, p < 0.001) and oxygen pulse, a surrogate for SV (16% lower, p = 0.005). Furthermore after detraining, SV on MRI decreased at rest (by 11 ml, p = 0.01) and during moderate-intensity exercise (by 16 ml, p = 0.04); inspiratory-dependent IVC blood return during exercise was 40% higher (p = 0.02). On CPAP, cardiac output was lower in the detrained state (101 vs. 77 ml/s, p = 0.03).

Conclusions

Resistance muscle training improves muscle mass, strength and is associated with improved cardiac filling, stroke volume, exercise capacity and cardiac output on CPAP, in adults with Fontan-type circulation.     

Irisin in patients with nonalcoholic fatty liver disease

Objective

Irisin is a recently discovered myokine proposed to increase thermogenesis-related energy expenditure and improve metabolism. We aimed to comparatively evaluate serum irisin levels in patients with biopsy-proven nonalcoholic fatty liver disease (NAFLD) vs. controls and study their association with disease severity.

Methods

Fifteen and 16 consecutively enrolled patients with biopsy-proven nonalcoholic simple steatosis (NAFL) and steatohepatitis (NASH), respectively, and 24 lean and 28 obese controls without NAFLD were recruited. Irisin, established adipokines and biochemical tests were measured.

Results

Serum irisin levels were statistically different in obese controls (33.7 ± 2.7 ng/mL; p < 0.001) and patients with NAFL (30.5 ± 1.5 ng/mL; p < 0.001) and NASH (35.8 ± 1.9 ng/mL; p = 0.001) compared with lean controls (47.7 ± 2.0 ng/mL), but were similar among patients with NAFL, NASH and obese controls. This difference remained significant after adjustment for body mass index (or waist circumference), gender, age, insulin resistance (assessed by HOMA-IR or QUICKI), exercise and time since blood collection. Serum leptin and adiponectin, but not irisin, levels were independently from BMI correlated with insulin resistance and cardiometabolic factors. Serum irisin tended to be higher in patients with (36.7 ± 2.4 ng/mL) than without (30.8 ± 1.2 ng/mL; p = 0.02) portal inflammation and independently associated with the latter; these data need to be confirmed by future studies.

Conclusions

Serum irisin levels differ between lean controls and obese controls or NAFLD patients. Despite similar circulating irisin levels between NAFL and NASH groups, irisin may be independently and positively associated with the presence of portal inflammation. Future clinical and mechanistic studies are needed to confirm and extend these data.     

Efficacy of exercise training in pulmonary arterial hypertension associated with congenital heart disease

Background

The objective of this prospective study was to assess the efficacy of exercise training as add-on to medical therapy in patients with congenital heart disease associated pulmonary arterial hypertension (CHD–APAH).

Methods

Patients with invasively confirmed CHD–APAH received in-hospital exercise training for 3 weeks and continued at home. Efficacy parameters were evaluated at baseline, after 3 and 15 weeks. Medical treatment remained unchanged. Worsening events and survival rate were assessed in a follow-up period of 21 ± 14 months.

Results

Twenty consecutive CHD–APAH patients (16 female, 4 male, mean pulmonary arterial pressure 60 ± 23 mm Hg) were included. Patients significantly improved the mean distance walked in 6 min compared to baseline by 63 ± 47 m after 3 weeks (p < 0.001) and by 67 ± 59 m after 15 weeks (p = 0.001). Quality of life-score (p = 0.05), peak oxygen consumption (p = 0.002) and maximal workload (p = 0.003) improved significantly by exercise training after 15 weeks. The 1- and 2‐year survival rates were 100%, the transplantation-free survival rate was 100% after 1 year and 93% after 2 years.

Conclusion

Exercise training as add-on to medical therapy may be effective in patients with CHD–APAH and improved work capacity, quality of life and further prognostic relevant parameters. It was associated with an excellent long-term survival. Further randomized controlled studies are needed to confirm these results.     

What can three-dimensional speckle-tracking echocardiography contribute to evaluate global left ventricular systolic performance in patients with heart failure?

Purpose

Three-dimensional speckle-tracking echocardiography (3D-STE) is a newly developed technique to evaluate left ventricular (LV) deformation by measuring the area strain (AS) of endocardial surface that combines information from both longitudinal (LS) and circumferential strain (CS). We performed a study to examine myocardial deformation in patients with heart failure (HF) using 3D-STE.

Method

A total of 149 subjects including 58 patients with HF and preserved ejection fraction (HFPEF), 45 patients with HF and reduced ejection fraction (HFREF), and 46 normal subjects were prospectively studied by 3D-STE.

Result

After adjusting for age, gender and BSA, global CS, LS, radial strain (RS) and AS derived from 3D-STE in patients with HFPEF were significantly higher than their counterparts in patients with HFREF (all p < 0.001), but lower than that in normal subjects (all p < 0.05). In addition, among all the strain parameters, global AS exhibited the highest correlation with LV ejection fraction (y = 1.243x + 6.332, r = 0.982, p < 0.001) and the best intra- (ICCs: 0.986, p < 0.001) and inter-observer variability (ICCs: 0.978, p < 0.001) than other parameters of 3D strain (CS: 0.981 and 0.974; LS: 0.908 and 0.841; RS: 0.946 and 0.915; all p < 0.001).

Conclusions

Measurement of endocardial surface AS based on 3D-STE technique is reproducible and proves to be accurate and comprehensive in assessing the global LV performance and multidirectional deformation of the LV myocardium in HF patients.     

Mismatch between heart failure patients in clinical trials and the real world

Background

Evidence-based medicine urges physicians to translate results from clinical trials to their patients. This, however, can only work, if real world patients are represented in clinical trials.

Methods

We searched the literature on chronic heart failure (1950-2/2011) for studies designed to detect effects on mortality (mortality studies, MS) and exercise training studies (ETS) as the leading non-pharmaceutical/non-surgical treatment option in order to compare their characteristics with European (Euro Heart Survey on Heart Failure, EHSHF) and North American (Framingham Heart Study, FHS) epidemiological studies.

Results

After an extensive literature search, we identified 207 ETS and 59 MS. Subjects enrolled in ETS were younger (ETS: 62.5 ± 6.6; MS: 63.9 ± 4.6; EHSHF: 71.0 ± 3.5; FHS: 78.0 years), more often male (ETS: 80.9%; MS: 77.3%; EHSHF: 53.0%; FHS: 49.6%; p < 0.001), and had substantially less comorbidities such as diabetes mellitus (ETS: 13.6%; MS: 22.5%; EHSHF: 27.0%; FHS: 25.3%; p < 0.001), or hypertension (ETS: 26.3%; MS: 39.1%; EHSHF: 53.0%; FHS: 46.9%; p < 0.001). Angiotensin converting enzyme-inhibitors, beta-blockers, and angiotensin-receptor-blockers were more commonly used in ETS than in EHSHF (all p < 0.001). Only 16 (10.6%) ETS and 20 (62.5%) MS reported ethnic background.

Conclusion

Heart failure patients in exercise training studies and mortality studies do not represent real world patients. In order to extrapolate data to the general population future exercise training studies as well as mortality studies need to include representative patients. Otherwise, knowledge gained can only be translated to a minority of our patients.     

Gender-related differences in patients with acute heart failure: Management and predictors of in-hospital mortality

Aim and methods

Gender-related differences in clinical phenotype, in-hospital management and prognosis of acute heart failure (AHF) patients have been previously reported in European and US registries. The ALARM-HF survey is the first to include a cohort of 4953 patients hospitalized for AHF in 666 hospitals in 6 European countries, Mexico and Australia.

Results

Women accounted for 37% of the study population, were older and had higher rates of de novo heart failure (45% vs 36%, p < 0.001) than men. An acute coronary syndrome (ACS) was the predominant precipitating factor in both genders, but to a lesser extent in females (30% vs 42%, p < 0.001). Between genders comparison showed higher incidence of atrial fibrillation, valvular heart disease, diabetes, obesity, anemia and depression in women (p < 0.05). Similarly, women had higher left ventricular ejection fraction (LVEF) on admission (42 ± 15% vs 36 ± 13%, p < 0.001) and systolic blood pressure (135 ± 40 mm Hg vs 131 ± 39 mm Hg, p = 0.001) than men. On the other hand, men had more often coronary artery disease, renal failure and chronic obstructive pulmonary disease (p < 0.05). Importantly, in-hospital mortality was similar in both genders (11.1% in females vs 10.5% in males, p = 0.475), and its common predictors were: systolic blood pressure at admission, creatinine > 1.5 mg/dL and diabetes. Furthermore, recent ACS, valvular heart disease and dementia contributed to prognosis in women, while LVEF, hypertension and anemia were independent predictors in men.

Conclusion

Among patients with AHF, there are significant differences in co-morbidities, precipitating factors and predictors of in-hospital mortality between genders. Nevertheless, in-hospital mortality remains similar between genders.     

The cardiovascular effects of premature ovarian failure

Background

Previous studies have shown that cardiovascular risk is increased in premature ovarian failure (POF). To determine the effects of POF on different parameters of cardiovascular health, we investigated the relationship between POF and circulating endothelial progenitor cells (EPC), endothelial function, carotid intima media thickness (CIMT) and left ventricular diastolic function.

Methods

We compared 23 female POF patients (mean age; 37.8 ± 10.8 years) with 20 gender and age-matched healthy controls. Circulating CD133(+)/34(+) and CD34(+)/KDR(+) EPCs were determined by using flow-cytometry. Ultrasound assessment of endothelial function by brachial artery flow-mediated dilatation (FMD) and CIMT was made. Left ventricular systolic and diastolic function was assessed by standard 2D and M-mode echocardiography and tissue Doppler velocities.

Results

Brachial artery FMD was significantly impaired in patients with POF compared with CG (6.3 ± 1.9% vs 10.4 ± 3.7%, p < 0.05). Furthermore, circulating EPCs were lower among patients with POF compared to controls for CD133(+)/34(+) and CD34(+)/KDR(+) cells (p < 0.05). There was a significant correlation between serum estradiol levels and EPC number (CD 133 +/34 +) (r = 0.329, p < 0.05). POF patients had increased CIMT compared to controls (0.67 ± 0.17 vs 0.43 ± 0.10, p < 0.05). When diastolic functions were assessed, patients with POF had lower E_peak, A_peak and mitral CP and higher DT and IVRT (p < 0.05, respectively).

Conclusion

Our findings indicate that endothelial function as well as circulating EPCs, CIMT and diastolic function are significantly affected in young women with POF which may have an adverse long-term effect on cardiovascular prognosis.     

Impaired cardiac reserve in asymptomatic patients with moderate pulmonary restenosis late after relief of severe pulmonary stenosis: Evidence for diastolic dysfunction

Background

Patients with moderate pulmonary valve restenosis late after relief of severe pulmonary stenosis (PS) may show decreased exercise tolerance. To elucidate the mechanism of decreased exercise tolerance, we evaluated cardiac response to physical and pharmacological stress in these patients and compared results with those of patients with native moderate PS.

Methods

Twenty asymptomatic patients with moderate PS were divided into 2 groups: Group I (late after relief of severe PS, n = 9), and Group II (no previous intervention, n = 11). All patients underwent an exercise test, dobutamine stress (DS) MRI, and delayed contrast enhanced MRI. The response to physical and pharmacological stress was compared between both groups.

Results

Group I showed impaired exercise capacity compared to Group II (VO₂max = 72.8% ± 3.5% vs. 102.5% ± 16.3%, p < 0.001). During DS-MRI, RV-SV increased in Group II, but not in Group I (+ 13 ± 8 ml, − 5 ± 8 ml, p < 0.001). RV end‐diastolic volume decreased significantly in Group I patients (p = 0.006) while it did not significantly change in Group II patients. The amount of RV-SV increase (? RV-SV) correlated negatively with the period of moderate PS existence and the current PG in Group I (r = − 0.82, p = 0.007, and r = − 0.68, p = 0.04, respectively) but not in Group II (r = 0.45, p = 0.1, and r = 0.40, p = 0.2, respectively). Furthermore, ? RV-SV correlated negatively with the PG before valvuloplasty (r = − 0.76, p = 0.02).

Conclusion

Impaired exercise capacity in patients with moderate pulmonary restenosis after relief of severe PS is probably caused by inability to increase RV-SV. Disturbed RV filling properties, worsening in time, might play a role.     

Myocardial alterations and clinical implications associated with recovery of cardiac function in dilated cardiomyopathy with obesity

Background

Obesity is associated with an increased risk of heart failure (HF) but the relationship between changes in cardiac function and the specific pathological features of dilated cardiomyopathy (DCM) with obesity, remains unknown.

Methods

Endomyocardial biopsies from the left ventricle (LV) were obtained from 50 patients with DCM, at the first-onset of decompensated HF. Thirty patients were obese (obese-group: body mass index > 30 kg/m²) and 20 were non-obese (lean-group). Clinical data were acquired at the admission, after one month and one year.

Results

The obese-group had higher systolic blood pressure (142.8 ± 33.9 vs 113.6 ± 18.7 mm Hg; p < 0.001) and serum troponin-T level (0.049 ± 0.07 vs 0.020 ± 0.03 ng/mL; p = 0.022) than the lean-group. LV ejection fraction (LVEF) was not significantly different between groups, but after one year the obese-group had an improved LVEF (57.0 ± 11.4 vs 44.3 ± 17.1; p = 0.003). Light microscopy revealed that the obese-group had larger cardiomyocytes (17.2 ± 1.7 vs 16.4 ± 1.4 μm; p = 0.033) and less myofilament lysis (37 vs 75%; p = 0.008) with a higher density of lipid droplets (1.93 ± 0.8 vs 0.94 ± 0.7 /μm²; p < 0.001). Multivariate regression analysis revealed that independent predictors of LVEF improvement after 12 months were diuretics use, nuclear diameter, and absence of myofilament lysis (p = 0.024, 0.012 and 0.028, respectively).

Conclusions

Cardiac function in most patients with DCM with obesity is reversible and myocardial structural changes are trivial even at the ultrastructural level.